- About
- Home
- Introduction
- Statistics
- Programs
- Dignet
- Gene
- GenePair
- BioSummarAI
- Help & Docs
- Documents
- Help
- FAQs
- Links
- Acknowledge
- Disclaimer
- Contact Us
Gene Information
Gene symbol: TNF
Gene name: tumor necrosis factor
HGNC ID: 11892
Synonyms: TNFSF2, DIF, TNF-alpha
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 24012111 | This study was planned to explore the possible association between tumor necrosis factor-alpha (TNF-α), urinary monocyte chemoattractant protein-1 (uMCP-1), high-sensitivity C-reactive protein (hsCRP) and parameters of oxidative stress in patients with Type 2 diabetes mellitus (DM) and diabetic chronic kidney disease (DM-CKD). |
| 2 | 24006180 | Also, tumor necrosis factor-alpha (TNF-α) and IL-1β levels were increased by diabetes, but not changed by training. |
| 3 | 24006180 | In conclusion, we found that in diabetic rats, resistance training increased muscle and serum IL-15 levels, decreased muscle IL-6 levels, and preserved FHL muscle mass. |
| 4 | 24001995 | Decreased SWS and increased REM density is correlated with an increase in proinflammatory cytokines (e.g., IL-6, tumor necrosis factor, etc.). |
| 5 | 23986664 | We thus evaluated in a cross-sectional study the circulating levels of leptin in 40 non-obese and 41 obese Mexican individuals, examining their relationship with tumor necrosis factor alpha (TNF-α), interleukin (IL) 12, IL-10, central obesity, serum glucose and insulin levels, and serum triglyceride and cholesterol concentrations. |
| 6 | 23986664 | Circulating levels of leptin, TNF-α, IL-12, IL-10, and insulin were measured by ELISA, while concentrations of glucose, triglyceride, and cholesterol were determined by enzymatic assays. |
| 7 | 23986664 | Furthermore, leptin also showed a strong relationship with serum TNF-α (r = 0.6989), IL-12 (r = 0.3093), and IL-10 (r = -0.5691). |
| 8 | 23986664 | Interestingly, leptin was also significantly related with high concentrations of fasting glucose (r = 0.5227) and insulin (r = 0.2229), as well as elevated levels of insulin resistance (r = 0.3611) and circulating triglyceride (r = 0.4135). |
| 9 | 23982206 | Activation of the transcriptional function of the NF-κB protein c-Rel by O-GlcNAc glycosylation. |
| 10 | 23982206 | Blocking the O-GlcNAcylation of this residue abrogated c-Rel-mediated expression of the cytokine-encoding genes IL2, IFNG, and CSF2 in response to T cell receptor (TCR) activation, whereas increasing the extent of O-GlcNAcylation of cellular proteins enhanced the expression of these genes. |
| 11 | 23982206 | TCR- or tumor necrosis factor (TNF)-induced expression of other NF-κB target genes, such as NFKBIA (which encodes IκBα) and TNFAIP3 (which encodes A20), occurred independently of the O-GlcNAcylation of c-Rel. |
| 12 | 23982203 | A study shows that O-GlcNAcylation of the nuclear factor κB (NF-κB) subunit c-Rel is required for its binding to the promoters of some, but not all, key T cell receptor-dependent genes; however, O-GlcNAcylation is dispensable for the binding of c-Rel to the promoters of tumor necrosis factor-α-dependent genes. |
| 13 | 23970879 | Macrophages play a role in the inflammatory process by secreting many cytokines such as tumor necrosis factor alpha, interleukin-6, resistin, and retinol binding protein-4. |
| 14 | 23970879 | More metabolic regulators, such as fibroblast growth factor (FGF)21, FGF19, FGF1, vaspin, and visfatin have now been discovered but their exact roles in human diseases are still unclear. |
| 15 | 23953853 | We sought to assess the relationship between cytokine tumor necrosis factor (TNF-α) and insulin resistance in a healthy, euglycemic population. |
| 16 | 23951179 | In obesity, high levels of tumor necrosis factor α (TNFα) stimulate lipolysis in adipocytes, leading to hyperlipidemia and insulin resistance. |
| 17 | 23951179 | Previous studies have revealed that in macrophages, the insulin-sensitizing effect of PPARγ may involve suppression of proinflammatory gene expression by recruiting the corepressor complex that contains corepressors and histone deacetylases (HDACs). |
| 18 | 23951179 | Finally, extracellular signal-related kinase 1/2 (ERK1/2) mediated TNFα-induced lipolysis, and TZDs suppressed TNFα-induced ERK phosphorylation. |
| 19 | 23948591 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been extensively studied for its preferential ability to induce apoptosis of cancer cells. |
| 20 | 23945602 | In the present study, we describe the inhibitory effect of crude extracts and steroids isolated from the starfish Astropecten polyacanthus on pro-inflammatory cytokine (Interleukin-12 (IL-12) p40, interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α)) production in lipopolysaccharide (LPS)-stimulated bone marrow-derived dendritic cells (BMDCs). |
| 21 | 23945602 | Potent inhibitory activities were also observed for compound 1 on the production of IL-12 p40 and IL-6 with values of 3.96 ± 0.12 and 4.07 ± 0.13 μM, respectively, and for compounds 3 and 4 on the production of IL-12 p40 with values of 6.55 ± 0.18 and 5.06 ± 0.16 μM, respectively. |
| 22 | 23945602 | Moreover, compounds 2 (IC50 = 34.86 ± 0.31 μM) and 6 (IC50 = 79.05 ± 2.05 μM) exhibited moderate inhibitory effects on the production of IL-12 p40, whereas compounds 3 (IC50 = 22.80 ± 0.21 μM) and 4 (IC50 = 16.73 ± 0.25 μM) moderately inhibited the production of TNF-α and IL-6, respectively. |
| 23 | 23925693 | The levels of circulating TRAIL at the onset of type 1 diabetes are markedly decreased in patients with ketoacidosis and with the highest insulin requirement. |
| 24 | 23925693 | Experimental evidence in animal models suggests that TNF-related apoptosis-inducing ligand (TRAIL), a member of the TNF superfamily, might play an important role in type 1 diabetes (T1D). |
| 25 | 23925693 | Moreover, the levels of TRAIL at diagnosis correlated inversely with the insulin requirement up to 21 months of follow-up. |
| 26 | 23925693 | This is the first study demonstrating that the levels of circulating TRAIL are significantly decreased in T1D, with the lowest levels of TRAIL being observed in patients with ketoacidosis at the onset and with the highest insulin requirement. |
| 27 | 23909556 | We have aimed to identify polymorphism genotype frequencies in genes related to the inflammatory response in the Brazilian population, namely, IκBL -62AT, IκBL -262CT, tumor necrosis factors alpha (TNFa) -238GA, TNFa -308GA, lymphotoxin-alpha (LTa) +80AC, LTa +252AG, FAS -670AG, and FASL -844TC, considering the white, black, and Pardo ethnicities of the São Paulo State. |
| 28 | 23904052 | Isoxanthohumol modulates angiogenesis and inflammation via vascular endothelial growth factor receptor, tumor necrosis factor alpha and nuclear factor kappa B pathways. |
| 29 | 23904052 | Angiogenic regulators, including vascular endothelial growth factor receptor 2 (HUVEC, 55%), angiopoietins 1 (HUVEC, 39%; HASMC, 35%), angiopoietin 2 (HUVEC, 38%), and Tie2 (HUVEC, 56%) were also inhibited by 10 µM of IXN treatments. |
| 30 | 23874021 | Inflammation contributes to all phases of the atherothrombotic process, patients with elevated inflammatory biomarkers such as high-sensitivity C-reactive protein (hsCRP) have increased cardiovascular risk, and recent work directly implicates the interleukin-1 (IL-1) and interleukin-6 (IL-6) pathways in atherogenesis. |
| 31 | 23874021 | CIRT is based, in part, on observational evidence of reduced vascular event rates among those treated with methotrexate in the setting of rheumatoid arthritis or psoriatic arthritis and on the ability of methotrexate to reduce TNF, IL-6, and CRP levels. |
| 32 | 23874021 | The second trial, the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS), will evaluate whether interleukin-1β (IL-1β) inhibition as compared to placebo can reduce rates of recurrent myocardial infarction, stroke, and cardiovascular death among stable coronary artery disease patients who remain at high vascular risk due to persistent elevations of hsCRP (_2 mg/L) despite contemporary secondary prevention strategies. |
| 33 | 23874021 | Canakinumab is a human monoclonal antibody that selectively neutralizes IL-1β, a pro-inflammatory cytokine that plays multiple roles in the atherothrombotic process and that undergoes activation by the NLRP3 inflammasome, a process promoted by cholesterol crystals that in turn leads directly to increased production of IL-1 and IL-6. |
| 34 | 23864495 | Thyroid-stimulating hormone induces the secretion of tumor necrosis factor-α from 3T3-L1 adipocytes via a protein kinase A-dependent pathway. |
| 35 | 23863813 | SNP also partly or fully reversed the inhibition of EC insulin uptake caused by L-NAME, wortmannin, the Src inhibitor PP1, and tumor necrosis factor-α. |
| 36 | 23863813 | In contrast, treatment with insulin and SNP significantly increased EC protein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1B (PTP1B), and Akt phosphorylation at Ser(473) and inhibited PTP1B activity. |
| 37 | 23863813 | Moreover, a high-fat diet significantly inhibited EC insulin-stimulated Akt phosphorylation and FITC-insulin uptake that was partially reversed by SNP in rats. |
| 38 | 23863813 | Finally, inhibition of S-nitrosylation by knockdown of thioredoxin-interacting protein completely eliminated SNP-enhanced FITC-insulin uptake. |
| 39 | 23863813 | NO also inhibits PTP1B activity, thereby enhancing insulin signaling. |
| 40 | 23840309 | Diabetes was confirmed by hyperglycemia and elevated glycated haemoglobin (HbA1c%), which were associated by weight loss, elevated tumor necrosis factor (TNF)-α and decreased insulin growth factor (IGF)-1β in the serum. |
| 41 | 23840309 | Such effects were associated by enhancement in both learning and memory as well as apparent normal cellularity in CA1and CA3 areas and reduced Casp-3 expression. |
| 42 | 23835343 | We have previously shown that several IRFs are regulators of adipogenesis and that IRF4 is a critical transcriptional regulator of adipocyte lipid handling. |
| 43 | 23835343 | Irf4(-/-) macrophages produce higher levels of proinflammatory cytokines, including interleukin-1β and tumor necrosis factor-α, in response to fatty acids. |
| 44 | 23835343 | In coculture experiments, IRF4 deletion in macrophages leads to reduced insulin signaling and glucose uptake in 3T3-L1 adipocytes. |
| 45 | 23835343 | To determine the macrophage-specific function of IRF4 in the context of obesity, we generated myeloid cell-specific IRF4 knockout mice, which develop significant insulin resistance on a high-fat diet, despite no difference in adiposity. |
| 46 | 23835343 | Furthermore, Irf4(-/-) ATMs express markers suggestive of enhanced M1 polarization. |
| 47 | 23816817 | The main mediators of such crosstalk include hormonal/cytokine signals from the bone (osteopontin, osteocalcin, and osteoprotegerin), the liver (fetuin-A), and adipose tissue [leptin, tumor necrosis factor-α (TNF-α), and adiponectin]. |
| 48 | 23797610 | We measured the levels of miRNAs, dicer, pro-inflammatory tumor necrosis factor alpha (TNFα), and anti-inflammatory interleukin 10 (IL-10) in C57BL/6J (WT) and Akita hearts. |
| 49 | 23797610 | The multiplex RT-PCR, qPCR, and immunoblotting showed up regulation of dicer, whereas miRNA array elicited spread down regulation of miRNAs in Akita including dramatic down regulation of let-7a, miR-130, miR-142-3p, miR-148, miR-338, miR-345-3p, miR-384-3p, miR-433, miR-450, miR-451, miR-455, miR-494, miR-499, miR-500, miR-542-3p, miR-744, and miR-872. |
| 50 | 23796217 | The effects of agaricoglycerides on tumor necrosis factor-α, interleukin-1β, vascular endothelial growth factor-α, interleukin-17, insulin secretion, adiponectin, leptin, hepatic glycogen, nuclear factor-κB activation, and total antioxidant activity were studied respectively. |
| 51 | 23780948 | Effects of a combined aerobic and resistance exercise program on C1q/TNF-related protein-3 (CTRP-3) and CTRP-5 levels. |
| 52 | 23769592 | Plasma concentrations of interleukin (IL)-5, IL-6, IL-7, tumor necrosis factor-α (TNF-α), and granulocyte-monocyte colony-stimulating factor (GM-CSF) were significantly higher in the prediabetic group, as compared to the control group (all p<0.05). |
| 53 | 23769592 | Plasma concentrations of all the other cytokines, interferon-γ (IFN-γ), IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and IL-13, seemed to be elevated in the prediabetic group, but failed to reach statistical significances. |
| 54 | 23769592 | Upon merging both groups, HbA1c was found to be positively correlated with IFN-γ, IL-1β, IL-2, IL-5, IL-7, IL-8, TNF-α and GM-CSF. |
| 55 | 23757408 | Thrombospondin-1 regulates adiposity and metabolic dysfunction in diet-induced obesity enhancing adipose inflammation and stimulating adipocyte proliferation. |
| 56 | 23757408 | Compared with corresponding wild-type animals, TSP-1-null mice had decreased insulin levels but exhibited elevated free fatty acid and triglyceride levels, suggesting impaired fatty acid uptake. |
| 57 | 23757408 | TSP-1 loss did not affect adipocyte size and had no effect on adipose vascular density. |
| 58 | 23757408 | However, TSP-1-null mice exhibited attenuated tumor necrosis factor-α mRNA expression and reduced macrophage infiltration, suggesting a role for TSP-1 in mediating obesity-associated inflammation. |
| 59 | 23757408 | The effects of TSP-1 may involve stimulation of adipocyte proliferation, activation of inflammatory signaling, and facilitated fatty acid uptake by adipocytes. |
| 60 | 23740954 | Differentiation of B cells into the MZ subset is governed by BCR signal strength and specificity, NF-κB activation through the B cell-activating factor belonging to the TNF family (BAFF) receptor, Notch2 signaling, and migration signals mediated by chemokine, integrin, and sphingosine-1-phosphate receptors. |
| 61 | 23740954 | Analysis of microarray expression data indicated that NOD MZ and precursor transitional 2-MZ subsets were particularly dysregulated for genes controlling cellular trafficking, including Apoe, Ccbp2, Cxcr7, Lgals1, Pla2g7, Rgs13, S1pr3, Spn, Bid, Cd55, Prf1, and Tlr3. |
| 62 | 23737649 | In addition, genistein treatment decreased inflammatory markers such as nuclear factor kappa B (p65), phosphorylated inhibitory kappa B alpha, C-reactive protein, monocyte chemotactic protein-1, cyclooxygenase-2, and tumor necrosis factor-alpha and improved oxidative stress markers (nuclear-related factor E2, heme oxygenase-1, glutathione peroxidase, and superoxide dismutase isoforms) in treatment groups, regardless of the genistein treatment dose. |
| 63 | 23737649 | Furthermore, genistein supplementation inhibited the fibrosis-related markers (protein kinase C, protein kinase C-beta II, and transforming growth factor-beta I) in the DN state. |
| 64 | 23735822 | As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. |
| 65 | 23735822 | Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. |
| 66 | 23735822 | As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. |
| 67 | 23735822 | Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. |
| 68 | 23735822 | The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. |
| 69 | 23735822 | Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. |
| 70 | 23725345 | Moreover, the old, infected mice exhibited significantly increased neutrophil recruitment and upregulation of both plasma interleukin-17α and tumor necrosis factor-α levels. |
| 71 | 23707905 | In the present study, the therapeutic effects of SGLT2 selective inhibitor ipragliflozin were examined in high-fat diet and streptozotocin-nicotinamide-induced type 2 diabetic mice which exhibit impaired insulin secretion, insulin resistance, hyperlipidemia, hepatic steatosis, and obesity. |
| 72 | 23707905 | In addition, ipragliflozin reduced plasma and liver levels of oxidative stress biomarkers (thiobarbituric acid reactive substances and protein carbonyl) and inflammatory markers (interleukin 6, tumor necrosis factor α, monocyte chemotactic protein-1, and c-reactive protein), and improved liver injury as assessed by plasma levels of aminotransferases. |
| 73 | 23698110 | Inhibition of the TNF-α-induced serine phosphorylation of IRS-1 at 636/639 by AICAR. |
| 74 | 23698110 | AMP-activated protein kinase (AMPK) contributes to the acceleration of insulin signaling. |
| 75 | 23698110 | However, the mechanism by which AMPK regulates insulin signaling remains unclear. |
| 76 | 23698110 | Here we investigated the role of AMPK in serine phosphorylation of IRS-1 at 636/639 and 307, which is induced by tumor necrosis factor (TNF)-α in 3T3L1 adipocytes. |
| 77 | 23698110 | We demonstrated that the AMPK activator 5-aminoimidazole-4-carboxamide-1-d-ribofuranoside (AICAR) significantly inhibited the TNF-α-induced serine phosphorylation of IRS-1 at 636/639 and 307 by suppression of extracellular signal-regulated kinase (ERK) phosphorylation but not c-Jun-NH2-terminal kinase (JNK) phosphorylation. |
| 78 | 23698110 | In addition, AICAR stimulation resulted in enhanced interaction between ERK and MAP kinase phosphatase-4 (DUSP9/MKP-4) without affecting DUSP9/MPK4 mRNA synthesis. |
| 79 | 23698110 | Moreover, intraperitoneal administration (0.25 g/kg) of AICAR to db/db mice improved blood glucose levels and inhibited the phosphorylation of ERK in adipose tissue. |
| 80 | 23698110 | In conclusion, we propose a new mechanism in which AICAR suppresses TNF-α-induced serine phosphorylation of IRS-1 at 636/639 and 307 by enhancing the interaction between ERK and DUSP9/MKP-4. |
| 81 | 23691063 | Several biomarkers in plasma, such as insulin, leptin, adiponectin, interleukin-6, tumor necrosis factor-α, high sensitivity-C-reactive protein, HbA1c, and glucose levels were measured during OGTT. |
| 82 | 23677182 | [Effect of metformin on the expression of tumor necrosis factor-α, Toll like receptors 2/4 and C reactive protein in obese type-2 diabetic patients]. |
| 83 | 23676315 | Altered lipid profile, oxidative stress, and increased levels of endothelin 1 (ET-1), tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) along with histological changes in heart and pancreas were observed in diabetic rats. |
| 84 | 23671886 | The ERK1/2 Inhibitor U0126 Attenuates Diabetes-Induced Upregulation of MMP-9 and Biomarkers of Inflammation in the Retina. |
| 85 | 23671886 | This study was conducted to determine the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in a time-dependent manner and the effect of extracellular-signal-regulated kinases-1/2 (ERK1/2) inhibition on the expressions of MMP-9, TIMP-1, and inflammatory biomarkers in the retinas of diabetic rats. |
| 86 | 23671886 | The expression of MMP-9 was quantified by zymography, and the mRNA level of MMP-9 and TIMP-1 was quantified by RT-PCR. |
| 87 | 23671886 | The expression of inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF- α ) was examined by Western blot analysis. |
| 88 | 23671886 | Intravitreal administration of the ERK1/2 inhibitor U0126 prior to induction of diabetes decreased ERK1/2 activation, attenuated diabetes-induced upregulation of MMP-9, iNOS, IL-6, and TNF- α and upregulated TIMP-1 expression. |
| 89 | 23671886 | In MMP-9 knockout mice, diabetes had no effect on retinal iNOS expression and its level remained unchanged. |
| 90 | 23671886 | These data provide evidence that ERK1/2 signaling pathway is involved in MMP-9, iNOS, IL-6, and TNF- α induction in diabetic retinas and suggest that ERK1/2 can be a novel therapeutic target in diabetic retinopathy. |
| 91 | 23670971 | Induction of cytosolic phospholipase a2α is required for adipose neutrophil infiltration and hepatic insulin resistance early in the course of high-fat feeding. |
| 92 | 23670971 | In the current study, we set out to explore whether adipose tissue infiltration by neutrophils that occurs early (3 days) after initiating a high-fat diet (HFD) could contribute to the early occurrence of hepatic insulin resistance and to determine the role of cytosolic phospholipase A2α (cPLA2α) in this process. |
| 93 | 23670971 | Adipose tissue secretion of tumor necrosis factor-α (TNF-α) was increased by the 3-day HFD, but not if mice were treated with AS or ICAM-1 antibodies. |
| 94 | 23657763 | Recently, serum concentrations of soluble tumor necrosis factor (TNF), receptor 1 (TNFR1), and TNFR2 have predicted future GFR loss and ESKD in patients of a wide variety of stages and both types of diabetes. |
| 95 | 23653387 | The (14)C-l-Met uptake by human trophoblasts (TBs) obtained from normal pregnancies (normal trophoblast [NTB] cells) is mainly system l-type amino acid transporter 1 (LAT1 [L])-mediated, although a small contribution of system y(+)LAT2 is also present. |
| 96 | 23653387 | Comparison of (14)C-l-Met uptake by NTB and by human TBs obtained from GDM pregnancies (diabetic trophoblast [DTB] cells) reveals similar kinetics, but a contribution of systems A, LAT2, and b(0+) and a greater contribution of system y(+)LAT1 appears to exist in DTB cells. |
| 97 | 23653387 | Short-term exposure to insulin and long-term exposure to high glucose, tumor necrosis factor-α, and leptin decrease (14)C-l-Met uptake in a human TB (Bewo) cell line. |
| 98 | 23653387 | The effect of leptin was dependent upon phosphoinositide 3-kinase, extracellular-signal-regulated kinase 1/2 (ERK/MEK 1/2), and p38 mitogen-activated protein kinase. |
| 99 | 23651237 | The purpose of this study was to understand the role of these cytokine gene polymorphisms in the tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and IL-6 genes with OLP in 101 individuals of Malayalam-speaking ethnicity from South India (Kerala). |
| 100 | 23644451 | Low C-peptide levels and decreased expression of TNF and CD45 in children with high risk of type 1 diabetes. |
| 101 | 23644451 | Low C-peptide levels and decreased expression of TNF and CD45 in children with high risk of type 1 diabetes. |
| 102 | 23644451 | Risk children had lower TNF and CD45, and although there were few differences between the groups, expression of many genes differed when comparing children with regard to residual insulin secretion. |
| 103 | 23644451 | Risk children had lower TNF and CD45, and although there were few differences between the groups, expression of many genes differed when comparing children with regard to residual insulin secretion. |
| 104 | 23643522 | The present randomized, double-blind, placebo-controlled, 12-week trial was designed to investigate the effects of zinc (40 mg/day) and α-linolenic acid (ALA; 2 g/day flaxseed oil) supplementation on markers of inflammation [interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, C-reactive protein (CRP)] and zinc transporter and metallothionein gene expression in 48 postmenopausal women with type 2 DM. |
| 105 | 23643522 | An impact of zinc treatment on zinc transporter gene expression was found; ZnT5 was positively correlated with Zip3 mRNA (P<.001) only in participants receiving zinc, while zinc supplementation abolished the relationship between ZnT5 and Zip10. |
| 106 | 23643522 | IL-6 predicted the expression levels and CRP predicted the fold change of the ZnT5, ZnT7, Zip1, Zip7 and Zip10 mRNA cluster (P<.001 and P=.031, respectively). |
| 107 | 23636268 | Zymography assay was utilized for the analysis of MMP-2 and MMP-9 activity. |
| 108 | 23636268 | TACE activity was evaluated by a specific fluorimetric assay. mRNA levels of MMPs as well as TIMPs were detected using quantitative real-time polymerase chain reaction. |
| 109 | 23636268 | The activity of MMP9 and A Disintegrin and A MetalloProtease Domain 17/TNF-Alpha Converting Enzyme (ADAM17/TACE) was significantly increased in ischemic compared to neuropathic biopsies. |
| 110 | 23636268 | The combination of increased activity of MMP9 and ADAM17/TACE with decreased concentrations of TIMP-3 mRNA expression in ischemic diabetic foot ulcers compared to neuropathic samples suggests that the increased proteolytic environment may represent a causative factor in the ulcer progression. |
| 111 | 23631205 | Obesity usually accompanies with an increase of the size of fat cells, which causes the changes of adipokines, such as the decrease of adiponectin and the increase of TNFalpha and free fatty acids, and leads to insulin resistance. |
| 112 | 23611575 | The administration of metformin reduced pain intensity from 9/10 to 3/10 and favorably affected the profile of inflammatory cytokines (i.e., TNF a, IL-1β, IL-6, and IL-10), adipokines (i.e., adiponectin, leptin, and resistin), and β-endorphin. |
| 113 | 23602201 | High tumor necrosis factor-α/interleukin-10 ratio is associated with hepatocellular carcinoma in patients with chronic hepatitis C. |
| 114 | 23602201 | High tumor necrosis factor-α/interleukin-10 ratio is associated with hepatocellular carcinoma in patients with chronic hepatitis C. |
| 115 | 23602201 | Two cytokines; tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) play key roles in the regulation of cellular immune response in HCV infection. |
| 116 | 23602201 | Two cytokines; tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) play key roles in the regulation of cellular immune response in HCV infection. |
| 117 | 23567861 | The results showed that levels of glucose, leptin, insulin, C-peptide, resistin, tumor necrosis factor-α, interleukin-6, triglycerides, total cholesterol, non-esterified fatty acids, high-density lipoprotein cholesterol, very low-density lipoprotein cholesterol/low-density lipoprotein cholesterol, reactive oxygen species (ROS), and thiobarbituric acid-reactive substance (TBARS) in serum were down-regulated, while adiponectin was augmented by GS treatment. |
| 118 | 23567861 | The administration of GS significantly decreased sterol regulatory element binding protein-1, nuclear factor-kappa ? |
| 119 | 23567861 | >Bp65, cyclooxygenase-2, inducible nitric oxide synthase, monocyte chemotactic protein-1, intracellular adhesion molecule-1, phosphor c-Jun N-terminal kinase, activator protein-1, transforming growth factor-β1, Bax, cytochrome c, and caspase-3 expressions. |
| 120 | 23566811 | In addition, the expression levels of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), interleukin-6 (IL-6) and cyclo-oxygenase-2 (COX-2) were effectively reduced in pancreas tissue by the treatments, respectively. |
| 121 | 23566811 | We also found that upon these treatments, the activities of manganese superoxide dismutase (MnSOD) and glutathione reductase (GSH-Rd) were increased; the content of malonaldehyde (MDA) was decreased in pancreas tissue; and the mRNA expression of heme oxygenase-1 (HO-1) was markedly increased in pancreas tissue. |
| 122 | 23566659 | Although synthesis of different pro- and anti-inflammatory cytokines has been implicated in this process, this low-grade inflammatory condition is characterized especially by an increase in Tumor Necrosis Factor alpha (TNF-α), a cytokine that has been associated to the development of insulin resistance and muscle wasting in the diabetic patients. |
| 123 | 23565185 | We demonstrated that angiotensin II type 2 (AT2) receptor-interacting protein (ATIP) 1 ameliorates inflammation-mediated vascular remodeling independent of the AT2 receptor, leading us to explore the possibility of whether ATIP1 could exert anti-inflammatory effects and play a role in other pathophysiological conditions. |
| 124 | 23565185 | We examined the possible anti-inflammatory effects of ATIP1 in adipose tissue associated with amelioration of insulin resistance. |
| 125 | 23565185 | In mice fed a high-cholesterol diet, adipose tissue macrophage (ATM) infiltration and M1-to-M2 ratio were decreased in ATIP1 transgenic mice (ATIP1-Tg) compared with wild-type mice (WT), with decreased expression of inflammatory cytokines such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in white adipose tissue (WAT), but an increase in interleukin-10, an anti-inflammatory cytokine. |
| 126 | 23565185 | ATM infiltration and M1-to-M2 ratio were decreased in ATIP1 chimera (ATIP1-tg as BM donor), with improvement of insulin-mediated 2-[(3)H]DG uptake and amelioration of inflammation in WAT. |
| 127 | 23565185 | Moreover, serum adiponectin concentration in ATIP1 chimera was significantly higher than that in WT chimera (WT as BM donor) and KKAy chimera (KKAy as BM donor). |
| 128 | 23565185 | These results indicate that ATIP1 could exert anti-inflammatory effects in adipose tissue via macrophage polarization associated with improvement of insulin resistance, and ATIP1 in hematopoietic cells may contribute to these beneficial effects on adipose tissue functions in type 2 diabetes. |
| 129 | 23563695 | Interleukin (IL)-10 protein levels and expression of most of the anti-inflammatory genes, including IL-10, macrophage mannose receptor (MMR), arginase, Dectin-1, YM-1 and YM-2, were significantly increased after treatment with APS for 24 h. |
| 130 | 23563695 | Furthermore, APS induced IL-10 protein production and anti-inflammatory gene expression of IL-10, MMR, Dectin-1, arginase, YM-1 and YM-2. |
| 131 | 23563695 | Additionally, APS inhibited IL-1β protein production and expression of most of the pro-inflammatory genes, such as IL-1β, iNOS, MCP-1, IL-6 and CD11c but not tumor necrosis factor (TNF)-α. |
| 132 | 23552726 | α1-Antitrypsin (AAT) is a member of the serine proteinase inhibitor family that impedes the enzymatic activity of serine proteinases, including human neutrophil elastase, cathepsin G and neutrophil proteinase 3. |
| 133 | 23552726 | Recombinant AAT-Fc protein was tested for antiinflammatory function and AAT-Fc sufficiently suppressed tumor necrosis factor (TNF)-α-induced interleukin (IL)-6 in human peripheral blood mononuclear cells (PBMCs) and inhibited cytokine-induced TNFα by different cytokines in mouse macrophage Raw 264.7 cells. |
| 134 | 23550407 | Genetic polymorphisms of the tumor necrosis factor and lymphotoxin alpha in type 2 diabetes. |
| 135 | 23530176 | Germline mutations in the SLC29A3 gene result in a range of recessive, clinically related syndromes: H syndrome, pigmented hypertrichosis with insulin-dependent diabetes mellitus syndrome, Faisalabad histiocytosis, and sinus histiocytosis with massive lymphadenopathy. |
| 136 | 23530176 | The febrile episodes did not respond to tumor necrosis factor α antagonists and interleukin-1. |
| 137 | 23528355 | Cilostazol ameliorates systemic insulin resistance in diabetic db/db mice by suppressing chronic inflammation in adipose tissue via modulation of both adipocyte and macrophage functions. |
| 138 | 23528355 | Cilostazol reduced the adipocyte size and suppressed mRNA expressions of monocyte chemoattractant protein 1, CD11c, and tumor necrosis factor α (TNFα) in the epididymal fat tissue of db/db mice. |
| 139 | 23528355 | Cilostazol also effectively ameliorated the TNFα-induced decrease of insulin-stimulated Akt phosphorylation and [(3)H]2-deoxyglucose uptake by suppressing c-Jun N terminal kinase-mediated serine phosphorylation of insulin receptor substrate 1 in 3T3-L1 adipocytes. |
| 140 | 23528355 | Importantly, the improvement of impaired insulin signaling was blunted by pretreatment with KT5720, a protein kinase A inhibitor, but not with GW9662, a peroxisome proliferator-activated receptor γ. |
| 141 | 23527709 | Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1. |
| 142 | 23527709 | Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1. |
| 143 | 23527709 | Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1. |
| 144 | 23527709 | Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits. |
| 145 | 23527709 | Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits. |
| 146 | 23527709 | Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits. |
| 147 | 23527709 | In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged. |
| 148 | 23527709 | In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged. |
| 149 | 23527709 | In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged. |
| 150 | 23527709 | These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice. |
| 151 | 23527709 | These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice. |
| 152 | 23527709 | These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice. |
| 153 | 23527709 | Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes. |
| 154 | 23527709 | Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes. |
| 155 | 23527709 | Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes. |
| 156 | 23510726 | The rationale and status of inhibitory therapy directed against IL-1, TNF, IL-12, IL-23, and IL-6 are discussed, towards a goal of using cytokine inhibition as a therapeutic platform to establish an in vivo milieu suitable for modulating the immune response in T1D. |
| 157 | 23495213 | Macrophages activated by dying or stressed cells, induce the transcription factor nuclear factor kappa-B leading to the production of pro-inflammatory cytokines including TNF and IL-6. |
| 158 | 23482247 | Obesity is a low-grade chronic inflammatory condition and obesity-related cytokines such as interleukin-6, adiponectin, leptin, and tumor necrosis factor-α may play important roles in the development of nonalcoholic fatty liver disease (NAFLD). |
| 159 | 23482247 | Fructose has a selective hepatic metabolism, and provokes a hepatic stress response involving activation of c-Jun N-terminal kinases and subsequent reduced hepatic insulin signaling. |
| 160 | 23480316 | Association between adiponectin and tumor necrosis factor-alpha levels at eight to fourteen weeks gestation and maternal glucose tolerance: the Parity, Inflammation, and Diabetes Study. |
| 161 | 23465589 | In the OZR, WB consumption resulted in decreased plasma concentrations of tumor necrosis factor (TNF)-α (-25.6%, P<.05), interleukin (IL)-6 (-14.9%, P<.05) and C-reactive protein (CRP) (-13.1%, P<.05) and increased adiponectin concentration (+21.8%, P<.05). |
| 162 | 23465589 | Furthermore, expression of IL-6, TNF-α and nuclear factor (NF)-kB was down-regulated in both the liver (-65%, -59% and -25%, respectively) and the abdominal adipose tissue (-64%, -52% and -65%), while CRP expression was down-regulated only in the liver (-25%). |
| 163 | 23465589 | In the abdominal adipose tissue, similar trends were also observed in LZR following WB treatment, with decreased liver expression of NF-kB, CRP, IL-6 and TNF-α (-24%, -16%, -21% and -50%) and increased adiponectin expression (+25%). |
| 164 | 23463119 | HCV core protein was shown to stimulate suppressor of cytokine signaling, resulting in ubiquitination and degradation of tyrosine kinase phosphorylated insulin receptor substrates (IRS1/2) in proteasomes. |
| 165 | 23463119 | HCV-nonstructural protein could increase protein phosphatase 2A which has been shown to inactivate the key enzyme Akt by dephosphorylating it. |
| 166 | 23463119 | Insulin signaling defects in hepatic IRS-1 tyrosine phosphorylation and PI3-kinase association/activation may contribute to IR, which leads to the development of T2D in patients with HCV infection. |
| 167 | 23463119 | PPARα upregulates glycerol-3-phosphate dehydrogenase, glycerol kinase, and glycerol transport proteins, which allows for glucose synthesis during fasting states. |
| 168 | 23463119 | It is speculated that TNF-alpha plays a major role in the pathogenesis of IR through lowering IRS1/2. |
| 169 | 23463119 | Furthermore, HCV infection- triggered ER stress could lead to the activation of PP2A, which inhibits both Akt and the AMP-activated kinase, the regulators of gluconeogenesis. |
| 170 | 23458195 | Aortic damage was observed through decreased endothelial nitric oxide synthase and increased NADPH oxidase mRNA expressions in CVD-induced rats. |
| 171 | 23458195 | KA treatment reduced the pro-inflammatory cytokines tumor necrosis factor-α and interleukin 6 in CVD-induced rats. |
| 172 | 23454694 | Several mechanisms, such as innate immune responses via Toll-like receptor-4, accumulation of diacylglycerols (DAG)/ceramides, and activation of protein kinase C (PKC), are considered to underlie skeletal muscle insulin resistance. |
| 173 | 23454694 | Only after LPS, circulating inflammatory markers (tumor necrosis factor-α, interleukin-6, and interleukin-1 receptor antagonist), their mRNA expression in subcutaneous adipose tissue, and circulating cortisol were elevated. |
| 174 | 23454256 | Interleukin-1 has opposing effects on connective tissue growth factor and tenascin-C expression in human cardiac fibroblasts. |
| 175 | 23454256 | We investigated the effects of pro-inflammatory cytokines on matricellular protein expression in cultured human CF. cDNA array analysis of matricellular proteins revealed that interleukin-1α (IL-1α, 10ng/ml, 6h) down-regulated connective tissue growth factor (CTGF/CCN2) mRNA by 80% and up-regulated tenascin-C (TNC) mRNA levels by 10-fold in human CF, without affecting expression of thrombospondins 1-3, osteonectin or osteopontin. |
| 176 | 23454256 | In contrast, tumor necrosis factor α (TNFα) did not modulate CCN2 expression and had only a modest stimulatory effect on TNC levels. |
| 177 | 23454256 | Signaling pathway inhibitor studies suggested an important role for the p38 MAPK pathway in suppressing CCN2 expression in response to IL-1α. |
| 178 | 23454256 | In contrast, multiple signaling pathways (p38, JNK, PI3K/Akt and NFκB) contributed to IL-1α-induced TNC expression. |
| 179 | 23454256 | In conclusion, IL-1α reduced CCN2 expression and increased TNC expression in human CF. |
| 180 | 23454064 | After 4 weeks of hyperglycemia, the mice were allocated to coenzyme Q10 supplementation (10mg/kg/day), treatment with the angiotensin-converting-enzyme inhibitor (ACE-I) ramipril (3mg/kg/day), treatment with olive oil vehicle, or no treatment for 8 weeks. |
| 181 | 23454064 | Type 1 diabetes upregulated LV NADPH oxidase (Nox2, p22(phox), p47(phox) and superoxide production), LV uncoupling protein UCP3 expression, and both LV and systemic oxidative stress (LV 3-nitrotyrosine and plasma lipid peroxidation). |
| 182 | 23454064 | Coenzyme Q10 substantially limited type 1 diabetes-induced impairments in LV diastolic function (E:A ratio and deceleration time by echocardiography, LV end-diastolic pressure, and LV -dP/dt by micromanometry), LV remodeling (cardiomyocyte hypertrophy, cardiac fibrosis, apoptosis), and LV expression of proinflammatory mediators (tumor necrosis factor-α, with a similar trend for interleukin IL-1β). |
| 183 | 23442249 | In ZDFs, hemin administration increased HO activity; normalized glycemia; potentiated insulin signaling by enhancing insulin receptor substrate 1(IRS-1), phosphatidylinositol-3-kinase (PI3K), and protein kinase B (PKB)/Akt; suppressed pericardial adiposity, cardiac hypertrophy, and left ventricular longitudinal muscle fiber thickness, a pathophysiological feature of cardiomyocyte hypertrophy; and correspondingly reduced systolic blood pressure, total peripheral resistance, and pro-inflammatory/oxidative mediators, including nuclear factor κB (NF-κB), cJNK, c-Jun-N-terminal kinase (cJNK), endothelin (ET-1), tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-1β, activating protein 1 (AP-1), and 8-isoprostane, whereas the HO inhibitor, stannous mesoporphyrin, nullified the effects. |
| 184 | 23442249 | Because NF-κB activates TNFα, IL-6, and IL-1β and TNF-α, cJNK, and AP-1 impair insulin signaling, the high levels of these cytokines in obesity/diabetes would create a vicious cycle that, together with 8-isoprostane and ET-1, exacerbates cardiac injury, compromising cardiac function. |
| 185 | 23442249 | Therefore, the concomitant reduction of pro-inflammatory cytokines and macrophage infiltration coupled to increased expressions of IRS-1, PI3K, and PKB may account for enhanced glucose metabolism and amelioration of cardiac injury and function in diabetic cardiomyopathy. |
| 186 | 23439570 | Quercetin but not quercitrin ameliorates tumor necrosis factor-alpha-induced insulin resistance in C2C12 skeletal muscle cells. |
| 187 | 23439570 | Quercetin, but not quercitrin moderately attenuated the effects of TNF-α and enhanced the basal and insulin stimulated uptake of glucose in a dose-dependent manner via the activation of the protein kinase B (Akt) and AMP-activated protein kinase (AMPK) pathways. |
| 188 | 23439570 | Furthermore, the underlying mechanism also involved the suppression of nuclear factor-κB (NF-κB) signaling and the nitric oxide (NO)/inducible nitric oxide synthase (iNOS) system, downstream of AMPK transduction. |
| 189 | 23439570 | In summary, quercetin exhibited its effect of improving glucose uptake and insulin sensitivity in skeletal muscle cells via the two independent signaling pathways of Akt and AMPK, and can be developed as a potential anti-diabetic agent. |
| 190 | 23434766 | We found that DMA inhibited inflammatory cytokine production via upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and alleviated oxidative stress through attenuation of p47phox translocation to the membrane of S100b-treated THP-1 monocytes. |
| 191 | 23434766 | We found that DMA activated Nrf2 mediated by the p38 kinase pathway in THP-1 monocytes. |
| 192 | 23434766 | The in vivo verification of anti-inflammation in peripheral blood mononuclear cells by DMA treatment was confirmed by tumor necrosis factor-α and interleukin-1β measurements. |
| 193 | 23430573 | Regulation and function of C1Q/TNF-related protein-5 (CTRP-5) in the context of adipocyte biology. |
| 194 | 23423575 | Furthermore, we traced CD68(+) macrophage accumulation and concomitant upregulation of tumor necrosis factor-α (TNF-α) levels in type 2 diabetic skin. |
| 195 | 23423575 | TNF-α treatment of LECs and its specific blockade in vitro reproduced differential regulation of a gene set that led to enhanced LEC mobility and macrophage attachment, which was mediated by the LEC-derived chemokine CXCL10. |
| 196 | 23412668 | The results showed that levels of glucose, leptin, insulin, C-peptide, resistin, tumor necrosis factor-α, and interleukin-6 in serum were down-regulated, while adiponectin was augmented by GS treatment. |
| 197 | 23412668 | Moreover, GS modulated protein expressions of pro-inflammatory nuclear factor-kappa Bp 65, cyclooxygenase-2, inducible nitric oxide synthase, c-Jun N-terminal kinase (JNK), phospho-JNK, activator protein-1, transforming growth factor-β1, and fibronectin. |
| 198 | 23385819 | Adipocytes subjected to oxidative stress also showed shortened telomeres and increased mRNA and protein expression of p53, p21, TNF alpha and IL-6. |
| 199 | 23376161 | Catalpol reduced the expression of pro-inflammatory mediates, such as monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), inducible NO synthase (iNOS), and receptor for AGE (RAGE). |
| 200 | 23365614 | Tumor necrosis factor alpha (TNFα) and vascular endothelial growth factor (VEGF) were also determined. |
| 201 | 23349496 | Here, we show that human mesenchymal stem/stromal cells (hMSCs) and tumor necrosis factor-α-stimulated gene 6 (TSG-6), a protein produced by hMSCs in response to signals from injured tissues, delayed the onset of spontaneous autoimmune diabetes in NOD mice by inhibiting insulitis and augmenting regulatory T cells (Tregs) within the pancreas. |
| 202 | 23349496 | TSG-6 inhibited the activation of both T cells and antigen-presenting cells (APCs) in a CD44-dependent manner. |
| 203 | 23349496 | Moreover, multiple treatments of TSG-6 rendered APCs more tolerogenic, capable of enhancing Treg generation and delaying diabetes in an adoptive transfer model. |
| 204 | 23341693 | The objective of the present study is to investigate the effect of dAGEs restriction on tumor necrosis factor-α (TNF-α), malondialdehyde, C-reactive protein (CRP), and insulin resistance in DM2 patients. |
| 205 | 23341693 | At the beginning and the end of study, we collected anthropometric measurements, and values of circulating glucose, HbA1c, lipids, insulin, serum AGEs, CRP, TNF-α and malondialdehyde. |
| 206 | 23333096 | In this report, we show that naringenin, a citrus flavonoid, inhibits TLR2 expression during adipocyte differentiation. |
| 207 | 23333096 | In addition, naringenin suppresses TLR2 expression induced by the co-culture of differentiated adipocytes and macrophages and also inhibits tumor necrosis factor-α (TNF-α)-induced TLR2 expression by inhibiting the activation of nuclear factor-κB and c-Jun NH2-terminal kinase pathways in differentiated adipocytes. |
| 208 | 23326455 | The levels of fasting blood glucose, serum insulin and glucose tolerance were measured and the relative levels of insulin-related phosphatidylinositol 3-kinase (PI3K)/Akt, insulin receptor (IR) and IR substrate 1 (IRS1) phosphorylation were determined. |
| 209 | 23326455 | The levels of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6- phosphatase (G6Pase), toll like receptor 4 (TLR4), tumor necrosis factor (TNF)-α and IL-6 expression and nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK), extracellular-signal-regulated kinase (ERK) and p38 MAPK activation in the liver were examined. |
| 210 | 23326455 | EPO treatment significantly reduced the body weights and the levels of fasting blood glucose and serum insulin and improved the HFD-induced glucose intolerance in mice. |
| 211 | 23326455 | EPO treatment significantly enhanced the levels of Akt, but not IR and IRS1, phosphorylation, accompanied by inhibiting the PEPCK and G6Pase expression in the liver. |
| 212 | 23326455 | Furthermore, EPO treatment mitigated the HFD-induced inflammatory TNF-α and IL-6 production, TLR4 expression, NF-κB and JNK, but not ERK and p38 MAPK, phosphorylation in the liver. |
| 213 | 23307037 | The expression of various pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1 and IL-6 is increased in adipose tissue and its expression linked to systemic inflammation and accompanying insulin resistance. |
| 214 | 23307037 | First clinical studies favor an important role for IL-1 family members and probably IL-6 but not for TNF-α in insulin-resistant states. |
| 215 | 23306763 | Marginal and not validated therapies are cyclosporine, somatostatin analogues, TNF-a inhibitors and rituximab. |
| 216 | 23262028 | CCL4 were examined in fracture calluses by immunohistochemistry and the role of TNF in diabetes-enhanced expression was investigated by treatment of animals with the TNF-specific inhibitor, pegsunercept. |
| 217 | 23262028 | CCL4 were examined in fracture calluses by immunohistochemistry and the role of TNF in diabetes-enhanced expression was investigated by treatment of animals with the TNF-specific inhibitor, pegsunercept. |
| 218 | 23262028 | Diabetes significantly upregulated mRNA levels of several chemokines in vivo including CCL4, CCL8, CCL6, CCL11, CCL20, CCL24, CXCL2, CXCL5 and chemokine receptors CCR5 and CXCR4. |
| 219 | 23262028 | Diabetes significantly upregulated mRNA levels of several chemokines in vivo including CCL4, CCL8, CCL6, CCL11, CCL20, CCL24, CXCL2, CXCL5 and chemokine receptors CCR5 and CXCR4. |
| 220 | 23262028 | Chondrocytes were identified as a significant source of CCL4 and its expression in diabetic fractures was dependent on TNF (P<0.05). |
| 221 | 23262028 | Chondrocytes were identified as a significant source of CCL4 and its expression in diabetic fractures was dependent on TNF (P<0.05). |
| 222 | 23255602 | Smad7 protein induces interferon regulatory factor 1-dependent transcriptional activation of caspase 8 to restore tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. |
| 223 | 23255602 | Smad7 protein induces interferon regulatory factor 1-dependent transcriptional activation of caspase 8 to restore tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. |
| 224 | 23255602 | Smad7 has been known as a negative regulator for the transforming growth factor-β (TGF-β) signaling pathway through feedback regulation. |
| 225 | 23255602 | Smad7 has been known as a negative regulator for the transforming growth factor-β (TGF-β) signaling pathway through feedback regulation. |
| 226 | 23255602 | By screening differentially regulated genes, we found that the caspase 8 gene was highly up-regulated in Smad7-expressing cells. |
| 227 | 23255602 | By screening differentially regulated genes, we found that the caspase 8 gene was highly up-regulated in Smad7-expressing cells. |
| 228 | 23255602 | Smad7 was able to activate the caspase 8 promoter through recruitment of the interferon regulatory factor 1 (IRF1) transcription factor to the interferon-stimulated response element (ISRE) site. |
| 229 | 23255602 | Smad7 was able to activate the caspase 8 promoter through recruitment of the interferon regulatory factor 1 (IRF1) transcription factor to the interferon-stimulated response element (ISRE) site. |
| 230 | 23255602 | Interaction of Smad7 on the caspase 8 promoter was confirmed with electrophoretic mobility shift assay and chromatin immunoprecipitation experiment. |
| 231 | 23255602 | Interaction of Smad7 on the caspase 8 promoter was confirmed with electrophoretic mobility shift assay and chromatin immunoprecipitation experiment. |
| 232 | 23255602 | Interestingly, Smad7 did not directly interact with the ISRE site, but it increased the binding activity of IRF1 with ISRE. |
| 233 | 23255602 | Interestingly, Smad7 did not directly interact with the ISRE site, but it increased the binding activity of IRF1 with ISRE. |
| 234 | 23255602 | These results support that Smad7 recruits IRF1 protein on the caspase 8 promoter and functions as a transcriptional coactivator. |
| 235 | 23255602 | These results support that Smad7 recruits IRF1 protein on the caspase 8 promoter and functions as a transcriptional coactivator. |
| 236 | 23255602 | To confirm the biological significance of caspase 8 up-regulation, we tested tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated cell death assay in breast cancer cells. |
| 237 | 23255602 | To confirm the biological significance of caspase 8 up-regulation, we tested tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated cell death assay in breast cancer cells. |
| 238 | 23255602 | Smad7 in apoptosis-resistant MCF7 cells markedly sensitized the cells to TRAIL-induced cell death by restoring the caspase cascade. |
| 239 | 23255602 | Smad7 in apoptosis-resistant MCF7 cells markedly sensitized the cells to TRAIL-induced cell death by restoring the caspase cascade. |
| 240 | 23255602 | In conclusion, we suggest a novel role for Smad7 as a transcriptional coactivator for caspase 8 through the interaction with IRF1 in regulation of the cell death pathway. |
| 241 | 23255602 | In conclusion, we suggest a novel role for Smad7 as a transcriptional coactivator for caspase 8 through the interaction with IRF1 in regulation of the cell death pathway. |
| 242 | 23251284 | TNF ligand-related molecule 1A (TL1A) and its receptor, death receptor 3 (DR3), belong to the TNF superfamily and have been implicated in chronic inflammatory diseases. |
| 243 | 23251284 | Bladder biopsies from 8 female patients clinically diagnosed with PBS/IC according to the National Institute for Diabetes and Digestive and Kidney Diseases criteria and 8 female bladder carcinoma control patients were investigated to test the protein and mRNA expression levels of TL1A and DR3 using western blotting and real-time RT-PCR. |
| 244 | 23251284 | The protein level ratio of TL1A to β-actin (IC, 0.65±0.03 vs. controls, 0.25±0.02, P<0.001) and of its receptor DR3 to β-actin (IC, 0.66±0.06 vs. controls, 0.27±0.02, P<0.001) were observed to be significantly higher in the patients with IC. |
| 245 | 23251284 | The real-time RT-PCR ΔCts of TL1A minus GAPDH (IC, 7.60±0.52 vs. controls, 10.08±0.32, P<0.001) and the DR3 minus GAPDH (IC, 6.68±0.60 vs. controls, 8.99±0.61, P=0.017) were observed to be significantly lower in the patients with IC, suggesting that the mRNA levels of TL1A and DR3 were higher in the PBS/IC patients. |
| 246 | 23251284 | The protein and mRNA expression of TL1A and DR3 are upregulated in the bladder tissues of PBS/IC patients and may be involved in inflammation and apoptosis in PBS/IC. |
| 247 | 23227456 | Circulating levels of oxidative stress markers [Nε-(carboxymethyl)lysine- advanced glycation end products (CML-AGEs) and advanced oxidation protein products-(AOPPs)], pro-inflammatory cytokines (interleukin-6, and tumor necrosis factor α), and high-sensitivity C-reactive protein (hsCRP) were assessed. |
| 248 | 23225194 | Flaxseed oil diet significantly up-regulated the key transcription factor peroxisome proliferator-activated receptor-α (PPAR-α ) and down-regulated sterol regulatory element-binding protein-1 (SREBP-1) in diabetic rats, which would have increased β-oxidation of fatty acids and concomitantly reduced lipogenesis respectively, thereby reducing TG levels. |
| 249 | 23225194 | We also observed down-regulation of atherogenic cytokines tumor necrosis factor-α and interleukin-6 by both the diets. |
| 250 | 23220232 | Furthermore, patients with inflammatory response show increased expression of miR-181a, which is strongly correlated with the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha. |
| 251 | 23212557 | Recently identified as adiponectin (APN) paralogs, C1q/TNF-related proteins (CTRPs) share similar metabolic regulatory functions as APN. |
| 252 | 23212557 | Recently identified as adiponectin (APN) paralogs, C1q/TNF-related proteins (CTRPs) share similar metabolic regulatory functions as APN. |
| 253 | 23212557 | In H9c2 cells, tumor necrosis factor-alpha (TNF-α) strongly inhibited CTRP9 expression (>60%), and significantly reduced peroxisome proliferator activated receptor-gamma (PPARγ), a known transcription factor promoting adiponectin expression. |
| 254 | 23212557 | In H9c2 cells, tumor necrosis factor-alpha (TNF-α) strongly inhibited CTRP9 expression (>60%), and significantly reduced peroxisome proliferator activated receptor-gamma (PPARγ), a known transcription factor promoting adiponectin expression. |
| 255 | 23212097 | Abnormal expression of tumor necrosis factor-α, interleukin-6, and lipid peroxidation endo products was observed in macrophages. |
| 256 | 23208607 | As early as 24 h postinfection, the expression of inflammatory (interleukin-1β [IL-1β], tumor necrosis factor alpha [TNF-α], and IL-6) and T(H)1 (IL-12 and gamma interferon [IFN-γ]) cytokines was impaired in diabetic mice compared to nondiabetic littermates. |
| 257 | 23195328 | Because telmisartan has also an agonistic action for peroxisome proliferators-activator receptor (PPAR)-γ, it is speculated that an effect of telmisartan on insulin sensitivity is different from that of valsartan, which lacks of PPAR-γ agonistic activity. |
| 258 | 23195328 | Insulin tolerance test was performed on day 14, and plasma adiponectin concentration and mRNA expression levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in adipose tissues were measured on day 21. |
| 259 | 23195328 | Telmisartan and valsartan elevated plasma adiponectin concentration and suppressed the mRNA expressions of TNF-α and IL-6 in adipose tissues. |
| 260 | 23170143 | Recent studies have shown that cerulein-activated nicotinamide adenine dinucleotide phosphate oxidase elicits reactive oxygen species, which trigger the phosphorylation of the JAK1, STAT1, and STAT3 proteins and induce the production of inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, in pancreatic acinar cells. |
| 261 | 23161002 | Lipopolysaccharide (LPS) induces many genes encoding inflammatory mediators, including cytokines such as tumor necrosis factor-α, interleukin-1β, (IL-1β), and IL-6, chemokines, and prostaglandins in microglial cells. |
| 262 | 23161002 | Among those, one of the strong mitogen-activated protein kinase (MAPK) regulator proteins, CMPK1 was highly upregulated after LPS stimulation in human microglial cells. |
| 263 | 23161002 | We detected and validated upregulation of MAPK including ERK1/2, p38, and SAPK/JNK by immunohistochemistry and Western blotting. |
| 264 | 23139599 | In this review, major literature data about the use of omega-3 polyunsaturated fatty acids (n-3 PUFAs) as a potential treatment of NAFLD have been described. n-3 PUFAs, besides having a beneficial impact on most of the cardio-metabolic risk factors (hypertension, hyperlipidemia, endothelial dysfunction and atherosclerosis) by regulating gene transcription factors [i.e., peroxisome proliferator-activated receptor (PPAR) α, PPARγ, sterol regulatory element-binding protein-1, carbohydrate responsive element-binding protein], impacts both lipid metabolism and on insulin sensitivity. |
| 265 | 23139599 | In addition to an enhancement of hepatic beta oxidation and a decrease of the endogenous lipid production, n-3 PUFAs are able to determine a significant reduction of the expression of pro-inflammatory molecules (tumor necrosis factor-α and interleukin-6) and of oxygen reactive species. |
| 266 | 23104422 | Small interfering-RNA to protein kinase C-delta reduces the proinflammatory effects of human C-reactive protein in biobreeding diabetic rats. |
| 267 | 23104422 | Previously we reported that human CRP accentuated macrophage activity in spontaneously diabetic biobreeding (BB) rats and also increased protein kinase C (PKC) delta. |
| 268 | 23104422 | Compared to scrambled siRNA, siRNA to PKC delta resulted in a significant decrease in biomediators of inflammation in plasma and from macrophages (IL-1, TNF-alpha, IL-6, MCP-1, KC/IL-8, and PAI -1). |
| 269 | 23097451 | The cytokine activation profile indicated a significant increase of MIG/CXCL9, IP-10/CXCL10, RANTES/CCL5, MIP1b/CCL4, Groa/CXCL1, interleukin 8 (IL-8)/CXCL8, tumor necrosis factor alpha (TNF-α), and IL-6. |
| 270 | 23080424 | These data indicate that endogenous CSE/H2 S system contributes to TNF-α-caused insulin resistance in 3T3-L1 adipocytes. |
| 271 | 23071669 | These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g. |
| 272 | 23071669 | MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g. |
| 273 | 23071669 | IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C). |
| 274 | 23071669 | Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR. |
| 275 | 23022408 | We observed that AK (10mg/kg bw) exerted peroxisome proliferator-activated receptor-γ (PPARγ) agonist activity, thereby enhancing insulin sensitivity (as indicated by hepatic GLUT2 translocation, PTP1B suppression, and glucose uptake) by downregulating blood glucose and upregulating pancreatic and duodenal homeobox-1 and Maf-A expression and increasing insulin production in MG-induced rats. |
| 276 | 23022408 | However, these effects were abolished by the administration of GW9662 (PPARγ antagonist), but the expression of hepatic heme oxygenase-1 (HO-1) and glutamate-cysteine ligase (GCL) was not suppressed in MG-induced rats. |
| 277 | 23022408 | AK did not affect hepatic Nrf2 mRNA or protein expression but significantly increased Nrf2 phosphorylation (serine 40), which was accompanied by increased transcriptional activation of hepatic HO-1 and GCL. |
| 278 | 23022408 | We also found that AK treatment reduced the production of inflammatory factors, such as tumor necrosis factor-α and interleukin-1β. |
| 279 | 23022408 | Taken together, the results of our mechanistic study of MG-induced rats suggest that the protective effects of AK against diabetes are mediated by the upregulation of the signaling pathway of Nrf2, which enhances antioxidant activity and serves as a PPARγ agonist to enhance insulin sensitivity. |
| 280 | 23020082 | Pro-inflammatory state was evaluated by plasma levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP). |
| 281 | 23020082 | ZDF rats exhibited higher levels of IL-6 (112.4 ± 1.5 pg/mL), TNF-α (11.0 ± 0.1 pg/mL) and CRP (828 ± 16.0 µg/mL) compared with lean rats (IL-6, 89.9 ± 1.0, P < 0.01; TNF-α, 9.7 ± 0.4, P < 0.01; CRP, 508 ± 21.5, P < 0.001). |
| 282 | 23020082 | Melatonin lowered IL-6 (10%, P < 0.05), TNF-α (10%, P < 0.05), and CRP (21%, P < 0.01). |
| 283 | 23019073 | Pigment epithelium-derived factor (PEDF) peptide eye drops reduce inflammation, cell death and vascular leakage in diabetic retinopathy in Ins2(Akita) mice. |
| 284 | 23019073 | Here, we evaluated intraocular deliverability features of two pigment epithelium-derived factor (PEDF) derivatives given as eye drops and their efficacy in modulating diabetes-induced retinal complications. |
| 285 | 23019073 | The antiangiogenic PEDF60-77 (P60) and neuroprotective PEDF78-121 (P78) derivatives were applied to Ins2(Akita) mouse eyes once a week for 15 wks at the onset of hyperglycemia. |
| 286 | 23019073 | Peak vitreous levels were 0.2 μg/mL for P60 and 0.9 μg/mL for P78 after 0.5 and 4 h, respectively. |
| 287 | 23019073 | Both peptides reduced vascular leakage by ~60% and increased zona occludens 1 (ZO1) and occludin expression in the microvasculature to nondiabetic levels. |
| 288 | 23019073 | P60 induced pERK1/2 and P78 promoted pAKT in Muller glia, two signals that were dampened in diabetic conditions. |
| 289 | 23019073 | Pharmacologically inhibiting AKT signaling in the retina blocked effects of the peptides on ZO1 and occludin expression. |
| 290 | 23019073 | P78 reduced levels of 9/20 cytokines in diabetic vitreous including interferon (IFN)-γ, interleukin (IL)-6, IL-3 and tumor necrosis factor (TNF)-α. |
| 291 | 23019073 | P60 lowered levels of 6/20 cytokines but was less effective than P78. |
| 292 | 23011592 | This is accompanied by decreased mRNA expression of the anti-inflammatory marker adiponectin in WAT and an increase of the proinflammatory monocyte chemoattractant protein-1 (MCP-1). |
| 293 | 23011592 | In vitro, activated Y1-deficient intraperitoneal macrophages display an increased inflammatory response, with exacerbated secretion of MCP-1 and tumor necrosis factor, whereas addition of neuropeptide Y to wild-type macrophages attenuates the release of these cytokines, this effect being blocked by Y1 but not Y2 receptor antagonism. |
| 294 | 23011592 | Importantly, treatment of adipocytes with the supernatant of activated Y1-deficient macrophages causes insulin resistance, as demonstrated by decreased insulin-induced phosphorylation of the insulin receptor and Akt as well as decreased expression of insulin receptor substrate 1. |
| 295 | 23002036 | Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression. |
| 296 | 23002036 | In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). |
| 297 | 23002036 | The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. |
| 298 | 23002036 | Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. |
| 299 | 23002036 | GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. |
| 300 | 23002036 | In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. |
| 301 | 23002036 | Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. |
| 302 | 23002036 | Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr. |
| 303 | 22988423 | The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1 alpha-hydroxylase gene. |
| 304 | 22988423 | Other roles have been proposed to involve immunoregulatory function by activating innate and adaptive immunity and cytokine release, activating inflammation by upregulation of nuclear factor κB and inducing tumor necrosis factor α, and other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity by a low calcium status, obesity, or by elevating serum levels of parathyroid hormone. |
| 305 | 22969920 | Polymerase chain reaction combined with restriction fragment length polymorphism (PCR-RFLP) was used to detect variation in the target genotype, and enzyme-linked immunosorbant assay (ELISA) was used to detect the cytokine [interleukin (IL)-1, IL-6 and tumor necrosis factor-α (TNF-α)] concentrations. |
| 306 | 22969920 | Furthermore, in the hypertensive subjects with the AGT gene 235T allele, the concentrations of IL-1 and TNF-α were significant higher than those in the controls. |
| 307 | 22969920 | High frequencies of the AGT gene 235T allele and high cytokine concentrations (IL-1 and TNF-α) may promote the transcription and expression of AGT, particularly in hypertensive patients with the 235TT genotype. |
| 308 | 22961079 | In this study, we show that in insulin-resistant high-fat diet-fed mice, the enhanced islet vascularization and inflammation was parallel to an increased expression of vascular endothelial growth factor A (VEGF). |
| 309 | 22961079 | We found that sustained increases in β-cell VEGF levels led to disorganized, hypervascularized, and fibrotic islets, progressive macrophage infiltration, and proinflammatory cytokine production, including tumor necrosis factor-α and interleukin-1β. |
| 310 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 311 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 312 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 313 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 314 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 315 | 22949029 | Glucocorticoids antagonize tumor necrosis factor-α-stimulated lipolysis and resistance to the antilipolytic effect of insulin in human adipocytes. |
| 316 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 317 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 318 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 319 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 320 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 321 | 22949029 | High concentrations of TNF within obese adipose tissue increase basal lipolysis and antagonize insulin signaling. |
| 322 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 323 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 324 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 325 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 326 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 327 | 22949029 | We tested the hypothesis that TNF decreases sensitivity to the antilipolytic effect of insulin and that GCs antagonize this effect in differentiated human adipocytes. |
| 328 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 329 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 330 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 331 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 332 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 333 | 22949029 | TNF not only increased basal lipolysis, it caused resistance to the antilipolytic effects of insulin in human adipocytes. |
| 334 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 335 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 336 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 337 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 338 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 339 | 22949029 | Cotreatment with DEX blocked TNF induction of basal lipolysis and insulin resistance by antagonizing TNF stimulation of PKA-mediated phosphorylation of hormone-sensitive lipase (HSL) at Ser⁵⁶³ and Ser⁶⁶⁰ and perilipin. |
| 340 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 341 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 342 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 343 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 344 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 345 | 22949029 | TNF did not affect perilipin, HSL, or phosphodiesterase-3B mass but paradoxically suppressed adipose tissue triglyceride lipase expression, and this effect was blocked by DEX. |
| 346 | 22948775 | Body weight, serum high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, tumor necrosis factor (TNF)-α, fasting glucose, and insulin were measured. |
| 347 | 22941040 | We tested expression levels of tumor necrosis factor α (TNFα) mRNA, glucose transporter 4 (GLUT4), peroxisome proliferator-activated receptor γ2 (PPARγ2) and phosphatidylinositol-3-kinase subunit p85α (PI3Kp85α) in the adipose tissues. |
| 348 | 22941040 | In conclusion, RYGB may improve insulin resistance and treat T2DM through upregulation of the PPARγ2 protein, downregulation of TNFα mRNA transcription, through the autocrine pathway, upregulation of PI3Kp85α expression, upregulation of GLUT4 mRNA transcripts and by inducing translocation of GLUT4 in adipose tissue. |
| 349 | 22939938 | Our study result showed that CAMFs reduced hyperglycemia by increasing serum insulin, C-peptide, total protein, and albumin levels, significantly. |
| 350 | 22939938 | Interestingly, CAMFs down-regulated elevated tumor necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 in the tissues and serum of the diabetic rats. |
| 351 | 22916281 | KIOM-79 strongly inhibited pericyte apoptosis, NF-κB activation and the expression of pro-apoptotic Bax and tumor necrosis factor-α. |
| 352 | 22912917 | Inflammation induces insulin resistance and hyperinsulinemia due to elevation of serum cytokines such as tumor necrosis factor-α and interleukins. |
| 353 | 22910140 | A large number of these mediators, called adipokines, such as tumor necrosis factor alpha (TNF-α), leptin, adiponectin, resistin, chemerin, interleukin-6 (IL-6), visfatin, and so on have been identified and studied widely. |
| 354 | 22896043 | The progression of diabetic renal injury was accompanied by the upregulation of fibrotic and inflammatory markers, increased production of reactive oxygen species and NADPH oxidase activity, and elevated activity of TNF-α-converting enzyme (TACE) in the TIMP3(-/-)/Akita kidneys. |
| 355 | 22891217 | Here, we evaluated the inhibitory effect of a monoclonal antibody (Mab) specific for the E1E2 domain of Wnt coreceptor low-density lipoprotein receptor-related protein 6, Mab2F1, on canonical Wnt signaling and its therapeutic potential for diabetic retinopathy. |
| 356 | 22891217 | In addition, Mab2F1 also attenuated the accumulation of β-catenin and overexpression of vascular endothelial growth factor, intercellular adhesion molecule-1, and tumor necrosis factor-α induced by high-glucose medium in retinal endothelial cells. |
| 357 | 22886693 | Endothelial hyperpermeability is increased by actomyosin contractile activity in response to phosphorylation of myosin light chain by myosin light chain kinase (MLCK). |
| 358 | 22886693 | MLCK-dependent endothelial hyperpermeability occurs in response to inflammatory mediators (e.g., activated neutrophils, thrombin, histamine, tumor necrosis factor alpha, etc.), through multiple cell signaling pathways and signaling molecules (e.g., Ca(++) , protein kinase C, Src kinase, nitric oxide synthase, etc.). |
| 359 | 22848037 | Sour cherry seed kernel extract increases heme oxygenase-1 expression and decreases representation of CD3+ TNF-α+ and CD3+IL-8+ subpopulations in peripheral blood leukocyte cultures from type 2 diabetes patients. |
| 360 | 22848037 | Cultures were evaluated by two-color flow cytometry for percent representation of CD3+ IL8+ and CD3+TNF-α cells which express interleukin-8 (IL-8), and tumor necrosis factor-α, (TNF-α+) respectively, and by enzyme-linked immunoassay for lymphocyte-associated heme oxygenase-1 (HO-1, known to be induced by SCE). |
| 361 | 22837306 | C1q/TNF-related protein-3 (CTRP-3) and pigment epithelium-derived factor (PEDF) concentrations in patients with type 2 diabetes and metabolic syndrome. |
| 362 | 22837306 | C1q/TNF-related protein-3 (CTRP-3) and pigment epithelium-derived factor (PEDF) concentrations in patients with type 2 diabetes and metabolic syndrome. |
| 363 | 22837306 | Recent studies have suggested that a novel adipokine, C1q/tumor necrosis factor-related protein-3 (CTRP-3), a paralog of adiponectin, may play an important role in the regulation of glucose metabolism and innate immunity. |
| 364 | 22837306 | Recent studies have suggested that a novel adipokine, C1q/tumor necrosis factor-related protein-3 (CTRP-3), a paralog of adiponectin, may play an important role in the regulation of glucose metabolism and innate immunity. |
| 365 | 22837306 | Pigment epithelium-derived factor (PEDF), a multifunctional protein with antioxidant and anti-inflammatory properties, is associated with insulin resistance and metabolic syndrome. |
| 366 | 22837306 | Pigment epithelium-derived factor (PEDF), a multifunctional protein with antioxidant and anti-inflammatory properties, is associated with insulin resistance and metabolic syndrome. |
| 367 | 22837306 | We examined circulating CTRP-3 and PEDF concentrations in 345 subjects with diverse glucose tolerance statuses. |
| 368 | 22837306 | We examined circulating CTRP-3 and PEDF concentrations in 345 subjects with diverse glucose tolerance statuses. |
| 369 | 22837306 | Furthermore, we evaluated the involvement of CTRP-3 and PEDF with cardiometabolic risk factors including insulin resistance, high-sensitivity C-reactive protein (hsCRP), estimated glomerular filtration rate (eGFR), and brachial-ankle pulse wave velocity (baPWV). |
| 370 | 22837306 | Furthermore, we evaluated the involvement of CTRP-3 and PEDF with cardiometabolic risk factors including insulin resistance, high-sensitivity C-reactive protein (hsCRP), estimated glomerular filtration rate (eGFR), and brachial-ankle pulse wave velocity (baPWV). |
| 371 | 22837306 | CTRP-3 concentrations were significantly higher in patients with type 2 diabetes or prediabetes than the normal glucose tolerance group, whereas PEDF levels were not different. |
| 372 | 22837306 | CTRP-3 concentrations were significantly higher in patients with type 2 diabetes or prediabetes than the normal glucose tolerance group, whereas PEDF levels were not different. |
| 373 | 22837306 | Subjects with metabolic syndrome showed significantly higher levels of both CTRP-3 and PEDF compared with subjects without metabolic syndrome. |
| 374 | 22837306 | Subjects with metabolic syndrome showed significantly higher levels of both CTRP-3 and PEDF compared with subjects without metabolic syndrome. |
| 375 | 22837306 | Both CTRP-3 and PEDF were significantly associated with cardiometabolic parameters, including waist-to-hip ratio, triglycerides, HDL-cholesterol, alanine aminotransferase, eGFR, hsCRP, and baPWV. |
| 376 | 22837306 | Both CTRP-3 and PEDF were significantly associated with cardiometabolic parameters, including waist-to-hip ratio, triglycerides, HDL-cholesterol, alanine aminotransferase, eGFR, hsCRP, and baPWV. |
| 377 | 22837306 | Both CTRP-3 and PEDF concentrations were increased in subjects with metabolic syndrome and associated with various cardiometabolic risk factors. |
| 378 | 22837306 | Both CTRP-3 and PEDF concentrations were increased in subjects with metabolic syndrome and associated with various cardiometabolic risk factors. |
| 379 | 22824914 | Intrahepatic triglyceride contents and expression of inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and monocyte chemo-attractant protein-1 (MCP-1) and also, PPAR-γ coactivator (PGC)-1α gene were evaluated in liver tissues of OLETF rats and HepG2 cells after GW0742 treatment. |
| 380 | 22824914 | In liver tissues, mRNA expressions of TNF-α, MCP-1, and PGC-1α were significantly decreased in diabetic rats treated with GW0742 compared to diabetic control rats. |
| 381 | 22824914 | The expression level of Akt and IRS-1 was significantly increased by treatment with GW0742. |
| 382 | 22824914 | The PPAR-δ agonist may attenuate hepatic fat accumulation through anti-inflammatory mechanism, reducing hepatic PGC-1α gene expression, and improvement of insulin signaling. |
| 383 | 22815043 | The serum levels of glucose, insulin, interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), MDA, SOD, and GSH-Px were determined. |
| 384 | 22815043 | Compared with diabetic rats receiving BMSCs, diabetic rats receiving EGB before BMSCs transplantation showed (1) significantly lower levels of blood glucose, serum MDA, IL-6, and TNF-α, and higher levels of insulin, SOD, and GSH-Px activities; (2) significantly lower PKCα expression and NF-κB activation in the kidney. |
| 385 | 22803952 | The effect of exercise on osteoprotegerin and TNF-related apoptosis-inducing ligand in obese patients. |
| 386 | 22774990 | The results indicated clearly that elevated MIF secretion preceded C57BL/6 pancreatic islets death induced by interferon (IFN)-γ + tumour necrosis factor (TNF)-α + interleukin (IL)-1β. |
| 387 | 22774990 | Furthermore, upon exposure to cytokines pancreatic islets from MIF-KO mice maintained normal insulin expression and produced less cyclooxygenase-2 (COX-2) than those from wild-type C57BL6 mice. |
| 388 | 22774990 | The final outcome of cytokine-induced islet apoptosis in islets from wild-type mice was the activation of mitochondrial membrane pore-forming protein Bcl-2-associated X protein and effector caspase 3. |
| 389 | 22773667 | We found that 1) the killing of β-cells by CD4⁺ T cells required activation of the recipient's own cytotoxic cells via tumor necrosis factor-α (TNF-α); 2) CD8⁺ T-cell cytotoxic mechanisms destroying β-cells were limited to perforin and Fas ligand, as double knockouts of these molecules abrogated the ability of T cells to cause diabetes; and 3) individual CD8⁺ T-cell clones chose their cytotoxic weaponry by a yet unknown mechanism and destroyed their targets via either Fas-independent or Fas-dependent (~40% of clones) pathways. |
| 390 | 22771801 | Quantitative real-time PCR analysis revealed that CRP inhibited adiponectin, leptin and peroxisome proliferator-activated receptor-gamma (PPAR-γ) genes expression and raised tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA levels in matured 3T3-L1 adipocytes in a dose and time-dependent manner. |
| 391 | 22771801 | Pharmacological inhibition of phosphatidylinositol (PI)-3 kinase by wortmannin partially reversed the effects of CRP on adiponectin, TNF-α and leptin genes expression. |
| 392 | 22771801 | These results collectively suggest that CRP regulates adiponectin, TNF-α, leptin, IL-6 and PPAR-γ genes expression, and that might represent a mechanism by which CRP regulates insulin resistance, obesity and metabolic syndrome. |
| 393 | 22743636 | Because in human umbilical vein endothelial cells (HUVEC), tumor necrosis factor alpha (TNFα)-induced sPLA2-V expression, and LPC content in LDL and monocyte chemoattractant protein-1 mRNA were enhanced by incubation of LDL with TNFα-stimulated HUVEC, we investigated whether an angiotensin II receptor type 1 blocker, telmisartan, or an antioxidant drug, N-acetylcysteine (NAC), suppressed TNFα-induced sPLA2-V expression. |
| 394 | 22743025 | Up-regulation of genes for insulin factors genes, peroxisome proliferative activity receptor were increased, and calcium channel gene and other genes for mitochondrial ribosomal protein S, and uncoupling protein 2. |
| 395 | 22743025 | Down-regulation of tumor necrosis factor alpha and interleukin 6 were demonstrated for this transformation. |
| 396 | 22733167 | Importantly, sitagliptin decreased mRNA expression of the inflammatory cytokines tumor necrosis factor-α (TNF-α) and transforming growth factor-β(1) (TGF-β(1)) in lung tissues as compared to the OVA group. |
| 397 | 22714715 | Recombinant PEDF activates macrophages to release tumor necrosis factor (TNF) and interleukin-1 (IL-1). |
| 398 | 22714715 | Recombinant PEDF activates macrophages to release tumor necrosis factor (TNF) and interleukin-1 (IL-1). |
| 399 | 22714715 | Recombinant PEDF activates macrophages to release tumor necrosis factor (TNF) and interleukin-1 (IL-1). |
| 400 | 22714715 | The PEDF receptor adipose triglyceride lipase (ATGL) is required for PEDF-mediated macrophage activation. |
| 401 | 22714715 | The PEDF receptor adipose triglyceride lipase (ATGL) is required for PEDF-mediated macrophage activation. |
| 402 | 22714715 | The PEDF receptor adipose triglyceride lipase (ATGL) is required for PEDF-mediated macrophage activation. |
| 403 | 22714715 | Selective inhibition of ATGL on macrophages attenuates PEDF-induced TNF production, and PEDF enhances the phosphorylation of p38 and extracellular signal-regulated kinase 1/2 mitogen-activated protein kinases. |
| 404 | 22714715 | Selective inhibition of ATGL on macrophages attenuates PEDF-induced TNF production, and PEDF enhances the phosphorylation of p38 and extracellular signal-regulated kinase 1/2 mitogen-activated protein kinases. |
| 405 | 22714715 | Selective inhibition of ATGL on macrophages attenuates PEDF-induced TNF production, and PEDF enhances the phosphorylation of p38 and extracellular signal-regulated kinase 1/2 mitogen-activated protein kinases. |
| 406 | 22714715 | PEDF administration to rats results in increased serum TNF levels, and insulin resistance. |
| 407 | 22714715 | PEDF administration to rats results in increased serum TNF levels, and insulin resistance. |
| 408 | 22714715 | PEDF administration to rats results in increased serum TNF levels, and insulin resistance. |
| 409 | 22689120 | The synthesis of the enzyme is regulated by interleukin 1 and tumor necrosis factor a. |
| 410 | 22688339 | There were no differences in the above parameters between the two groups, but patients whose ulcers failed to heal had higher tumor necrosis factor-α, monocyte chemoattractant protein-1, matrix metallopeptidase 9 (MMP-9), and fibroblast growth factor 2 serum levels when compared with those who healed. |
| 411 | 22688339 | Skin biopsy analysis showed that compared with control subjects, diabetic patients had increased immune cell infiltration, expression of MMP-9, and protein tyrosine phosphatase-1B (PTP1B), which negatively regulates the signaling of insulin, leptin, and growth factors. |
| 412 | 22688339 | We conclude that increased inflammation, expression of MMP-9, PTP1B, and aberrant growth factor levels are the main factors associated with failure to heal DFUs. |
| 413 | 22688336 | TNF-α augmented the contraction of primary cultured bladder smooth muscle cells through upregulating Rho kinase activity and phosphorylating myosin light chain. |
| 414 | 22688336 | Systemic treatment of DKO animals with soluble TNF receptor 1 (TNFRI) prevented upregulation of Rho A signaling and reversed the bladder dysfunction, without affecting hyperglycemia. |
| 415 | 22683870 | Insulin resistance is a causative factor for type 2 diabetes, whereas the development of insulin resistance is closely related to chronic inflammation induced by factors such as tumor necrosis factor-α (TNF-α). |
| 416 | 22683870 | Consequently, the expression of inflammatory markers including inducible nitric oxide synthase (iNOS), the p65 subunit of nuclear factor-κB (NF-κB), protein-tyrosine phosphatase-1B, TNF-α and interleukin-1β were significantly elevated by TNF-α in the cell, and EMCD obviously suppressed the TNF-α-induced expression of these markers. |
| 417 | 22666480 | Five hundred human islets were co-cultured with 0.5 or 1.0 × 10(6) human MSCs derived from bone marrow or pancreas for 24 hours followed by 48 hour exposure to interferon-γ, tumor necrosis factor-α and interleukin 1β. |
| 418 | 22644855 | In addition, the levels of RAGE protein, transcription factor NF-κB p65, and the p22phox subunit of NADPH oxidase were increased, as were the serum levels of malondialdehyde and tumor necrosis factor-alpha (TNF-α; p < 0.01 vs control), suggesting that the mechanisms of oxidative stress contributed to vascular injury in the diabetic model group. |
| 419 | 22615828 | Combined use of serum adiponectin and tumor necrosis factor-alpha receptor 2 levels was comparable to 2-hour post-load glucose in diabetes prediction. |
| 420 | 22596052 | Analysis of secreted cytokines and chemokines by Luminex technology confirmed production and secretion of proinflammatory cytokines (e.g., interleukin [IL]-6 and tumor necrosis factor-α) as well as various chemotactic proteins, such as IFN-γ-induced protein 10, macrophage inflammatory protein (MIP)-1α, MIP-1β, and IL-8. |
| 421 | 22586584 | The inhibitory molecule lymphocyte activation gene 3 (LAG-3) and metalloprotease tumor necrosis factor-α converting enzyme (TACE) work together to regulate TH1 responses. |
| 422 | 22586584 | The aim of this study was to determine if regulating redox using a catalytic antioxidant (CA) could modulate TACE-mediated LAG-3 shedding to impede diabetogenic T-cell activation and progression to disease. |
| 423 | 22586584 | A combination of in vitro experiments and in vivo analyses using NOD mouse strains was conducted to test the effect of redox modulation on LAG-3 shedding, TACE enzymatic function, and disease onset. |
| 424 | 22586584 | Disease prevention correlated with decreased activation, proliferation, and effector function of diabetogenic T cells; reduced insulin-specific T-cell frequency; and enhanced LAG-3(+) cells. |
| 425 | 22585450 | In aortic rings, relaxation to acetylcholine and vasoreactivity to noradrenaline were impaired, whereas aortic iNOS expression and plasma tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), total nitrite-nitrate, and malondialdehite levels were increased in diabetic rats compared with controls. |
| 426 | 22585450 | These results suggest that chronic in vivo treatment of CM preserves endothelium-dependent relaxation and vascular contraction in STZ-induced diabetes, possibly by reducing iNOS expression in the aorta and by decreasing plasma levels of TNF-α and IL-6 and by preventing lipid peroxidation. |
| 427 | 22556082 | However, LF infection was associated with augmented levels of tumor necrosis factor-α and interleukin-6 among CAD(+) subjects. |
| 428 | 22527888 | The levels of malondialdehyde (MDA), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) in kidney were determined. |
| 429 | 22527888 | Compared to diabetic rats treated with insulin alone, the diabetic rats treated with combination of insulin and RA showed: (1) significantly lower levels of MDA, IL-6, TNF-α, and Scr (p < 0.05); (2) significantly higher SOD and GSH-Px activities (p < 0.05); (3) significantly lower NF-κB activation and lower expression levels of PKCα (p < 0.05); (4) significantly smaller kidney-to-body weight ratio (p < 0.05). |
| 430 | 22522614 | Obese rodents were treated by intracerebroventricular injections, with immunoneutralizing antibodies against Toll-like receptor (TLR)4 or tumor necrosis factor (TNF)α, and insulin signal transduction, hepatic steatosis, and gluconeogenesis were evaluated. |
| 431 | 22522614 | The inhibition of either TLR4 or TNFα reduced hypothalamic inflammation, which was accompanied by the reduction of hypothalamic resistance to leptin and improved insulin signal transduction in the liver. |
| 432 | 22522145 | Since tumor necrosis factor-α (TNF-α) has been shown to trigger the death of perycites and endothelial cells as well as the breakdown of the blood-retinal barrier, we set out to investigate whether TNF-α acting through tumor necrosis factor receptor 1 (TNFR1), the major receptor responsible for mediating TNF-induced cell death, could also be responsible for the early neuronal cell death observed in DR. |
| 433 | 22511336 | Potential anti-diabetic mechanisms were investigated with blood glucose, serum insulin, serum adiponectin, hemoglobin A1c (HbA1c), glucose tolerance, insulin secretion assay, quantitative real-time polymerase chain reaction, and hematoxylin-eosin staining. |
| 434 | 22511336 | Compared with the control group, the FGE group had lower levels of blood glucose after 6 and 9 h fasting, HbA1c, and the area under the curve in an oral glucose tolerance test and higher levels of adiponectin and serum insulin (p < 0.05). |
| 435 | 22511336 | The FGE group had higher levels of peroxisome proliferator-activated receptor gamma 2 and glucose transporter protein 2 mRNAs, a lower level of tumor necrosis factor-α (TNF-α) (p < 0.05), and less lymphocytes in pancreas than the control group had. |
| 436 | 22492942 | Also, renal levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), ED-1, hypoxia-inducible factor-1α (HIF-1α), and neutrophil gelatinase-associated lipocalin (NGAL) were determined by immunohistochemistry and immunoblotting. |
| 437 | 22492942 | Additionally, ANG-(1-7) reduced renal fibrosis, decreased thiobarbituric acid-reactive substances, and restored the activity of both renal superoxide dismutase and catalase in ZDF. |
| 438 | 22492942 | This attenuation of renal oxidative stress proceeded with decreased renal immunostaining of IL-6, TNF-α, ED-1, HIF-1α, and NGAL to values similar to those displayed by LZR. |
| 439 | 22492942 | Angiotensin-converting enzyme type 2 (ACE2) and ANG II levels remained unchanged after treatment with ANG-(1-7). |
| 440 | 22476617 | Adipose tissue secretes numerous pro-inflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α that can lead to insulin resistance (IR). |
| 441 | 22476617 | In the liver, both IL-6 and TNF-α induce IR by inhibiting phosphorylation or ubiquitination of IRS1. |
| 442 | 22476617 | We measured intracellular Fe levels and the relative expression of hepcidin, NF-κB, IL-6, TNF-α, hypoxia inducible factor 1α (HIF-1α), and mitofusin 2 (Mfn-2) mRNA using qRT-PCR. |
| 443 | 22476617 | HepG2 cells incubated with 40 μM Fe alone or Fe/glucose and challenged with IL-6 and/or CoCl(2) showed increased IL-6, NF-κB, and TNF-α mRNA expression and decreased mRNA expression of Mfn-2 in all experimental conditions. 3T3-L1 cells incubated with 40 μM Fe alone or Fe/glucose and challenged with IL-6 showed increased NF-κB mRNA expression and decreased Mfn-2 expression in all experimental conditions. |
| 444 | 22474026 | Fifteen cytokines, chemokines, and growth factors were elevated (P ≤ 0.01) in Ab(+) versus Ab(-) children (interleukin [IL]-1β, IL-5, IL-7, IL-12(p70), IL-16, IL-17, IL-20, IL-21, IL-28A, tumor necrosis factor-α, chemokine C-C motif ligand [CCL]13, CCL26, chemokine C-X-C motif ligand 5, granulocyte-macrophage colony-stimulating factor, and thrombopoietin); most have proinflammatory effects. |
| 445 | 22474026 | In EV(+) versus EV(-) children, IL-10 was higher (P = 0.005), while IL-21 was lower (P = 0.008). |
| 446 | 22474026 | Apart from differences in IL-10 and IL-21, EV infection was not associated with a specific cytokine profile. |
| 447 | 22473609 | Oxidative burst, myeloperoxidase (MPO) release, expression of pathogen recognition receptors (TLR2, TLR4, and CD14), and activation markers (CD11b and HLA-DR) were measured on polymorphonuclear (PMN) leukocytes and monocytes. |
| 448 | 22473609 | Concentrations of plasma inflammatory cytokine (interleukin-6 [IL-6], IL-12p70, tumor necrosis factor alpha [TNF-α], monocyte chemoattractant protein 1 [MCP-1], IL-8, IL-1β, and IL-10) were also determined. |
| 449 | 22473609 | Differences were also observed in expression of Toll-like receptor 2 (TLR2), CD14, and CD11b on phagocytes from T2D and ND individuals. |
| 450 | 22473609 | Levels of IL-12p70, MCP-1, and IL-8 were significantly elevated in blood from PC-T2D subjects compared to ND individuals. |
| 451 | 22451521 | The induction of tumor necrosis factor alpha (TNF-α) was evaluated by immunohistochemistry and of apoptotic cells by a TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay. |
| 452 | 22451385 | Moreover, the hepatic expression of such inflammatory genes as tumor necrosis factor-alpha and monocyte chemoattractant protein-1 were markedly suppressed by the Lotus diet. |
| 453 | 22446096 | Circulating soluble tumor necrosis factor related apoptosis inducing-ligand (TRAIL) is decreased in type-2 newly diagnosed, non-drug using diabetic patients. |
| 454 | 22437419 | Tristetraprolin, a downstream product of NF-κB activation, may mediate destabilization of ANKH mRNA as its knockdown by shRNA increased ANKH expression and decreased calcification. |
| 455 | 22437419 | Furthermore, a rat chronic renal failure model, with increased serum TNF levels, activated NF-κB and decreased ANKH levels. |
| 456 | 22426798 | OBDM patients with or without anemia had higher levels of ferritin and high-sensitivity C-reactive protein than the Cn group. mRNA relative abundance of nuclear factor kappa-light-chain-enhancer of activated B cells was elevated in OBDM with anemia, and mRNA expression of interleukin-6 and toll-like receptor (TLR) 2 was increased in OBDM group in basal high Fe and high glucose concentrations. |
| 457 | 22426798 | The expression of tumor necrosis factor alpha and TLR-4 was increased in OBDM with anemia in all experimental conditions. |
| 458 | 22418727 | Galectin-3, a unique chimera-type member of the β-galactoside-binding soluble lectin family, is widely expressed in numerous cells. |
| 459 | 22418727 | In addition, experiments in Galectin-3-"knock-out" mice indicate that Galectin-3 is also involved in immune-mediated β-cell damage and is required for diabetogenesis in MLD-STZ model by promoting the expression of IFN-gamma, TNF-alpha, IL-17 and iNOS in immune and accessory effector cells. |
| 460 | 22418727 | Next, our data demonstrated that Galectin-3 plays an important disease-exacerbating role in EAE through its multifunctional roles in preventing cell apoptosis and increasing IL-17 and IFN-gamma synthesis, but decreasing IL-10 production. |
| 461 | 22408428 | The -308G/A of Tumor Necrosis Factor (TNF)-α and 825C/T of Guanidine Nucleotide Binding Protein 3 (GNB3) are associated with the onset of acute myocardial infarction and obesity in Taiwan. |
| 462 | 22408428 | The -308G/A of Tumor Necrosis Factor (TNF)-α and 825C/T of Guanidine Nucleotide Binding Protein 3 (GNB3) are associated with the onset of acute myocardial infarction and obesity in Taiwan. |
| 463 | 22408428 | To discriminate obesity- and inflammation-related genes and the onset of acute myocardial infarction (AMI), a case-control study was conducted to investigate the association of the -308G/A polymorphisms of tumor necrosis factor (TNF)-α and the C825T polymorphism of guanidine nucleotide binding protein 3 (GNB3) with the onset of AMI among Taiwanese cohorts. |
| 464 | 22408428 | To discriminate obesity- and inflammation-related genes and the onset of acute myocardial infarction (AMI), a case-control study was conducted to investigate the association of the -308G/A polymorphisms of tumor necrosis factor (TNF)-α and the C825T polymorphism of guanidine nucleotide binding protein 3 (GNB3) with the onset of AMI among Taiwanese cohorts. |
| 465 | 22406002 | In the Sydney Memory and Aging Study, the relationships between remitted depression, current and first onset of symptoms of depression or anxiety (Geriatric Depression Scale and Goldberg Anxiety Scale (GDS, GAS), and markers of systemic inflammation (C-reactive protein (CRP), interleukins-1β, -6, -8, -10, -12, plasminogen activator inhibitor-1 (PAI-1), serum amyloid A, tumor necrosis factor-α, and vascular adhesion molecule-1) were investigated. |
| 466 | 22406002 | The results show a significant linear relationship between increasing levels of IL-6 and depressive symptoms at baseline only, whereas IL-8 was associated with depressed symptoms at baseline and at 2 years follow-up. |
| 467 | 22406002 | The findings are suggestive of IL-6 and IL-8 being associated with current symptoms and IL-8 being associated with first onset of depressive symptoms, whereas PAI-1 could be regarded as a marker of remitted depression. |
| 468 | 22396205 | Stress augments insulin resistance and prothrombotic state: role of visceral adipose-derived monocyte chemoattractant protein-1. |
| 469 | 22396205 | Expression of plasma lipids, monocyte/macrophage markers (CD11b, CD68, and F4/80), proinflammatory cytokines (monocyte chemoattractant protein-1 [MCP-1], tumor necrosis factor-α, and interleukin-6), adiponectin, heat shock protein 70.1 (HSP70.1), and coagulation factors (plasminogen activation inhibitor-1 [PAI-1] and tissue factor [TF]) in blood and inguinal white adipose tissue (WAT) was determined using immunohistochemistry, enzyme-linked immunosorbent assay, and RT-PCR, respectively. |
| 470 | 22396205 | Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests, and expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. |
| 471 | 22396205 | Stress increased monocyte accumulation, free fatty acids, proinflammatory cytokine, and HSP70.1 and reduced adiponectin. |
| 472 | 22396205 | Without any changes in GTT, stress worsened insulin sensitivity and decreased IRS-1 and GLUT4 in WAT. |
| 473 | 22396205 | Stress evoked adipose inflammation to increase coagulation factors and impair insulin sensitivity through adipose-derived MCP-1. |
| 474 | 22394022 | SAC or SPC intake significantly reduced the plasma blood urea nitrogen level and increased creatinine clearance (P < 0.05). |
| 475 | 22394022 | These treatments significantly lowered the renal level of reactive oxygen species, nitric oxide, interleukin-6, tumor necrosis factor-α, and prostaglandin E(2) in diabetic mice (P < 0.05). |
| 476 | 22394022 | Renal mRNA expression of inducible nitric oxide synthase, cyclooxygenase-2, protein kinase C (PKC)-α, PKC-β, and PKC-γ was enhanced in diabetic mice (P < 0.05); however, SAC or SPC treatments dose dependently declined mRNA expression of these factors (P < 0.05). |
| 477 | 22394022 | SAC or SPC intake dose dependently suppressed NF-κB activity, NF-κB p65 mRNA expression, and protein level (P < 0.05). |
| 478 | 22394022 | SAC and SPC, only at a high dose, significantly suppressed protein production of p-p38 and p-ERK1/2 (P < 0.05). |
| 479 | 22394022 | Renal mRNA expression and protein generation of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ were significantly down-regulated in diabetic mice (P < 0.05), but the intake of SAC or SPC at high dose up-regulated PPAR-α and PPAR-γ (P < 0.05). |
| 480 | 22394022 | These findings support that SAC and SPC are potent anti-inflammatory agents against diabetic kidney diseases. |
| 481 | 22385239 | In this study we showed that peripheral sera cytokines [interleukin (IL)-12, IL-6, II-1β, tumour necrosis factor (TNF)-α, IL-10] and chemokines (CXCL10, CXCL8, CXCL9, CCL2) measured were significantly higher in newly diagnosed T1AD patients when compared to healthy controls (P < 0·001). |
| 482 | 22385239 | Among T1AD, we found a positive correlation between CXCL10 and CCL-2 (r = 0·80; P = 0·000), IL-8 and TNF-α (r = 0·60; P = 0·000); IL-8 and IL-12 (r = 0·57; P = 0·001) and TNF-α and IL-12 (r = 0·93; P = 0·000). |
| 483 | 22385239 | Glutamic acid decarboxylase-65 (GAD-65) autoantibodies (GADA) were associated negatively with CXCL10 (r = -0·45; P = 0·011) and CCL2 (r = -0·65; P = 0·000), while IA-2A showed a negative correlation with IL-10 (r = -0·38; P = 0·027). |
| 484 | 22385239 | Human leucocyte antigen (HLA) DR3, DR4 or DR3/DR4 and PTPN22 polymorphism did not show any association with pancreatic islet cell antibodies or cytokines studied. |
| 485 | 22384308 | Exercise did not change body weight of db/db, but superoxide dismutase (SOD1 and SOD2) and phosphorylated- eNOS protein (Ser1177) expression in heart tissue was up-regulated whereas tumor necrosis factor-alpha (TNF-α) protein level was decreased by ET. |
| 486 | 22362176 | HS+MES treatment or HSP72 overexpression increased HSP72 protein levels and decreased tumor necrosis factor (TNF)-α-induced Jun NH(2)-terminal kinase (JNK) phosphorylation, endoplasmic reticulum (ER) stress, and proapoptotic signal in MIN6 cells. |
| 487 | 22362176 | Compared with sham treatment, levels of HSP72, insulin, pancreatic duodenal homeobox-1, GLUT2, and insulin receptor substrate-2 were upregulated in the pancreatic islets of HS+MES-treated mice, whereas JNK phosphorylation, nuclear translocation of forkhead box class O-1, and nuclear factor-κB p65 were reduced. |
| 488 | 22362176 | Thus, HSP72 induction by HS+MES treatment protects β-cells from apoptosis by attenuating JNK activation and cell stresses. |
| 489 | 22362175 | In the hippocampus of HFD-fed mice, the protein levels of tumor necrosis factor-α and Iba-1 expression were reduced by RES treatment. |
| 490 | 22362175 | Choline acetyltransferase was increased, and the phosphorylation of tau was decreased in the hippocampus of HFD-fed mice upon RES treatment. |
| 491 | 22362099 | White adipose tissue (WAT) is more than a mere organ for storage of energy; it is also a highly active metabolic and endocrine organ that secretes physiologically active substances collectively known as adipokines, including tumor necrosis factor-α and adiponectin. |
| 492 | 22350950 | Rosiglitazone ameliorates diabetic nephropathy by reducing the expression of Chemerin and ChemR23 in the kidney of streptozotocin-induced diabetic rats. |
| 493 | 22350950 | This study aims to determine whether rosiglitazone and pioglitazone ameliorate renal function through an effect on the expression of chemerin and ChemR23 in streptozotocin-induced diabetic rats. |
| 494 | 22350950 | The expression level of chemerin and ChemR23 in the renal tissues was significantly elevated in the diabetic group compared with the control group. |
| 495 | 22350950 | Rosiglitazone inhibited the overexpression of chemerin and ChemR23, while pioglitazone inhibited the overexpression of ChemR23 in the kidney of diabetic rats. |
| 496 | 22350950 | In addition, chemerin expression level was positively correlated with transforming growth factor-β1, connective tissue growth factor, tumor necrosis factor-α, and intracellular cell adhesion molecule-1 expression in diabetic rats. |
| 497 | 22350950 | Rosiglitazone ameliorates diabetic nephropathy by reducing the expression of chemerin and ChemR23 in diabetic rats. |
| 498 | 22344597 | Janex-1, a JAK3 inhibitor, ameliorates tumor necrosis factor-α-induced expression of cell adhesion molecules and improves myocardial vascular permeability in endotoxemic mice. |
| 499 | 22344597 | Janex-1, a JAK3 inhibitor, ameliorates tumor necrosis factor-α-induced expression of cell adhesion molecules and improves myocardial vascular permeability in endotoxemic mice. |
| 500 | 22344597 | The purpose of this study was to investigate the effect of JAK3 inhibition on the expression of tumor necrosis factor (TNF)-α-induced cell adhesion molecules in vascular endothelial cells and to evaluate the therapeutic potential of JAK3 for myocardial vascular permeability in endotoxemic mice. |
| 501 | 22344597 | The purpose of this study was to investigate the effect of JAK3 inhibition on the expression of tumor necrosis factor (TNF)-α-induced cell adhesion molecules in vascular endothelial cells and to evaluate the therapeutic potential of JAK3 for myocardial vascular permeability in endotoxemic mice. |
| 502 | 22344597 | A JAK3 inhibitor, JANEX-1, decreased the TNF-α-induced expression of intercellular adhesion molecule (ICAM)-1, VCAM (vascular cell adhesion molecule)-1 and fractalkine in human umbilical vein endothelial cells (HUVECs). |
| 503 | 22344597 | A JAK3 inhibitor, JANEX-1, decreased the TNF-α-induced expression of intercellular adhesion molecule (ICAM)-1, VCAM (vascular cell adhesion molecule)-1 and fractalkine in human umbilical vein endothelial cells (HUVECs). |
| 504 | 22344560 | Metformin induced a marked activation of AMP-activated protein kinase, endothelial nitric oxide synthase, and vascular endothelial growth factor and reduced tumor necrosis factor-α expression and myocyte apoptosis. |
| 505 | 22331607 | Oxidation and glycation enhance foam cell formation via MAPK/JNK in euglycemic and diabetic subjects. |
| 506 | 22331607 | Glc-oxLDL induced a broad cascade of MAPK/JNK-dependent signaling transduction pathways and the AP-1 complex. |
| 507 | 22331607 | In glc-oxLDL treated coronary arterioles, tumor necrosis factor (TNF) α increased JNK phosphorylation, whereas protein kinase inhibitor dimethylaminopurine (DMAP) prevented the TNF-induced increase in JNK phosphorylation. |
| 508 | 22331607 | The role of MKK4 and JNK were then investigated in vivo, using apolipoprotein E knockout (ApoE(-/-)) mice. |
| 509 | 22331607 | Compared to streptozotocin-treated diabetic C57BL6 and nondiabetic C57BL6 Wt mice, in streptozotocin-diabetic ApoE(-/-) mice, the increment of foam cell formation corresponded to an increment of phosphorylation of JNK1, JNK2, and MMK4. |
| 510 | 22326465 | Major systemic and liver-specific molecular mechanisms involved include insulin resistance and hyperinsulinemia, increased TNF signaling pathways, and alterations in cellular lipid metabolism. |
| 511 | 22303583 | Interleukin 6 (IL-6), Tumor Necrosis Factor-alpha (TNF-alpha), High Sensitive C-Reactive protein (hs-CRP) and Fasting Insulin concentration were measured. |
| 512 | 22288305 | Biological drugs include TNF-alpha inhibitors (etanercept, infliximab and adalimumab) and ustekinumab which is an anti-IL 2/23 monoclonal antibody. |
| 513 | 22275362 | C1q/TNF-related protein-12 (CTRP12), a novel adipokine that improves insulin sensitivity and glycemic control in mouse models of obesity and diabetes. |
| 514 | 22266664 | Elevated plasma concentrations of TNF receptors 1 and 2 (TNFR1 and TNFR2) predict development of ESRD in patients with type 2 diabetes without proteinuria, suggesting these markers may contribute to the pathogenesis of renal decline. |
| 515 | 22266664 | Concentrations of TNFR1 and TNFR2 were strongly associated with risk for early renal decline. |
| 516 | 22266663 | Of the examined markers, only TNF receptors 1 and 2 (TNFR1 and TNFR2) associated with risk for ESRD. |
| 517 | 22261190 | Adiponectin, a member of the C1q/TNF-related protein (CTRP) family, has attracted much interest because of its anti-inflammatory and insulin-sensitizing effects. |
| 518 | 22227604 | Both sc insulin and oral nanoparticle insulin partially attenuated hyperglycemia-induced inflammation caused by tumor necrosis factor α, but not by interleukin-6 or C-reactive protein; on the other hand, subcutaneous insulin was found to be more effective on lipid profile measured in the form of high density lipoprotein, cholesterol and triglyceride. |
| 519 | 22220267 | Induction of protective genes in the recipient (e.g., heme oxygenase-1 (HO-1), A20/tumor necrosis factor alpha inducible protein3 (tnfaip3), biliverdin reductase (BVR), Bcl2, and others) or administration of one or more of the products of HO-1 to the donor, the islets themselves, and/or the recipient offers an alternative or synergistic approach to improve islet graft survival and function. |
| 520 | 22220267 | In this perspective, we summarize studies describing the protective effects of these genes on islet survival and function in rodent allogeneic and xenogeneic transplantation models and the prevention of onset of diabetes, with emphasis on HO-1, A20, and BVR. |
| 521 | 22210749 | On the one hand, most adipokines [including tumor necrosis factor-α, resistin, adipocyte fatty acid binding protein (A-FABP), and lipocalin-2] are proinflammatory and causally associated with endothelial and cardiac dysfunction by their endocrine/paracrine actions. |
| 522 | 22210749 | This review provides an update in understanding the roles of adipokines in the pathogenesis of cardiovascular disorders associated with obesity and diabetes and focuses on the two most abundant adipokines, adiponectin and A-FABP. |
| 523 | 22210320 | Potential role of tumor necrosis factor-α in downregulating sex hormone-binding globulin. |
| 524 | 22210320 | Potential role of tumor necrosis factor-α in downregulating sex hormone-binding globulin. |
| 525 | 22210320 | The aim of the current study is to explore whether tumor necrosis factor-α (TNF-α) rather than insulin could be the main factor accounting for low SHBG levels in obesity. |
| 526 | 22210320 | The aim of the current study is to explore whether tumor necrosis factor-α (TNF-α) rather than insulin could be the main factor accounting for low SHBG levels in obesity. |
| 527 | 22210320 | In addition, a cross-sectional study to explore the relationship between TNF-α and SHBG in obese patients and an interventional study to examine the effect of insulin administration on circulating SHBG in type 2 diabetic patients were performed. |
| 528 | 22210320 | In addition, a cross-sectional study to explore the relationship between TNF-α and SHBG in obese patients and an interventional study to examine the effect of insulin administration on circulating SHBG in type 2 diabetic patients were performed. |
| 529 | 22210320 | We provide evidence that TNF-α, but not insulin, is the main factor by which SHBG is reduced in obesity. |
| 530 | 22210320 | We provide evidence that TNF-α, but not insulin, is the main factor by which SHBG is reduced in obesity. |
| 531 | 22210320 | Plasma SHBG was significantly increased rather than decreased after insulin treatment in diabetic patients. |
| 532 | 22210320 | Plasma SHBG was significantly increased rather than decreased after insulin treatment in diabetic patients. |
| 533 | 23510213 | In addition, CC treatment significantly decreased mitogen-stimulated tumor necrosis factor (TNF)-α and interleukin (IL)-6 production in leukocytes as well as the numbers of total and B splenocytes. |
| 534 | 22200617 | Described herein are the traditional as well as endocrine roles of adipose tissue in controlling energy metabolism and their dysregulation in obesity that leads to development of cardiometabolic disorders, with a focus on what is currently known regarding the characteristics and roles in both health and disease of the adipocyte-derived adipokines, adiponectin, leptin, resistin, and retinol binding protein 4, and the resident macrophage-derived adipokines, tumor necrosis factor-α and interleukin-6. |
| 535 | 22186136 | These effects were accompanied by age-dependent changes in peripheral secretion of proinflammatory (interleukin [IL]-6 and tumor necrosis factor [TNF]-α) and T cell-related (IL-2 and interferon [IFN]-γ) cytokines and by increased release of the stress hormone corticosterone in periadolescence. |
| 536 | 22181071 | Among these gut hormones are ghrelin, glucagon-like peptide 1, peptide YY, and cholecystokinin. |
| 537 | 22181071 | Some of the most relevant adipocytokines include adiponectin, leptin, tumor necrosis factor-α, and interleukin-6. |
| 538 | 22179526 | Interferon-γ (IFN-γ), TNF-α, interleukin-1 β (IL-1β), fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFβ-1), bone morphogenetic protein-2 (BMP-2), and BMP-6 were measured by real-time RT-PCR, and histological sections were examined for leukocyte infiltration and several parameters related to bone resorption and formation. |
| 539 | 22179526 | TNF inhibition in diabetic animals also reduced apoptosis, increased proliferation of bone-lining cells, and increased mRNA levels of FGF-2, TGFβ-1, BMP-2, and BMP-6. |
| 540 | 22178943 | Significant p-p38 MAPK activation in DN 14-3-3 mice compared to wild type mice (WT) after diabetes induction and with a corresponding up regulation of its downstream effectors, p-MAPK activated protein kinase 2 (MAPKAPK-2). |
| 541 | 22178943 | Marked increases in cardiac hypertrophy, fibrosis and inflammation were observed with a corresponding up-regulation of atrial natriuretic peptide, osteopontin, connective tissue growth factor, tumor necrosis factor α, interleukin (IL)-1β, IL-6 and cellular adhesion molecules. |
| 542 | 22178943 | Moreover, reactive oxygen species, left ventricular expression of NADPH oxidase subunits, p22 phox, p67 phox, and Nox4, and lipid peroxidation levels were significantly increased in diabetic DN 14-3-3mice compared to diabetic WT mice. |
| 543 | 22178943 | In conclusion, our data suggests that depletion of 14-3-3 protein induces cardiac oxidative stress, inflammation and remodeling after experimental diabetes induction mediated through p38 MAPK, MAPKAPK-2 and NF-κB signaling. |
| 544 | 22178606 | We report here that high glucose (HG) treatment stimulated astrocytic morphological alteration coupled with changes in glial fibrillary acidic protein (GFAP) and vimentin expression. |
| 545 | 22178606 | Additionally, HG upregulated the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-4 (IL-4), and vascular endothelial growth factor (VEGF); however, its effects on transforming growth factor-β (TGF-β) expression were not evident. |
| 546 | 22178606 | HG treatment induced increased production of reactive oxygen species (ROS) as well as activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator transcription 3 (STAT 3). |
| 547 | 22178606 | HG-induced expression of TNF-α, IL-6, IL-1β, IL-4, and VEGF was blocked by ROS scavenger and inhibitors specific for NF-κB and STAT 3, respectively. |
| 548 | 22155554 | Among serum proteins albumin and transferrin have attracted the most interest as drug carriers in the past two decades. |
| 549 | 22155554 | Meanwhile intensive pursuit of exploiting transferrin, but above all albumin as an exogenous or endogenous carrier protein for treating various diseases, primarily cancer, rheumatoid arthritis, diabetes and hepatitis has resulted in several marketed products and numerous clinical trials. |
| 550 | 22155554 | While the use of transferrin has clinically been primarily restricted to immunotoxins, albumin-based drug delivery systems ranging from albumin drug nanoparticles, albumin fusion protein, prodrugs and peptide derivatives that bind covalently to albumin as well as physically binding antibody fragments and therapeutically active peptides are in advanced clinical trials or approved products. |
| 551 | 22155554 | For treating diabetes, Levemir and Victoza that are myristic acid derivatives of human insulin or glucagon-like peptide 1 (GLP-1) act as long-acting peptides by binding to the fatty acid binding sites on circulating albumin to control glucose levels. |
| 552 | 22155554 | The most advanced antibody of this kind is ATN-103 (Ozoralizumab), a trivalent albumin-binding nanobody that neutralizes the pro-inflammatory tumor necrosis factor alpha (TNF-α) as a causative agent for exacerbating rheumatoid arthritis. |
| 553 | 22144989 | TRAIL and DcR1 expressions are differentially regulated in the pancreatic islets of STZ- versus CY-applied NOD mice. |
| 554 | 22144989 | TNF-related apoptosis-inducing ligand (TRAIL) is an important component of the immune system. |
| 555 | 22144989 | Specific increases observed in TRAIL ligand and DcR1 expressions may be part of a defensive strategy of the beta islets against the infiltrating leukocytes, while the immune-suppressive agent CY may partly hold down this defense, contributing further to diabetes development. |
| 556 | 22131032 | In vitro exposure of beta cells to the cytokines interleukin(IL)-1β + interferon(IFN)-γ or to tumor necrosis factor(TNF)-α + IFN-γ induces beta cell dysfunction and ultimately apoptosis. |
| 557 | 22128263 | Interleukin-1β (IL-1β), tumor necrosis factor-α, and glycated albumin (AGE-BSA) were identified as inducers of RCAN1.4 in mesangial cells. |
| 558 | 22110480 | LYR motif containing 1 (LYRM1) is a novel gene that is abundantly expressed in the adipose tissue of obese subjects and is involved in insulin resistance. |
| 559 | 22110480 | In this study, free fatty acids (FFAs) and tumor necrosis factor-α (TNF-α) are shown to upregulate LYRM1 mRNA expression in 3T3-L1 adipocytes. |
| 560 | 22110480 | Conversely, resistin and rosiglitazone exert an inhibitory effect on LYRM1 mRNA expression. |
| 561 | 22110480 | These results suggest that the expression of LYRM1 mRNA is affected by a variety of factors that are related to insulin sensitivity. |
| 562 | 22110480 | LYRM1 may be an important mediator in the development of obesity-related insulin resistance. |
| 563 | 22094062 | Apocynin significantly attenuates the impaired glomerular function, concentration of Na(+), K(+), alpha glutathione S-transferase levels in urine and neutrophil gelatinase-associated lipocalin levels in plasma caused by iomeprol. |
| 564 | 22094062 | In kidney, immunohistochemical analysis of some inflammatory mediators, such as nitrotyrosine, poly-ADP-ribosyl polymerase, tumor necrosis factor-α, interleukin-1β as well as apoptosis (evaluated as terminal deoxynucleotidyltransferase-mediated UTP end labeling assay) revealed positive staining in tissue obtained from iomeprol group. |
| 565 | 22092703 | We analyzed the change of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leptin from pre- to immediately post-race in 15 male runners (age 43 ± 10.9 years and body mass index 24.5 ± 2.7 kg/m(2) ) both on the protein level in the plasma and on the messenger ribonucleic acid (mRNA) level in blood mononuclear cells (BMNC). |
| 566 | 22092703 | We observed a significant increase of IL-6 (prerace 2.08 ± 0.10 ng/L and postrace 40.14 ± 24.85 ng/L, P < 0.001) and TNF-α (prerace 8.14 ± 1.38 ng/L and postrace 12.40 ± 3.15 ng/L, P < 0.001) and a decrease of leptin (prerace 1.64 ± 2.64 μg/L and postrace 0.80 ± 1.70 μg/L, P = 0.04) serum levels after the marathon race. |
| 567 | 22092703 | Furthermore, TNF-α, IL-6, and leptin were expressed (mRNA level) in BMNC. |
| 568 | 22087354 | Non-alcoholic fatty liver disease (NAFLD) is a low-grade systemic inflammatory condition, since liver and adipose tissue tumor necrosis factor-α (TNF-α) and TNF receptor 1 transcripts and serum TNF-α levels are increased and IL-6(-/-) mice are less prone to NAFLD. |
| 569 | 22083962 | First, we revealed that excess palmitate (PA), but not hyperglycemia, hyperinsulinemia, or elevated tumor necrosis factor alpha, induced mitochondrial fragmentation and increased mitochondrion-associated Drp1 and Fis1 in differentiated C2C12 muscle cells. |
| 570 | 22083962 | Both genetic and pharmacological inhibition of Drp1 attenuated PA-induced mitochondrial fragmentation, mitochondrial depolarization, and insulin resistance in C2C12 cells. |
| 571 | 22075749 | We studied normal and streptozotocin-induced diabetic (DM) Sprague-Dawley rats treated for 6 weeks with vehicle, ALISK, HCTZ, or AMLO individually and combined and evaluated the effects of treatments on BP, urine albumin to creatinine ratio, renal interstitial fluid levels of angiotensin II, tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) and renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B. |
| 572 | 22075749 | Renal interstitial fluid TNF-α and IL-6, and the renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B were increased in DM rats. |
| 573 | 22075273 | Short-term walnut consumption increases circulating total adiponectin and apolipoprotein A concentrations, but does not affect markers of inflammation or vascular injury in obese humans with the metabolic syndrome: data from a double-blinded, randomized, placebo-controlled study. |
| 574 | 22075273 | Consumption of walnuts was associated with a statistically significant increase in serum apolipoprotein A concentrations (P = .03), but did not affect circulating levels of fetuin A, resistin, C-reactive protein, serum amyloid A, soluble intercellular adhesion molecules 1 and 3, soluble vascular cell adhesion protein 1, interleukins 6 and 8, tumor necrosis factor α, E-selectin, P-selectin, and thrombomodulin. |
| 575 | 22046428 | Atrophied cerebella exhibited significant loss of Purkinje cells, as well as reactive astrogliosis, the activation of microglial cells, and the pronounced up-regulation of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). |
| 576 | 22037824 | Risk factors that increase risk for future CVD among women with a history of GDM include postpartum progression to T2DM; metabolic syndrome; obesity; hypertension; and altered levels of circulating inflammatory markers, specifically, adiponectin, C-reactive protein, and tumor necrosis factor-α. |
| 577 | 23554718 | Results show that the combination of pioglitazone with glimepiride is more effective in amelioration of diabetic nephropathy than rosiglitazone with glimepiride drug therapy due to glycemic control, suppressing albumin excretion rate, total protein excretion rate and augmented TNF-a signaling during the development of streptozotocin induced type 2 diabetic nephropathy. |
| 578 | 22023613 | Antioxidant effect of sulforaphane is derived from nuclear erythroid 2-related factor 2 (Nrf2) activation as demonstrated by increased expression of Nrf2 and downstream targets hemeoxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO-1) in neuro2a cells and sciatic nerve of diabetic animals. |
| 579 | 22023613 | Nuclear factor-kappa B (NF-κB) inhibition seemed to be responsible for antiinflammatory activity of sulforaphane as there was reduction in NF-κB expression and IκB kinase (IKK) phosphorylation along with abrogation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression and tumor necrosis factor-α (TNF-α) and interleukine-6 (IL-6) levels. |
| 580 | 22023146 | Here, we attempted to identify and characterize the members of the skeletal muscle secretome in response to tumor necrosis factor-alpha (TNF-α)-induced insulin resistance. |
| 581 | 21993838 | PAI-1 is the fast acting and specific inhibitor of tissue plasminogen activator (tPA) and urokinase (uPA), the activators of plasminogen and consequently of fibrinolysis. |
| 582 | 21993838 | These molecules include transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α), angiotensin II and interleukin 6 (IL-6), all of which up-regulate PAI-1 in various cell types or can be up-regulated by PAI-1. |
| 583 | 21993838 | Thus, PAI-1 plays a critical role in the insulin resistance syndrome, which leads to type 2 diabetes mellitus, and is associated with its side effects such as an increased risk of diabetic nephropathy, atherosclerotic cardiovascular disease and others. |
| 584 | 21984724 | Once considered to be physiologically inert, adipose tissue is an active producer of hormones, such as leptin and resistin, and cytokines, including many inflammatory cytokines such as tumor necrosis factor-α, IL-1β and IL-6, and C-reactive protein. |
| 585 | 21984724 | Once considered to be physiologically inert, adipose tissue is an active producer of hormones, such as leptin and resistin, and cytokines, including many inflammatory cytokines such as tumor necrosis factor-α, IL-1β and IL-6, and C-reactive protein. |
| 586 | 21984724 | For example, tumor necrosis factor-α alters insulin sensitivity by blocking activation of insulin receptors. |
| 587 | 21984724 | For example, tumor necrosis factor-α alters insulin sensitivity by blocking activation of insulin receptors. |
| 588 | 21977173 | The selected inflammatory markers are associated with different pathogenic steps in atherogenesis: acute phase reactants (C-reactive protein); pro-inflammatory cytokines (TNF-alpha, interleukin-6 and -18); endothelium activation markers (soluble VCAM-1, ICAM-1); and specific factors (anticardiolipinic antibodies). |
| 589 | 21965021 | TNF-related apoptosis-inducing ligand (TRAIL) protects against diabetes and atherosclerosis in Apoe ⁻/⁻ mice. |
| 590 | 21957201 | We found that incubation of 1-palmitoyl-2-(5'-oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC) with THP-1-derived macrophages upregulated the expression of cytokine genes, including granulocyte/macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor (TNF)-α, monocyte chemotactic protein 1 (MCP-1), interleukin (IL)-1β, IL-6, and IL-8. |
| 591 | 21954641 | The use of metformin during the first month of treatment of patients with coronary artery disease and diabetes type 2 led to the decrease of insulin resistance and reduced activity of systemic inflammation (significant decrease in the concentrations of IL-1, IL-6, IL-8 and TNF-alpha). |
| 592 | 21937453 | Cytokines tumor necrosis factor-α and interferon-γ induce pancreatic β-cell apoptosis through STAT1-mediated Bim protein activation. |
| 593 | 21937453 | Cytokines tumor necrosis factor-α and interferon-γ induce pancreatic β-cell apoptosis through STAT1-mediated Bim protein activation. |
| 594 | 21937453 | Here we clarify the molecular mechanism of β-cell death triggered by the pro-inflammatory cytokines tumor necrosis factor (TNF)-α and interferon (IFN)-γ. |
| 595 | 21937453 | Here we clarify the molecular mechanism of β-cell death triggered by the pro-inflammatory cytokines tumor necrosis factor (TNF)-α and interferon (IFN)-γ. |
| 596 | 21937453 | The combination of TNF-α + IFN-γ induced DP5, p53 up-regulated modulator of apoptosis (PUMA), and Bim expression in human islets and rodent β-cells. |
| 597 | 21937453 | The combination of TNF-α + IFN-γ induced DP5, p53 up-regulated modulator of apoptosis (PUMA), and Bim expression in human islets and rodent β-cells. |
| 598 | 21937453 | DP5 and PUMA inactivation by RNA interference partially protected against TNF-α + IFN-γ-induced β-cell apoptosis. |
| 599 | 21937453 | DP5 and PUMA inactivation by RNA interference partially protected against TNF-α + IFN-γ-induced β-cell apoptosis. |
| 600 | 21937453 | Bim expression was transcriptionally regulated by STAT1, and its activation triggered cleavage of caspases. |
| 601 | 21937453 | Bim expression was transcriptionally regulated by STAT1, and its activation triggered cleavage of caspases. |
| 602 | 21925162 | To examine the direct effects of EGCG on β-cells, insulin-producing RINm5F cells were exposed to a combination of recombinant interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ), with or without EGCG pretreatment for 24h. |
| 603 | 21925162 | The expression of cytochrome c, Bax, Bcl-2, and iNOS proteins was measured by western blotting. |
| 604 | 21925162 | EGCG reduced the cytokine-induced generation of reactive oxygen species, the loss of mitochondrial membrane potential (Δψm), the release of cytochrome c from the mitochondria, and translocation of Bax protein to the mitochondria from the cytosol. |
| 605 | 21902468 | Insulin-stimulated glucose uptake from the medium was assessed with and without TNF-alpha. 3D adipose tissue was generated in the 3D-bioreactors. |
| 606 | 21902468 | Insulin-stimulated glucose uptake from the medium was assessed with and without TNF-alpha. 3D adipose tissue was generated in the 3D-bioreactors. |
| 607 | 21902468 | Importantly, TNF-alpha inhibited glucose uptake, an indication of the metabolic activity of the tissue. 3D bioreactors allow more mature adipocyte differentiation of ASCs compared with traditional 2D culture and generate adipose tissue in vitro for up to 2 months. |
| 608 | 21902468 | Importantly, TNF-alpha inhibited glucose uptake, an indication of the metabolic activity of the tissue. 3D bioreactors allow more mature adipocyte differentiation of ASCs compared with traditional 2D culture and generate adipose tissue in vitro for up to 2 months. |
| 609 | 21894153 | The HTR2C and leptin genes are among the most promising, and new evidence suggests that the DRD2, TNF, SNAP-25 and MC4R genes are also prominent risk factors. |
| 610 | 21894153 | Further promising findings have been reported in novel susceptibility genes, such as CNR1, MDR1, ADRA1A and INSIG2. |
| 611 | 21886908 | In all patients, lipid profile, oxidative stress, and inflammatory mediators were assessed by measuring serum concentrations of triglycerides, low density lipoprotein, hydrogen preroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6, respectively. |
| 612 | 21886908 | In all patients, lipid profile, oxidative stress, and inflammatory mediators were assessed by measuring serum concentrations of triglycerides, low density lipoprotein, hydrogen preroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6, respectively. |
| 613 | 21886908 | In all patients, lipid profile, oxidative stress, and inflammatory mediators were assessed by measuring serum concentrations of triglycerides, low density lipoprotein, hydrogen preroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6, respectively. |
| 614 | 21886908 | In the studied population, it was found that the presence of type 2 diabetes mellitus-induced hyperglycemia significantly impaired lipid profile, and significantly enhanced the formation of hydrogen preroxide and malondialdehyde as well as significantly increased the release of tumor necrosis factor-alpha and interleukin-6 in the second group of patients. |
| 615 | 21886908 | In the studied population, it was found that the presence of type 2 diabetes mellitus-induced hyperglycemia significantly impaired lipid profile, and significantly enhanced the formation of hydrogen preroxide and malondialdehyde as well as significantly increased the release of tumor necrosis factor-alpha and interleukin-6 in the second group of patients. |
| 616 | 21886908 | In the studied population, it was found that the presence of type 2 diabetes mellitus-induced hyperglycemia significantly impaired lipid profile, and significantly enhanced the formation of hydrogen preroxide and malondialdehyde as well as significantly increased the release of tumor necrosis factor-alpha and interleukin-6 in the second group of patients. |
| 617 | 21886908 | In addition, plasma glucose level showed significant positive correlation with hydrogen peroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6. |
| 618 | 21886908 | In addition, plasma glucose level showed significant positive correlation with hydrogen peroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6. |
| 619 | 21886908 | In addition, plasma glucose level showed significant positive correlation with hydrogen peroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6. |
| 620 | 21881808 | On the other hand, sleep deprivation stress affects adipokines - increasing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and decreasing leptin and adiponectin -, thus establishing a possible association between sleep-debt, adipokines and glucose metabolism. |
| 621 | 21850156 | Increased tumor necrosis factor-α, cleaved caspase 3 levels and insulin receptor substrate-1 phosphorylation in the β₁-adrenergic receptor knockout mouse. |
| 622 | 21841823 | Pancreatic β-cells activate a JunB/ATF3-dependent survival pathway during inflammation. |
| 623 | 21841823 | Histochemical analysis of pancreases from non-obese diabetic mice indicated activation of the transcription factor JunB/AP-1 (activator protein-1) after autoimmune infiltration of the islets. |
| 624 | 21841823 | In vitro studies demonstrated that the cytokines tumor necrosis factor (TNF)-α and interferon (IFN)-γ induce JunB expression as a protective mechanism against apoptosis in both human and rodent β-cells. |
| 625 | 21841823 | The gene network affected was studied by microarray analysis showing that JunB regulates nearly 20% of the cytokine-modified β-cell genes, including the transcription factor ATF3. |
| 626 | 21841823 | Direct transcriptional induction of ATF3 by JunB is a key event for β-cell survival after TNF-α+IFN-γ treatment. |
| 627 | 21841823 | Moreover, pharmacological upregulation of JunB/ATF3 via increased cAMP protected rodent primary β-cells and human islet cells against pro-inflammatory mediators. |
| 628 | 21841823 | Our findings identify ATF3 as a novel downstream target of JunB in the survival mechanism of β-cells under inflammatory stress. |
| 629 | 21833742 | In 562 subjects aged 85 years old of the general population, venous blood samples were taken for measurement of morning glucose, C-reactive protein (CRP) and glycated hemoglobin (HbA1c). |
| 630 | 21833742 | The innate immune response was assessed by performing ex vivo whole blood lipopolysaccharide (LPS) stimulation for production capacity of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1-beta (IL1-β), interleukin 10 (IL-10) and interleukin 1 receptor antagonist (IL-1Ra). |
| 631 | 21811392 | High TNF-alpha plasma levels and macrophages iNOS and TNF-alpha expression as risk factors for painful diabetic neuropathy. |
| 632 | 21797106 | Serum inflammatory cytokines IL-1beta, IL-6, TNF-alpha and VEGF have influence on the development of diabetic retinopathy. |
| 633 | 21783017 | Activation of p38 in spinal microglia results in increased synthesis and release of the neurotrophin brain-derived neurotrophic factor and the proinflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α. |
| 634 | 21780542 | By measuring the values of TNF-a, fibrinogen, high sensitive capsule reactive protein (hs-CRP), IL-4, IL-6, IL-8, IL-10, at the beginning of non-surgical periodontal therapy and it has been after 3 months of treatment, noticed a relevant reduction only of TNF-a and fibrinogen. |
| 635 | 21738955 | Potential role of leptin, adiponectin and three novel adipokines--visfatin, chemerin and vaspin--in chronic hepatitis. |
| 636 | 21738955 | Visfatin exerts insulin-mimetic effects, decreases plasma glucose levels and regulates cell energy balance. |
| 637 | 21738955 | Vaspin expression in human adipose tissue seems to be a compensatory mechanism associated with obesity and insulin resistance. |
| 638 | 21738955 | Vaspin suppresses leptin, tumor necrosis factor (TNF)-α and resistin expression. |
| 639 | 21738950 | The aim of this study was to determine the circulating concentrations and expression levels of calprotectin subunits (S100A8 and S100A9) in visceral adipose tissue (VAT), exploring its impact on insulin resistance and inflammation and the effect of weight loss. |
| 640 | 21738950 | Calprotectin was mainly expressed by SVFCs, and its expression was significantly correlated (P < 0.01) with mRNA levels of the monocyte-macrophage-related molecules macrophage-specific antigen CD68 (CD68), monocyte chemotactic protein 1 (MCP1), integrin α-M (CD11B), and NADPH oxidase 2 (NOX2). |
| 641 | 21738950 | Tumor necrosis factor-α treatment significantly enhanced (P < 0.05) the mRNA levels of S100 calcium-binding protein A8 (S100A8) of human visceral adipocytes. |
| 642 | 21716679 | The RMD-treated diabetic rats showed higher activities of glutathione disulfide reductase, glutathione reductase, catalase and superoxide dismutase (P < .05) in the pancreas compared with the diabetic control rats. |
| 643 | 21716679 | RMD also inhibited diabetes-induced elevation in the levels of interleukin (IL)-1β, IL-6, interferon-γ and tumor necrosis factor-α. |
| 644 | 21679694 | More vascular protective effects of telmisartan than losartan were associated with greater anti-inflammatory effects of telmisartan, as shown by attenuation of vascular nuclear factor kappa B (NFκB) activation and tumor necrosis factor α. |
| 645 | 21678423 | We found that F4/80(+) peritoneal exudate macrophages (PEMs) from mice with diabetes for 4 months displayed significantly reduced CD86 and CD54 expression and tumor necrosis factor (TNF)-α and IL-6 production but enhanced nitric oxide (NO) secretion compared with control mice when treated with interferon (IFN)-γ and lipopolysaccharide (LPS), while the activity of arginase in PEMs from diabetic mice was significantly higher than control mice when stimulating with IL-4. |
| 646 | 21678423 | In an in vitro culture system, high glucose and insulin significantly altered TNF-α, IL-6, and NO production and arginase activity of macrophages, which was reversed by the treatment with AKT and ERK inhibitors. |
| 647 | 21655062 | We hypothesized that aspirin improves insulin resistance in type 2 diabetes by inhibiting hepatic nuclear factor kappa-β (NF-κB) activation and serum tumor necrosis factor-α (TNF-α). |
| 648 | 21653631 | Anastrozole treatment also attenuated urine albumin excretion by 42%, glomerulosclerosis by 30%, tubulointerstitial fibrosis by 32%, along with a decrease in the density of renal cortical CD68-positive cells by 50%, and protein expression of transforming growth factor-β by 20%, collagen type IV by 29%, tumor necrosis factor-α by 28%, and interleukin-6 by 25%. |
| 649 | 21641234 | Anti-TNF rescue CD4+Foxp3+ regulatory T cells in patients with type 1 diabetes from effects mediated by TNF. |
| 650 | 21641234 | Anti-TNF rescue CD4+Foxp3+ regulatory T cells in patients with type 1 diabetes from effects mediated by TNF. |
| 651 | 21641234 | It indicates that TNF reduces the number and frequency of regulatory CD4(+)Foxp3(+) T cells in children with diabetes type 1 and that in vitro treatment with anti-TNF antibody seems to rescue this cell subset from its defective effects. |
| 652 | 21641234 | It indicates that TNF reduces the number and frequency of regulatory CD4(+)Foxp3(+) T cells in children with diabetes type 1 and that in vitro treatment with anti-TNF antibody seems to rescue this cell subset from its defective effects. |
| 653 | 21631419 | It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitricoxide synthases. |
| 654 | 21631419 | However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α). |
| 655 | 21626279 | Induction of HS did not affect the aberrant NOD-MΦ cytokine profile, which is characterized by elevated IL-10 levels and normal tumor necrosis factor alpha. |
| 656 | 21606463 | Microarray and quantitative PCR analyses of livers from Ins2(Akita)Ldlr⁻/⁻ mice revealed altered expression of lipid homeostatic genes, including sterol-regulatory element binding protein (Srebp)1, liver X receptor (Lxr)α, Abca1, Cyp7b1, Cyp27a1, and Lpl, along with increased expression of pro-inflammatory cytokine genes, including interleukin (Il)1α, Il1β, Il2, tumor necrosis factor (Tnf)α, and Mcp1. |
| 657 | 21593803 | At the same time, both plasma oxidative products (malondialdehyde (MDA), 8-iso-prostaglandin) and inflammatory markers (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)) were remarkably decreased (P < 0.01), while adiponectin was increased (P < 0.01). |
| 658 | 21593803 | There are significant negative correlations between ISI and plasma FFAs, sd-LDL-Chol, ox-LDL-Chol, MDA, 8-iso-prostaglandin, TNF-α, and IL-6, and positive correlations with HDL-Chol and adiponectin in obese-IGT patients. |
| 659 | 21590648 | We evaluated glycemic-metabolic parameters [glycated hemoglobin (HbA (1c)), fasting plasma glucose (FPG), fasting plasma insulin (FPI), homeostasis model assessment (Homa) index], total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), triglycerides (Tgs), interleukin-6 (IL-6), high sensitivity C-reactive protein (Hs-CRP), tumor necrosis factor-α (TNF-α), and adiponectin (ADN). |
| 660 | 21562638 | Stress- and inflammation-related p38 mitogen-activated protein kinase activity and tumor necrosis factor-α production of diabetic rats were significantly depressed by Ipomoea batatas administration. |
| 661 | 21555997 | Cell-specific effects of TNF-α and IL-1β on alkaline phosphatase: implication for syndesmophyte formation and vascular calcification. |
| 662 | 21555997 | Tumor necrosis factor (TNF)-α and interleukin (IL)-1β stimulate tissue non-specific alkaline phosphatase (TNAP) activity and mineralization in cultures of vascular smooth muscle cells (VSMCs). |
| 663 | 21555997 | In this context, our aims were to compare the effects of TNF-α and IL-1β on TNAP activity and mineralization in entheseal cells and VSMCs. |
| 664 | 21555997 | In conclusion, whereas TNF-α and IL-1β stimulate TNAP activity in VSMCs, they inhibit it in entheseal cells in situ and on chondrocytes in vitro. |
| 665 | 21554121 | In the experiments on carrageenan-induced paw edema, paws were dissected for hematoxylin-eosin staining and immunohistochemistry determinations of tumor necrosis factor-α and inducible nitric oxide synthase. |
| 666 | 21554121 | In the experiments on carrageenan-induced paw edema, paws were dissected for hematoxylin-eosin staining and immunohistochemistry determinations of tumor necrosis factor-α and inducible nitric oxide synthase. |
| 667 | 21554121 | It also significantly decreased neutrophil infiltration and partially decreased immunostaining for tumor necrosis factor-α and inducible nitric oxide synthase. |
| 668 | 21554121 | It also significantly decreased neutrophil infiltration and partially decreased immunostaining for tumor necrosis factor-α and inducible nitric oxide synthase. |
| 669 | 21550076 | The gene expression of inflammatory cytokines including interleukin-6, tumor necrosis factor-α, and interferon-γ in peripheral leukocytes gradually increased during the development of diabetes in control rats, but not in miglitol-treated rats. |
| 670 | 21546935 | At 6 months, the improvement in insulin sensitivity correlated with the change in total ceramide levels (r = -0.68, P = 0.02), and with plasma tumor necrosis factor-α (TNF-α) (r = -0.62, P = 0.04). |
| 671 | 21537437 | The purpose of this review will be to examine the reported effects of commonly used lipid-lowering drugs (statins, fibrates, niacin and omega-3-fatty acids) on the circulating concentrations of leptin, adiponectin, tumor necrosis-factor-α (TNF-α), Retinol binding protein 4 (RBP4) and resistin. |
| 672 | 21537437 | Overall, the lipid-lowering drugs reviewed have minimal effects on leptin and resistin concentrations.Conversely, circulating adiponectin concentrations are consistently increased by each lipid-lowering drug reviewed with the greatest effects produced by niacin. |
| 673 | 21537437 | Niacin and fibrates appear to lower RBP4 but not resistin concentrations. |
| 674 | 21537349 | This Review, therefore, focuses on key proinflammatory molecules and pathways implicated in the development and progression of diabetic nephropathy: the chemokines CCL2, CX3CL1 and CCL5 (also known as MCP-1, fractalkine and RANTES, respectively); the adhesion molecules intercellular adhesion molecule 1, vascular cell adhesion protein 1, endothelial cell-selective adhesion molecule, E-selectin and α-actinin 4; the transcription factor nuclear factor κB; and the inflammatory cytokines IL-1, IL-6, IL-18 and tumor necrosis factor. |
| 675 | 21536024 | In addition, minocyline treatment reduced the levels of interleukin-1β and tumor necrosis factor-α, lipid peroxidation, nitrite and also improved antioxidant defense in spinal cords of diabetic rats as compared to diabetic control animals. |
| 676 | 21510113 | Proposed biological mechanisms in experimental animals included up regulation of inflammatory signals like cytokines and TNF-alpha, oxidative stress, hypomethylation, decreased DNA repair and apoptosis, cell proliferation, angiogenesis, activation of several enzymes like methyl transferase which converts inorganic arsenic to MMA and DMA, and GSH in in-vivo and in-vitro in experimental rat liver slices. |
| 677 | 21498926 | Adipose tissue gene expression of adiponectin, tumor necrosis factor-α and leptin in metabolic syndrome patients with coronary artery disease. |
| 678 | 21488367 | The role of some adipocytokines such as IL-6, TNF-alpha, leptin, adiponectin, visfatin and resistin was demonstrated in these processes. |
| 679 | 21488132 | Elevated soluble CD40 ligand in diabetic patients with painless myocardial infarction. |
| 680 | 21488132 | In addition to baseline parameters, cytokine levels, including plasma high sensitivity C-reactive protein (HsCRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and soluble CD40 ligand (sCD40L) levels, were analyzed using enzyme-linked immunosorbent assays (ELISAs). |
| 681 | 21483749 | Anthropometrics were evaluated and metabolic measures such as fasting serum glucose, lipid profiles, insulin, leptin, adiponectin, resistin, tumor necrosis factor alpha (TNFα), activated plasminogen activator inhibitor 1 (aPAI1), high sensitivity C-reactive protein (hsCRP) and angiotensin II were also assessed. |
| 682 | 21483749 | PC1, which explained 21% of the variation, was most strongly loaded on levels of leptin, TNFα, insulin, and aPAI1, and inversely with adiponectin. |
| 683 | 21483233 | Rosiglitazone attenuates tumor necrosis factor-α-induced protein-tyrosine phosphatase-1B production in HepG2 cells. |
| 684 | 21483233 | Rosiglitazone attenuates tumor necrosis factor-α-induced protein-tyrosine phosphatase-1B production in HepG2 cells. |
| 685 | 21483233 | Tumor necrosis factor (TNF)-α impairs insulin signaling and plays an important role in the development of insulin resistance. |
| 686 | 21483233 | Tumor necrosis factor (TNF)-α impairs insulin signaling and plays an important role in the development of insulin resistance. |
| 687 | 21483233 | TNF-α up-regulates PTP- 1B expression in a dose-dependent manner and decreases insulin-stimulated phosphorylation of IR and insulin receptor substrate-1 in HepG2 cells. |
| 688 | 21483233 | TNF-α up-regulates PTP- 1B expression in a dose-dependent manner and decreases insulin-stimulated phosphorylation of IR and insulin receptor substrate-1 in HepG2 cells. |
| 689 | 21478880 | Interleukin (IL)-1β plays a role in insulin resistance, yet how IL-1β is induced by the fatty acids in an HFD, and how this alters insulin signaling, is unclear. |
| 690 | 21478880 | We show that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1β and IL-18 production. |
| 691 | 21478880 | This pathway involves mitochondrial reactive oxygen species and the AMP-activated protein kinase and unc-51-like kinase-1 (ULK1) autophagy signaling cascade. |
| 692 | 21478880 | Furthermore, IL-1β affects insulin sensitivity through tumor necrosis factor-independent and dependent pathways. |
| 693 | 21440948 | C-reactive protein (CRP), lipoprotein-associated phospholipase A2 (Lp-PLA2), secretory phospholipase A2 (sPLA2), interleukin 8 (IL8), monocyte chemotactic protein 1 (MCP1) and tumor necrosis factor α (TNFα) were measured. |
| 694 | 21439758 | The adipose tissue of obese humans contains increased numbers of macrophages, and once activated, these macrophages are responsible for the expression of most of the tissue's tumor necrosis factor (TNF)-α and interleukin (IL)-6. |
| 695 | 21439758 | Adipocytes secrete a variety of hormones, cytokines, growth factors, and other bioactive substances, conceptualized as adipocytokines, including plasminogen activator inhibitor 1 (PAI-1), TNF-α, leptin, and adiponectin. |
| 696 | 21431832 | Several proinflammatory cytokines, acute-phase proteins, and cell adhesion molecules, such as C-reactive protein (CRP), interleukines (IL), and tumor necrosis factor alpha (TNF-α), seem to play a role in the low-grade systemic inflammation observed in these subjects. |
| 697 | 21431832 | Recent research showed that combined exercise has greater anti-inflammatory effects than aerobic or resistance exercise alone causing a deepest decrease in CRP, IL-6, IL-1β, TNF-α, leptin, and resistin and a higher increase in anti-inflammatory cytokines such as IL-4, IL-10, and adiponectin. |
| 698 | 21420073 | Differential cytokine secretion results from p65 and c-Rel NF-κB subunit signaling in peripheral blood mononuclear cells of TNF receptor-associated periodic syndrome patients. |
| 699 | 21420073 | Differential cytokine secretion results from p65 and c-Rel NF-κB subunit signaling in peripheral blood mononuclear cells of TNF receptor-associated periodic syndrome patients. |
| 700 | 21420073 | Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an autosomal dominant autoinflammatory condition caused by mutations in the TNFRSF1A gene which encodes the tumor necrosis factor (TNF) receptor, TNFR1. |
| 701 | 21420073 | Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an autosomal dominant autoinflammatory condition caused by mutations in the TNFRSF1A gene which encodes the tumor necrosis factor (TNF) receptor, TNFR1. |
| 702 | 21420073 | Interestingly, high p65 activity was associated with elevated IL-8 secretion, whereas high c-Rel activity increased IL-1β and IL-12 secretion. |
| 703 | 21420073 | Interestingly, high p65 activity was associated with elevated IL-8 secretion, whereas high c-Rel activity increased IL-1β and IL-12 secretion. |
| 704 | 21388274 | Diabetes caused significant increases in cardiac inflammation, shown by time-dependent increases in mRNA and protein expressions of interleukin 18 (IL-18), tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule 1 (ICAM-1), plasminogen activator inhibitor 1 (PAI-1), and monocyte chemoattractant protein 1 (MCP-1). |
| 705 | 21388274 | Repeated exposure of diabetic mice to low-dose radiation significantly reduced diabetes-increased cardiac expression of IL-18, TNF-α, MCP-1 and PAI-1 at both the mRNA and protein levels. |
| 706 | 21377179 | Fasting and postprandial blood glucose, glycated hemoglobin, lipid profile, insulin resistance index (homeostasis model assessment of insulin resistance), adipocytokines (adiponectin, visfatin, and resistin), tumor necrosis factor, interleukin, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline and at the end of the study. |
| 707 | 21374991 | [Changes of leptin, tumor necrosis factor-alpha, neuropeptide Y levels and their association with insulin resistance and insulin secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees]. |
| 708 | 21374991 | [Changes of leptin, tumor necrosis factor-alpha, neuropeptide Y levels and their association with insulin resistance and insulin secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees]. |
| 709 | 21374991 | [Changes of leptin, tumor necrosis factor-alpha, neuropeptide Y levels and their association with insulin resistance and insulin secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees]. |
| 710 | 21374991 | [Changes of leptin, tumor necrosis factor-alpha, neuropeptide Y levels and their association with insulin resistance and insulin secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees]. |
| 711 | 21374991 | This investigation was made in regard to the changes of plasma Leptin, Tumor Necrosis Factor-alpha (TNF-alpha) and Neuropeptide Y (NPY) levels and their association with insulin resistance and beta-cell secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees in Chengdu area. |
| 712 | 21374991 | This investigation was made in regard to the changes of plasma Leptin, Tumor Necrosis Factor-alpha (TNF-alpha) and Neuropeptide Y (NPY) levels and their association with insulin resistance and beta-cell secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees in Chengdu area. |
| 713 | 21374991 | This investigation was made in regard to the changes of plasma Leptin, Tumor Necrosis Factor-alpha (TNF-alpha) and Neuropeptide Y (NPY) levels and their association with insulin resistance and beta-cell secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees in Chengdu area. |
| 714 | 21374991 | This investigation was made in regard to the changes of plasma Leptin, Tumor Necrosis Factor-alpha (TNF-alpha) and Neuropeptide Y (NPY) levels and their association with insulin resistance and beta-cell secretion function in normal glucose tolerant first-degree relatives of familial type 2 diabetic pedigrees in Chengdu area. |
| 715 | 21374991 | Levels of Leptin, TNF-alpha, NPY and lipids (TG, TC, HDL-C) were determined in 86 type 2 diabetic mellitus (DM) patients, 73 normal glucose tolerant (NGT) first-degree relatives in familial type 2 diabetic pedigrees and 65 normal controls (NC) from non-diabetic families. |
| 716 | 21374991 | Levels of Leptin, TNF-alpha, NPY and lipids (TG, TC, HDL-C) were determined in 86 type 2 diabetic mellitus (DM) patients, 73 normal glucose tolerant (NGT) first-degree relatives in familial type 2 diabetic pedigrees and 65 normal controls (NC) from non-diabetic families. |
| 717 | 21374991 | Levels of Leptin, TNF-alpha, NPY and lipids (TG, TC, HDL-C) were determined in 86 type 2 diabetic mellitus (DM) patients, 73 normal glucose tolerant (NGT) first-degree relatives in familial type 2 diabetic pedigrees and 65 normal controls (NC) from non-diabetic families. |
| 718 | 21374991 | Levels of Leptin, TNF-alpha, NPY and lipids (TG, TC, HDL-C) were determined in 86 type 2 diabetic mellitus (DM) patients, 73 normal glucose tolerant (NGT) first-degree relatives in familial type 2 diabetic pedigrees and 65 normal controls (NC) from non-diabetic families. |
| 719 | 21374991 | Leptin was positively correlated with age, BMI, waist, A1c, fasting and OGTT-2h glucose, OGTT-2h TI and TNF-alpha in all subjects, and was negatively correlated with HOMA-B in females. |
| 720 | 21374991 | Leptin was positively correlated with age, BMI, waist, A1c, fasting and OGTT-2h glucose, OGTT-2h TI and TNF-alpha in all subjects, and was negatively correlated with HOMA-B in females. |
| 721 | 21374991 | Leptin was positively correlated with age, BMI, waist, A1c, fasting and OGTT-2h glucose, OGTT-2h TI and TNF-alpha in all subjects, and was negatively correlated with HOMA-B in females. |
| 722 | 21374991 | Leptin was positively correlated with age, BMI, waist, A1c, fasting and OGTT-2h glucose, OGTT-2h TI and TNF-alpha in all subjects, and was negatively correlated with HOMA-B in females. |
| 723 | 21354119 | We have demonstrated that AKR1B1 inhibitor, fidarestat, significantly prevents tumor necrosis factor-alpha (TNF-α)-, growth factors-, lipopolysachharide (LPS)-, and environmental allergens-induced inflammatory signals that cause various inflammatory diseases. |
| 724 | 21321581 | Protection against diabetes was accompanied by histone hyperacetylation in pancreas and spleen, enhanced frequency of CD4(+) CD62L(+) cells in the spleen, reduction in cellular infiltration of islets, restoration of normoglycemia and glucose-induced insulin release by beta cells. |
| 725 | 21321581 | Activation of splenic T lymphocytes derived from protected mice in vitro with pharmacological agents that bypass the antigen receptor or immobilized anti-CD3 antibody resulted in enhanced expression of Ifng mRNA and protein without altering the expression of Il4, Il17, Il18, Inos and Tnfa genes nor the secretion of IL-2, IL-4, IL-17 and TNF-α proteins. |
| 726 | 21321581 | Consistently, expression of the transcription factor involved in Ifng transcription, Tbet/Tbx21 but not Gata3 and Rorgt, respectively, required for the transcription of Il4 and Il17, was upregulated in activated splenocytes of protected mice. |
| 727 | 21317853 | The systemic inflammation in psoriasis generates elevation of C-reactive protein, homocysteine, and inflammatory cytokines such as TNF-a, IL-6, IL-17, IL-20, IL-22, and IL-23, which may contribute to the overall morbidity and mortality in these patients. |
| 728 | 21290055 | Gold nanoparticles were attached to antibodies against interleukin-12 and tumor necrosis factor-α, typical inflammatory markers found with near overlapping responses, on an impedance spectroscopy based biosensor. |
| 729 | 21290055 | Gold nanoparticles were attached to antibodies against interleukin-12 and tumor necrosis factor-α, typical inflammatory markers found with near overlapping responses, on an impedance spectroscopy based biosensor. |
| 730 | 21290055 | This was accomplished without significantly altering the lower limits of detection (<4 pg ml(-1) and ∼60 pg ml(-1) for interleukin-12 and tumor necrosis factor-α, respectively), no cross-reactivity and specificity as determined by ELISAs. |
| 731 | 21290055 | This was accomplished without significantly altering the lower limits of detection (<4 pg ml(-1) and ∼60 pg ml(-1) for interleukin-12 and tumor necrosis factor-α, respectively), no cross-reactivity and specificity as determined by ELISAs. |
| 732 | 21290055 | Although interleukin-12 and TNF-α equivalent circuit calculations were modeled here, a sensor with the potential to measure multiple markers at once might offer a solution on the sensor front for simplified management of conditions such as diabetes, where both glucose and hemoglobin A1c values could be obtained. |
| 733 | 21290055 | Although interleukin-12 and TNF-α equivalent circuit calculations were modeled here, a sensor with the potential to measure multiple markers at once might offer a solution on the sensor front for simplified management of conditions such as diabetes, where both glucose and hemoglobin A1c values could be obtained. |
| 734 | 21289599 | Urinary albumin excretion increased in vehicle-treated diabetic rats (single injection of streptozotocin), compared with controls, and was associated with tubule injury and increased urinary tumor necrosis factor-α (TNF-α) at 9 weeks. |
| 735 | 21289599 | Further, both agonists restored WT-1 staining along with podocin and nephrin mRNA expression, suggesting podocyte protection. |
| 736 | 21286214 | In addition, increased circulating levels of pro-inflammatory cytokines, such as tumor necrosis factor α, interleukin-6 and C-reactive protein, are closely related to morbidity and mortality of cardiovascular complications. |
| 737 | 21286214 | Emerging evidence suggests that interventions including nutrition, pharmacology and exercise may activate expression of cellular anti-oxidant systems via the nuclear factor erythroid 2-related factor 2-Kelch-like ECH-associated protein 1 signaling pathway and play a role in preventing inflammatory processes in CVD. |
| 738 | 21266511 | In Wistar rats, hypothalamic TNFα blunts the anorexigenic effect of leptin, which is accompanied by reduced leptin signaling and increased expression of suppressor of cytokine signaling 3. |
| 739 | 21266511 | The use of intracerebroventricular infliximab restores O(2) consumption in obese rats, whereas TNF receptor 1-knockout mice are protected from diet-induced reduced thermogenesis and defective insulin signal transduction. |
| 740 | 21264951 | The number of microglia time dependently increased at demyelinative lesion sites, proliferated, and expressed tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, inducible nitric oxide synthase, and MMP2, 9, and 12 at the early phase. |
| 741 | 21264951 | The number of astrocytes time dependently increased around demyelinative lesions, extended processes to lesions, proliferated, and expressed nerve growth factor and glial cell line-derived neurotrophic factor at the late phase. |
| 742 | 21262584 | The macrophage Ox-LDL receptor, CD36 and its association with type II diabetes mellitus. |
| 743 | 21262584 | In addition to Ox-LDL, raised levels of glucose, insulin resistance, low HDL cholesterol, increased levels of free fatty acid (FFA) all result in increased expression of CD36, thereby contributing to T2DM and related atherosclerosis. |
| 744 | 21262584 | Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis. |
| 745 | 21257748 | Intracerebroventricular injection of a low dose of tumor necrosis factor α leads to a dysfunctional increase in insulin secretion and activates the expression of a number of markers of apoptosis in pancreatic islets. |
| 746 | 21257748 | In addition, the injection of stearic acid intracerebroventricularly, which leads to hypothalamic inflammation through the activation of tau-like receptor-4 and endoplasmic reticulum stress, produces an impairment of insulin secretion, accompanied by increased expression of markers of apoptosis. |
| 747 | 21257748 | The defective insulin secretion, in this case, is partially dependent on sympathetic signal-induced peroxisome proliferator receptor-γ coactivator Δα and uncoupling protein-2 expression and is restored after sympathectomy or following PGC1α expression inhibition by an antisense oligonucleotide. |
| 748 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 749 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 750 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 751 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 752 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 753 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 754 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 755 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 756 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 757 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 758 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 759 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 760 | 21244505 | This was associated with increased expression of factors involved in osteoclast activity and recruitment (Rankl, Csf1, Ccl2, Ccl5, and Tnfa) in DB mice. |
| 761 | 21233809 | Therefore, we characterized levels of acute-phase reactants (C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), white blood cell (WBC) count), adhesion molecules (E-selectin, vascular cell adhesion molecule-1), and coagulation products (fibrinogen, plasminogen activator inhibitor-1 (PAI-1)) among four body size phenotypes (normal weight with 0/1 vs. ≥2 metabolic syndrome components/diabetes and overweight/obesity with 0/1 vs. ≥2 metabolic syndrome components/diabetes) in cross-sectional analyses of 1,889 postmenopausal women from the Women's Health Initiative Observational Study (WHI-OS) nested case-control stroke study. |
| 762 | 21204649 | We measured levels of glycosylated hemoglobin (HbA1c), plasma lipid peroxides, superoxide dismutase, glutathione peroxidase, total antioxidants, and tumor necrosis factor-alpha (TNF-α). |
| 763 | 21197110 | Age-related factors contributing to glucose intolerance, which may be improved with RT, include improvements in insulin signaling defects, reductions in tumor necrosis factor-α, increases in adiponectin and insulin-like growth factor-1 concentrations, and reductions in total and abdominal visceral fat. |
| 764 | 21196299 | The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal. |
| 765 | 21196299 | The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal. |
| 766 | 21196299 | The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal. |
| 767 | 21196299 | The elevated TNF-alpha and IL-1beta, but not IL-6 and VEGF, were decreased by 2 U/ml EPO as detected by real-time PCR and ELISA. |
| 768 | 21196299 | The elevated TNF-alpha and IL-1beta, but not IL-6 and VEGF, were decreased by 2 U/ml EPO as detected by real-time PCR and ELISA. |
| 769 | 21196299 | The elevated TNF-alpha and IL-1beta, but not IL-6 and VEGF, were decreased by 2 U/ml EPO as detected by real-time PCR and ELISA. |
| 770 | 21196299 | Moreover, the activity of AP-1 but not NF-kappaB was modulated by glyoxal and EPO. |
| 771 | 21196299 | Moreover, the activity of AP-1 but not NF-kappaB was modulated by glyoxal and EPO. |
| 772 | 21196299 | Moreover, the activity of AP-1 but not NF-kappaB was modulated by glyoxal and EPO. |
| 773 | 21196299 | Intravitreal injection of EPO performed 24 h prior to sacrifice significantly reduced TNF-alpha and IL-1beta production while moderately attenuating IL-6 and VEGF in the retinas of streptozotocin-induced diabetic rats. |
| 774 | 21196299 | Intravitreal injection of EPO performed 24 h prior to sacrifice significantly reduced TNF-alpha and IL-1beta production while moderately attenuating IL-6 and VEGF in the retinas of streptozotocin-induced diabetic rats. |
| 775 | 21196299 | Intravitreal injection of EPO performed 24 h prior to sacrifice significantly reduced TNF-alpha and IL-1beta production while moderately attenuating IL-6 and VEGF in the retinas of streptozotocin-induced diabetic rats. |
| 776 | 21196299 | Furthermore, Muller cells were identified as the main source of IL-1beta production as indicated by co-localization of IL-1beta and CRALBP in situ. |
| 777 | 21196299 | Furthermore, Muller cells were identified as the main source of IL-1beta production as indicated by co-localization of IL-1beta and CRALBP in situ. |
| 778 | 21196299 | Furthermore, Muller cells were identified as the main source of IL-1beta production as indicated by co-localization of IL-1beta and CRALBP in situ. |
| 779 | 22519279 | In psoriasis there is an increased synthesis of proinflammatory proteins, such as: C-reactive protein (CRP), interleukin 1 (IL-1), IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), alpha2-macroglobulin, alpha1-antitrypsin and ceruloplasmin. |
| 780 | 21180596 | These include weight loss agents, bariatric surgery, insulin-sensitizing agents, lipid-lowering agents, antioxidants, probiotics, anti-tumor necrosis factor agents, cytoprotective and other novel agents. |
| 781 | 21175000 | Results showed that PCB77 induced the expression of proinflammatory cytokines including IL-6 and TNFalpha and induced U937 adhesion to HUVEC cells consistent with increased NFkappaB transcription activity. |
| 782 | 21175000 | Results showed that PCB77 induced the expression of proinflammatory cytokines including IL-6 and TNFalpha and induced U937 adhesion to HUVEC cells consistent with increased NFkappaB transcription activity. |
| 783 | 21175000 | Results showed that PCB77 induced the expression of proinflammatory cytokines including IL-6 and TNFalpha and induced U937 adhesion to HUVEC cells consistent with increased NFkappaB transcription activity. |
| 784 | 21175000 | On the other hand, PCB77 blocked insulin-activated Akt signaling pathway, which was restored by pretreatment with TNFalpha neutralization antibody. |
| 785 | 21175000 | On the other hand, PCB77 blocked insulin-activated Akt signaling pathway, which was restored by pretreatment with TNFalpha neutralization antibody. |
| 786 | 21175000 | On the other hand, PCB77 blocked insulin-activated Akt signaling pathway, which was restored by pretreatment with TNFalpha neutralization antibody. |
| 787 | 21175000 | And PCB77 was observed to alter insulin-activated Akt signaling by TNFalpha secretion for the first time. |
| 788 | 21175000 | And PCB77 was observed to alter insulin-activated Akt signaling by TNFalpha secretion for the first time. |
| 789 | 21175000 | And PCB77 was observed to alter insulin-activated Akt signaling by TNFalpha secretion for the first time. |
| 790 | 21147643 | Adipokines such as leptin, resistin, tumor necrosis factor-α, interleukin-6, adipsin, visfatin, and adiponectin are biologically active molecules produced by adipose tissue. |
| 791 | 21147643 | Adiponectin has been associated with both central obesity and increased visceral adipose tissue and it has anti-inflammatory, anti-atherogenic, and potent insulin-sensitizing (anti-diabetic) effects. |
| 792 | 21147639 | Serious consequences accompanying obesity, e.g., type 2 diabetes and lipid abnormalities may be caused by increased level of proinflammatory cytokines, such as IL-1, IL-6, and TNF. |
| 793 | 21150875 | When TNFα-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFα action was through TNF receptor-1 (TNFR1). |
| 794 | 21150875 | In response to tunicamycin-induced acute ER stress, kidneys from neither TNFα-/- nor TNFR1-/- mice showed a significant increase in phosphorylated eukaryotic translation initiation factor 2α (eIF2α), a key step in ER stress regulation. |
| 795 | 21150875 | Moreover, proximal tubular cells from TNFR1-/- mice did not show increased eIF2α phosphorylation in response to tunicamycin and were susceptible to ER stress-induced cell death. |
| 796 | 21150875 | Finally, treatment of proximal tubule cells isolated from TNFR1-/- mice with an inhibitor of eIF2α phosphatase increased the levels of phosphorylated eIF2α and substantially reduced tunicamycin-induced cell death. |
| 797 | 21150875 | Thus, disruption of TNFR1 signaling leads to dysregulation of eIF2α and increased susceptibility to acute ER stress injury in the kidney. |
| 798 | 21149504 | Common variations in the genes encoding C-reactive protein, tumor necrosis factor-alpha, and interleukin-6, and the risk of clinical diabetes in the Women's Health Initiative Observational Study. |
| 799 | 21144822 | In vitro, exendin-4 reduced β-cell apoptosis, and tumor necrosis factor α (TNFα), interleukin β (IL-β), and inducible nitric oxide synthase (iNOS) production of infected or lipopolysaccharide (LPS)-stimulated macrophages. |
| 800 | 21144584 | We tested the hypothesis that interleukin (IL)-6 and tumor necrosis factor (TNF)-α stimulate placental fatty acid transport, as these pro-inflammatory cytokines have been shown to affect lipid metabolism in other tissues. |
| 801 | 21144584 | The increased fatty acid accumulation could not be explained by an increased expression of key components in placental fatty acid transport, such as adipophilin, fatty acid transport protein (FATP)1, FATP4, or lipoprotein lipase. |
| 802 | 21144584 | In a cohort of lean and overweight/obese pregnant women, increasing maternal third trimester IL-6 plasma concentrations correlated with decreasing placental lipoprotein lipase activity. |
| 803 | 21144584 | However, as no effect on lipoprotein lipase activity was observed in cultured trophoblast cells after exposure to either IL-6 or TNF-α, the correlation between maternal circulatory IL-6 levels and placental lipoprotein lipase activity at term is unlikely to represent a cause-and-effect relationship. |
| 804 | 21138840 | However, ER stress preconditioning almost completely abolished TNF-α-elicited NF-κB activation and adhesion molecule ICAM-1 and VCAM-1 expression. |
| 805 | 21138840 | Moreover, loss of XBP1 led to an increase in ICAM-1 and VCAM-1 expression. |
| 806 | 21138840 | Conversely, overexpression of spliced XBP1 attenuated TNF-α-induced phosphorylation of IKK, IκBα, and NF-κB p65, accompanied by decreased NF-κB activity and reduced adhesion molecule expression. |
| 807 | 21138840 | Finally, in vivo studies show that activation of XBP1 by ER stress preconditioning prevents TNF-α-induced ICAM-1 and VCAM-1 expression, leukostasis, and vascular leakage in mouse retinas. |
| 808 | 21127808 | These studies specifically show effects on the glucose transporter (GLUT-4) gene and protein; insulin-like growth factor binding protein-1 (IGFBP-1); nuclear transcription factor kappa B (NFκB); tumor necrosis factor alpha (TNF-α); and insulin production. |
| 809 | 21104585 | The lipocalins retinol-binding protein-4, lipocalin-2 and lipocalin-type prostaglandin D2-synthase correlate with markers of inflammatory activity, alcohol intake and blood lipids, but not with insulin sensitivity in metabolically healthy 58-year-old Swedish men. |
| 810 | 21104585 | The lipocalins retinol-binding protein (RBP)-4, lipocalin-2 and lipocalin-type prostaglandin D-synthase (L-PGDS) have been suggested to mediate obesity-associated insulin resistance and other metabolic co-morbidities. |
| 811 | 21104585 | Therefore, we examined the correlations between serum levels of RBP-4, L-PGDS and lipocalin-2 and insulin sensitivity and other metabolic parameters in non-diabetic subjects selected to display variations in insulin sensitivity. 100 clinically healthy 58-year-old Swedish men were selected by stratified sampling among 818 screened subjects to represent quintiles of varying degrees of insulin sensitivity. |
| 812 | 21104585 | However, we found that lipocalin-2 and L-PGDS were correlated with each other, but not with RBP-4. |
| 813 | 21104585 | Lipocalin-2 and L-PGDS were positively correlated with soluble TNF- receptors 1 and 2 and negatively with alcohol consumption and serum HDL. |
| 814 | 21104585 | Further, lipocalin-2 was correlated with interleukin-6 whereas RBP-4 was negatively correlated with TNF-α. |
| 815 | 21104585 | □These results suggest that RBP-4, lipocalin-2 and L-PGDS do not regulate insulin sensitivity in healthy men. |
| 816 | 21104585 | Rather the expression levels of lipocalin-2 and L-PGDS, but not RBP-4, seemed to reflect inflammatory activity and were inversely correlated with alcohol intake and serum HDL levels. |
| 817 | 21103795 | Many obesity-related factors are responsible, including increased blood levels of insulin/IGF, IL-6, TNF-alpha, and leptin, and decreased blood levels of adiponectin. |
| 818 | 21103795 | IL-17 could activate Src/PI3K, MAPK, Stat3, and PKC, resulting in carcinogenesis. |
| 819 | 21099113 | CD4+CD25+Foxp3+ Tregs play a major role in prevention of autoimmune diseases. |
| 820 | 21099113 | In vivo experiments showed that this Treg boost was partially dependent on TNF but not on IL-2. |
| 821 | 21088675 | Interleukin-6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) levels increased during the study period but were not affected by lipid-heparin infusion. |
| 822 | 21081794 | Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems. |
| 823 | 21081794 | With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases. |
| 824 | 21081660 | We describe a novel strategy, using large-scale gene expression profiling, to develop a gene expression signature (GES) that reflects the overall state of insulin resistance in cells and patients. |
| 825 | 21081660 | The GES was developed from 3T3-L1 adipocytes that were made "insulin resistant" by treatment with tumor necrosis factor-α (TNF-α) and then reversed with aspirin and troglitazone ("resensitized"). |
| 826 | 21081660 | The GES consisted of five genes whose expression levels best discriminated between the insulin-resistant and insulin-resensitized states. |
| 827 | 21081660 | We then used this GES to screen a compound library for agents that affected the GES genes in 3T3-L1 adipocytes in a way that most closely resembled the changes seen when insulin resistance was successfully reversed with aspirin and troglitazone. |
| 828 | 21081660 | We tested the biological relevance of this GES in participants in the San Antonio Family Heart Study (n = 1,240) and showed that patients with the lowest GES scores were more insulin resistant (according to HOMA_IR and fasting plasma insulin levels; P < 0.001). |
| 829 | 21081660 | These findings show that GES technology can be used for both the discovery of insulin-sensitizing compounds and the characterization of patients into subtypes of insulin resistance according to GES scores, opening the possibility of developing a personalized medicine approach to type 2 diabetes. |
| 830 | 21046484 | In the observational study that the authors conducted, plasma concentrations of 25(OH) D, leptin, resistin, adiponectin and interleukine-18 were determined in 134 healthy men and 127 women. |
| 831 | 21046484 | In the observational study that the authors conducted, plasma concentrations of 25(OH) D, leptin, resistin, adiponectin and interleukine-18 were determined in 134 healthy men and 127 women. |
| 832 | 21046484 | In the population consisting of 44 patients with morbid obesity, plasma concentrations of 25(OH) D, leptin, resistin, adiponectin, interleukine-18, soluble tumor necrosis factor receptors 1 and 2 and C-reactive protein were analysed. |
| 833 | 21046484 | In the population consisting of 44 patients with morbid obesity, plasma concentrations of 25(OH) D, leptin, resistin, adiponectin, interleukine-18, soluble tumor necrosis factor receptors 1 and 2 and C-reactive protein were analysed. |
| 834 | 21046484 | However, no significant associations were found amongst 25(OH) D and plasma concentrations of resistin, adiponectin or interleukine-18. |
| 835 | 21046484 | However, no significant associations were found amongst 25(OH) D and plasma concentrations of resistin, adiponectin or interleukine-18. |
| 836 | 21046484 | In the morbidly obese subjects, 25(OH) D did not correlate with leptin, resistin, adiponectin, interleukine-18, soluble tumor necrosis factor receptors 1 and 2 or with C-reactive protein. |
| 837 | 21046484 | In the morbidly obese subjects, 25(OH) D did not correlate with leptin, resistin, adiponectin, interleukine-18, soluble tumor necrosis factor receptors 1 and 2 or with C-reactive protein. |
| 838 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 839 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 840 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 841 | 21038470 | Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF. |
| 842 | 21038470 | They inhibit CD4(+) T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2. |
| 843 | 21038470 | They inhibit CD4(+) T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2. |
| 844 | 21038470 | They inhibit CD4(+) T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2. |
| 845 | 21038470 | They inhibit CD4(+) T-cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL-2. |
| 846 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 847 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 848 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 849 | 21038470 | The induction of CD8(+) Treg by anti-CD3 mAb requires TNF and signaling through the NF-κB cascade. |
| 850 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 851 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 852 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 853 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 854 | 21033373 | Such signal molecules as tumor necrosis factor (TNF-alpha), interleukins-1,6 (IL-1,6) take part in these processes. |
| 855 | 20972877 | We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. |
| 856 | 20972877 | We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. |
| 857 | 20972877 | We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. |
| 858 | 20972877 | We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. |
| 859 | 20972877 | We hypothesized that PAR2 regulates tumor necrosis factor-alpha (TNF-α)-induced coronary arteriolar dysfunction in type 2 diabetic (db/db) mice. |
| 860 | 20972877 | To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH₂ (db/db+FSLLRY-NH₂) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH₂O) without flow. |
| 861 | 20972877 | To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH₂ (db/db+FSLLRY-NH₂) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH₂O) without flow. |
| 862 | 20972877 | To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH₂ (db/db+FSLLRY-NH₂) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH₂O) without flow. |
| 863 | 20972877 | To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH₂ (db/db+FSLLRY-NH₂) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH₂O) without flow. |
| 864 | 20972877 | To test this, coronary arterioles from WT control, db/db, db/db mice treated with PAR2 antagonist FSLLRY-NH₂ (db/db+FSLLRY-NH₂) and db/db mice null for TNF (db(TNF-)/db(TNF-)) were isolated and pressurized (60 cmH₂O) without flow. |
| 865 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH₂ and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 866 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH₂ and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 867 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH₂ and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 868 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH₂ and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 869 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH₂ and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 870 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 871 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 872 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 873 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 874 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 875 | 20972877 | Protein expressions of TNF-α, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. |
| 876 | 20972877 | Protein expressions of TNF-α, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. |
| 877 | 20972877 | Protein expressions of TNF-α, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. |
| 878 | 20972877 | Protein expressions of TNF-α, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. |
| 879 | 20972877 | Protein expressions of TNF-α, PAR2, gp91(phox) and p47(phox) in the heart and isolated coronary arterioles were higher in db/db mice compared to WT mice. |
| 880 | 20972877 | Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91(phox) and PAR2. |
| 881 | 20972877 | Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91(phox) and PAR2. |
| 882 | 20972877 | Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91(phox) and PAR2. |
| 883 | 20972877 | Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91(phox) and PAR2. |
| 884 | 20972877 | Administration of PAR2 antagonist to db/db mice reduced protein expression of TNF-α, gp91(phox) and PAR2. |
| 885 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 886 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 887 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 888 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 889 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 890 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47(phox). |
| 891 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47(phox). |
| 892 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47(phox). |
| 893 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47(phox). |
| 894 | 20972877 | These results indicate that PAR2 plays a pivotal role in endothelial dysfunction in type 2 diabetes by up-regulating the expression/production of TNF-α and activating NAD(P)H oxidase subunit p47(phox). |
| 895 | 20964459 | With respect to molecular targets, evidence has been adduced for the roles of vascular endothelial growth factor (VEGF), tumour necrosis factor (TNF)-α and protein kinase C (PKC)-β2 in the pathogenesis of DR, and agents targeting these factors are under intense investigation. |
| 896 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 897 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 898 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 899 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 900 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 901 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 902 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 903 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 904 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 905 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 906 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 907 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 908 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 909 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 910 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 911 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 912 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 913 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 914 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 915 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 916 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 917 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 918 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 919 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 920 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 921 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 922 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 923 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 924 | 20885391 | Concerning the inflammatory status, EPA treatment resulted in a decreased gene expression for both tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) both in skeletal muscle and adipose tissue. |
| 925 | 20872723 | Quantitative RT-PCR was used to measure viral RNA and mRNA of cytokines interferon (IFN)-α, IFN-β, IFN-γ, tumor necrosis factor (TNF)-α, and chemokine (C-X-C motif) ligand 10 (CXCL10), chemokine (C-C motif) ligand 2 (CCL2), and chemokine (C-C motif) ligand 5 (CCL5) in infected INS-1 cells. |
| 926 | 20872723 | IFN-γ, CXCL10, and CCL5 mRNA levels all increased significantly following infection with CVB2, 4, 5, and 6 (P<0.05). |
| 927 | 20854863 | Samples were typed for 38 tumor necrosis factor (TNF) block single nucleotide polymorphisms (SNP), human leukocyte antigen (HLA)-B and HLA-DRB1 alleles. |
| 928 | 20854863 | Samples were typed for 38 tumor necrosis factor (TNF) block single nucleotide polymorphisms (SNP), human leukocyte antigen (HLA)-B and HLA-DRB1 alleles. |
| 929 | 20854863 | FV16 appears to be the best MHC and TNF block marker of susceptibility. |
| 930 | 20854863 | FV16 appears to be the best MHC and TNF block marker of susceptibility. |
| 931 | 20847810 | The aim of this study was to evaluate the effects of moderate-intensity exercise on plasma levels of C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) as markers of low-grade inflammation and endothelial function in diabetic (db/db) mice. |
| 932 | 20846161 | The exercise decreased serum levels of tumour necrosis factor (TNF)-α (6%), cytokine-induced neutrophil chemotactic factor 2 alpha/beta (CINC-2α/β) (9%), interleukin (IL)-1β (34%), IL-6 (86%), C-reactive protein (CRP) (41%) and FFA (40%) in diabetic rats when compared with sedentary diabetic animals. |
| 933 | 20838752 | Serum leptin, adiponectin and tumor necrosis factor-α in hyperlipidemic rats with/without concomitant diabetes mellitus. |
| 934 | 20838752 | Serum leptin, adiponectin and tumor necrosis factor-α in hyperlipidemic rats with/without concomitant diabetes mellitus. |
| 935 | 20838752 | We compared the lipid profiles and serum levels of leptin, adiponectin and tumor necrosis factor-α (TNF-α) in rats with/without hyperlipidemia and with/without concomitant diabetes mellitus. |
| 936 | 20838752 | We compared the lipid profiles and serum levels of leptin, adiponectin and tumor necrosis factor-α (TNF-α) in rats with/without hyperlipidemia and with/without concomitant diabetes mellitus. |
| 937 | 20838752 | Our data suggest that serum leptin, adiponectin and TNF-α levels may serve as markers of obesity and type I diabetes mellitus. |
| 938 | 20838752 | Our data suggest that serum leptin, adiponectin and TNF-α levels may serve as markers of obesity and type I diabetes mellitus. |
| 939 | 20829804 | Vascular endothelial growth factor (VEGF) was higher in the obese nondiabetic subjects (P < 0.05), tumor necrosis factor-α was higher in the obese diabetic patients (P < 0.0001) and C-reactive protein was higher in both the obese nondiabetic and diabetic subjects (P < 0.0001). |
| 940 | 20826789 | In transfected HEK293 cells, we find that plasma kallikrein directly activates G protein-coupled protease-activated receptors (PARs) 1 and 2, which possess consensus kallikrein cleavage sites, but not PAR4. |
| 941 | 20826789 | In vascular smooth muscles, KK stimulates ADAM (a disintegrin and metalloprotease) 17 activity via a PAR1/2 receptor-dependent mechanism, leading sequentially to release of the endogenous ADAM17 substrates, amphiregulin and tumor necrosis factor-α, metalloprotease-dependent transactivation of epidermal growth factor receptors, and metalloprotease and epidermal growth factor receptor-dependent ERK1/2 activation. |
| 942 | 20814070 | The aim of the present study was: 1) to compare the effects of treatment with PPARg ligand (pioglitazone) on healing of acetic acid-induced gastric ulcers and prevention of acute water immersion and restraint stress (WRS)-induced gastric lesions in normal rats and those with streptozotocin (STZ)-induced diabetes mellitus; 2) to assess the effects of pioglitazone on the mRNA expression of cyclooxygenase-2 (COX-2), c-NOS, interleukin-1beta and hypoxia inducible factor-1 alpha (HIF-1alpha) in the gastric mucosa of rats with or without STZ-induced diabetes mellitus; 3) to investigate the involvement of endogenous NO and proinflammatory cytokines (IL-1beta, TNF-alpha) in healing of chronic gastric ulcers and in prevention of acute stress lesions by pioglitazone in rats with or without STZ-induced diabetes mellitus. |
| 943 | 20814070 | The aim of the present study was: 1) to compare the effects of treatment with PPARg ligand (pioglitazone) on healing of acetic acid-induced gastric ulcers and prevention of acute water immersion and restraint stress (WRS)-induced gastric lesions in normal rats and those with streptozotocin (STZ)-induced diabetes mellitus; 2) to assess the effects of pioglitazone on the mRNA expression of cyclooxygenase-2 (COX-2), c-NOS, interleukin-1beta and hypoxia inducible factor-1 alpha (HIF-1alpha) in the gastric mucosa of rats with or without STZ-induced diabetes mellitus; 3) to investigate the involvement of endogenous NO and proinflammatory cytokines (IL-1beta, TNF-alpha) in healing of chronic gastric ulcers and in prevention of acute stress lesions by pioglitazone in rats with or without STZ-induced diabetes mellitus. |
| 944 | 20814070 | In rats with chronic ulcers, the mRNA expression of HIF-1alpha, IL-1beta and COX-2 was assessed by RT-PCR and protein expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), COX-2 and cNOS was examined by Western blot. |
| 945 | 20814070 | In rats with chronic ulcers, the mRNA expression of HIF-1alpha, IL-1beta and COX-2 was assessed by RT-PCR and protein expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), COX-2 and cNOS was examined by Western blot. |
| 946 | 20814070 | In rats with stress lesions, the protein expression of COX-2, cNOS, catalase, PPAR and heat shock protein 70 (HSP70) was examined by Western blot. |
| 947 | 20814070 | In rats with stress lesions, the protein expression of COX-2, cNOS, catalase, PPAR and heat shock protein 70 (HSP70) was examined by Western blot. |
| 948 | 20814070 | Interestingly, the ulcer healing and gastroprotective effects of pioglitazone were weak under diabetic conditions, and this effect on ulcer healing was accompanied by impaired angiogenesis due to decreased PECAM-1 expression, attenuated expression of COX-2 and the increased expression of proinflammatory cytokines compared to those in diabetic rats treated with vehicle. |
| 949 | 20814070 | Interestingly, the ulcer healing and gastroprotective effects of pioglitazone were weak under diabetic conditions, and this effect on ulcer healing was accompanied by impaired angiogenesis due to decreased PECAM-1 expression, attenuated expression of COX-2 and the increased expression of proinflammatory cytokines compared to those in diabetic rats treated with vehicle. |
| 950 | 20814070 | We conclude that: 1) experimental diabetes in rats impairs healing of chronic ulcers and enhances acute stress lesions due to an increase in the expression and release of proinflammatory cytokines such as TNF-alpha and IL-1beta; 2) the ulcer healing effect of pioglitazone, which is, at least in part, mediated by endogenous NO, is significantly attenuated by L-NNA in diabetic rats despite increased COX-2 expression at the ulcer edge; 3) the formation of acute gastric lesions induced by WRS is also attenuated by pretreatment with pioglitazone due to increased GBF probably mediated by NO, as the administration of L-NNA reversed, in part, the preventive action induced by this PPARgamma ligand, and 4) pioglitazone is effective both in healing of chronic ulcers and protection against WRS lesions though its action under diabetic conditions seems to be attenuated, possibly due to reduction in NOS-NO system, angiogenesis and increased expression and release of proinflammatory cytokines. |
| 951 | 20814070 | We conclude that: 1) experimental diabetes in rats impairs healing of chronic ulcers and enhances acute stress lesions due to an increase in the expression and release of proinflammatory cytokines such as TNF-alpha and IL-1beta; 2) the ulcer healing effect of pioglitazone, which is, at least in part, mediated by endogenous NO, is significantly attenuated by L-NNA in diabetic rats despite increased COX-2 expression at the ulcer edge; 3) the formation of acute gastric lesions induced by WRS is also attenuated by pretreatment with pioglitazone due to increased GBF probably mediated by NO, as the administration of L-NNA reversed, in part, the preventive action induced by this PPARgamma ligand, and 4) pioglitazone is effective both in healing of chronic ulcers and protection against WRS lesions though its action under diabetic conditions seems to be attenuated, possibly due to reduction in NOS-NO system, angiogenesis and increased expression and release of proinflammatory cytokines. |
| 952 | 20814014 | Coronary and aortic endothelial function affected by feedback between adiponectin and tumor necrosis factor α in type 2 diabetic mice. |
| 953 | 20800281 | We examined mouse islets treated overnight with a low-dose cytokine combination commonly associated with inflammation (TNF-alpha, IL-1 beta, and IFN-gamma). |
| 954 | 20795368 | Effect of Cyclea peltata Lam. roots aqueous extract on glucose levels, lipid profile, insulin, TNF-alpha and skeletal muscle glycogen in type 2 diabetic rats. |
| 955 | 20795368 | Effect of Cyclea peltata Lam. roots aqueous extract on glucose levels, lipid profile, insulin, TNF-alpha and skeletal muscle glycogen in type 2 diabetic rats. |
| 956 | 20795368 | In view of multi-dimensional activity of plant drugs beneficial to complex disorders like diabetes, the present study has been undertaken to evaluate the effect of aqueous extract of C. peltata roots on serum glucose, lipid profile, insulin, inflammatory marker namely tumour necrosis factor (TNF)-alpha and muscle glycogen in type 2 diabetic rats. |
| 957 | 20795368 | In view of multi-dimensional activity of plant drugs beneficial to complex disorders like diabetes, the present study has been undertaken to evaluate the effect of aqueous extract of C. peltata roots on serum glucose, lipid profile, insulin, inflammatory marker namely tumour necrosis factor (TNF)-alpha and muscle glycogen in type 2 diabetic rats. |
| 958 | 20720210 | Nasal anti-CD3 induced a LAP(+) regulatory T cell that secreted high levels of IL-10 and suppressed collagen-specific T cell proliferation and anti-collagen Ab production. |
| 959 | 20720210 | Suppression of arthritis by mucosal anti-CD3 was associated with less joint damage, a decrease of TNF-alpha and IFN-gamma mRNA expression in joints, and a reduction in anti-collagen Abs. |
| 960 | 20717728 | Screening of dried plant seed extracts for adiponectin production activity and tumor necrosis factor-alpha inhibitory activity on 3T3-L1 adipocytes. |
| 961 | 20717728 | Screening of dried plant seed extracts for adiponectin production activity and tumor necrosis factor-alpha inhibitory activity on 3T3-L1 adipocytes. |
| 962 | 20717728 | Screening of dried plant seed extracts for adiponectin production activity and tumor necrosis factor-alpha inhibitory activity on 3T3-L1 adipocytes. |
| 963 | 20717728 | Screening of dried plant seed extracts for adiponectin production activity and tumor necrosis factor-alpha inhibitory activity on 3T3-L1 adipocytes. |
| 964 | 20717728 | To search for dried plant seeds with potent anti-diabetes activity, we conducted a large scale screening for inhibitory activity on tumor necrosis factor-alpha and facilitating activity on adiponectin production in vitro. |
| 965 | 20717728 | To search for dried plant seeds with potent anti-diabetes activity, we conducted a large scale screening for inhibitory activity on tumor necrosis factor-alpha and facilitating activity on adiponectin production in vitro. |
| 966 | 20717728 | To search for dried plant seeds with potent anti-diabetes activity, we conducted a large scale screening for inhibitory activity on tumor necrosis factor-alpha and facilitating activity on adiponectin production in vitro. |
| 967 | 20717728 | To search for dried plant seeds with potent anti-diabetes activity, we conducted a large scale screening for inhibitory activity on tumor necrosis factor-alpha and facilitating activity on adiponectin production in vitro. |
| 968 | 20717728 | All adiponectin-production-enhancing seeds except spinach (2.7 pg/ml) and okra (Abelmoschus esculentus) (6.6 pg/ml) effectively decreased tumor necrosis factor-alpha levels (0.0 pg/ml). |
| 969 | 20717728 | All adiponectin-production-enhancing seeds except spinach (2.7 pg/ml) and okra (Abelmoschus esculentus) (6.6 pg/ml) effectively decreased tumor necrosis factor-alpha levels (0.0 pg/ml). |
| 970 | 20717728 | All adiponectin-production-enhancing seeds except spinach (2.7 pg/ml) and okra (Abelmoschus esculentus) (6.6 pg/ml) effectively decreased tumor necrosis factor-alpha levels (0.0 pg/ml). |
| 971 | 20717728 | All adiponectin-production-enhancing seeds except spinach (2.7 pg/ml) and okra (Abelmoschus esculentus) (6.6 pg/ml) effectively decreased tumor necrosis factor-alpha levels (0.0 pg/ml). |
| 972 | 20717728 | These results point to the potential of dried seed extracts as a means to modify the activity of tumor necrosis factor-alpha for the adiponectin production. |
| 973 | 20717728 | These results point to the potential of dried seed extracts as a means to modify the activity of tumor necrosis factor-alpha for the adiponectin production. |
| 974 | 20717728 | These results point to the potential of dried seed extracts as a means to modify the activity of tumor necrosis factor-alpha for the adiponectin production. |
| 975 | 20717728 | These results point to the potential of dried seed extracts as a means to modify the activity of tumor necrosis factor-alpha for the adiponectin production. |
| 976 | 20703212 | The expression of TNF-related apoptosis-inducing ligand (TRAIL), its decoy receptor osteoprotegerin, and receptors Fas (a Fas ligand receptor) and CD74 (a migration inhibitory factor (MIF) receptor) were induced in human diabetic nephropathy. |
| 977 | 20686866 | Polymorphisms in the genes encoding TGF-beta1, TNF-alpha, and IL-6 show association with type 1 diabetes mellitus in the Slovak population. |
| 978 | 20686866 | Polymorphisms in the genes encoding TGF-beta1, TNF-alpha, and IL-6 show association with type 1 diabetes mellitus in the Slovak population. |
| 979 | 20686866 | Polymorphisms in the genes encoding TGF-beta1, TNF-alpha, and IL-6 show association with type 1 diabetes mellitus in the Slovak population. |
| 980 | 20686866 | Furthermore, tumor necrosis factor (TNF)-alpha -308 A allele carriers were also significantly overrepresented among the diabetics (P (c) = 0.0031, OR = 2.62); however, the association of the -308 A allele with T1D might be due to its strong linkage disequilibrium with the susceptibility allele HLA-DRB1*0301. |
| 981 | 20686866 | Furthermore, tumor necrosis factor (TNF)-alpha -308 A allele carriers were also significantly overrepresented among the diabetics (P (c) = 0.0031, OR = 2.62); however, the association of the -308 A allele with T1D might be due to its strong linkage disequilibrium with the susceptibility allele HLA-DRB1*0301. |
| 982 | 20686866 | Furthermore, tumor necrosis factor (TNF)-alpha -308 A allele carriers were also significantly overrepresented among the diabetics (P (c) = 0.0031, OR = 2.62); however, the association of the -308 A allele with T1D might be due to its strong linkage disequilibrium with the susceptibility allele HLA-DRB1*0301. |
| 983 | 20686866 | Moreover, a possible role of TNF-alpha and IL-6 SNPs cannot be ruled out, although their association with T1D was due to strong LD with the HLA class II susceptibility allele or did not withstand statistical correction, respectively. |
| 984 | 20686866 | Moreover, a possible role of TNF-alpha and IL-6 SNPs cannot be ruled out, although their association with T1D was due to strong LD with the HLA class II susceptibility allele or did not withstand statistical correction, respectively. |
| 985 | 20686866 | Moreover, a possible role of TNF-alpha and IL-6 SNPs cannot be ruled out, although their association with T1D was due to strong LD with the HLA class II susceptibility allele or did not withstand statistical correction, respectively. |
| 986 | 20679400 | Low-dose IL-2 increases the number of T reg cells in the pancreas and induces expression of T reg cell-associated proteins including Foxp3, CD25, CTLA-4, ICOS (inducible T cell costimulator), and GITR (glucocorticoid-induced TNF receptor) in these cells. |
| 987 | 20675566 | Resveratrol increased NO production by enhancing endothelial NO synthase (eNOS) expression and reduced O(2)(·-) production by inhibiting NAD(P)H oxidase activity and gp91(phox) mRNA and protein expression. |
| 988 | 20675566 | The increased nitrotyrosine (N-Tyr) protein expression in Lepr(db) mice was prevented by the inducible NO synthase (iNOS) inhibitor 1400W. |
| 989 | 20675566 | Resveratrol reduced both N-Tyr and iNOS expression in Lepr(db) mice. |
| 990 | 20675566 | Both Lepr(db) mice null for TNF-α (db(TNF-)/db(TNF-) mice) and Lepr(db) mice treated with the NF-κB inhibitor MG-132 showed decreased NAD(P)H oxidase activity and iNOS expression as well as elevated eNOS expression, whereas m-Lepr(db) mice treated with TNF-α showed the opposite effects. |
| 991 | 20675566 | This improvement is due to the role of resveratrol in inhibiting TNF-α-induced NF-κB activation, therefore subsequently inhibiting the expression and activation of NAD(P)H oxidase and iNOS as well as increasing eNOS expression in type 2 diabetes. |
| 992 | 20674184 | Many studies have provided evidence for a role of inflammation and inflammatory cytokines such as tumour necrosis factor (TNF)-α and interleukin (IL)-1β in the vascular calcification process. |
| 993 | 20674184 | TNF-α and IL-1β have indeed been shown to stimulate in vitro the expression by vascular smooth muscle cells (VSMCs) of tissue-non specific alkaline phosphatase (TNAP), a key enzyme in the mineralization process, and to trigger the trans-differentiation of VSMCs into osteoblast-like cells, expressing the master transcription factor RUNX2. |
| 994 | 20674184 | We propose that cytokines block bone formation by decreasing RUNX2-mediated type I collagen production in osteoblasts, whereas they induce vascular ossification by the mere stimulation of TNAP by VSMCs, independently of RUNX2. |
| 995 | 20674184 | We propose that this stimulation of TNAP in VSMCs in vitro and in vivo may be sufficient to induce the calcification of collagen fibrils, and that the absence of crystal clearance, in turn, induces the differentiation of VSMCs and/or mesenchymal stem cells into bone-forming cells, eventually leading to formation of a bone-like tissue. |
| 996 | 20665664 | Hepatic expression profiling shows involvement of PKC epsilon, DGK eta, Tnfaip, and Rho kinase in type 2 diabetic nephropathy rats. |
| 997 | 20665664 | Gene expression profiling data revealed dramatic increase in expression of PKC epsilon, TNF-alpha-induced protein (four- to seven-folds), and decrease in the expression of DGK eta in the liver of diabetic nephropathic rats. |
| 998 | 20665664 | To the best of our knowledge, this is the first report which shows the involvement of PKC epsilon, DGK eta, Tnfaip, and Rho kinase in the liver of type 2 diabetic rats and its association with diabetic nephropathy. |
| 999 | 20655188 | HG significantly induced histone acetylation, NF-κB activity and proinflammatory cytokine (interleukin 6, tumor necrosis factor α and MCP-1) release from THP-1 cells. |
| 1000 | 20655188 | Also, since p300 histone acetyltransferase is a coactivator of NF-κB, we examined its acetylation. |
| 1001 | 20655188 | Curcumin treatment also significantly reduced HAT activity, level of p300 and acetylated CBP/p300 gene expression, and induced HDAC2 expression by curcumin. |
| 1002 | 20649096 | Pro-insulin, C peptide, glucagon, adiponectin, TNF alpha, AMPK: neglected players in type 2 diabetes mellitus. |
| 1003 | 20649096 | Pro-insulin, C peptide, glucagon, adiponectin, TNF alpha, AMPK: neglected players in type 2 diabetes mellitus. |
| 1004 | 20649096 | This article emphasizes (1) the utility of routine measurement of pro-insulin to insulin ratio as a specific marker of insulin resistance and predictor of future T2DM, HT and CAD, (2) routine C-Peptide estimation to determine which T2DM needs insulin and to monitor the effect of newer drugs which promote beta cell regeneration, (3) routine estimation of adiponectin and TNF alpha and monitor response to thiozolidine drugs which increases adiponectin and decreases TNF alpha production by adipocytes, (4) crucial role of AMPK--Cellular energy sensor in mediating the beneficial effects of exercise as well as drugs (adiponectin, metformin) in T2DM, (5) Availability of glucogon suppressors will eliminate the need for giving insulin to T2 DM with normal C Pepetide levels which inevitably causes undesirable weight gain & hypoglycemia. |
| 1005 | 20649096 | This article emphasizes (1) the utility of routine measurement of pro-insulin to insulin ratio as a specific marker of insulin resistance and predictor of future T2DM, HT and CAD, (2) routine C-Peptide estimation to determine which T2DM needs insulin and to monitor the effect of newer drugs which promote beta cell regeneration, (3) routine estimation of adiponectin and TNF alpha and monitor response to thiozolidine drugs which increases adiponectin and decreases TNF alpha production by adipocytes, (4) crucial role of AMPK--Cellular energy sensor in mediating the beneficial effects of exercise as well as drugs (adiponectin, metformin) in T2DM, (5) Availability of glucogon suppressors will eliminate the need for giving insulin to T2 DM with normal C Pepetide levels which inevitably causes undesirable weight gain & hypoglycemia. |
| 1006 | 20646763 | CD40 glycoforms and TNF-receptors 1 and 2 in the formation of CD40 receptor(s) in autoimmunity. |
| 1007 | 20646763 | CD40 glycoforms and TNF-receptors 1 and 2 in the formation of CD40 receptor(s) in autoimmunity. |
| 1008 | 20646763 | We described a CD4(+)CD40(+) T cell (Th40) subset which is expanded in autoimmunity and is necessary and sufficient in transferring type 1 diabetes. |
| 1009 | 20646763 | We described a CD4(+)CD40(+) T cell (Th40) subset which is expanded in autoimmunity and is necessary and sufficient in transferring type 1 diabetes. |
| 1010 | 20646763 | Here we demonstrate that several CD40 receptor constellations exist on CD4 T cells. |
| 1011 | 20646763 | Here we demonstrate that several CD40 receptor constellations exist on CD4 T cells. |
| 1012 | 20646763 | Interestingly, CD40 stimulation induces some CD40 receptor constellations that contain TNF-receptors 1 and 2 and targeting of those alters CD40 signaling outcomes in NOD Th40 cells. |
| 1013 | 20646763 | Interestingly, CD40 stimulation induces some CD40 receptor constellations that contain TNF-receptors 1 and 2 and targeting of those alters CD40 signaling outcomes in NOD Th40 cells. |
| 1014 | 20633104 | Diminished serotonin production is associated with mental depression while increased formation of kynurenines might contribute to development of MetS/AAND via their apoptotic, neurotoxic, and pro-oxidative effects, and upregulation of inducible nitric oxide synthase, phospholipase A2, arachidonic acid, prostaglandin, 5-lipoxygenase, and leukotriene cascade. |
| 1015 | 20633104 | The combined presence of high producers of alleles of polymorphic PIC genes (e.g., interferon-gamma and tumor necrosis factor alpha) might account for the genetic predisposition to high levels of PIC production, leading to "superinduction" of IDO. |
| 1016 | 20632297 | Serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and adiponectin were measured by enzyme-linked immunosorbent assay. |
| 1017 | 20620534 | We evaluated the islet xenograft mean survival time as well as changes in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) levels in transplanted mice. |
| 1018 | 20620534 | We evaluated the islet xenograft mean survival time as well as changes in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) levels in transplanted mice. |
| 1019 | 20620534 | Within 1 week after transplantation the levels of IL-2 and TNF-alpha showed sharp increases in the untreated group, being significantly higher than those observed prior to transplantation. |
| 1020 | 20620534 | Within 1 week after transplantation the levels of IL-2 and TNF-alpha showed sharp increases in the untreated group, being significantly higher than those observed prior to transplantation. |
| 1021 | 20608029 | The results of our studies testify that insulin resistance in patients with MS and type 2 DM is associated by the decrease in the level of adiponectin and increase in the level of resistin. |
| 1022 | 20608029 | Lower level of adiponectin and higher level of resistin in blood serum can be examined as markers of the metabolic syndrome. |
| 1023 | 20608029 | Content of adiponectin in blood serum negatively correlates with an insulin resistance index HOMA IR, the level of TSH, proinflammatory cytokines-tumor necrosis factor alpha (TNFa) and cortisol. |
| 1024 | 20608029 | The author showed direct correlations between the TSH level and proinflammatory cytokines--TNFalpha, IL-6, CRP and negative correlations between HOMA IR indexes and iodinuria. |
| 1025 | 20599720 | Pharmacologic experiments suggested that TRPV family members, but neither TRPC nor TRPM family members, are involved in the LPS-induced TNFalpha and IL-6 production in RAW264 macrophages. |
| 1026 | 20599720 | Pharmacologic experiments suggested that TRPV family members, but neither TRPC nor TRPM family members, are involved in the LPS-induced TNFalpha and IL-6 production in RAW264 macrophages. |
| 1027 | 20599720 | Pharmacologic experiments suggested that TRPV family members, but neither TRPC nor TRPM family members, are involved in the LPS-induced TNFalpha and IL-6 production in RAW264 macrophages. |
| 1028 | 20599720 | Pharmacologic experiments suggested that TRPV family members, but neither TRPC nor TRPM family members, are involved in the LPS-induced TNFalpha and IL-6 production in RAW264 macrophages. |
| 1029 | 20599720 | ShRNA against TRPV2 inhibited the LPS-induced TNFalpha and IL-6 production as well as IkappaBalpha degradation. |
| 1030 | 20599720 | ShRNA against TRPV2 inhibited the LPS-induced TNFalpha and IL-6 production as well as IkappaBalpha degradation. |
| 1031 | 20599720 | ShRNA against TRPV2 inhibited the LPS-induced TNFalpha and IL-6 production as well as IkappaBalpha degradation. |
| 1032 | 20599720 | ShRNA against TRPV2 inhibited the LPS-induced TNFalpha and IL-6 production as well as IkappaBalpha degradation. |
| 1033 | 20599720 | BAPTA/AM abolished LPS-induced TNFalpha and IL-6 production, while EGTA only partially suppressed LPS-induced IL-6 production, but not TNFalpha production. |
| 1034 | 20599720 | BAPTA/AM abolished LPS-induced TNFalpha and IL-6 production, while EGTA only partially suppressed LPS-induced IL-6 production, but not TNFalpha production. |
| 1035 | 20599720 | BAPTA/AM abolished LPS-induced TNFalpha and IL-6 production, while EGTA only partially suppressed LPS-induced IL-6 production, but not TNFalpha production. |
| 1036 | 20599720 | BAPTA/AM abolished LPS-induced TNFalpha and IL-6 production, while EGTA only partially suppressed LPS-induced IL-6 production, but not TNFalpha production. |
| 1037 | 20599720 | In addition to Ca2+ mobilization through the IP3-receptor, TRPV2-mediated intracellular Ca2+ mobilization is involved in NFkappaB-dependent TNFalpha and IL-6 expression, while extracellular Ca2+ entry is involved in NFkappaB-independent IL-6 production. |
| 1038 | 20599720 | In addition to Ca2+ mobilization through the IP3-receptor, TRPV2-mediated intracellular Ca2+ mobilization is involved in NFkappaB-dependent TNFalpha and IL-6 expression, while extracellular Ca2+ entry is involved in NFkappaB-independent IL-6 production. |
| 1039 | 20599720 | In addition to Ca2+ mobilization through the IP3-receptor, TRPV2-mediated intracellular Ca2+ mobilization is involved in NFkappaB-dependent TNFalpha and IL-6 expression, while extracellular Ca2+ entry is involved in NFkappaB-independent IL-6 production. |
| 1040 | 20599720 | In addition to Ca2+ mobilization through the IP3-receptor, TRPV2-mediated intracellular Ca2+ mobilization is involved in NFkappaB-dependent TNFalpha and IL-6 expression, while extracellular Ca2+ entry is involved in NFkappaB-independent IL-6 production. |
| 1041 | 20586146 | Evaluation of the relationship between insulin resistance and plasma tumor necrosis factor-alpha, interleukin-6 and C-reactive protein levels in obese women. |
| 1042 | 20560108 | We evaluated body weight, body mass index (BMI), glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), fasting plasma insulin (FPI), homeostasis model assessment insulin resistance index (HOMA-IR), homeostasis model assessment beta-cell function index (HOMA-beta), fasting plasma proinsulin (FPPr), proinsulin/fasting plasma insulin ratio (Pr/FPI ratio), adiponectin (ADN), resistin (R), tumor necrosis factor-alpha (TNF-alpha), and high sensitivity C-reactive protein (Hs-CRP) at their baseline values, and after 3, 6, 9, and 12 months of treatment. |
| 1043 | 20560108 | We evaluated body weight, body mass index (BMI), glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), fasting plasma insulin (FPI), homeostasis model assessment insulin resistance index (HOMA-IR), homeostasis model assessment beta-cell function index (HOMA-beta), fasting plasma proinsulin (FPPr), proinsulin/fasting plasma insulin ratio (Pr/FPI ratio), adiponectin (ADN), resistin (R), tumor necrosis factor-alpha (TNF-alpha), and high sensitivity C-reactive protein (Hs-CRP) at their baseline values, and after 3, 6, 9, and 12 months of treatment. |
| 1044 | 20560108 | Fasting plasma insulin, FPPr, Pr/FPI ratio, R, and TNF-alpha were significantly decreased and ADN was significantly increased with pioglitazone plus vildagliptin, but not with glimepiride plus vildagliptin. |
| 1045 | 20560108 | Fasting plasma insulin, FPPr, Pr/FPI ratio, R, and TNF-alpha were significantly decreased and ADN was significantly increased with pioglitazone plus vildagliptin, but not with glimepiride plus vildagliptin. |
| 1046 | 20559450 | We hypothesized that impairment in coronary endothelial function in type 2 diabetes is due to the overexpression of TNF and TNF receptors (TNFRs). |
| 1047 | 20559450 | We hypothesized that impairment in coronary endothelial function in type 2 diabetes is due to the overexpression of TNF and TNF receptors (TNFRs). |
| 1048 | 20559450 | We hypothesized that impairment in coronary endothelial function in type 2 diabetes is due to the overexpression of TNF and TNF receptors (TNFRs). |
| 1049 | 20559450 | We hypothesized that impairment in coronary endothelial function in type 2 diabetes is due to the overexpression of TNF and TNF receptors (TNFRs). |
| 1050 | 20559450 | Neutralizing antibodies to TNF, or blockade of NAD(P)H and xanthine oxidase, partially restored endothelium-dependent, NO-mediated vasodilation in isolated coronary arteries in ZDF rats, but anti-TNF did not alter endothelium-dependent vasodilation in lean rats. |
| 1051 | 20559450 | Neutralizing antibodies to TNF, or blockade of NAD(P)H and xanthine oxidase, partially restored endothelium-dependent, NO-mediated vasodilation in isolated coronary arteries in ZDF rats, but anti-TNF did not alter endothelium-dependent vasodilation in lean rats. |
| 1052 | 20559450 | Neutralizing antibodies to TNF, or blockade of NAD(P)H and xanthine oxidase, partially restored endothelium-dependent, NO-mediated vasodilation in isolated coronary arteries in ZDF rats, but anti-TNF did not alter endothelium-dependent vasodilation in lean rats. |
| 1053 | 20559450 | Neutralizing antibodies to TNF, or blockade of NAD(P)H and xanthine oxidase, partially restored endothelium-dependent, NO-mediated vasodilation in isolated coronary arteries in ZDF rats, but anti-TNF did not alter endothelium-dependent vasodilation in lean rats. |
| 1054 | 20559450 | The mRNA expression of TNF receptor 1 (TNFR1, but not TNFR2) significantly increased in coronary arteries in ZDF rats. |
| 1055 | 20559450 | The mRNA expression of TNF receptor 1 (TNFR1, but not TNFR2) significantly increased in coronary arteries in ZDF rats. |
| 1056 | 20559450 | The mRNA expression of TNF receptor 1 (TNFR1, but not TNFR2) significantly increased in coronary arteries in ZDF rats. |
| 1057 | 20559450 | The mRNA expression of TNF receptor 1 (TNFR1, but not TNFR2) significantly increased in coronary arteries in ZDF rats. |
| 1058 | 20559450 | These results demonstrate the endothelial dysfunction occurring in type 2 diabetes is the result of effects of the inflammatory cytokine TNF that activates NAD(P)H oxidase and xanthine oxidase; and perhaps acts mainly through the overexpression of TNFR1. |
| 1059 | 20559450 | These results demonstrate the endothelial dysfunction occurring in type 2 diabetes is the result of effects of the inflammatory cytokine TNF that activates NAD(P)H oxidase and xanthine oxidase; and perhaps acts mainly through the overexpression of TNFR1. |
| 1060 | 20559450 | These results demonstrate the endothelial dysfunction occurring in type 2 diabetes is the result of effects of the inflammatory cytokine TNF that activates NAD(P)H oxidase and xanthine oxidase; and perhaps acts mainly through the overexpression of TNFR1. |
| 1061 | 20559450 | These results demonstrate the endothelial dysfunction occurring in type 2 diabetes is the result of effects of the inflammatory cytokine TNF that activates NAD(P)H oxidase and xanthine oxidase; and perhaps acts mainly through the overexpression of TNFR1. |
| 1062 | 20558911 | The WY14643-treated mice showed reduced body weight and blood glucose, improved myocardial pathological changes, lower cardiac TNF-alpha expression, and significantly higher adiponectin expression, whereas the LW/LC ratio was lower and cardiac UCP3 mRNA expression higher in the WY14643 treatment groups than in the vehicle group on day 4. |
| 1063 | 20558911 | The cardioprotective effect may be due to its anti-inflammatory properties and its ability to increase cardiac adiponectin expression, whereas the reduced cardiac efficiency may be due to its enhancement of cardiac UCP3 mRNA expression. |
| 1064 | 20558773 | In previous work, we found that toxic AGEs, AGE-2 and AGE-3, induced the expression of intracellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, production of interferon-gamma and tumor necrosis factor alpha, and lymphocyte proliferation during human mixed lymphocyte reaction. |
| 1065 | 20558773 | The effects of PGE2 were mimicked by an EP2 receptor agonist, ONO-AE1-259-01 (11,15-O-dimethyl PGE2), and an EP4 receptor agonist, ONO-AE1-329 [16-(3-methoxymethyl)phenyl-omega-tetranor-3,7dithia PGE1]. |
| 1066 | 20558773 | An EP2 receptor antagonist, AH6809 (6-isopropoxy-9-oxaxanthene-2-carboxylic acid), and an EP4 receptor antagonist, AH23848 [(4Z)-7-[(rel-1S,2S,5R)-5-((1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid], inhibited the actions of PGE2. |
| 1067 | 20558773 | The stimulation of EP2 and EP4 receptors is reported to increase cAMP levels. |
| 1068 | 20558773 | The effects of PGE2 were reversed by protein kinase A (PKA) inhibitors and mimicked by dibutyryl cAMP and an adenylate cyclase activator, forskolin. |
| 1069 | 20558773 | These results as a whole indicate that PGE2 inhibited the actions of AGE-2 and AGE-3 via EP2/EP4 receptors and the cAMP/PKA pathway. |
| 1070 | 20555424 | Regulation of IRS-2 signaling by IGF-1 receptor in the diabetic rat heart. |
| 1071 | 20555424 | Since insulin/insulin-like growth factor 1 receptor (IGF-1R) can activate vascular endothelial growth factor to promote vascular growth, reduced IGF-1R signaling in the type I diabetic heart could be detrimental, leading to reduced, collateral blood vessel growth. |
| 1072 | 20555424 | Diabetes increased TNF-alpha, interleukin-6 (IL-6), and IL-1alpha levels in the heart. |
| 1073 | 20555424 | JNK and p42/p44 activity was significantly increased in the diabetic heart, while IGF-1R phosphorylation, IRS-2 tyrosine phosphorylation, and Akt activities were reduced. |
| 1074 | 20555424 | These results suggest that diabetes activates multiple inflammatory markers in the heart, which then signal a decrease in the activities of key players in the insulin-signaling cascade, namely IGF-1R, IRS-2, and Akt, to regulate apoptosis. |
| 1075 | 20529823 | The aim of our study was to test the hypothesis that T regulatory cells express pro- and anti-inflammatory cytokines, elements of cytotoxicity and OX40/4-1BB molecules. |
| 1076 | 20529823 | Concurrently with the flow cytometric assessment of Tregs we separated CD4+CD25+CD127dim/- cells for further mRNA analysis. mRNA levels for transcription factor FoxP3, pro- and anti-inflammatory cytokines (interferon gamma, interleukin-2, interleukin-4, interleukin-10, transforming growth factor beta1 and tumor necrosis factor alpha), activatory molecules (OX40, 4-1BB) and elements of cytotoxicity (granzyme B, perforin 1) were determined by real-time PCR technique. |
| 1077 | 20529823 | Lower OX40 and higher 4-1BB mRNA but not protein levels in Treg cells in diabetic patients compared to the healthy children were noted. |
| 1078 | 20529823 | Our observations confirm the presence of mRNA for pro- and anti-inflammatory cytokines in CD4+CD25+CD127dim/- cells in the peripheral blood of children with T1DM. |
| 1079 | 20521979 | All 21 subset samples inhibited TNFalpha-stimulated free fatty acid release and attenuated TNFalpha inhibition of adiponectin secretion. |
| 1080 | 20519551 | Peroxisome proliferator-activated receptor (PPAR)-gamma modulators, a class of antidiabetic drugs, have been associated with cardiovascular risks in type 2 diabetes in humans. |
| 1081 | 20519551 | Biomarkers for potential cardiovascular risks were assessed, including 1) ultrasound for cardiac structure and function; 2) neuroendocrine and hormonal plasma biomarkers of cardiovascular risk; 3) pharmacogenomic profiling of cardiac and renal tissue by targeted tissue low-density gene array representing ion channels and transporters, and components of the renin-angiotensin-aldosterone system; and 4) immunohistochemistry for cardiac fibrosis, hypertrophy, and inflammation (macrophages and tumor necrosis factor-alpha). |
| 1082 | 20519180 | Advanced glycation endproducts increase the activity of the nuclear-factor kappa-B, as well as the production of vasoactive factors and cytokines (interleukin-1, -6, tumor necrosis factor alpha). |
| 1083 | 20519180 | On one hand, transketolase-activator benfotiamine inhibits alternative pathways induced by hyperglycemia (the polyol-, hexosamine-, diacilglycerol protein kinase-C-, and advanced glycation pathways), while, on the other hand, it increases the activity of the pentose-phosphate-shunt. |
| 1084 | 20512929 | Our findings also demonstrate that berberine significantly down-regulates LPS- or interferon (IFN)-gamma-induced nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) expression in BV-2 microglia cells. |
| 1085 | 20512929 | Berberine also inhibited LPS- or IFN-gamma-induced nitric oxide production. |
| 1086 | 20512929 | In addition, berberine effectively inhibited proinflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6 expression. |
| 1087 | 20512929 | On the other hand, upon various inflammatory stimulus including LPS and IFN-gamma, berberine suppressed the phosphorylated of ERK but not p38 and JNK in BV-2 microglia. |
| 1088 | 20512929 | AMPK activation is catalyzed by upstream kinases such as LKB1 and Ca2+/calmodulin-dependent protein kinase kinase-II (CaMKK II). |
| 1089 | 20512929 | Moreover, berberine induced LKB1 (Ser428), CaMKII (Thr286), and AMPK (Thr172) phosphorylation, but not AMPK (Ser485). |
| 1090 | 20512929 | Furthermore, the inhibitory effect of berberine on iNOS and COX-2 expression was abolished by AMPK inhibition via Compound C, an AMPK inhibitor. |
| 1091 | 20508722 | A common denominator of these chronic conditions is the enhanced the levels of cytokines like tumour necrosis factor-alpha (TNF-alpha), interleukin (IL-6), IL-1beta and resistin, which in turn activates the c-Jun-N-terminal kinase (JNK) and NF-kappaB pathways, creating a vicious cycle that exacerbates insulin resistance, type-2 diabetes and related complications. |
| 1092 | 20508722 | Importantly, the HO system abates inflammation through several mechanisms including the suppression of macrophage-infiltration and abrogation of oxidative/inflammatory transcription factors like NF-kappaB, JNK and activating protein-1. |
| 1093 | 20501676 | Changes in gene and protein expression of cytokines, CD8 markers, monocyte chemoattractant protein-1, inducible NO synthase, and caspase 3 were evaluated. |
| 1094 | 20501676 | However, six of 12 treated animals showed increased gene expression of IL-1beta, TNF-alpha, and CD8 markers in pancreas-draining lymph nodes, indicating immune cell activation. |
| 1095 | 20501675 | Contribution of TNF-alpha and nuclear factor-kappaB signaling to type 2 iodothyronine deiodinase activation in the mediobasal hypothalamus after lipopolysaccharide administration. |
| 1096 | 20501675 | Contribution of TNF-alpha and nuclear factor-kappaB signaling to type 2 iodothyronine deiodinase activation in the mediobasal hypothalamus after lipopolysaccharide administration. |
| 1097 | 20501675 | Contribution of TNF-alpha and nuclear factor-kappaB signaling to type 2 iodothyronine deiodinase activation in the mediobasal hypothalamus after lipopolysaccharide administration. |
| 1098 | 20501675 | To determine whether signaling through TNF and/or nuclear factor-kappaB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Ikappa-Balpha expression in tanycytes were studied. |
| 1099 | 20501675 | To determine whether signaling through TNF and/or nuclear factor-kappaB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Ikappa-Balpha expression in tanycytes were studied. |
| 1100 | 20501675 | To determine whether signaling through TNF and/or nuclear factor-kappaB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Ikappa-Balpha expression in tanycytes were studied. |
| 1101 | 20501675 | Animals treated with soluble, rat, polyethylene glycol-conjugated TNF receptor type 1 (4 mg/kg body weight) before a single ip injection of LPS showed a significant reduction in circulating IL-6 levels but no effect on LPS-induced D2 mRNA in the majority of tanycytes with the exception of a subpopulation of alpha tanycytes in the wall of the third ventricle. |
| 1102 | 20501675 | Animals treated with soluble, rat, polyethylene glycol-conjugated TNF receptor type 1 (4 mg/kg body weight) before a single ip injection of LPS showed a significant reduction in circulating IL-6 levels but no effect on LPS-induced D2 mRNA in the majority of tanycytes with the exception of a subpopulation of alpha tanycytes in the wall of the third ventricle. |
| 1103 | 20501675 | Animals treated with soluble, rat, polyethylene glycol-conjugated TNF receptor type 1 (4 mg/kg body weight) before a single ip injection of LPS showed a significant reduction in circulating IL-6 levels but no effect on LPS-induced D2 mRNA in the majority of tanycytes with the exception of a subpopulation of alpha tanycytes in the wall of the third ventricle. |
| 1104 | 20501675 | The LPS-induced increase in Ikappa-Balpha in the pars tuberalis was associated with increased TSHbeta gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of alpha tanycytes. |
| 1105 | 20501675 | The LPS-induced increase in Ikappa-Balpha in the pars tuberalis was associated with increased TSHbeta gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of alpha tanycytes. |
| 1106 | 20501675 | The LPS-induced increase in Ikappa-Balpha in the pars tuberalis was associated with increased TSHbeta gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of alpha tanycytes. |
| 1107 | 20499416 | Tumor necrosis factor (TNF-alpha) and C-reactive protein (CRP) are positively associated with the risk of chronic kidney disease in patients with type 2 diabetes. |
| 1108 | 20493839 | Western blotting was done for insulin receptor signaling and Akt and ELISA analyses for TNFalpha concentration and cleavage of caspase 3 at 2- and 8-months of diabetes. |
| 1109 | 20483768 | The TNF alpha-induced protein 3 (TNFAIP3) is an ubiquitin-modifying enzyme and an essential negative regulator of inflammation. |
| 1110 | 20481343 | These are achieved predominantly through release of adipocytokines, which include several novel molecules released by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells, like TNF-alpha and IL-6. |
| 1111 | 20481316 | Serum creatine (Scr) and 24 hours urine protein, cross reaction protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured at the end of the study. |
| 1112 | 20481316 | Serum creatine (Scr) and 24 hours urine protein, cross reaction protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured at the end of the study. |
| 1113 | 20481316 | The mRNA of transforming growth factor-beta1 (TGF-beta1) was measured by real-time PCR (RT-PCR), and the protein expression of TGF-beta1 was surveyed by Enzyme-Linked Immunosorbent Assay (ELISA). |
| 1114 | 20481316 | The mRNA of transforming growth factor-beta1 (TGF-beta1) was measured by real-time PCR (RT-PCR), and the protein expression of TGF-beta1 was surveyed by Enzyme-Linked Immunosorbent Assay (ELISA). |
| 1115 | 20481316 | The renal pathological changes in DN rats given ginsenoside Rg1 treatment were ameliorated, and the expression levels of 24 h urine protein, serum creatinine, CRP, TNF-alpha, ED-1 and TGF-beta1 were significantly lower than those in the diabetic nephropathy group (P < 0.05). |
| 1116 | 20481316 | The renal pathological changes in DN rats given ginsenoside Rg1 treatment were ameliorated, and the expression levels of 24 h urine protein, serum creatinine, CRP, TNF-alpha, ED-1 and TGF-beta1 were significantly lower than those in the diabetic nephropathy group (P < 0.05). |
| 1117 | 20464496 | Incubation of betaTC-6 cells with cytokine mixture (IL-1beta, TNF-alpha, and IFN-gamma) or exogenous peroxynitrite significantly increased apoptotic cell percentage, elevated PTEN and p-PTEN levels, and inhibited Akt activation. |
| 1118 | 20464496 | Transfection with PTEN-specific siRNA protected betaTC-6 cells from cytokine or peroxynitrite-mediated cell apoptosis and partially reversed Akt inhibition. |
| 1119 | 20464496 | Preventing peroxynitrite formation by administrating NAC/L: -NMMA, or scavenging peroxynitrite directly by UA, attenuated cytokine-induced PTEN upregulation, Akt inhibition, and beta-cell apoptosis. |
| 1120 | 20460908 | The pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are critically involved in the pathophysiology of various aspects of human NAFLD. |
| 1121 | 20460908 | The pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are critically involved in the pathophysiology of various aspects of human NAFLD. |
| 1122 | 20460908 | The pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) are critically involved in the pathophysiology of various aspects of human NAFLD. |
| 1123 | 20460908 | Serum levels of this cytokine correlate remarkably well with the presence of IR, and adipose tissue-derived IL-6 has been shown to regulate hepatic IR via upregulation of SOCS3. |
| 1124 | 20460908 | Serum levels of this cytokine correlate remarkably well with the presence of IR, and adipose tissue-derived IL-6 has been shown to regulate hepatic IR via upregulation of SOCS3. |
| 1125 | 20460908 | Serum levels of this cytokine correlate remarkably well with the presence of IR, and adipose tissue-derived IL-6 has been shown to regulate hepatic IR via upregulation of SOCS3. |
| 1126 | 20460908 | Adiponectin is a potent TNF-alpha-neutralizing and anti-inflammatory adipocytokine, and in vitro and experimental animal studies have proven the importance of this mediator in counteracting inflammation and IR. |
| 1127 | 20460908 | Adiponectin is a potent TNF-alpha-neutralizing and anti-inflammatory adipocytokine, and in vitro and experimental animal studies have proven the importance of this mediator in counteracting inflammation and IR. |
| 1128 | 20460908 | Adiponectin is a potent TNF-alpha-neutralizing and anti-inflammatory adipocytokine, and in vitro and experimental animal studies have proven the importance of this mediator in counteracting inflammation and IR. |
| 1129 | 20460908 | Anti-inflammatory effects of adiponectin are mediated via suppression of TNF-alpha synthesis as well as induction of anti-inflammatory cytokines such as IL-10 or IL-1 receptor antagonist. |
| 1130 | 20460908 | Anti-inflammatory effects of adiponectin are mediated via suppression of TNF-alpha synthesis as well as induction of anti-inflammatory cytokines such as IL-10 or IL-1 receptor antagonist. |
| 1131 | 20460908 | Anti-inflammatory effects of adiponectin are mediated via suppression of TNF-alpha synthesis as well as induction of anti-inflammatory cytokines such as IL-10 or IL-1 receptor antagonist. |
| 1132 | 20452384 | In contrast, high glucose, insulin or EGF failed to affect ACE expression. |
| 1133 | 20452384 | The effect of TNF-alpha was abated by etanercept, the IKK2 inhibitor TPCA-1, or a p38 inhibitor while that of PMA was reduced by inhibitors of PKC isoforms sensitive to phorbol esters and calcium. |
| 1134 | 20452384 | The short-term PKC- and MEK1-dependent increase of c-Fos expression was best correlated to PMA-induced ACE upregulation. |
| 1135 | 20451496 | TRAIL upregulates decoy receptor 1 and mediates resistance to apoptosis in insulin-secreting INS-1 cells. |
| 1136 | 20451496 | TRAIL/Apo2L (tumor necrosis factor-related apoptosis-inducing ligand) is a multifunctional protein regulating the homeostasis of the immune system, infection, autoimmune diseases, and apoptosis. |
| 1137 | 20451496 | A previous study found that TRAIL did not have significant cytotoxic effects on the insulin-secreting pancreatic beta cell line, INS-1. |
| 1138 | 20451496 | TRAIL treatment showed NF-kappaB translocation to the nucleus in TRAIL-resistant INS-1 cells, and TRAIL-induced NF-kappaB activation was preceded by IkappaBalpha degradation. |
| 1139 | 20451496 | A pharmacological inhibitor of NF-kappaB, Bay 11-7082, blocked TRAIL-induced NF-kappaB translocation to the nucleus and IkappaBalpha degradation. |
| 1140 | 20451496 | Four related receptors bind TRAIL: two death receptors (DR4 and DR5) that promote apoptosis, and two decoy receptors (DcR1 and DcR2) that act as dominant-negative inhibitors of TRAIL-mediated apoptosis. |
| 1141 | 20451496 | In the present study, TRAIL treatment in INS-1 cells upregulated DcR1 and downregulated DR5 without altering the expression of DcR2 and DR4. |
| 1142 | 20451496 | The resistance to apoptosis in INS-1 cells might therefore, be a consequence of DcR1 upregulation and DR5 downregulation, and the transcription factor, NF-kappaB, could regulate the sensitivity of cells to TRAIL by controlling the ratio of decoy to death receptors. |
| 1143 | 20451496 | Thus, TRAIL may play an important role in the survival of pancreatic beta cells by regulating receptor expression in an NF-kappaB-dependent manner. |
| 1144 | 20442404 | R-spondin-1 is a novel beta-cell growth factor and insulin secretagogue. |
| 1145 | 20442404 | R-spondin-1 (Rspo1) is an intestinal growth factor known to exert its effects through activation of the canonical Wnt (cWnt) signaling pathway and subsequent expression of cWnt target genes. |
| 1146 | 20442404 | Rspo1 activated cWnt signaling in MIN6 beta-cells by increasing nuclear beta-catenin and c-myc, a cWnt target gene. |
| 1147 | 20442404 | Rspo1 also induced insulin mRNA expression in MIN6 cells. |
| 1148 | 20442404 | Incubation of MIN6 and mouse beta-cells with cytokines (IL1beta/TNFalpha/interferon-gamma) significantly increased cellular apoptosis; this increase was abolished by pretreatment with Rspo1. |
| 1149 | 20442404 | Rspo1 also stimulated insulin secretion in a glucose-independent fashion. |
| 1150 | 20442404 | We further demonstrated that the glucagon-like peptide-1 receptor agonist, exendin4 (EX4), stimulated Rspo1 mRNA transcript levels in MIN6 cells in a glucose-, time-, dose-, and PI3-kinase-dependent fashion. |
| 1151 | 20442404 | Together, these studies demonstrate that Rspo1 is a novel beta-cell growth factor and insulin secretagogue that is regulated by EX4. |
| 1152 | 20442402 | Orosomucoid (ORM), also called alpha-1 acid glycoprotein, is an abundant plasma protein that is an immunomodulator induced by stressful conditions such as infections. |
| 1153 | 20442402 | Orosomucoid (ORM), also called alpha-1 acid glycoprotein, is an abundant plasma protein that is an immunomodulator induced by stressful conditions such as infections. |
| 1154 | 20442402 | Adipose Orm levels were elevated by metabolic signals, including insulin, high glucose, and free fatty acid, as well as by the proinflammatory cytokine tumor necrosis factor-alpha, which is found in increased levels in the adipose tissue of morbid obese subjects. |
| 1155 | 20442402 | Adipose Orm levels were elevated by metabolic signals, including insulin, high glucose, and free fatty acid, as well as by the proinflammatory cytokine tumor necrosis factor-alpha, which is found in increased levels in the adipose tissue of morbid obese subjects. |
| 1156 | 20442402 | In both adipocytes and macrophages, ORM suppressed proinflammatory gene expression and pathways such as NF-kappaB and mitogen-activated protein kinase signalings and reactive oxygen species generation. |
| 1157 | 20442402 | In both adipocytes and macrophages, ORM suppressed proinflammatory gene expression and pathways such as NF-kappaB and mitogen-activated protein kinase signalings and reactive oxygen species generation. |
| 1158 | 20442402 | Concomitantly, ORM relieved hyperglycemia-induced insulin resistance as well as tumor necrosis factor-alpha-mediated lipolysis in adipocytes. |
| 1159 | 20442402 | Concomitantly, ORM relieved hyperglycemia-induced insulin resistance as well as tumor necrosis factor-alpha-mediated lipolysis in adipocytes. |
| 1160 | 20442402 | Accordingly, ORM improved glucose and insulin tolerance in obese and diabetic db/db mice. |
| 1161 | 20442402 | Accordingly, ORM improved glucose and insulin tolerance in obese and diabetic db/db mice. |
| 1162 | 20427484 | Although FK506-binding protein 52 (FKBP52) is an established positive regulator of glucocorticoid receptor (GR) activity, an in vivo role for FKBP52 in glucocorticoid control of metabolism has not been reported. |
| 1163 | 20427484 | To address this question, FKBP52(+/-) mice were placed on a high-fat (HF) diet known to induce obesity, hepatic steatosis, and insulin resistance. |
| 1164 | 20427484 | In response to HF, FKBP52(+/-) mice demonstrated a susceptibility to hyperglycemia and hyperinsulinemia that correlated with reduced insulin clearance and reduced expression of hepatic CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1), a mediator of clearance. |
| 1165 | 20427484 | Livers of HF-fed mutant mice had high lipid content and elevated expression of lipogenic genes (peroxisome proliferator-activated receptor gamma, fatty acid synthase, and sterol regulatory element-binding protein 1c) and inflammatory markers (TNFalpha). |
| 1166 | 20427484 | Interestingly, mutant mice under HF showed elevated serum corticosterone, but their steatotic livers had reduced expression of gluconeogenic genes (phosphoenolpyruvate carboxy kinase, glucose 6 phosphatase, and pyruvate dehydrogenase kinase 4), whereas muscle and adipose expressed normal to elevated levels of glucocorticoid markers. |
| 1167 | 20427484 | Consistent with this hypothesis, reduced expression of gluconeogenic genes and CEACAM1 was observed in dexamethasone-treated FKBP52-deficient mouse embryonic fibroblast cells. |
| 1168 | 20424670 | Fasting plasma glucose, HbA1c, tumor necrosis factor (TNF)alpha, free fatty acid, leptin, adiponectin and plasma 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha) levels as a marker of oxidative stress were measured on admission, just before and 2 weeks after local heating of the leg. |
| 1169 | 20424670 | On the other hand, glucose, HbA1c, free fatty acid, leptin and adiponectin levels were not changed during the study period. |
| 1170 | 20420526 | There, it suppresses the proinflammatory transcription factors nuclear factor-kappa B, signal transducer and activators of transcription-3, and Wnt/beta-catenin, and it activates peroxisome proliferator-activated receptor-gamma and Nrf2 cell-signaling pathways, thus leading to the downregulation of adipokines, including tumor necrosis factor, interleukin-6, resistin, leptin, and monocyte chemotactic protein-1, and the upregulation of adiponectin and other gene products. |
| 1171 | 20417247 | Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor alpha (TNFalpha), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. |
| 1172 | 20417247 | Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor alpha (TNFalpha), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. |
| 1173 | 20417247 | This includes the observations that: (1) people with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; (2) many people administered inflammatory cytokines such as interferon alpha develop depression that is indistinguishable from depression in non-medically ill populations; (3) a significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFalpha; (4) inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. |
| 1174 | 20417247 | This includes the observations that: (1) people with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; (2) many people administered inflammatory cytokines such as interferon alpha develop depression that is indistinguishable from depression in non-medically ill populations; (3) a significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFalpha; (4) inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. |
| 1175 | 20388942 | Moderating the secretion of adipocytokines like leptin, adiponectin, plasminogen activator inhibitor 1 (PAI-1), tumor necrosis factor alfa (TNF-alfa), interleukin-6 (IL-6) and resistin, it is associated with the processes of inflammation, endothelial dysfunction, hypertension and atherogenesis. |
| 1176 | 20405946 | White adipose tissue mRNA levels of inflammatory cytokines (MCP-1, IL-6, and TNFalpha), adipose tissue MCP-1 concentration, and serum IL-6 concentration in the coffee group were lower than the control group. |
| 1177 | 20399771 | Also, telmisartan significantly reduced the elevations of total gastric acid output, pepsin activity, gastric ulcer index and gastric mucosal tumor necrosis factor-alpha, nitric oxide, malondialdehyde and caspase-3 activity, and restored the depleted antioxidant defenses (reduced glutathione level, and superoxide dismutase and catalase activities) caused by indomethacin administration in diabetic rats. |
| 1178 | 20399771 | Immunohistochemical analysis revealed that telmisartan markedly attenuated the reduction in insulin content of pancreatic islet beta-cells, and prevented the indomethacin-induced overexpression of inducible nitric oxide synthase and nuclear factor-kappaB in gastric mucosa of diabetic rats. |
| 1179 | 20399204 | Rimonabant, a cannabinoid CB1 receptor antagonist, attenuates mechanical allodynia and counteracts oxidative stress and nerve growth factor deficit in diabetic mice. |
| 1180 | 20399204 | Rimonabant is a selective cannabinoid CB(1) receptor antagonist that produces a significant increase in insulin sensitivity and a reduction of HbA(1c) in diabetic patients. |
| 1181 | 20399204 | The same repeated treatment inhibited tumor necrosis factor (TNFalpha) overproduction in the spinal cord and increased the NGF support. |
| 1182 | 20387643 | In addition, circulating concentrations of inflammatory cytokines (e.g., TNF-alpha, IL-6) as well as decreased antiinflammatory factors (e.g., adiponectin, IL-10) are not only implicated in the development of insulin resistance and type 2 diabetes, but are also related to NAFLD. |
| 1183 | 20379144 | CM from LPS-stimulated THP1 inhibited insulin-induced AKT phosphorylation in adipocytes, in contrast to CM from nonactivated THP1. |
| 1184 | 20379144 | Moreover, it contained higher concentrations of tumor necrosis factor-α (TNFα) and lower levels of the anti-inflammatory cytokine IL-10. |
| 1185 | 20379144 | SR141716 reduced TNFα production and increased IL-10 secretion, resulting in a rescue of insulin signaling in adipocytes. |
| 1186 | 20378819 | In a subset analysis of 362 women who also had measurements of inflammatory and endothelial biomarkers, plasma resistin levels significantly correlated with IL-6, soluble TNF receptor 2, intercellular adhesion molecule 1, vascular adhesion molecule 1, and E-selectin after controlling for age and body mass index. |
| 1187 | 20378819 | After further adjustment for these biomarkers and C-reactive protein, resistin levels remained significantly associated with incident hypertension. |
| 1188 | 20370675 | Visceral fat accumulation is associated with hypersecretion of adipocytokines such as tumor necrosis factor-alpha and plasminogen activator inhibitor-1 which may regulate inflammatory and atherogenic diseases. |
| 1189 | 20370670 | For several adipocytokines such as leptin, adiponectin, tumor necrosis factor-alpha, retinol binding protein 4 (RBP4) or fetuin-A a crucial role in the development and progression of fatty liver disease has been suggested. |
| 1190 | 20370563 | Oral administration of D-pinitol (50 mg/kg b.w.) resulted in significant (p < 0.05) attenuation in blood glucose, glycosylated haemoglobin and pro-inflammatory markers such as TNF-alpha, IL-1beta, IL-6, NF-kappaB p65 unit and NO and significant (p < 0.05) elevation in the plasma insulin level. |
| 1191 | 20361391 | The rs1800629 polymorphism in the TNF gene interacts with physical activity on the changes in C-reactive protein levels in the Finnish Diabetes Prevention Study. |
| 1192 | 20361391 | The rs1800629 polymorphism in the TNF gene interacts with physical activity on the changes in C-reactive protein levels in the Finnish Diabetes Prevention Study. |
| 1193 | 20361391 | The rs1800629 polymorphism in the TNF gene interacts with physical activity on the changes in C-reactive protein levels in the Finnish Diabetes Prevention Study. |
| 1194 | 20361391 | The rs1800629 polymorphism in the TNF gene interacts with physical activity on the changes in C-reactive protein levels in the Finnish Diabetes Prevention Study. |
| 1195 | 20361391 | In particular, the rs1800629 single-nucleotide polymorphism (SNP) in the tumor necrosis factor ( TNF) gene and the rs1800795 SNP in the interleukin-6 ( IL6) gene have been found to modify the effect of exercise training on circulating levels of C-reactive protein (CRP) and IL-6, respectively. |
| 1196 | 20361391 | In particular, the rs1800629 single-nucleotide polymorphism (SNP) in the tumor necrosis factor ( TNF) gene and the rs1800795 SNP in the interleukin-6 ( IL6) gene have been found to modify the effect of exercise training on circulating levels of C-reactive protein (CRP) and IL-6, respectively. |
| 1197 | 20361391 | In particular, the rs1800629 single-nucleotide polymorphism (SNP) in the tumor necrosis factor ( TNF) gene and the rs1800795 SNP in the interleukin-6 ( IL6) gene have been found to modify the effect of exercise training on circulating levels of C-reactive protein (CRP) and IL-6, respectively. |
| 1198 | 20361391 | In particular, the rs1800629 single-nucleotide polymorphism (SNP) in the tumor necrosis factor ( TNF) gene and the rs1800795 SNP in the interleukin-6 ( IL6) gene have been found to modify the effect of exercise training on circulating levels of C-reactive protein (CRP) and IL-6, respectively. |
| 1199 | 20361391 | We assessed whether rs1800629 and rs1800795 modified the effect of moderate-to-vigorous physical activity on changes in serum levels of high-sensitivity CRP and IL-6 in the Finnish Diabetes Prevention Study (DPS). |
| 1200 | 20361391 | We assessed whether rs1800629 and rs1800795 modified the effect of moderate-to-vigorous physical activity on changes in serum levels of high-sensitivity CRP and IL-6 in the Finnish Diabetes Prevention Study (DPS). |
| 1201 | 20361391 | We assessed whether rs1800629 and rs1800795 modified the effect of moderate-to-vigorous physical activity on changes in serum levels of high-sensitivity CRP and IL-6 in the Finnish Diabetes Prevention Study (DPS). |
| 1202 | 20361391 | We assessed whether rs1800629 and rs1800795 modified the effect of moderate-to-vigorous physical activity on changes in serum levels of high-sensitivity CRP and IL-6 in the Finnish Diabetes Prevention Study (DPS). |
| 1203 | 20361391 | Genotype and 1-year data on changes in physical activity, serum CRP and IL-6 were available for 390 overweight subjects with impaired glucose tolerance. |
| 1204 | 20361391 | Genotype and 1-year data on changes in physical activity, serum CRP and IL-6 were available for 390 overweight subjects with impaired glucose tolerance. |
| 1205 | 20361391 | Genotype and 1-year data on changes in physical activity, serum CRP and IL-6 were available for 390 overweight subjects with impaired glucose tolerance. |
| 1206 | 20361391 | Genotype and 1-year data on changes in physical activity, serum CRP and IL-6 were available for 390 overweight subjects with impaired glucose tolerance. |
| 1207 | 20361391 | The rs1800629 SNP in TNF interacted with the 1-year change in moderate-to-vigorous physical activity on changes in CRP among those who had high (≥3 mg/L) baseline CRP levels ( P = 0.034 for interaction). |
| 1208 | 20361391 | The rs1800629 SNP in TNF interacted with the 1-year change in moderate-to-vigorous physical activity on changes in CRP among those who had high (≥3 mg/L) baseline CRP levels ( P = 0.034 for interaction). |
| 1209 | 20361391 | The rs1800629 SNP in TNF interacted with the 1-year change in moderate-to-vigorous physical activity on changes in CRP among those who had high (≥3 mg/L) baseline CRP levels ( P = 0.034 for interaction). |
| 1210 | 20361391 | The rs1800629 SNP in TNF interacted with the 1-year change in moderate-to-vigorous physical activity on changes in CRP among those who had high (≥3 mg/L) baseline CRP levels ( P = 0.034 for interaction). |
| 1211 | 20361391 | In conclusion, the rs1800629 SNP in the TNF gene may modify the effect of moderate-to-vigorous physical activity on serum levels of CRP. |
| 1212 | 20361391 | In conclusion, the rs1800629 SNP in the TNF gene may modify the effect of moderate-to-vigorous physical activity on serum levels of CRP. |
| 1213 | 20361391 | In conclusion, the rs1800629 SNP in the TNF gene may modify the effect of moderate-to-vigorous physical activity on serum levels of CRP. |
| 1214 | 20361391 | In conclusion, the rs1800629 SNP in the TNF gene may modify the effect of moderate-to-vigorous physical activity on serum levels of CRP. |
| 1215 | 20357221 | New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}. |
| 1216 | 20357221 | New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}. |
| 1217 | 20357221 | New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}. |
| 1218 | 20357221 | New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}. |
| 1219 | 20357221 | This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease. |
| 1220 | 20357221 | This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease. |
| 1221 | 20357221 | This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease. |
| 1222 | 20357221 | This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease. |
| 1223 | 20357221 | A PARP inhibitor treatment counteracted diabetes-induced motor and sensory nerve conduction slowing, axonal atrophy of large myelinated fibers, and increase in sciatic nerve and spinal cord NT and TNF-alpha concentrations. |
| 1224 | 20357221 | A PARP inhibitor treatment counteracted diabetes-induced motor and sensory nerve conduction slowing, axonal atrophy of large myelinated fibers, and increase in sciatic nerve and spinal cord NT and TNF-alpha concentrations. |
| 1225 | 20357221 | A PARP inhibitor treatment counteracted diabetes-induced motor and sensory nerve conduction slowing, axonal atrophy of large myelinated fibers, and increase in sciatic nerve and spinal cord NT and TNF-alpha concentrations. |
| 1226 | 20357221 | A PARP inhibitor treatment counteracted diabetes-induced motor and sensory nerve conduction slowing, axonal atrophy of large myelinated fibers, and increase in sciatic nerve and spinal cord NT and TNF-alpha concentrations. |
| 1227 | 20357221 | The findings identify PARP as a compelling drug target for prevention and treatment of both functional and structural manifestations of peripheral diabetic neuropathy and provide rationale for detailed evaluation of NT and TNF-alpha as potential biomarkers of its presence, severity, and progression. |
| 1228 | 20357221 | The findings identify PARP as a compelling drug target for prevention and treatment of both functional and structural manifestations of peripheral diabetic neuropathy and provide rationale for detailed evaluation of NT and TNF-alpha as potential biomarkers of its presence, severity, and progression. |
| 1229 | 20357221 | The findings identify PARP as a compelling drug target for prevention and treatment of both functional and structural manifestations of peripheral diabetic neuropathy and provide rationale for detailed evaluation of NT and TNF-alpha as potential biomarkers of its presence, severity, and progression. |
| 1230 | 20357221 | The findings identify PARP as a compelling drug target for prevention and treatment of both functional and structural manifestations of peripheral diabetic neuropathy and provide rationale for detailed evaluation of NT and TNF-alpha as potential biomarkers of its presence, severity, and progression. |
| 1231 | 20354158 | Hypothalamic inflammation induced by high-fat feeding causes insulin and leptin resistance and contributes to the pathogenesis of obesity. |
| 1232 | 20354158 | Insulin-treated cells were evaluated for induction of markers of insulin receptor signaling (p-IRS, p-Akt). |
| 1233 | 20354158 | In both hypothalamic cell lines, inflammation was induced by prototypical inflammatory mediators LPS and TNFalpha, as judged by induction of IkappaBalpha (3- to 5-fold) and IL-6 (3- to 7-fold) mRNA and p-IkappaBalpha protein, and TNFalpha pretreatment reduced insulin-mediated p-Akt activation by 30% (P < 0.05). |
| 1234 | 20333650 | Oral administration of resveratrol (5 mg/kg body weight) to diabetic rats for 30 days showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), TNF-alpha, IL-1beta, IL-6, NF-kappaB p65 unit and nitric oxide (NO) with concomitant elevation in plasma insulin. |
| 1235 | 20333650 | The diminished activities of pancreatic superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione-S-transferase (GST) as well as the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were reverted to near normalcy by resveratrol administration. |
| 1236 | 20308528 | Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. |
| 1237 | 20308528 | Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. |
| 1238 | 20308528 | Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. |
| 1239 | 20308528 | Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. |
| 1240 | 20308528 | Treatment of VSMC with AR inhibitor sorbinil prevented HG- as well as TNF-alpha-induced phosphorylation of retinoblastoma protein and activation of E2F-1. |
| 1241 | 20308528 | Treatment of VSMC with AR inhibitor sorbinil prevented HG- as well as TNF-alpha-induced phosphorylation of retinoblastoma protein and activation of E2F-1. |
| 1242 | 20308528 | Treatment of VSMC with AR inhibitor sorbinil prevented HG- as well as TNF-alpha-induced phosphorylation of retinoblastoma protein and activation of E2F-1. |
| 1243 | 20308528 | Treatment of VSMC with AR inhibitor sorbinil prevented HG- as well as TNF-alpha-induced phosphorylation of retinoblastoma protein and activation of E2F-1. |
| 1244 | 20308528 | Inhibition of AR also prevented HG- and TNF-alpha-induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. |
| 1245 | 20308528 | Inhibition of AR also prevented HG- and TNF-alpha-induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. |
| 1246 | 20308528 | Inhibition of AR also prevented HG- and TNF-alpha-induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. |
| 1247 | 20308528 | Inhibition of AR also prevented HG- and TNF-alpha-induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. |
| 1248 | 20308528 | Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. |
| 1249 | 20308528 | Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. |
| 1250 | 20308528 | Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. |
| 1251 | 20308528 | Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. |
| 1252 | 20307516 | After the experimental period of 30 days, the pathophysiological markers such as serum bilirubin and hepatic aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) were studied in addition to hepatic TNF-alpha, IL-1 beta, IL-6, NF-kappaB p65 and nitric oxide (NO) levels in control and experimental groups of rats. |
| 1253 | 20307516 | The levels of vitamin C, vitamin E and reduced glutathione (GSH) and activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR) were determined in the liver tissues. |
| 1254 | 20307255 | Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF). |
| 1255 | 20304443 | No effect of BBR was observed on plasma levels of insulin, adipokines (leptin and adiponectin), or inflammatory cytokines (tumor necrosis factor-α and C-reactive protein). |
| 1256 | 20228013 | The secretion of various effectors such as adipokines, interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha (TNF-alpha), beta-adrenergics and reactive oxygen species (ROS) involved in insulin resistance is enhanced in Mg deficiency and obesity. |
| 1257 | 20224659 | By mediating anti-inflammatory effects in the muscle itself, myokines may also counteract TNF-driven insulin resistance. |
| 1258 | 20211973 | Concomitantly HFFD feeding markedly up-regulated hepatic mRNA expression of proinflammatory cytokines (TNFalpha, IL-6, and monocyte chemoattractant protein-1), gluconeogenic gene phosphoenolpyruvate carboxykinase, transcription factor carbohydrate response element binding protein, and its downstream lipogenic enzymes, all of which were significantly suppressed by spironolactone. |
| 1259 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1260 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1261 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1262 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1263 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1264 | 20208423 | S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 1265 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1266 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1267 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1268 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1269 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1270 | 20208423 | The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. |
| 1271 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1272 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1273 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1274 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1275 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1276 | 20208423 | We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. |
| 1277 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1278 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1279 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1280 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1281 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1282 | 20208423 | SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. |
| 1283 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1284 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1285 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1286 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1287 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1288 | 20208423 | The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. |
| 1289 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1290 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1291 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1292 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1293 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1294 | 20208423 | In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. |
| 1295 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1296 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1297 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1298 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1299 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1300 | 20208423 | These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus. |
| 1301 | 20204165 | Evidence for increased inflammation includes: increased levels of plasma C-reactive protein, the prototypic marker of inflammation; increased levels of plasminogen-activator inhibitor; increased monocyte superoxide and proinflammatory cytokine release (IL-1, IL-6 and TNF-alpha); increased monocyte adhesion to endothelium; increased NF-kappaB activity; and increased Toll-like receptor 2 and 4 expression and activity in diabetes. |
| 1302 | 20203087 | Macrophage migration inhibitory factor is a therapeutic target in treatment of non-insulin-dependent diabetes mellitus. |
| 1303 | 20203087 | Here, we investigated the role of MIF in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) using MIF(-/-) mice and a mouse model of streptozotocin (STZ)-induced NIDDM. |
| 1304 | 20203087 | These mice produced significantly less inflammatory cytokines and resistin as compared with MIF(+/+) mice and failed to develop clinical disease. |
| 1305 | 20203087 | Finally, oral administration of a small-molecule MIF antagonist, CPSI-1306, to outbred ICR mice following induction of NIDDM significantly lowered blood glucose levels in the majority of animals, which was also associated with a significant reduction in the levels of the proinflammatory cytokines IL-6 and TNF-alpha in the sera. |
| 1306 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1307 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1308 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1309 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1310 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1311 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1312 | 20200974 | TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1. |
| 1313 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1314 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1315 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1316 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1317 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1318 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1319 | 20200974 | Tumor necrosis factor alpha (TNF-alpha) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. |
| 1320 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1321 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1322 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1323 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1324 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1325 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1326 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 1327 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1328 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1329 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1330 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1331 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1332 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1333 | 20200974 | This coincided with elevated TNF-alpha protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). |
| 1334 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1335 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1336 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1337 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1338 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1339 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1340 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 1341 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1342 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1343 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1344 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1345 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1346 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1347 | 20200974 | The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. |
| 1348 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1349 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1350 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1351 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1352 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1353 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1354 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 1355 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1356 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1357 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1358 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1359 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1360 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1361 | 20200974 | Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. |
| 1362 | 20200812 | The following parameters were measured every 4-8 weeks: BMI, body fat proportion, waist and hip circumference, HOMA insulin resistance, fasting serum-/plasma concentrations of adiponectin, leptin, ghrelin, vascular endothelial growth factor (VEGF), cortisol, interleukin-6 and tumor necrosis factor (TNF)-alpha. |
| 1363 | 20200812 | The following parameters were measured every 4-8 weeks: BMI, body fat proportion, waist and hip circumference, HOMA insulin resistance, fasting serum-/plasma concentrations of adiponectin, leptin, ghrelin, vascular endothelial growth factor (VEGF), cortisol, interleukin-6 and tumor necrosis factor (TNF)-alpha. |
| 1364 | 20200812 | Compared with the baseline value, 20 weeks of treatment reduced the BMI by 7.2+/-1.4%, body fat proportion by 11.6+/-3.6%, waist circumference by 4.2+/-1.2%, leptin by 39.2+/-6.5% and HOMA insulin resistance by 37.3+/-5%, while adiponectin was increased by 69.9+/-17.3% (P<0.05, respectively). |
| 1365 | 20200812 | Compared with the baseline value, 20 weeks of treatment reduced the BMI by 7.2+/-1.4%, body fat proportion by 11.6+/-3.6%, waist circumference by 4.2+/-1.2%, leptin by 39.2+/-6.5% and HOMA insulin resistance by 37.3+/-5%, while adiponectin was increased by 69.9+/-17.3% (P<0.05, respectively). |
| 1366 | 20200812 | There were trends for a reduction in ghrelin concentration, whereas cortisol, interleukin-6 and TNF-alpha values were unchanged. |
| 1367 | 20200812 | There were trends for a reduction in ghrelin concentration, whereas cortisol, interleukin-6 and TNF-alpha values were unchanged. |
| 1368 | 20200812 | In summary, in this small sample of migraine patients topiramate treatment was associated with increased insulin sensitivity, increased adiponectin concentration and a reduction of body fat in all treated patients. |
| 1369 | 20200812 | In summary, in this small sample of migraine patients topiramate treatment was associated with increased insulin sensitivity, increased adiponectin concentration and a reduction of body fat in all treated patients. |
| 1370 | 20184396 | Since its debut as the tumor necrosis factor converting enzyme (TACE), ADAM-17 has been reported to be an indispensible regulator of almost every cellular event from proliferation to migration. |
| 1371 | 20177654 | Six common genetic variants (rs2229094, rs1041981, rs1800630, rs1800629, rs361525, and rs1800610) in the TNF-LTA locus encoding the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and lymphotoxin-alpha have been shown to be associated with various metabolic traits including susceptibility to type 2 diabetes, metabolic syndrome, insulin resistance, and increased body mass index (BMI) in Caucasians from different geographic locations and have yielded mixed results. |
| 1372 | 20177654 | Six common genetic variants (rs2229094, rs1041981, rs1800630, rs1800629, rs361525, and rs1800610) in the TNF-LTA locus encoding the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and lymphotoxin-alpha have been shown to be associated with various metabolic traits including susceptibility to type 2 diabetes, metabolic syndrome, insulin resistance, and increased body mass index (BMI) in Caucasians from different geographic locations and have yielded mixed results. |
| 1373 | 20177654 | We report the association of a promoter region variant of TNF: rs1800630 and non-synonymous LTA variant: rs2229094 with type 2 diabetes [OR = 0.83 (95% CI 0.72-0.95), P = 0.005 and OR = 0.86 (95% CI 0.75-0.98), P = 0.02, respectively]. |
| 1374 | 20177654 | We report the association of a promoter region variant of TNF: rs1800630 and non-synonymous LTA variant: rs2229094 with type 2 diabetes [OR = 0.83 (95% CI 0.72-0.95), P = 0.005 and OR = 0.86 (95% CI 0.75-0.98), P = 0.02, respectively]. |
| 1375 | 20173393 | TNF-alpha is expressed in and secreted by adipose tissue, its levels correlating with the degree of adiposity and the associated insulin resistance. |
| 1376 | 20173393 | TNF-alpha is expressed in and secreted by adipose tissue, its levels correlating with the degree of adiposity and the associated insulin resistance. |
| 1377 | 20173393 | TNF-alpha is expressed in and secreted by adipose tissue, its levels correlating with the degree of adiposity and the associated insulin resistance. |
| 1378 | 20173393 | Targeting TNF-alpha and/or its receptors has been suggested as a promising treatment for insulin resistance and type 2 diabetes. |
| 1379 | 20173393 | Targeting TNF-alpha and/or its receptors has been suggested as a promising treatment for insulin resistance and type 2 diabetes. |
| 1380 | 20173393 | Targeting TNF-alpha and/or its receptors has been suggested as a promising treatment for insulin resistance and type 2 diabetes. |
| 1381 | 20173393 | This review will summarize the available knowledge on the role of TNF-alpha in obesity and related processes and the potential implications of the above in the development of new therapeutic approaches for obesity and insulin resistance. |
| 1382 | 20173393 | This review will summarize the available knowledge on the role of TNF-alpha in obesity and related processes and the potential implications of the above in the development of new therapeutic approaches for obesity and insulin resistance. |
| 1383 | 20173393 | This review will summarize the available knowledge on the role of TNF-alpha in obesity and related processes and the potential implications of the above in the development of new therapeutic approaches for obesity and insulin resistance. |
| 1384 | 20170650 | Continuous high glucose exposure for 2-12 days significantly elevated gene expressions and protein concentrations of IL-1 beta, NF-kB, VEGF, TNF-alpha, TGF-beta and ICAM-1 in retinal pericytes. |
| 1385 | 20164427 | Induction of genes implicated in diabetes, such as Il18, Tnfa, and Inos but not Il4, Il17 or Ifng, was repressed in splenocytes derived from protected mice. |
| 1386 | 20146878 | Compared with lean control subjects, patients with metabolic syndrome and type 2 diabetes had lower circulating levels of total adiponectin and high molecular weight (HMW) adiponectin, and higher levels of leptin and interleukin-6 (IL-6). |
| 1387 | 20146878 | After adjusting for age and sex, leptin, IL-6 and tumour necrosis factor-alpha (TNF-alpha) were positively correlated with HOMA-IR. |
| 1388 | 20146878 | In conclusion, decreased total adiponectin and HMW adiponectin and increased leptin and IL-6 levels are characteristic of patients with metabolic syndrome and type 2 diabetes. |
| 1389 | 20144589 | Role of modulation of vascular endothelial growth factor and tumor necrosis factor-alpha in gastric ulcer healing in diabetic rats. |
| 1390 | 20144589 | Role of modulation of vascular endothelial growth factor and tumor necrosis factor-alpha in gastric ulcer healing in diabetic rats. |
| 1391 | 20144589 | Role of modulation of vascular endothelial growth factor and tumor necrosis factor-alpha in gastric ulcer healing in diabetic rats. |
| 1392 | 20144589 | Role of modulation of vascular endothelial growth factor and tumor necrosis factor-alpha in gastric ulcer healing in diabetic rats. |
| 1393 | 20144589 | The aim of the present study was to assess the effect of drugs that increase gastric vascular endothelial growth factor (VEGF) and suppress gastric tumor necrosis factor-alpha (TNF-alpha) in gastric ulcer healing in streptozotocin-induced diabetic rats. |
| 1394 | 20144589 | The aim of the present study was to assess the effect of drugs that increase gastric vascular endothelial growth factor (VEGF) and suppress gastric tumor necrosis factor-alpha (TNF-alpha) in gastric ulcer healing in streptozotocin-induced diabetic rats. |
| 1395 | 20144589 | The aim of the present study was to assess the effect of drugs that increase gastric vascular endothelial growth factor (VEGF) and suppress gastric tumor necrosis factor-alpha (TNF-alpha) in gastric ulcer healing in streptozotocin-induced diabetic rats. |
| 1396 | 20144589 | The aim of the present study was to assess the effect of drugs that increase gastric vascular endothelial growth factor (VEGF) and suppress gastric tumor necrosis factor-alpha (TNF-alpha) in gastric ulcer healing in streptozotocin-induced diabetic rats. |
| 1397 | 20144589 | The use of insulin, combinations of insulin and pentoxifylline or simvastatin resulted in a significant decrease in gastric ulcer area, significant increase in epithelial regeneration assessed histologically, significant increase in gastric VEGF concentration, and gastric von Willebrand factor (vWF) as well as significant decrease in gastric TNF-alpha. |
| 1398 | 20144589 | The use of insulin, combinations of insulin and pentoxifylline or simvastatin resulted in a significant decrease in gastric ulcer area, significant increase in epithelial regeneration assessed histologically, significant increase in gastric VEGF concentration, and gastric von Willebrand factor (vWF) as well as significant decrease in gastric TNF-alpha. |
| 1399 | 20144589 | The use of insulin, combinations of insulin and pentoxifylline or simvastatin resulted in a significant decrease in gastric ulcer area, significant increase in epithelial regeneration assessed histologically, significant increase in gastric VEGF concentration, and gastric von Willebrand factor (vWF) as well as significant decrease in gastric TNF-alpha. |
| 1400 | 20144589 | The use of insulin, combinations of insulin and pentoxifylline or simvastatin resulted in a significant decrease in gastric ulcer area, significant increase in epithelial regeneration assessed histologically, significant increase in gastric VEGF concentration, and gastric von Willebrand factor (vWF) as well as significant decrease in gastric TNF-alpha. |
| 1401 | 20144589 | A significant difference in gastric ulcer area as well as in gastric TNF-alpha, VEGF and vWF levels could be observed between rats that received combinations of insulin and pentoxifylline or simvastatin compared to rats that received either drug alone. |
| 1402 | 20144589 | A significant difference in gastric ulcer area as well as in gastric TNF-alpha, VEGF and vWF levels could be observed between rats that received combinations of insulin and pentoxifylline or simvastatin compared to rats that received either drug alone. |
| 1403 | 20144589 | A significant difference in gastric ulcer area as well as in gastric TNF-alpha, VEGF and vWF levels could be observed between rats that received combinations of insulin and pentoxifylline or simvastatin compared to rats that received either drug alone. |
| 1404 | 20144589 | A significant difference in gastric ulcer area as well as in gastric TNF-alpha, VEGF and vWF levels could be observed between rats that received combinations of insulin and pentoxifylline or simvastatin compared to rats that received either drug alone. |
| 1405 | 20143002 | [TNF-alpha and insulin-resistance: metabolic effects of in vivo therapeutic blockade]. |
| 1406 | 20143002 | [TNF-alpha and insulin-resistance: metabolic effects of in vivo therapeutic blockade]. |
| 1407 | 20143002 | [TNF-alpha and insulin-resistance: metabolic effects of in vivo therapeutic blockade]. |
| 1408 | 20143002 | TNF-alpha, a proinflammatory cytokine, plays an important role in the pathogenesis of insulin resistance associated with inflammation during the course of rheumatic diseases. |
| 1409 | 20143002 | TNF-alpha, a proinflammatory cytokine, plays an important role in the pathogenesis of insulin resistance associated with inflammation during the course of rheumatic diseases. |
| 1410 | 20143002 | TNF-alpha, a proinflammatory cytokine, plays an important role in the pathogenesis of insulin resistance associated with inflammation during the course of rheumatic diseases. |
| 1411 | 20143002 | In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in rheumatic patients without diabetes. |
| 1412 | 20143002 | In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in rheumatic patients without diabetes. |
| 1413 | 20143002 | In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in rheumatic patients without diabetes. |
| 1414 | 20134408 | Significant increases in triglycerides, plasminogen activator inhibitor-I (PAI-I), leptin, and tumor necrosis factor-alpha (TNF-alpha) were observed. |
| 1415 | 20134099 | Atorvastatin downregulates monocyte CD36 expression, nuclear NFkappaB and TNFalpha levels in type 2 diabetes. |
| 1416 | 20131064 | Basal blood samples were collected to determine plasma leptin, adiponectin, resistin, tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP) and FFA concentrations. |
| 1417 | 20131064 | Basal blood samples were collected to determine plasma leptin, adiponectin, resistin, tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP) and FFA concentrations. |
| 1418 | 20131064 | Plasma FFA, inflammatory marker (hsCRP, IL-6, TNFalpha), adipokine (adiponectin, resistin, leptin), and triglyceride concentrations did not differ between non-obese diabetes patients and healthy, normoglycemic controls. |
| 1419 | 20131064 | Plasma FFA, inflammatory marker (hsCRP, IL-6, TNFalpha), adipokine (adiponectin, resistin, leptin), and triglyceride concentrations did not differ between non-obese diabetes patients and healthy, normoglycemic controls. |
| 1420 | 20131064 | Plasma FFA, IL-6, hsCRP, leptin, and triglyceride levels were significantly higher in the obese diabetes patients when compared with the healthy normoglycemic controls (P < 0.05). |
| 1421 | 20131064 | Plasma FFA, IL-6, hsCRP, leptin, and triglyceride levels were significantly higher in the obese diabetes patients when compared with the healthy normoglycemic controls (P < 0.05). |
| 1422 | 20131064 | Elevated plasma leptin, hsCRP, IL-6, and FFA concentrations are associated with obesity and not necessarily with the type 2 diabetic state. |
| 1423 | 20131064 | Elevated plasma leptin, hsCRP, IL-6, and FFA concentrations are associated with obesity and not necessarily with the type 2 diabetic state. |
| 1424 | 20130740 | The aim of this study was to determine the antidiabetic properties of 4 purified fractions of different molecular weight range HPSs (HPS1, HPS2, HPS3, HPS4). |
| 1425 | 20130740 | The interleukin-6, tumor necrosis factor-alpha, leptin, and free fatty acid levels were significantly lower in the HPS3-treated groups and HPS3 + metformin (HPS3+MET) group than in the DM control group, while plasma insulin, hepatic glycogen, superoxide dismutase, and nitric oxide synthetase activity were significantly higher. |
| 1426 | 20122988 | Confocal microscopy revealed abounden GPR30 expression in insulin, glucagon and somatostatin cells. |
| 1427 | 20122988 | Dose-response studies of G-1 vs 17beta-estradiol in isolated islets at 1 or 12 mM glucose showed an almost identical pattern in that both compounds increased insulin and inhibited glucagon and somatostatin secretion. |
| 1428 | 20122988 | ICI-182,780 and EM-652, potent antagonists of the 17beta-estradiol receptors (ER alpha and ER beta) did not influence the amplifying effect of G-1 or 17beta-estradiol on cAMP content or insulin secretion from isolated islets. |
| 1429 | 20122988 | Cytokine-induced (IL-1 beta+TNFalpha+INF gamma) apoptosis in islets, cultured for 24h at 5mM glucose, was almost abolished by G-1 or 17beta-estradiol treatment. |
| 1430 | 20120526 | Retinopathy and nephropathy in type 1 diabetic patients--association with polymorphysms of vitamin D-receptor, TNF, Neuro-D and IL-1 receptor 1 genes. |
| 1431 | 20120526 | Retinopathy and nephropathy in type 1 diabetic patients--association with polymorphysms of vitamin D-receptor, TNF, Neuro-D and IL-1 receptor 1 genes. |
| 1432 | 20120526 | We genotyped variants in vitamin D receptor (VDR) and tumor necrosis factor (TNF) genes in 47 patients and in NeuroD1 and interleukin-1 receptor 1 (IL1R1) genes in 35 patients. |
| 1433 | 20120526 | We genotyped variants in vitamin D receptor (VDR) and tumor necrosis factor (TNF) genes in 47 patients and in NeuroD1 and interleukin-1 receptor 1 (IL1R1) genes in 35 patients. |
| 1434 | 20111020 | Adipocypte fatty acid-binding protein-4 (FABP4/adipocyte P2) may play a central role in energy metabolism and inflammation. |
| 1435 | 20111020 | In animal models, defects of the aP2 gene (aP2(-/-)) partially protected against the development of obesity-related insulin resistance, dyslipidemia, and atherosclerosis. |
| 1436 | 20111020 | There were no significant associations between SNPs and plasma levels of inflammatory and endothelial biomarkers, including C-reactive protein, tumor necrosis factor (TNF), interleukin-6 (IL-6), E-selectin, and intercellular adhesion molecule (ICAM-1). |
| 1437 | 20111020 | The observed significant association between reduced VCAM-1 levels and FABP4 genotypes in African-American women warrant further confirmation. |
| 1438 | 20108212 | The immune molecular mechanisms involved were preliminarily regarded as downregulation of the expression of pathogenic T-helper 1 lymphocyte (Th1) cytokine tumor necrosis factor-alpha (TNF-alpha) (p<0.01) along with upregulation of the expression of protective T-helper 2 lymphocyte Th2 cytokine interleukin 10 (IL-10) (p<0.01) which ameliorates the Th1/Th2 imbalance in diabetes. |
| 1439 | 20107818 | Most PD patients respond to bacterial invaders by mobilizing their defensive cells and releasing cytokines such as interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha, and IL-6, which ultimately causes tissue destruction by stimulating the production of collagenolytic enzymes, such matrix metalloproteinases. |
| 1440 | 20100990 | Valsartan treatment also blocked Western diet-induced increases in serum levels of the proinflammatory cytokines interferon-gamma and monocyte chemotactic protein 1. |
| 1441 | 20100990 | In isolated adipocytes, valsartan treatment blocked or attenuated Western diet-induced changes in expression of several key inflammatory signals: interleukin 12p40, interleukin 12p35, tumor necrosis factor-alpha, interferon-gamma, adiponectin, platelet 12-lipoxygenase, collagen 6, inducible NO synthase, and AT1R. |
| 1442 | 20098632 | Obesity and type 2 diabetes are characterized by a diminished production of protective factors such as adiponectin and increased detrimental adipocytokines such as leptin, resistin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFα), and monocyte chemoattractant protein-1 (MCP-1) by adipose tissue. |
| 1443 | 20098449 | In addition, two components of the TNF superfamily, namely TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) and osteoprotegerin, may be involved in the pathogenesis of diabetic angiopathy. |
| 1444 | 20095809 | In this article we compare the two main methods of dissolving FAs for work in vitro, (i) dissolution in dimethylsulfoxide (DMSO) and (ii) conjugation with bovine serum albumin (BSA), and describe the effects of the solvent on cytotoxicity (determination of viability) and bioavailability (as shown by the impact on the gene expression of TNF-alpha). |
| 1445 | 20089301 | NEFA also promoted trophoblast syncytialisation and TNFalpha, IL-1beta, IL-6 and IL-10 production without effects on cell viability, apoptosis or hormone secretion. |
| 1446 | 20070992 | Blood pressure, glucose, insulin, adiponectin, leptin, and tumor necrosis factor alpha were examined. |
| 1447 | 20070992 | Blood pressure, glucose, insulin, adiponectin, leptin, and tumor necrosis factor alpha were examined. |
| 1448 | 20070992 | The telmisartan-induced increase in adiponectin was most probably associated with a decrease in glucose and tumor necrosis factor alpha levels. |
| 1449 | 20070992 | The telmisartan-induced increase in adiponectin was most probably associated with a decrease in glucose and tumor necrosis factor alpha levels. |
| 1450 | 20069130 | Infected mice that received MLDS did not show an increase in their regulatory T cell population, however, they had a greater number of alternatively activated macrophages, higher levels of the cytokine IL-4, and lower levels of TNF-alpha. |
| 1451 | 20061825 | NKG2D is a surface receptor expressed on NK cells but also on CD8(+) T cells, gammadelta T cells, and auto-reactive CD4(+)/CD28(-) T cells of patients with rheumatoid arthritis. |
| 1452 | 20061825 | MAb E4 potently antagonized the cytolytic activity of NKL cells against BaF/3-MICA cells expressing NKG2D ligand, and blocked the NKG2D ligand-induced secretion of TNFalpha, IFNgamma and GM-CSF, as well as surface expression of CRTAM by NK cells cultured on immobilized MICA or ULBP-1 ligands. |
| 1453 | 20060507 | TNF-alpha, a proinflammatory cytokine, plays a pivotal role in the pathogenesis of inflammation-associated insulin resistance during the course of rheumatic diseases. |
| 1454 | 20060507 | TNF-alpha, a proinflammatory cytokine, plays a pivotal role in the pathogenesis of inflammation-associated insulin resistance during the course of rheumatic diseases. |
| 1455 | 20060507 | In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in non-diabetic rheumatic patients. |
| 1456 | 20060507 | In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in non-diabetic rheumatic patients. |
| 1457 | 20058158 | This study was designed to investigate plasma circulating pro-inflammatory cytokines, adiponectin and high-sensitive C-reactive protein (hsCRP) in young men with type 2 diabetes. |
| 1458 | 20058158 | Hemoglobin A1c, fasting glycemic index, lipids, adiponectin, hsCRP, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined. |
| 1459 | 20058158 | There were significantly lower plasma adiponectin and higher hsCRP and TNF-α levels in OBYDM, whereas higher TNF-α and IL-6 were shown in NOYDM. |
| 1460 | 20058158 | Spearman rank correlation analysis demonstrated significant correlations between BMI and adiponectin (R = -0.44, P < 0.005), CRP (R = 0.28, P < 0.05), TNF-α (R = 0.42, P < 0.005) and IL-6 (R = 0.33, P < 0.01) in all YDM. |
| 1461 | 20053369 | STZ administration elevated the levels of IL-2 as well as IFN-gamma and attenuated the level of TNF-alpha in the sera of diabetic animals. |
| 1462 | 20053369 | Investigating the oxidative stress responsive cell signaling pathways, increased expressions (immunoreactive concentrations) of phosphorylated p65 as well as its inhibitor protein phospho IkappaBalpha and phosphorylated mitogen activated protein kinases (MAPKs) have been observed in diabetic spleen tissue. |
| 1463 | 20053369 | Studies on isolated splenocytes revealed that hyperglycemia caused disruption of mitochondrial membrane potential, elevation in the concentration of cytosolic cytochrome c as well as activation of caspase 3 leading to apoptotic cell death. |
| 1464 | 20043993 | Downregulated expression of the secreted glycoprotein follistatin-like 1 (Fstl1) is a robust hallmark of preadipocyte to adipocyte conversion. |
| 1465 | 20043993 | Time course studies in multiple adipogenesis models reveal downregulation of Fstl1 is a hallmark of white and brown adipocyte conversion. |
| 1466 | 20043993 | By Western blot, we show culture media of 3T3-L1 preadipocytes contains high levels of Fstl1 protein that rapidly decline in adipocyte conversion. |
| 1467 | 20043993 | Moreover, we observe a correlation between preadipocyte phenotype and Fstl1 expression in that TNFalpha-mediated de-differentiation of 3T3-L1 adipocytes is accompanied by re-expression of Fstl1 transcript and protein. |
| 1468 | 20043993 | Furthermore, of 10 additional preadipocyte-expressed genes analyzed we find Pref-1, Col1A1, Sca-1/Ly6a, Lox and Thbs2, are also downregulated by 5-aza-cytidine. |
| 1469 | 20043993 | Using luciferase reporter constructs containing 791 or 3922 bp of the Fstl1 5' flanking region, we determine negative transcriptional regulation by Kruppel-like factor 15. |
| 1470 | 20043993 | Together, our data suggest downregulation of Fstl1 expression may be an important feature of preadipocyte to adipocyte conversion. |
| 1471 | 21814537 | Cord blood IL-6, IL-8, TNF-alpha and RANTES levels were analyzed from a larger panel of immune biomarkers measured using multiplex immunoassay. |
| 1472 | 21437105 | At month 6, weight, leptin, adiponectin, and tumor necrosis factor-α concentrations did not differ significantly between groups (P > 0.05 for all variables). |
| 1473 | 21437105 | However, significant changes in leptin and adiponectin occurred over time (P < 0.001 and P < 0.012, respectively). |
| 1474 | 21437105 | Modest weight loss, rather than macronutrient composition, likely accounted for the favorable changes observed in leptin and adiponectin over time. |
| 1475 | 21437087 | In obesity, this activation leads to the release of pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin-1β and interleukin-6 that block major anabolic cascades downstream of insulin signaling and thus disrupt insulin homeostasis and action. |
| 1476 | 21437087 | Cytokines also trigger the production of acute-phase reactants such as C-reactive protein, plasminogen activator inhibitor-1, serum amyloid-A, and haptoglobin. |
| 1477 | 20039009 | The glomerular hypertrophy and mesangial matrix expansion seen in early diabetes can be reduced or prevented by C-peptide administration, possibly via interference with TGF-beta1 and TNFalpha signaling. |
| 1478 | 20038749 | Interleukin 17 promotes angiotensin II-induced hypertension and vascular dysfunction. |
| 1479 | 20038749 | We found that angiotensin II infusion increased IL-17 production from T cells and IL-17 protein in the aortic media. |
| 1480 | 20038749 | The initial hypertensive response to angiotensin II infusion was similar in IL-17(-/-) and C57BL/6J mice. |
| 1481 | 20038749 | However, hypertension was not sustained in IL-17(-/-) mice, reaching levels 30-mm Hg lower than in wild-type mice by 4 weeks of angiotensin II infusion. |
| 1482 | 20038749 | Vessels from IL-17(-/-) mice displayed preserved vascular function, decreased superoxide production, and reduced T-cell infiltration in response to angiotensin II. |
| 1483 | 20038749 | Gene array analysis of cultured human aortic smooth muscle cells revealed that IL-17, in conjunction with tumor necrosis factor-alpha, modulated expression of >30 genes, including a number of inflammatory cytokines/chemokines. |
| 1484 | 20038749 | We conclude that IL-17 is critical for the maintenance of angiotensin II-induced hypertension and vascular dysfunction and might be a therapeutic target for this widespread disease. |
| 1485 | 20030175 | Examination to be necessary for a pathologic classification of DM is islet-associated antibody, namely, GAD antibody, IA-2 antibody and the measurement of IRI, blood/urinary C-peptide to evaluate insulin secretory ability. |
| 1486 | 20030175 | TNF-alpha and leptin levels as insulin resistance advances and adiponectin levels as insulin resistance improves are measured as adipocytokines secreted by visceral fat tissue. |
| 1487 | 20025835 | This interference was reflected in NO-mediated suppression of T lymphocyte proliferation and lower production of the proinflammatory cytokines interferon-gamma, IL-17 and TNF-alpha in the spleen, with subsequent blockade of beta-cell destruction. |
| 1488 | 20020468 | The results showed that induction of HO-1 inhibited the maturation of osteoblasts including mineralized bone nodule formation, alkaline phosphatase activity and decreased mRNA expression of several differentiation markers such as alkaline phosphatase, osteocalcin, and RUNX2. |
| 1489 | 20020468 | HO-1 can be induced by H(2)O(2), lipopolysaccharide and inflammatory cytokines such as TNF-alpha and IL-1beta in osteoblasts and also in STZ-induced diabetic mice. |
| 1490 | 20019678 | Subjects with T2D had higher VAT expression of molecules regulating inflammation (tumor necrosis factor-alpha (TNFalpha), macrophage inflammatory protein (MIP), interleukin-8 (IL-8)). |
| 1491 | 20019678 | Subjects with T2D had higher VAT expression of molecules regulating inflammation (tumor necrosis factor-alpha (TNFalpha), macrophage inflammatory protein (MIP), interleukin-8 (IL-8)). |
| 1492 | 20019678 | Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor. |
| 1493 | 20019678 | Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor. |
| 1494 | 20019678 | Abdominal fat mass was related to VAT expression of MIP, SAA, cAMP response element-binding protein (CREBP), IL-1beta, and IL-8. |
| 1495 | 20019678 | Abdominal fat mass was related to VAT expression of MIP, SAA, cAMP response element-binding protein (CREBP), IL-1beta, and IL-8. |
| 1496 | 20019678 | There were depot-specific differences in expression of serum T2D predictors: VAT expressed higher levels of complement C3; SAT expressed higher levels of retinol-binding protein-4 (RBP4), adiponectin, and leptin. |
| 1497 | 20019678 | There were depot-specific differences in expression of serum T2D predictors: VAT expressed higher levels of complement C3; SAT expressed higher levels of retinol-binding protein-4 (RBP4), adiponectin, and leptin. |
| 1498 | 20007938 | This study was designed to evaluate the relationship between the TNF-alpha-C-857T polymorphism and LDL cholesterol levels according to statin treatment in subjects with type 2 diabetes. |
| 1499 | 20007581 | DcR3 protects islet beta cells from apoptosis through modulating Adcyap1 and Bank1 expression. |
| 1500 | 20007581 | The transgenically expressed DcR3 protected islets from IFN-gamma plus IL-1beta- or TNF-alpha plus IL-1beta-induced dysfunction and apoptosis in vitro. |
| 1501 | 20007581 | Recombinant LIGHT- and TL1A-induced islet apoptosis in the absence of the FasL/Fas pathway, as well as DcR3, could block such induction. |
| 1502 | 20007581 | These results for the first time demonstrated that LIGHT and TL1A were capable of inducing islet apoptosis in addition to FasL, while DcR3 protected the islets by blocking all three apoptosis pathways. |
| 1503 | 20007364 | Association of reduced tumor necrosis factor alpha, gamma interferon, and interleukin-1beta (IL-1beta) but increased IL-10 expression with improved chest radiography in patients with pulmonary tuberculosis. |
| 1504 | 20007364 | Association of reduced tumor necrosis factor alpha, gamma interferon, and interleukin-1beta (IL-1beta) but increased IL-10 expression with improved chest radiography in patients with pulmonary tuberculosis. |
| 1505 | 20007364 | The objective of the present study was to correlate the modulation of cytokine expression (interleukin-1 [IL-1], IL-6, IL-8, IL-10, IL-12, gamma interferon [IFN-gamma], interferon-inducible protein [IP-10], and monocyte chemotactic protein 1 [MCP-1]) with the clinical response to 2 months of intensive therapy. |
| 1506 | 20007364 | The objective of the present study was to correlate the modulation of cytokine expression (interleukin-1 [IL-1], IL-6, IL-8, IL-10, IL-12, gamma interferon [IFN-gamma], interferon-inducible protein [IP-10], and monocyte chemotactic protein 1 [MCP-1]) with the clinical response to 2 months of intensive therapy. |
| 1507 | 20007364 | The levels of expression of TNF-alpha, MCP-1, IFN-gamma, and IL-1beta were decreased; and the level of IL-10 increased in early responders. |
| 1508 | 20007364 | The levels of expression of TNF-alpha, MCP-1, IFN-gamma, and IL-1beta were decreased; and the level of IL-10 increased in early responders. |
| 1509 | 20007364 | After adjustment for age, gender, and the result of sputum culture for M. tuberculosis, significant differences in the levels of MCP-1 and IP-10 expression were observed between the early and the late responders after 2 months of intensive anti-M. tuberculosis therapy. |
| 1510 | 20007364 | After adjustment for age, gender, and the result of sputum culture for M. tuberculosis, significant differences in the levels of MCP-1 and IP-10 expression were observed between the early and the late responders after 2 months of intensive anti-M. tuberculosis therapy. |
| 1511 | 20005389 | At week three after transplantation, the concentrations of monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-1 beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha in intraperitoneal fluid were determined using ELISA. |
| 1512 | 20005389 | At week three after transplantation, the concentrations of monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-1 beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha in intraperitoneal fluid were determined using ELISA. |
| 1513 | 20005389 | Also, the concentrations of cytokines IL-1beta, IFN-gamma, and TNF-alpha were decreased significantly. |
| 1514 | 20005389 | Also, the concentrations of cytokines IL-1beta, IFN-gamma, and TNF-alpha were decreased significantly. |
| 1515 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1516 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1517 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1518 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1519 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1520 | 20004646 | Tumor necrosis factor-alpha increases alkaline phosphatase expression in vascular smooth muscle cells via MSX2 induction. |
| 1521 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1522 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1523 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1524 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1525 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1526 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 1527 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1528 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1529 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1530 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1531 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1532 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 1533 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1534 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1535 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1536 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1537 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1538 | 20004646 | MSX2 over-expression alone induced ALP expression, whereas knockdown of MSX2 with small interfering RNA completely blocked TNF-alpha-induced ALP expression. |
| 1539 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1540 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1541 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1542 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1543 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1544 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 1545 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1546 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1547 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1548 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1549 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1550 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 1551 | 19996381 | SIRT1 inhibits inflammatory pathways in macrophages and modulates insulin sensitivity. |
| 1552 | 19996381 | SIRT1 inhibits inflammatory pathways in macrophages and modulates insulin sensitivity. |
| 1553 | 19996381 | The mammalian silent information regulator 2 homolog SIRT1 modulates several physiological processes important for life span, and a potential role of SIRT1 in the regulation of insulin sensitivity has been shown. |
| 1554 | 19996381 | The mammalian silent information regulator 2 homolog SIRT1 modulates several physiological processes important for life span, and a potential role of SIRT1 in the regulation of insulin sensitivity has been shown. |
| 1555 | 19996381 | Here, we show that knockdown of SIRT1 in the mouse macrophage RAW264.7 cell line and in intraperitoneal macrophages broadly activates the JNK and IKK inflammatory pathways and increases LPS-stimulated TNFalpha secretion. |
| 1556 | 19996381 | Here, we show that knockdown of SIRT1 in the mouse macrophage RAW264.7 cell line and in intraperitoneal macrophages broadly activates the JNK and IKK inflammatory pathways and increases LPS-stimulated TNFalpha secretion. |
| 1557 | 19996381 | We also demonstrate that SIRT1 activators inhibit LPS-stimulated inflammatory pathways, as well as secretion of TNFalpha, in a SIRT1-dependent manner in RAW264.7 cells and in primary intraperitoneal macrophages. |
| 1558 | 19996381 | We also demonstrate that SIRT1 activators inhibit LPS-stimulated inflammatory pathways, as well as secretion of TNFalpha, in a SIRT1-dependent manner in RAW264.7 cells and in primary intraperitoneal macrophages. |
| 1559 | 19996381 | Treatment of Zucker fatty rats with a SIRT1 activator leads to greatly improved glucose tolerance, reduced hyperinsulinemia, and enhanced systemic insulin sensitivity during glucose clamp studies. |
| 1560 | 19996381 | Treatment of Zucker fatty rats with a SIRT1 activator leads to greatly improved glucose tolerance, reduced hyperinsulinemia, and enhanced systemic insulin sensitivity during glucose clamp studies. |
| 1561 | 19996381 | These in vivo insulin-sensitizing effects were accompanied by a reduction in tissue inflammation markers and a decrease in the adipose tissue macrophage proinflammatory state, fully consistent with the in vitro effects of SIRT1 in macrophages. |
| 1562 | 19996381 | These in vivo insulin-sensitizing effects were accompanied by a reduction in tissue inflammation markers and a decrease in the adipose tissue macrophage proinflammatory state, fully consistent with the in vitro effects of SIRT1 in macrophages. |
| 1563 | 19996381 | In conclusion, these results define a novel role for SIRT1 as an important regulator of macrophage inflammatory responses in the context of insulin resistance and raise the possibility that targeting of SIRT1 might be a useful strategy for treating the inflammatory component of metabolic diseases. |
| 1564 | 19996381 | In conclusion, these results define a novel role for SIRT1 as an important regulator of macrophage inflammatory responses in the context of insulin resistance and raise the possibility that targeting of SIRT1 might be a useful strategy for treating the inflammatory component of metabolic diseases. |
| 1565 | 19959191 | In addition, levels of serum HMGB1, tumor necrosis factor-α, and interleukin-6 were increased in diabetic rats. |
| 1566 | 19947950 | TZDs (thiazolidinediones) are prescribed as anti-Type II diabetes drugs, but little is known regarding whether TZDs regulate the expression of sPLA2 (secretory phospholipase A2) in macrophages. |
| 1567 | 19947950 | We have investigated the effects of pioglitazone on LPS (lipopolysaccharide)-induced production of TNF-alpha (tumour necrosis factor alpha), sPLA2-V and -X (groups V and X sPLA2) in RAW 264.7 macrophages. |
| 1568 | 19947910 | Throughout the differentiation, AP-18 cells expressed Pref-1, LPL, C/EBP beta, C/EBP delta, RXR alpha, C/EBP alpha, PPAR gamma, RXR gamma, aP2, GLUT4, SCD1, UCP2, UCP3, TNFalpha, resistin, leptin, adiponectin and PAI-1 genes, but not the UCP1 gene, indicating that the cell is derived from WAT (white adipose tissue). |
| 1569 | 19940327 | Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis. |
| 1570 | 19940327 | In human studies, the influence of resistin on the development of insulin resistance is controversial. |
| 1571 | 19929783 | Branched-chain amino acids and pigment epithelium-derived factor: novel therapeutic agents for hepatitis c virus-associated insulin resistance. |
| 1572 | 19929783 | HCV directly causes insulin resistance through HCV core protein-elicited proteasomal degradation of insulin receptor substrates and subsequent inactivation of intracellular insulin signaling molecules such as Akt. |
| 1573 | 19929783 | Furthermore, tumor necrosis factor-alpha (TNF-alpha) and/or triglyceride accumulation-induced nuclear factor-kappaB (NF-kappaB) activation in the liver is shown to play a role in insulin resistance in patients with HCV-related chronic liver disease as well. |
| 1574 | 19929783 | We, along with others, have recently found that branched-chain amino acids (BCAAs) and pigment epithelium-derived factor (PEDF) could improve the HCV-associated insulin resistance via suppression of NF-kappaB and preservation of insulin signaling pathway. |
| 1575 | 19929783 | In this review, we discuss the mechanisms for the actions of BCAAs and PEDF, and their clinical implications in insulin resistance of chronic liver disease in patients with HCV infection. |
| 1576 | 19917698 | Activation of TLRs, particularly TLR2 and TLR4, promotes chronic systemic inflammation. |
| 1577 | 19917698 | However, recent work showed that an increased percentage of circulating B cells from inflammatory disease patients express TLR2 and TLR4, and that TLR engagement on B cells resulted in unexpected changes in gene expression. |
| 1578 | 19917698 | Some cytokines (IL-1beta and IL-10) are predominantly regulated by TLR4, but others (IL-8 and TNF-alpha) are predominantly regulated by TLR2, due in part to TLR-dictated changes in transcription factor/promoter association. |
| 1579 | 19917698 | TLR2 and TLR9 also regulate B cell TLR4 expression, demonstrating that TLR cross-talk controls B cell responses at multiple levels. |
| 1580 | 19914138 | We investigated the effect of four distinct AGE subtypes (AGE-2/AGE-3/AGE-4/AGE-5) on the expressions of intracellular adhesion molecule (ICAM)-1, B7.1, B7.2 and CD40 on monocytes, the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha and the proliferation of T-cells during human mixed lymphocyte reaction (MLR). |
| 1581 | 19902175 | Impaired wound healing in mouse models of diabetes is mediated by TNF-alpha dysregulation and associated with enhanced activation of forkhead box O1 (FOXO1). |
| 1582 | 19885845 | CA or EA at 5% significantly decreased the levels of plasma HbA1c, urinary glycated albumin, renal carboxymethyllysine, pentosidine, sorbitol and fructose (p<0.05), and significantly diminished renal activity of aldose reductase and sorbitol dehydrogenase, as well as suppressed renal aldose reductase mRNA expression (p<0.05). |
| 1583 | 19885845 | CA or EA at 5% significantly decreased the levels of plasma HbA1c, urinary glycated albumin, renal carboxymethyllysine, pentosidine, sorbitol and fructose (p<0.05), and significantly diminished renal activity of aldose reductase and sorbitol dehydrogenase, as well as suppressed renal aldose reductase mRNA expression (p<0.05). |
| 1584 | 19885845 | CA or EA dose dependently lowered renal levels of IL-6, IL-1beta, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein 1 (MCP-1) (p<0.05). |
| 1585 | 19885845 | CA or EA dose dependently lowered renal levels of IL-6, IL-1beta, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein 1 (MCP-1) (p<0.05). |
| 1586 | 19885845 | Furthermore, CA or EA dose dependently down-regulated tumor necrosis factor-alpha and monocyte chemoattractant protein-1 mRNA expression in kidney (p<0.05). |
| 1587 | 19885845 | Furthermore, CA or EA dose dependently down-regulated tumor necrosis factor-alpha and monocyte chemoattractant protein-1 mRNA expression in kidney (p<0.05). |
| 1588 | 19861974 | In this study, we investigated the actions of the peroxisome proliferator-activated receptor (PPAR)-gamma agonist darglitazone in treating diabetes and promoting recovery after a hypoxic-ischemic (H/I) insult in the diabetic ob/ob mouse. |
| 1589 | 19861974 | Microglial and astrocytic activation monitored by cytokine expression (interleukin-1beta and tumor necrosis factor-alpha) and in situ hybridization studies (bfl1 and glial fibrillary acidic protein) suggest a biphasic inflammatory response, with darglitazone restoring the compromised proinflammatory response(s) in the diabetic mouse at 4 h but suppressing subsequent inflammatory responses at 8 and 24 h in both control and diabetic mice. |
| 1590 | 19860210 | The interaction of adipocytokines (TNF-alpha, adiponectin) with oxidative stress and lipid peroxidation has been postulated to play a key role in NASH. |
| 1591 | 19857486 | Cell-to-cell interaction through binding of intercellular adhesion molecule-1 (ICAM-1) and CD40 on monocytes to their ligands on T-cells plays crucial roles in cytokine production. |
| 1592 | 19857486 | In a previous study, we found that glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells. beta(2)-adrenoceptor stimulation has been demonstrated to modulate the production of inflammatory mediators. |
| 1593 | 19857054 | Tart cherry intake was associated with reduced hyperlipidemia, percentage fat mass, abdominal fat (retroperitoneal) weight, retroperitoneal interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) expression, and plasma IL-6 and TNF-alpha. |
| 1594 | 19857054 | Tart cherry intake was associated with reduced hyperlipidemia, percentage fat mass, abdominal fat (retroperitoneal) weight, retroperitoneal interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) expression, and plasma IL-6 and TNF-alpha. |
| 1595 | 19857054 | Tart cherry diet also increased retroperitoneal fat PPAR-alpha and PPAR-gamma mRNA (P = .12), decreased IL-6 and TNF-alpha mRNA, and decreased nuclear factor kappaB activity. |
| 1596 | 19857054 | Tart cherry diet also increased retroperitoneal fat PPAR-alpha and PPAR-gamma mRNA (P = .12), decreased IL-6 and TNF-alpha mRNA, and decreased nuclear factor kappaB activity. |
| 1597 | 19854869 | Renal concentrations of TGF-beta(1), vascular endothelial growth factor, endothelin-1, TNF-alpha, monocyte chemoattractant protein-1, lipid peroxidation products, and nitrotyrosine were increased in diabetic rats, and all these changes as well as an increase in urinary TNF-alpha excretion were completely or partially prevented by ISO and GPI-15427. |
| 1598 | 19848310 | The association between the increase in life expectancy in humans and age-related changes in the immune system promotes that individuals are exposed longer to endogenous and environment antigens which allows an activation of the innate immune system and the subsequent establishment of a low grade chronic inflammation state with an increased expression of proinflammatory cytokines (tumor necrosis factor alpha, interleukin 6, etc.). |
| 1599 | 19848310 | This inflammatory state referred as inflammaging is characterized by a inflammatory origin of aging given by the activation of cellular systems responsible of gene promotion and suppression as the nuclear factor kappa B, sirtuins, forkhead box O and KLOTHO, who are directly or indirectly involved in cellular mechanisms of resistance to oxidative stress, apoptosis and nucleic acids transcriptional mistakes repair. |
| 1600 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1601 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1602 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1603 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1604 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1605 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1606 | 19846171 | The association of tumor necrosis factor alpha receptor 2 and tumor necrosis factor alpha with insulin resistance and the influence of adipose tissue biomarkers in humans. |
| 1607 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1608 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1609 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1610 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1611 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1612 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1613 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 1614 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1615 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1616 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1617 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1618 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1619 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1620 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 1621 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1622 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1623 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1624 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1625 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1626 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1627 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 1628 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1629 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1630 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1631 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1632 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1633 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1634 | 19846171 | Tumor necrosis factor alpha activity was measured by plasma tumor necrosis factor alpha receptor 2 (TNFr2) or TNFalpha; possible confounders included adipose tissue biomarkers (plasma adiponectin, resistin, and triglycerides). |
| 1635 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1636 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1637 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1638 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1639 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1640 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1641 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 1642 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1643 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1644 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1645 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1646 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1647 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1648 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 1649 | 19845893 | AMP deaminase-1 (AMPD1, C34T) and adenosine deaminase (ADA, G22A), were analyzed. |
| 1650 | 19845893 | There were no associations between AMPD1 C34T or ADA G22A genotypes and TNF-alpha or its receptors. |
| 1651 | 19845868 | Generally, there are significant correlations between body mass index and increased c-reactive protein and decreased adiponectin levels in children; these levels tend to be improved in interventions resulting in approximately 5% weight loss, regardless of the type or length of intervention. |
| 1652 | 19845868 | There is a need for further research measuring other inflammatory mediators (e.g. tumour necrosis factor (TNF)-alpha, IL-6, IL-8) and histological studies examining immune cell infiltration in adipose tissue depots in obese children. |
| 1653 | 19845589 | Pancreatic insulin secretion, hepatic insulin uptake, pancreatic antibodies and proinflammatory cytokines in serum (tumor necrosis factor-alpha, intereukin-6, high-sensitive C-reactive protein) were also assessed. |
| 1654 | 19837795 | Insulin resistance in hyperthyroidism: the role of IL6 and TNF alpha. |
| 1655 | 19820199 | The expression of profibrotic factors, transforming growth factor-beta (TGF-beta1), connective tissue growth factor, and matrix proteins was increased, and the TGF-beta1-linked transcription factors phospho-Smad3/4 and activator protein-1 were activated in the DM1 myocardium. |
| 1656 | 19820199 | Proapoptotic molecules FasL, Fas, Bax, and cleaved caspase-3 were also augmented. |
| 1657 | 19820199 | In addition, hypertension was associated with activation of NF-kappaB, increased inflammatory cell infiltrate, and expression of the mediators [interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, monocyte chemoattractant protein 1, vascular cell adhesion molecule 1, angiotensinogen, and oxidants], which were absent in long-term DM1. |
| 1658 | 19820199 | In cultured cardiomyocytes, IL-10, TGF-beta1, and catalase blocked the glucose-stimulated expression of proinflammatory genes. |
| 1659 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1660 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1661 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1662 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1663 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1664 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1665 | 19819972 | Short-term regulation of tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes is mediated through the inducible nitric oxide synthase/nitric oxide-dependent pathway. |
| 1666 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1667 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1668 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1669 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1670 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1671 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1672 | 19819972 | HBr), an adenylyl cyclase inhibitor (SQ22536), and a guanylyl cyclase inhibitor (LY83583) were used to investigate the involvement of iNOS, cAMP, and cGMP in TNF-alpha-induced lipolysis. |
| 1673 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1674 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1675 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1676 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1677 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1678 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1679 | 19819972 | Transient transfection with iNOS short hairpin RNA was performed to confirm the involvement of iNOS in TNF-alpha-induced lipolysis. |
| 1680 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1681 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1682 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1683 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1684 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1685 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1686 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 1687 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1688 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1689 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1690 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1691 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1692 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1693 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 1694 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1695 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1696 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1697 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1698 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1699 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1700 | 19819972 | Suppression of TNF-alpha-induced iNOS expression using short hairpin RNA significantly reduced TNF-alpha-induced lipolysis. |
| 1701 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1702 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1703 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1704 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1705 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1706 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1707 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 1708 | 19808894 | Tpl2 kinase is upregulated in adipose tissue in obesity and may mediate interleukin-1beta and tumor necrosis factor-{alpha} effects on extracellular signal-regulated kinase activation and lipolysis. |
| 1709 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1710 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1711 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1712 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1713 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1714 | 19801900 | Vaspin can not inhibit TNF-alpha-induced inflammation of human umbilical vein endothelial cells. |
| 1715 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1716 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1717 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1718 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1719 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1720 | 19801900 | We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. |
| 1721 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1722 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1723 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1724 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1725 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1726 | 19801900 | Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. |
| 1727 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1728 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1729 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1730 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1731 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1732 | 19801900 | Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt. |
| 1733 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1734 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1735 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1736 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1737 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1738 | 19801900 | Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. |
| 1739 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1740 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1741 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1742 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1743 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1744 | 19801900 | The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury. |
| 1745 | 19798065 | Transient receptor potential vanilloid type-1 (TRPV-1), peroxisome proliferator-activated receptor (PPAR)-alpha, and PPARgamma coactivator-1alpha (PGC-1alpha) mRNAs were also measured by RT-PCR, and PPARalpha luciferase assays were performed. |
| 1746 | 19798065 | Dietary capsaicin lowered fasting glucose, insulin, leptin levels, and markedly reduced the impairment of glucose tolerance in obese mice. |
| 1747 | 19798065 | Levels of tumor necrosis factor-alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), and interleukin (IL)-6 mRNAs and proteins in adipose tissue and liver decreased markedly, as did macrophage infiltration, hepatic triglycerides, and TRPV-1 expression in adipose tissue. |
| 1748 | 19798065 | At the same time, the mRNA/protein of adiponectin in the adipose tissue and PPARalpha/PGC-1alpha mRNA in the liver increased. |
| 1749 | 19798065 | The effects of capsaicin in adipose tissue and liver are related to its dual action on PPARalpha and TRPV-1 expression/activation. |
| 1750 | 19789291 | Furthermore, LDR protection against diabetes-induced renal dysfunction and pathological changes was associated with a significant suppression of diabetes-increased systemic and renal inflammation, shown by significant increases in serum and renal TNFalpha, ICAM-1, IL-18, MCP-1, and PAI-1 contents. |
| 1751 | 19789062 | Key proinflammatory cytokines secreted by adipocytes include tumor necrosis factor-alpha, interleukin-6, leptin, resistin, and plasminogen activator inhibitor-1. |
| 1752 | 19789061 | Excess adipose tissue acts as an endocrine organ to produce excess free fatty acids, as well as tumor necrosis factor-alpha, interleukin-6, leptin, and plasminogen activator inhibitor-1. |
| 1753 | 19786623 | Oral administration of TC-7020 reduced weight gain and food intake, reduced elevated glucose and glycated hemoglobin levels, and lowered elevated plasma levels of triglycerides and the proinflammatory cytokine tumor necrosis factor-alpha. |
| 1754 | 19786623 | Prevention of weight gain, decreased food intake, and normalization of glucose levels were also blocked by the Janus kinase 2 (JAK2) inhibitor alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide (AG-490), suggesting that these effects involve linkage of alpha7 nAChRs to the JAK2-signal transducer and activator of transcription 3 signaling pathway. |
| 1755 | 19782393 | We demonstrated that a poly(ethylene glycol)-containing hydrogel network, formed by native chemical ligation and presenting an inhibitory peptide for islet cell surface IL-1 receptor, was able to maintain the viability of encapsulated islet cells in the presence of a combination of cytokines including IL-1 beta, TNF-alpha, and INF-gamma. |
| 1756 | 19776662 | The inflammatory response was manifested by increased gene expression of tumor necrosis factor-alpha and intercellular adhesion molecule-1 (ICAM-1) as well as elevated protein levels of soluble ICAM-1. |
| 1757 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1758 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1759 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1760 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1761 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1762 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1763 | 19769745 | Circulating tumour necrosis factor-alpha (TNFalpha) levels, which are elevated in obesity-associated insulin resistance and diabetes, inhibit insulin signalling at several points in the signalling cascade. |
| 1764 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1765 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1766 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1767 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1768 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1769 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1770 | 19769745 | As the transcription factor Foxa2 has been implicated, in part, in the regulation of gluconeogenic genes, we studied the effects of TNFalpha and/or insulin on its cellular status in hepatocytes, followed by an assessment of its occupancy on the phosphoenolpyruvate carboxykinase (PEPCK) promoter. |
| 1771 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1772 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1773 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1774 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1775 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1776 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1777 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 1778 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1779 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1780 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1781 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1782 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1783 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1784 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 1785 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1786 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1787 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1788 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1789 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1790 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1791 | 19769745 | TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. |
| 1792 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1793 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1794 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1795 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1796 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1797 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1798 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 1799 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1800 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1801 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1802 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1803 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1804 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1805 | 19769745 | Several other well-known mediators of insulin action in the liver in general and of gluconeogenic genes in particular include Foxo1, PGC-1 and SREBP-1c. |
| 1806 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1807 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1808 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1809 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1810 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1811 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1812 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 1813 | 19769609 | (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II-dependent and -independent effects. |
| 1814 | 19769609 | (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II-dependent and -independent effects. |
| 1815 | 19769609 | (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II-dependent and -independent effects. |
| 1816 | 19769609 | (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II-dependent and -independent effects. |
| 1817 | 19769609 | (Pro)renin receptor (PRR) binding to renin or prorenin mediates angiotensin (Ang) II-dependent and -independent effects. |
| 1818 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 1819 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 1820 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 1821 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 1822 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 1823 | 19769609 | Compared with values in normoglycaemic control rats, UACR and RIF AngII, TNF-alpha and IL-1beta were significantly higher in untreated diabetic rats. |
| 1824 | 19769609 | Compared with values in normoglycaemic control rats, UACR and RIF AngII, TNF-alpha and IL-1beta were significantly higher in untreated diabetic rats. |
| 1825 | 19769609 | Compared with values in normoglycaemic control rats, UACR and RIF AngII, TNF-alpha and IL-1beta were significantly higher in untreated diabetic rats. |
| 1826 | 19769609 | Compared with values in normoglycaemic control rats, UACR and RIF AngII, TNF-alpha and IL-1beta were significantly higher in untreated diabetic rats. |
| 1827 | 19769609 | Compared with values in normoglycaemic control rats, UACR and RIF AngII, TNF-alpha and IL-1beta were significantly higher in untreated diabetic rats. |
| 1828 | 19769609 | Treatment of diabetic rats with the PRRB or valsartan alone and in combination significantly reduced UACR and RIF TNF-alpha and IL-1beta levels. |
| 1829 | 19769609 | Treatment of diabetic rats with the PRRB or valsartan alone and in combination significantly reduced UACR and RIF TNF-alpha and IL-1beta levels. |
| 1830 | 19769609 | Treatment of diabetic rats with the PRRB or valsartan alone and in combination significantly reduced UACR and RIF TNF-alpha and IL-1beta levels. |
| 1831 | 19769609 | Treatment of diabetic rats with the PRRB or valsartan alone and in combination significantly reduced UACR and RIF TNF-alpha and IL-1beta levels. |
| 1832 | 19769609 | Treatment of diabetic rats with the PRRB or valsartan alone and in combination significantly reduced UACR and RIF TNF-alpha and IL-1beta levels. |
| 1833 | 19769609 | Renal expression of TNF-alpha and IL-1beta was higher in untreated diabetic rats than in control rats, but was reduced significantly following treatment with PRRB or valsartan alone and in combination. |
| 1834 | 19769609 | Renal expression of TNF-alpha and IL-1beta was higher in untreated diabetic rats than in control rats, but was reduced significantly following treatment with PRRB or valsartan alone and in combination. |
| 1835 | 19769609 | Renal expression of TNF-alpha and IL-1beta was higher in untreated diabetic rats than in control rats, but was reduced significantly following treatment with PRRB or valsartan alone and in combination. |
| 1836 | 19769609 | Renal expression of TNF-alpha and IL-1beta was higher in untreated diabetic rats than in control rats, but was reduced significantly following treatment with PRRB or valsartan alone and in combination. |
| 1837 | 19769609 | Renal expression of TNF-alpha and IL-1beta was higher in untreated diabetic rats than in control rats, but was reduced significantly following treatment with PRRB or valsartan alone and in combination. |
| 1838 | 19769609 | The PRRB had no effect on RIF AngII levels, whereas valsartan alone and in combination with the PRRB significantly increased AngII levels. 4. |
| 1839 | 19769609 | The PRRB had no effect on RIF AngII levels, whereas valsartan alone and in combination with the PRRB significantly increased AngII levels. 4. |
| 1840 | 19769609 | The PRRB had no effect on RIF AngII levels, whereas valsartan alone and in combination with the PRRB significantly increased AngII levels. 4. |
| 1841 | 19769609 | The PRRB had no effect on RIF AngII levels, whereas valsartan alone and in combination with the PRRB significantly increased AngII levels. 4. |
| 1842 | 19769609 | The PRRB had no effect on RIF AngII levels, whereas valsartan alone and in combination with the PRRB significantly increased AngII levels. 4. |
| 1843 | 19769609 | In conclusion, the PRR is involved in the development and progression of kidney disease in diabetes by enhancing renal production of the inflammatory cytokines TNF-alpha and IL-1beta, independent of renal AngII effects. |
| 1844 | 19769609 | In conclusion, the PRR is involved in the development and progression of kidney disease in diabetes by enhancing renal production of the inflammatory cytokines TNF-alpha and IL-1beta, independent of renal AngII effects. |
| 1845 | 19769609 | In conclusion, the PRR is involved in the development and progression of kidney disease in diabetes by enhancing renal production of the inflammatory cytokines TNF-alpha and IL-1beta, independent of renal AngII effects. |
| 1846 | 19769609 | In conclusion, the PRR is involved in the development and progression of kidney disease in diabetes by enhancing renal production of the inflammatory cytokines TNF-alpha and IL-1beta, independent of renal AngII effects. |
| 1847 | 19769609 | In conclusion, the PRR is involved in the development and progression of kidney disease in diabetes by enhancing renal production of the inflammatory cytokines TNF-alpha and IL-1beta, independent of renal AngII effects. |
| 1848 | 19768249 | Mature adipocytes secrete adipokines, such as TNFalpha, IL-6, leptine and adiponectin, and lipokine, the palmitoleic acid omega-7. |
| 1849 | 19764353 | Compared with the diabetic (STZ-treated) controls, the diabetic-heatstroke rats displayed higher levels of body temperature, intracranial pressure, serum nitric oxide metabolite, tumor necrosis factor-alpha and dihydroxybenzoic acid, blood urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. |
| 1850 | 19763396 | Pancreatic beta cell damage caused by proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumor necrosis factor-alpha (TNFalpha) is a key event in the pathogenesis of type 1 diabetes. |
| 1851 | 19763396 | Pancreatic beta cell damage caused by proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumor necrosis factor-alpha (TNFalpha) is a key event in the pathogenesis of type 1 diabetes. |
| 1852 | 19763396 | The suppressor of cytokine signaling-1 (SOCS-1) blocks IFNgamma-induced signaling and prevents diabetes in the non-obese diabetic mouse. |
| 1853 | 19763396 | The suppressor of cytokine signaling-1 (SOCS-1) blocks IFNgamma-induced signaling and prevents diabetes in the non-obese diabetic mouse. |
| 1854 | 19763396 | We demonstrate that SOCS-1 does not prevent increase in NO production and decrease in glucose-stimulated insulin secretion in the presence of IL-1beta, IFNgamma, TNFalpha. |
| 1855 | 19763396 | We demonstrate that SOCS-1 does not prevent increase in NO production and decrease in glucose-stimulated insulin secretion in the presence of IL-1beta, IFNgamma, TNFalpha. |
| 1856 | 19763396 | Our data suggest that SOCS-1 overexpression may not be sufficient in preventing all the biological activities of IFNgamma in beta cells. |
| 1857 | 19763396 | Our data suggest that SOCS-1 overexpression may not be sufficient in preventing all the biological activities of IFNgamma in beta cells. |
| 1858 | 19763396 | In summary, we show that interference with IFNgamma signal transduction pathways by SOCS-1 inhibits cytokine-stimulated pancreatic beta cell death. |
| 1859 | 19763396 | In summary, we show that interference with IFNgamma signal transduction pathways by SOCS-1 inhibits cytokine-stimulated pancreatic beta cell death. |
| 1860 | 19758820 | Association of serum amyloid A levels with adipocyte size and serum levels of adipokines: differences between men and women. |
| 1861 | 19758820 | The aim of this study was to characterize the association between adipocyte enlargement and circulating levels of serum amyloid A (SAA). |
| 1862 | 19758820 | Adipocyte diameter as well as circulating levels of SAA, C-reactive protein (CRP), adiponectin, leptin, interleukin-6, tumor necrosis factor alpha, glucose and insulin were measured. |
| 1863 | 19758820 | SAA levels were weakly but positively correlated with BMI (p=0.043) and % body fat (p=0.027) in all subjects as well as subcutaneous adipocyte diameter (p=0.034) in women. |
| 1864 | 19758820 | Furthermore, in all subjects we found correlations between SAA levels and levels of CRP (p<0.001), interleukin-6 (p<0.001), leptin (p=0.003), insulin (p=0.006), HbA1c (p=0.02) and HOMA-IR (p=0.002). |
| 1865 | 19753653 | It was shown that the DAA treatment suppressed the production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNFalpha) (proinflammatory cytokines) and increased that of adiponectin (an anti-inflammatory cytokine). |
| 1866 | 19745063 | The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. |
| 1867 | 19745063 | The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. |
| 1868 | 19745063 | The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. |
| 1869 | 19745063 | The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. |
| 1870 | 19745063 | FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. |
| 1871 | 19745063 | FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. |
| 1872 | 19745063 | FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. |
| 1873 | 19745063 | FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. |
| 1874 | 19745063 | An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. |
| 1875 | 19745063 | An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. |
| 1876 | 19745063 | An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. |
| 1877 | 19745063 | An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. |
| 1878 | 19745063 | These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage. |
| 1879 | 19745063 | These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage. |
| 1880 | 19745063 | These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage. |
| 1881 | 19745063 | These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage. |
| 1882 | 19722571 | PA treatments at 2% and 4% significantly lowered plasminogen activator inhibitor-1 activity and fibrinogen level; increased plasma activity of antithrombin-III and protein C; decreased triglyceride content in plasma, heart, and liver; elevated glutathione level and the retention of glutathione peroxidase and catalase activities in heart and kidney. |
| 1883 | 19722571 | PA treatments at 2% and 4% also significantly lowered plasma C-reactive protein and von Willebrand factor levels and reduced interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 levels in heart and kidney. |
| 1884 | 19721920 | At the first stage, the fat tissue of the obese patient becomes resistant to the action of insulin due to the effect of some of these adipokines such as tumour necrosis alpha (TNF-alpha) or interleukine-6 (IL-6). |
| 1885 | 19721200 | Periodontal pathogens such as P. gingivalis lipopolysaccharide (P-LPS) and several cytokines (TNF-alpha, IL-1 and IL-6) stimulate osteoclast differentiation in gingival connective tissue. |
| 1886 | 19721200 | Periodontal pathogens such as P. gingivalis lipopolysaccharide (P-LPS) and several cytokines (TNF-alpha, IL-1 and IL-6) stimulate osteoclast differentiation in gingival connective tissue. |
| 1887 | 19721200 | Recently, many researches demonstrated that periodontitis affected diabetic condition, in which periodontal pathogen like P-LPS and TNF-alpha possibly elevated insulin resistance by inhibiting glucose incorporation into smooth muscle cells. |
| 1888 | 19721200 | Recently, many researches demonstrated that periodontitis affected diabetic condition, in which periodontal pathogen like P-LPS and TNF-alpha possibly elevated insulin resistance by inhibiting glucose incorporation into smooth muscle cells. |
| 1889 | 19707732 | They were found to be considerably more active in inhibiting this interaction than the tumor necrosis factor (TNF)-R1-TNF-alpha or B cell-activating factor (BAFF)-R-BAFF interaction, which are members of the same family. |
| 1890 | 19707732 | They specifically inhibited CD154-induced cell responses in human B cells as well as in THP-1 myeloid cells, which can serve as surrogate dendritic cells, at concentrations well below their cytotoxic concentrations determined in the same cells. |
| 1891 | 19707732 | Flow cytometry experiments confirmed their ability to inhibit the CD154-induced, but not the Staphylococcus aureus Cowan I- or phorbol 12-myristate 13-acetate-induced increase in the surface expression of CD54, CD40, and major histocompatibility complex class II. |
| 1892 | 19700629 | Because the engagement of intercellular adhesion molecule-1 (ICAM-1), B7.1, B7.2, and CD40 on monocytes with their ligands on T cells plays roles in cytokine production, we investigated the effects of AGE-2 and AGE-3 on the expressions of ICAM-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon gamma and tumor necrosis factor alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells and their modulation by prostaglandin E(2) (PGE(2)). |
| 1893 | 19700629 | The stimulation of EP(2) and EP(4) receptors is reported to increase cAMP levels. |
| 1894 | 19700629 | The effects of PGE(2) were reversed by a protein kinase A (PKA) inhibitor, H89, and mimicked by a dibutyryl cAMP and an adenylate cyclase activator, forskolin. |
| 1895 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1896 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1897 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1898 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1899 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1900 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1901 | 19690174 | Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. |
| 1902 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1903 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1904 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1905 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1906 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1907 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1908 | 19690174 | In healthy humans, TNF-alpha infusion induces skeletal muscle insulin resistance. |
| 1909 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1910 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1911 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1912 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1913 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1914 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1915 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 1916 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1917 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1918 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1919 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1920 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1921 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1922 | 19690174 | Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. |
| 1923 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1924 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1925 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1926 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1927 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1928 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1929 | 19690174 | This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. |
| 1930 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1931 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1932 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1933 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1934 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1935 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1936 | 19690174 | Strikingly, TNF-alpha treatment decreased IRS-2 protein level by 46 +/- 7% versus control, although mRNA expression was unchanged. |
| 1937 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1938 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1939 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1940 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1941 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1942 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1943 | 19690174 | While TNF-alpha treatment increased MAP4K4 mRNA expression by 33 +/- 5%, knockdown of MAP4K4 by siRNA-protected beta cells against the detrimental effects of TNF-alpha on both insulin secretion and signaling. |
| 1944 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1945 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1946 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1947 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1948 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1949 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1950 | 19690174 | We thus identify MAP4K4 as a key upstream mediator of TNF-alpha action on the beta cell, making it a potential therapeutic target for preservation of beta cell function in type 2 diabetes. |
| 1951 | 19684849 | Risk factors were compared according to current use of corticosteroids, methotrexate, antimalarials, NSAIDs, COX-2 inhibitors, leflunomide and TNF-alpha blockers. |
| 1952 | 19684849 | Risk factors were compared according to current use of corticosteroids, methotrexate, antimalarials, NSAIDs, COX-2 inhibitors, leflunomide and TNF-alpha blockers. |
| 1953 | 19684849 | RESULTS: No cardiovascular risk factor differed significantly among current users and non-users of NSAIDs, COX-2 inhibitors, methotrexate and TNF-alpha blockers. |
| 1954 | 19684849 | RESULTS: No cardiovascular risk factor differed significantly among current users and non-users of NSAIDs, COX-2 inhibitors, methotrexate and TNF-alpha blockers. |
| 1955 | 19680232 | Herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF14), which serves as a receptor for herpes viruses and cytokines such as lymphotoxin-alpha (LT-alpha) and LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for herpes virus entry on T cells). |
| 1956 | 19680232 | Herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF14), which serves as a receptor for herpes viruses and cytokines such as lymphotoxin-alpha (LT-alpha) and LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for herpes virus entry on T cells). |
| 1957 | 19680232 | HVEM -241GA and -14AG gene polymorphisms were associated with obesity, diastolic pressure, several inflammatory parameters (C-reactive protein and interleukin 18 (IL-18)), and circulating LIGHT concentrations. |
| 1958 | 19680232 | HVEM -241GA and -14AG gene polymorphisms were associated with obesity, diastolic pressure, several inflammatory parameters (C-reactive protein and interleukin 18 (IL-18)), and circulating LIGHT concentrations. |
| 1959 | 19680232 | These results provide evidences of an existing relationship between HVEM and obesity, which suggest that this TNF superfamily receptor could be involved in the pathogenesis of obesity and inflammation-related activity. |
| 1960 | 19680232 | These results provide evidences of an existing relationship between HVEM and obesity, which suggest that this TNF superfamily receptor could be involved in the pathogenesis of obesity and inflammation-related activity. |
| 1961 | 19674864 | Weight loss also led to notable decreases in plasma tumor necrosis factor-alpha (TNF-alpha), haptoglobin, and C-reactive protein concentrations (P<0.05 for all), suggesting improvement of a subclinical inflammatory state associated with obesity. |
| 1962 | 19674864 | Weight loss also led to notable decreases in plasma tumor necrosis factor-alpha (TNF-alpha), haptoglobin, and C-reactive protein concentrations (P<0.05 for all), suggesting improvement of a subclinical inflammatory state associated with obesity. |
| 1963 | 19674864 | Concurrent decreases in TNF-alpha and adipose tissue mass suggest that in dogs, as in humans, this adipokine may be implicated in the insulin resistance of obesity. |
| 1964 | 19674864 | Concurrent decreases in TNF-alpha and adipose tissue mass suggest that in dogs, as in humans, this adipokine may be implicated in the insulin resistance of obesity. |
| 1965 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1966 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1967 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1968 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1969 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1970 | 19666844 | Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. |
| 1971 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1972 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1973 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1974 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1975 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1976 | 19666844 | Tumor necrosis factor-alpha (TNF-alpha) upregulates the expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in type 2 diabetes. |
| 1977 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1978 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1979 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1980 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1981 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1982 | 19666844 | We hypothesized that TNF-alpha and MCP-1 may interact to contribute to the evolution of vascular inflammation and endothelial dysfunction in coronary arterioles in type 2 diabetes. |
| 1983 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1984 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1985 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1986 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1987 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1988 | 19666844 | Anti-TNF-alpha or anti-MCP-1 markedly reduced macrophage infiltration and the number of MCP-1-positive endothelium in Lepr(db) mice. |
| 1989 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1990 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1991 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1992 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1993 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1994 | 19666844 | The neutralization of TNF-alpha or anti-MCP-1 reduced the expression of adhesion molecules, suggesting that proinflammatory cytokines interact to amplify the signaling process that leads to vascular dysfunction. |
| 1995 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 1996 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 1997 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 1998 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 1999 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 2000 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 2001 | 19666548 | Specific blockade of IL-1 activity by the IL-1 receptor antagonist (IL-1Ra) reduced the release of inflammatory cytokines/chemokines from GK islets in vitro and from mouse islets exposed to metabolic stress. |
| 2002 | 19666548 | Islets from mice deficient in IL-1beta or MyD88 challenged with glucose and palmitate in vitro also produced significantly less IL-6 and chemokines. |
| 2003 | 19666548 | In addition, islet-derived proinflammatory cytokines/chemokines (IL-1beta, IL-6, TNFalpha, KC, MCP-1, and MIP-1alpha) and islet CD68(+), MHC II(+), and CD53(+) immune cell infiltration were reduced by IL-1Ra treatment. |
| 2004 | 19666548 | Rather than being directly cytotoxic, IL-1beta may drive tissue inflammation that impacts on both beta cell functional mass and insulin sensitivity in type 2 diabetes. |
| 2005 | 19651784 | C1q tumor necrosis factor alpha-related protein isoform 5 is increased in mitochondrial DNA-depleted myocytes and activates AMP-activated protein kinase. |
| 2006 | 19651784 | C1q tumor necrosis factor alpha-related protein isoform 5 is increased in mitochondrial DNA-depleted myocytes and activates AMP-activated protein kinase. |
| 2007 | 19651784 | Here we show that the expression of C1q tumor necrosis factor alpha-related protein isoform 5 (C1QTNF5) is drastically increased following depletion of mtDNA in myocytes. |
| 2008 | 19651784 | Here we show that the expression of C1q tumor necrosis factor alpha-related protein isoform 5 (C1QTNF5) is drastically increased following depletion of mtDNA in myocytes. |
| 2009 | 19651784 | C1QTNF5 is homologous to adiponectin in respect to domain structure, and its expression and secretion from myocytes correlated negatively with the cellular mtDNA content. |
| 2010 | 19651784 | C1QTNF5 is homologous to adiponectin in respect to domain structure, and its expression and secretion from myocytes correlated negatively with the cellular mtDNA content. |
| 2011 | 19651784 | Similar to adiponectin, C1QTNF5 induced the phosphorylation of AMP-activated protein kinase (AMPK), leading to increased cell surface recruitment of GLUT4 and increased glucose uptake. |
| 2012 | 19651784 | Similar to adiponectin, C1QTNF5 induced the phosphorylation of AMP-activated protein kinase (AMPK), leading to increased cell surface recruitment of GLUT4 and increased glucose uptake. |
| 2013 | 19651784 | C1QTNF5-mediated phosphorylation of AMPK or acetyl-CoA carboxylase was unaffected by depletion of adiponectin receptors such as AdipoR1 or AdipoR2, which indicated that adiponectin receptors do not participate in C1QTNF5-induced activation of AMPK. |
| 2014 | 19651784 | C1QTNF5-mediated phosphorylation of AMPK or acetyl-CoA carboxylase was unaffected by depletion of adiponectin receptors such as AdipoR1 or AdipoR2, which indicated that adiponectin receptors do not participate in C1QTNF5-induced activation of AMPK. |
| 2015 | 19651784 | These results highlight C1QTNF5 as a putative biomarker for mitochondrial dysfunction and a potent activator of AMPK. |
| 2016 | 19651784 | These results highlight C1QTNF5 as a putative biomarker for mitochondrial dysfunction and a potent activator of AMPK. |
| 2017 | 19642305 | Overproduction of cytokines IL-1 alpha, IL-1 beta and TNF-alpha increases bone resorption, which is further accelerated by hyperparathyroidism connected with malabsorption of calcium and vitamin D. |
| 2018 | 19633828 | Impaired regulation of the TNF-alpha converting enzyme/tissue inhibitor of metalloproteinase 3 proteolytic system in skeletal muscle of obese type 2 diabetic patients: a new mechanism of insulin resistance in humans. |
| 2019 | 19629935 | Reconsideration of insulin signals induced by improved laboratory animal diets, Japanese and American diets, in IRS-2 deficient mice. |
| 2020 | 19629935 | Therefore, changes in insulin signals caused by current Japanese and American diets were examined using IRS-2 deficient mice ( IRS2(-/-) mice) and mechanisms of aggravation of type 2 diabetes due to modern diets were examined. |
| 2021 | 19629935 | When the IRS2(-/-) mice reached 6 weeks of age, the glucose tolerance test (GTT), insulin tolerance test (ITT) and organ sampling were performed. |
| 2022 | 19629935 | These results were caused an increase in fat accumulation and adipocytes in the peritoneal cavity by lipogenic enzyme activity in the liver and muscle, and the increase in TNFalpha of hypertrophic adipocyte origin further aggravated insulin resistance and the increase in resistin also aggravated the impaired glucose tolerance, leading to aggravation of type 2 diabetes. |
| 2023 | 19629935 | The Japanese and American diets given to the IRS2(-/-) mice, which we developed, showed abnormal findings in some IRS2(-/-) mice but inhibited excessive reactions of insulin signals as diets used in ordinary nutritional management. |
| 2024 | 19629054 | We hypothesized that weight loss in patients with type 2 diabetes mellitus (T2DM) predominantly decreases the size of large and very-large adipocyte subfractions in parallel with beneficial changes in serum adipokines and improved insulin sensitivity. |
| 2025 | 19629054 | A 13% weight loss was accompanied by 46% improvement in insulin sensitivity (increased glucose disposal rate from 5.9+/-2.2 to 8.6+/-2.7 mg/min/kg fat-free mass, P<0.05) in parallel with a 36% increase in plasma adiponectin concentration (6.1+/-3.1 to 8.3+/-3.9 microg/ml, P<0.05], but no changes in the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha. |
| 2026 | 19629054 | Our data suggest that change in the large adipocyte subfraction may contribute to the improvement in insulin sensitivity via an increase in serum adiponectin. |
| 2027 | 19628894 | Selected biochemical markers (high sensitivity C-reactive protein (hsCRP), soluble vascular cell adhesion molecules (sVCAM), soluble intercellular adhesion molecules (sICAM), soluble E-selectin (sE-selectin), nitrotyrosine, superoxide anion (O2-), interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha)) were used for correlation. |
| 2028 | 19627007 | [Effect of ginsenoside Rgl on the expression of TNF-alpha and MCP-1 in rats with diabetic nephropathy]. |
| 2029 | 19621420 | Since CD154 is a member of the tumor necrosis factor (TNF) superfamily of cell surface interaction molecules, inhibitory activities on the TNF-R1-TNF-alpha interactions were also determined to test for specificity, and the compounds selected here all showed more than 30-fold selectivity toward the CD40-CD154 interaction. |
| 2030 | 19608431 | Association of tumor necrosis factor alpha, interferon gamma and interleukin 10 gene polymorphisms with peripheral neuropathy in South Indian patients with type 2 diabetes. |
| 2031 | 19597296 | Retinol binding protein-4 is associated with TNF-alpha and not insulin resistance in subjects with type 2 diabetes mellitus and coronary heart disease. |
| 2032 | 19597296 | Retinol binding protein-4 is associated with TNF-alpha and not insulin resistance in subjects with type 2 diabetes mellitus and coronary heart disease. |
| 2033 | 19597296 | Retinol binding protein-4 is associated with TNF-alpha and not insulin resistance in subjects with type 2 diabetes mellitus and coronary heart disease. |
| 2034 | 19597296 | We studied the association between RBP4 and various markers related to insulin resistance and diabetic complications as well as inflammatory markers in Saudi population suffering from type 2 diabetes and coronary heart disease. |
| 2035 | 19597296 | We studied the association between RBP4 and various markers related to insulin resistance and diabetic complications as well as inflammatory markers in Saudi population suffering from type 2 diabetes and coronary heart disease. |
| 2036 | 19597296 | We studied the association between RBP4 and various markers related to insulin resistance and diabetic complications as well as inflammatory markers in Saudi population suffering from type 2 diabetes and coronary heart disease. |
| 2037 | 19597296 | Serum RBP4, TNF-alpha, insulin, CRP, resistin, leptin and adiponectin were analysed in all samples. |
| 2038 | 19597296 | Serum RBP4, TNF-alpha, insulin, CRP, resistin, leptin and adiponectin were analysed in all samples. |
| 2039 | 19597296 | Serum RBP4, TNF-alpha, insulin, CRP, resistin, leptin and adiponectin were analysed in all samples. |
| 2040 | 19597296 | No correlations were found between RBP4 levels and insulin resistance in all studied groups. |
| 2041 | 19597296 | No correlations were found between RBP4 levels and insulin resistance in all studied groups. |
| 2042 | 19597296 | No correlations were found between RBP4 levels and insulin resistance in all studied groups. |
| 2043 | 19597296 | Our findings suggest that serum RBP4 levels is associated with pro-inflammatory cytokine (TNF-alpha) and is not associated with insulin resistance among patients with type 2 diabetes and coronary heart disease. |
| 2044 | 19597296 | Our findings suggest that serum RBP4 levels is associated with pro-inflammatory cytokine (TNF-alpha) and is not associated with insulin resistance among patients with type 2 diabetes and coronary heart disease. |
| 2045 | 19597296 | Our findings suggest that serum RBP4 levels is associated with pro-inflammatory cytokine (TNF-alpha) and is not associated with insulin resistance among patients with type 2 diabetes and coronary heart disease. |
| 2046 | 19567513 | c-Jun N-terminal kinase 1/2 activation by tumor necrosis factor-alpha induces insulin resistance in human visceral but not subcutaneous adipocytes: reversal by liver X receptor agonists. |
| 2047 | 19557294 | These changes were associated with increased expression of TNF-alpha, IL-1beta, IL-2 and IL-6 in hippocampi of diabetic rats. |
| 2048 | 19553520 | TNF receptor 1 can activate signaling pathways leading to the activation of NF-kappaB. |
| 2049 | 19553520 | A20, an NF-kappaB-inducible protein, negatively regulates these signaling pathways and acts as an anti-inflammatory mediator. |
| 2050 | 19381127 | HCV infection promotes IR mainly through increased TNF-a and cytokine suppressor (SOCS-3) production. |
| 2051 | 19381127 | Both events inhibit insulin receptor and IRS-1 (insulin receptor substrate) tyrosine phosphorylation. |
| 2052 | 19530270 | The cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene was recently associated with AITD and PGA, and the CTLA-4 protein is a strong inhibitor of T-cells.The tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine. |
| 2053 | 19530270 | The cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene was recently associated with AITD and PGA, and the CTLA-4 protein is a strong inhibitor of T-cells.The tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine. |
| 2054 | 19530270 | The cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene was recently associated with AITD and PGA, and the CTLA-4 protein is a strong inhibitor of T-cells.The tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine. |
| 2055 | 19530270 | The cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene was recently associated with AITD and PGA, and the CTLA-4 protein is a strong inhibitor of T-cells.The tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine. |
| 2056 | 19530270 | This study aimed to analyze the association of the CTLA-4 CT60 and TNF-alpha-863 polymorphisms with PGA. |
| 2057 | 19530270 | This study aimed to analyze the association of the CTLA-4 CT60 and TNF-alpha-863 polymorphisms with PGA. |
| 2058 | 19530270 | This study aimed to analyze the association of the CTLA-4 CT60 and TNF-alpha-863 polymorphisms with PGA. |
| 2059 | 19530270 | This study aimed to analyze the association of the CTLA-4 CT60 and TNF-alpha-863 polymorphisms with PGA. |
| 2060 | 19530270 | Homogeneous groups of 70 patients with AITD, 70 with type 1 diabetes (T1D), 70 with both AITD and T1D (PGA), and 100 healthy controls were genotyped for the CTLA-4 CT60 and TNF-alpha-863 polymorphisms by minisequencing on an ABI PRISM-3100 genetic analyzer. |
| 2061 | 19530270 | Homogeneous groups of 70 patients with AITD, 70 with type 1 diabetes (T1D), 70 with both AITD and T1D (PGA), and 100 healthy controls were genotyped for the CTLA-4 CT60 and TNF-alpha-863 polymorphisms by minisequencing on an ABI PRISM-3100 genetic analyzer. |
| 2062 | 19530270 | Homogeneous groups of 70 patients with AITD, 70 with type 1 diabetes (T1D), 70 with both AITD and T1D (PGA), and 100 healthy controls were genotyped for the CTLA-4 CT60 and TNF-alpha-863 polymorphisms by minisequencing on an ABI PRISM-3100 genetic analyzer. |
| 2063 | 19530270 | Homogeneous groups of 70 patients with AITD, 70 with type 1 diabetes (T1D), 70 with both AITD and T1D (PGA), and 100 healthy controls were genotyped for the CTLA-4 CT60 and TNF-alpha-863 polymorphisms by minisequencing on an ABI PRISM-3100 genetic analyzer. |
| 2064 | 19530270 | For TNF-alpha-863, carriers of the minor A allele occurred more frequently in the T1D group than in controls (47.1 % vs. 33 % , OR = 1.81, 95 % CI = 0.97-3.39, p = 0.079), but no differences in allele or genotype distribution were noted between PGA patients and controls (p = 0.886 and 0.389, respectively). |
| 2065 | 19530270 | For TNF-alpha-863, carriers of the minor A allele occurred more frequently in the T1D group than in controls (47.1 % vs. 33 % , OR = 1.81, 95 % CI = 0.97-3.39, p = 0.079), but no differences in allele or genotype distribution were noted between PGA patients and controls (p = 0.886 and 0.389, respectively). |
| 2066 | 19530270 | For TNF-alpha-863, carriers of the minor A allele occurred more frequently in the T1D group than in controls (47.1 % vs. 33 % , OR = 1.81, 95 % CI = 0.97-3.39, p = 0.079), but no differences in allele or genotype distribution were noted between PGA patients and controls (p = 0.886 and 0.389, respectively). |
| 2067 | 19530270 | For TNF-alpha-863, carriers of the minor A allele occurred more frequently in the T1D group than in controls (47.1 % vs. 33 % , OR = 1.81, 95 % CI = 0.97-3.39, p = 0.079), but no differences in allele or genotype distribution were noted between PGA patients and controls (p = 0.886 and 0.389, respectively). |
| 2068 | 19530270 | In conclusion the CTLA-4 CT60 polymorphism is associated with PGA. |
| 2069 | 19530270 | In conclusion the CTLA-4 CT60 polymorphism is associated with PGA. |
| 2070 | 19530270 | In conclusion the CTLA-4 CT60 polymorphism is associated with PGA. |
| 2071 | 19530270 | In conclusion the CTLA-4 CT60 polymorphism is associated with PGA. |
| 2072 | 19521344 | When 3T3-L1 adipocytes were treated with the 12/15-LO products, 12-hydroxyeicosatetranoic acid (12(S)-HETE) and 12-hydroperoxyeicosatetraenoic acid (12(S)-HPETE), expression of proinflammatory cytokine genes, including tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein 1 (MCP-1), interleukin 6 (IL-6), and IL-12p40, was upregulated whereas anti-inflammatory adiponectin gene expression was downregulated. 12/15-LO products also augmented c-Jun N-terminal kinase 1 (JNK-1) phosphorylation, a known negative regulator of insulin signaling. |
| 2073 | 19521344 | Consistent with impaired insulin signaling, we found that insulin-stimulated 3T3-L1 adipocytes exhibited decreased IRS-1(Tyr) phosphorylation, increased IRS-1(Ser) phosphorylation, and impaired Akt phosphorylation when treated with 12/15-LO product. |
| 2074 | 19507273 | The expressions of nephrin, tumor necrosis factor-alpha (TNF-alpha), NF-kappaB p65 and 3-nitrotyrosine (3-NT) protein were determined by immunoinfluorescence or Western blot analysis in the kidneys. |
| 2075 | 19507273 | The expressions of nephrin, tumor necrosis factor-alpha (TNF-alpha), NF-kappaB p65 and 3-nitrotyrosine (3-NT) protein were determined by immunoinfluorescence or Western blot analysis in the kidneys. |
| 2076 | 19507273 | The expressions of TNF-alpha, NF-kappaB p65 and 3-NT protein were significantly increased in the kidneys of diabetic rats, which were all significantly inhibited by TGP treatment. |
| 2077 | 19507273 | The expressions of TNF-alpha, NF-kappaB p65 and 3-NT protein were significantly increased in the kidneys of diabetic rats, which were all significantly inhibited by TGP treatment. |
| 2078 | 19505724 | Protease-resistant human GAD-derived altered peptide ligands decrease TNF-alpha and IL-17 production in peripheral blood cells from patients with type 1 diabetes mellitus. |
| 2079 | 19505724 | Protease-resistant human GAD-derived altered peptide ligands decrease TNF-alpha and IL-17 production in peripheral blood cells from patients with type 1 diabetes mellitus. |
| 2080 | 19505724 | Glutamic acid decarboxylase 65 (GAD) and proinsulin are major diabetes-associated autoantigens that drive autoreactive T cells. |
| 2081 | 19505724 | Glutamic acid decarboxylase 65 (GAD) and proinsulin are major diabetes-associated autoantigens that drive autoreactive T cells. |
| 2082 | 19505724 | Likewise, the production of IL-17, TNF-alpha, and secretion of IL-6 by peripheral blood lymphocytes from patients with type 1 diabetes mellitus (T1D) was reduced, when stimulated with both GAD and GAD-derived prAPL. |
| 2083 | 19505724 | Likewise, the production of IL-17, TNF-alpha, and secretion of IL-6 by peripheral blood lymphocytes from patients with type 1 diabetes mellitus (T1D) was reduced, when stimulated with both GAD and GAD-derived prAPL. |
| 2084 | 19505724 | Thus, prAPL with high affinity for HLA-DRB1(*)0401 mitigate the response of GAD-reactive human Th17 cells. |
| 2085 | 19505724 | Thus, prAPL with high affinity for HLA-DRB1(*)0401 mitigate the response of GAD-reactive human Th17 cells. |
| 2086 | 19494326 | We provide evidence that metformin attenuates the induction of EAE by restricting the infiltration of mononuclear cells into the CNS, down-regulating the expression of proinflammatory cytokines (IFN-gamma, TNF-alpha, IL-6, IL-17, and inducible NO synthase (iNOS)), cell adhesion molecules, matrix metalloproteinase 9, and chemokine (RANTES). |
| 2087 | 19494326 | It also attenuated IFN-gamma and IL-17-induced iNOS and cyclooxygenase 2 expression in RAW267.4 cells, further supporting its anti-inflammatory property. |
| 2088 | 19492335 | We show that LPS greatly increased the secretion levels of pro-inflammatory adipokines including IL-6, IL-8, GRO, and MCP-1. |
| 2089 | 19492335 | Macrophage-conditioned medium also upregulated IL-6, IL-8, GRO, and MCP-1 mRNA expression and protein levels and led to the novo secretion of ICAM-1, IL-1 beta, IP-10, MIP-1 alpha, MIP-1 beta, VEGF, and TNFalpha. |
| 2090 | 19492335 | Human differentiated adipocytes treated by macrophage-conditioned medium displayed marked reduction of adipocyte function as assessed by decreased phosphorylation levels of ERK1, ERK2, and p38 alpha and reduced gene expression of lipogenic markers including PPAR-gamma and fatty acid synthase. |
| 2091 | 19488738 | Coupling factor 6 (CF6) is composed of 76 amino acids and is present in the peripheral stalk of mitochondrial ATP synthase. |
| 2092 | 19488738 | The generation of CF6 is positively regulated by tumor necrosis factor alpha and shear stress via nuclear factor kappaB, and by high glucose via protein kinase C and p38 mitogen-activated protein kinase. |
| 2093 | 19488738 | CF6 also suppresses nitric oxide synthase activity via an increase in asymmetric dimethylarginine and a decrease in platelet/endothelial cell adhesion molecule-1. |
| 2094 | 19488738 | CF6 induces the gene and protein expression of proatherogenic molecules such as endothelin 2, urokinase type plasminogen activator receptor, estrogen receptor beta, a soluble short form of vascular endothelial growth factor receptor-1, and lectin-like oxidized low-density lipoprotein receptor-1. |
| 2095 | 19482369 | Serum levels of adiponectin and tumor necrosis factor (TNF)-alpha were determined. |
| 2096 | 19482369 | Serum levels of adiponectin and tumor necrosis factor (TNF)-alpha were determined. |
| 2097 | 19482369 | Serum levels of adiponectin and tumor necrosis factor (TNF)-alpha were determined. |
| 2098 | 19482369 | Serum levels of adiponectin and tumor necrosis factor (TNF)-alpha were determined. |
| 2099 | 19482369 | Male gender, HOMA, serum non-HDL-Cholesterol (Chol) and TNF-alpha/adiponectin ratio were higher, and VFA was larger in DM than in C. |
| 2100 | 19482369 | Male gender, HOMA, serum non-HDL-Cholesterol (Chol) and TNF-alpha/adiponectin ratio were higher, and VFA was larger in DM than in C. |
| 2101 | 19482369 | Male gender, HOMA, serum non-HDL-Cholesterol (Chol) and TNF-alpha/adiponectin ratio were higher, and VFA was larger in DM than in C. |
| 2102 | 19482369 | Male gender, HOMA, serum non-HDL-Cholesterol (Chol) and TNF-alpha/adiponectin ratio were higher, and VFA was larger in DM than in C. |
| 2103 | 19482369 | VFA was positively correlated with TNF-alpha/adiponectin ratio and serum non-HDL-Chol in DM. |
| 2104 | 19482369 | VFA was positively correlated with TNF-alpha/adiponectin ratio and serum non-HDL-Chol in DM. |
| 2105 | 19482369 | VFA was positively correlated with TNF-alpha/adiponectin ratio and serum non-HDL-Chol in DM. |
| 2106 | 19482369 | VFA was positively correlated with TNF-alpha/adiponectin ratio and serum non-HDL-Chol in DM. |
| 2107 | 19482369 | Furthermore, multiple regression analysis revealed that, in DM, serum non-HDL-Chol was associated with IMT, VFA probably via an increase in TNF-alpha/adiponectin ratio was associated with stiffness index beta, and 24-h sBP, HOMA and VFA were associated with plaque formation independently of age and sex, respectively, although any association was not observed in C. |
| 2108 | 19482369 | Furthermore, multiple regression analysis revealed that, in DM, serum non-HDL-Chol was associated with IMT, VFA probably via an increase in TNF-alpha/adiponectin ratio was associated with stiffness index beta, and 24-h sBP, HOMA and VFA were associated with plaque formation independently of age and sex, respectively, although any association was not observed in C. |
| 2109 | 19482369 | Furthermore, multiple regression analysis revealed that, in DM, serum non-HDL-Chol was associated with IMT, VFA probably via an increase in TNF-alpha/adiponectin ratio was associated with stiffness index beta, and 24-h sBP, HOMA and VFA were associated with plaque formation independently of age and sex, respectively, although any association was not observed in C. |
| 2110 | 19482369 | Furthermore, multiple regression analysis revealed that, in DM, serum non-HDL-Chol was associated with IMT, VFA probably via an increase in TNF-alpha/adiponectin ratio was associated with stiffness index beta, and 24-h sBP, HOMA and VFA were associated with plaque formation independently of age and sex, respectively, although any association was not observed in C. |
| 2111 | 19477937 | TNF-alpha signals through two receptors, TNFR1 and TNFR2. |
| 2112 | 19477937 | Obese RKO mice were markedly insulin resistant, suggesting that intact TNFR signaling is not required for the effect of obesity to impair glucose metabolism. |
| 2113 | 19477937 | Despite these effects, TNFRs are not required for obesity-induced insulin resistance. |
| 2114 | 19474523 | Serum amyloid A attenuates cellular insulin sensitivity by increasing JNK activity in 3T3-L1 adipocytes. |
| 2115 | 19474523 | A permanent increase in acute-phase serum amyloid A (A-SAA) level is observed in obesity and insulin resistance. |
| 2116 | 19474523 | In this study, we used two cellular models of insulin resistance, one induced by treatment with tumor necrosis factor-alpha (TNF-alpha) and the other with the glucocorticoid dexamethasone. |
| 2117 | 19474523 | Gene expression analysis showed that SAA3 mRNA levels were increased in both models of insulin resistance, and ELISA showed that A-SAA levels were increased in both models too. |
| 2118 | 19474523 | To assess the potential impact of A-SAA on insulin resistance, we treated 3T3-L1 adipocytes with recombinant human SAA (Rh-SAA) and found that Rh-SAA attenuated cellular insulin sensitivity, up-regulated the level of phosphor-JNK, and down-regulated the level of phosphotyrosine-IRS-1 and the expression of glucose transporter 4 (GLUT4) in 3T3-L1 adipocytes. |
| 2119 | 19474523 | Pre-treatment of cells with C-Jun amino-terminal kinases (JNK) inhibitor brought about partial restoration of Rh-SAA-induced insulin resistance. |
| 2120 | 19474523 | In sum, our findings suggest that serum amyloid A might be a marker of insulin resistance, and it might play a major role in the development of obesity-related insulin resistance. |
| 2121 | 19474523 | Moreover, in our study it has been proved that JNK is indeed a crucial component of the pathway responsible for SAA-induced insulin resistance in 3T3-L1 adipocytes, which suggests that a selective interference with JNK activity might be a useful strategy in the treatment of Type 2 diabetes and other insulin-resistant states. |
| 2122 | 19474287 | Adipocytokines, including leptin, adiponectin, tumor necrosis factor alpha, interleukin 6, as well as the newly discovered resistin, visfatin, and apelin, are also known to be produced within the intrauterine environment. |
| 2123 | 19474287 | Focus will be placed on the functions and other potential roles of the novel adipocytokines resistin, visfatin, and apelin. |
| 2124 | 19463916 | Twenty-three retinal genes, mainly from TNF ligand and receptor, caspase, Bcl-2 and death domain subfamilies that were upregulated by least a two-fold in PC rats remain upregulated after reversal of hyperglycemia. |
| 2125 | 19449282 | LPS significantly increased the serum levels of TNF-alpha and IL-6 in normal and diabetic rats; LPS also dramatically increased the plasma concentrations of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone. |
| 2126 | 19449282 | LPS significantly increased the serum levels of TNF-alpha and IL-6 in normal and diabetic rats; LPS also dramatically increased the plasma concentrations of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone. |
| 2127 | 19449282 | Both 0.1 and 1 mg/kg MLT doses significantly decreased the serum levels of TNF-alpha and IL-6. |
| 2128 | 19449282 | Both 0.1 and 1 mg/kg MLT doses significantly decreased the serum levels of TNF-alpha and IL-6. |
| 2129 | 19449282 | Significant inhibitory effects of MLT (1 mg/kg) were observed on the plasma concentrations of CRH, ACTH, and corticosterone of the HPA axis. |
| 2130 | 19449282 | Significant inhibitory effects of MLT (1 mg/kg) were observed on the plasma concentrations of CRH, ACTH, and corticosterone of the HPA axis. |
| 2131 | 19447618 | Among the compounds that were tested, compounds 8 and 9 reduced the LPS-induced secretion of IL-6, as well as TNF-alpha, in a mouse RAW264.7 macrophage cell line. |
| 2132 | 19433255 | Islets were exposed to hIL-1beta (25U/ml) alone or in combination with hTNF-alpha (1000U/ml)+mIFN-gamma (1000U/ml) for 48h, whereupon islet functions were assessed. |
| 2133 | 19424605 | The Chi-square test, multivariable logistic regression analysis with adjustment for covariates, as well as a stepwise forward selection procedure revealed that ten different polymorphisms were associated (P<0.05) with the prevalence of CKD in high- or low-risk subjects: the -519Aright curved arrow G polymorphism of MMP1, the 1061Aright curved arrow G (Ile405Val) polymorphism of CETP, the Aright curved arrow G (Lys45Glu) polymorphism of MMP3, the -219Gright curved arrow T polymorphism of APOE, the Aright curved arrow G (Ile1205Val) polymorphism of COL3A1, the -863Cright curved arrow A polymorphism of TNF, and the 1454Cright curved arrow G (Leu125Val) polymorphism of PECAM1 in high-risk subjects; and the 1167Cright curved arrow T (Asn389Asn) polymorphism of TGFBR2, the 2386Aright curved arrow G (Ile796Val) polymorphism of SCAP, and the TAAAright curved arrow del polymorphism of PDE4D in low-risk subjects. |
| 2134 | 19424163 | When compared to OZR-RD animals, OZR-HFD animals exhibited significantly higher levels of total renal cortical reactive oxygen species (ROS) production, plasma lipids, insulin, C-reactive protein, blood urea nitrogen (BUN), creatinine (Cr), and urinary albumin excretion (P < 0.05); these changes were accompanied by a significant decrease in plasma high-density lipoprotein levels (P < 0.05). |
| 2135 | 19424163 | The mRNA expression levels of desmin, tumor necrosis factor-alpha (TNF-alpha), nuclear factor kappaB (NFkappaB), and NAD(P)H oxidase-1 (NOX-1) were significantly higher in the renal cortical tissues of OZR-HFD animals; NFkappaB p65 DNA binding activity as determined by electrophoretic mobility shift assay was also significantly higher in these animals. |
| 2136 | 19414540 | TNF-alpha, IL-6, PTX3, CCL3, and CCL5 levels. |
| 2137 | 19414540 | TNF-alpha, IL-6, PTX3, CCL3, and CCL5 levels. |
| 2138 | 19414540 | By depleting peritoneal resident Mphi using clodronate liposomes prior to the application of hCG and the TG trigger, we established that Mphi are the main responsive cells to hCG, as the suppressed TNF-alpha and IL-6 production and increased PMN influx are abolished in their absence. |
| 2139 | 19414540 | By depleting peritoneal resident Mphi using clodronate liposomes prior to the application of hCG and the TG trigger, we established that Mphi are the main responsive cells to hCG, as the suppressed TNF-alpha and IL-6 production and increased PMN influx are abolished in their absence. |
| 2140 | 19407801 | Importantly, silencing Map4k4 in macrophages in vivo protected mice from lipopolysaccharide-induced lethality by inhibiting Tnf-alpha and interleukin-1beta production. |
| 2141 | 19406980 | TIMP3 is the most highly expressed tissue inhibitor of metalloproteinase (TIMP) in the kidney, but its function in renal disease is incompletely understood. |
| 2142 | 19406980 | TIMP3 is the most highly expressed tissue inhibitor of metalloproteinase (TIMP) in the kidney, but its function in renal disease is incompletely understood. |
| 2143 | 19406980 | In addition, TIMP3-/- mice had greater interstitial fibrosis; increased synthesis and deposition of type I collagen; increased activation of fibroblasts; enhanced apoptosis; and greater activation of MMP2, but not MMP9, after UUO. |
| 2144 | 19406980 | In addition, TIMP3-/- mice had greater interstitial fibrosis; increased synthesis and deposition of type I collagen; increased activation of fibroblasts; enhanced apoptosis; and greater activation of MMP2, but not MMP9, after UUO. |
| 2145 | 19406980 | TIMP3 deficiency also led to accelerated processing of TNFalpha, demonstrated by significantly higher TACE activity and greater soluble TNFalpha levels by 3 d after UUO. |
| 2146 | 19406980 | TIMP3 deficiency also led to accelerated processing of TNFalpha, demonstrated by significantly higher TACE activity and greater soluble TNFalpha levels by 3 d after UUO. |
| 2147 | 19406980 | Moreover, inhibition of MMPs in TIMP3-/-/TNFalpha-/- mice further abrogated postobstructive injury and prevented tubulointerestitial fibrosis. |
| 2148 | 19406980 | Moreover, inhibition of MMPs in TIMP3-/-/TNFalpha-/- mice further abrogated postobstructive injury and prevented tubulointerestitial fibrosis. |
| 2149 | 19393643 | To address potential mechanisms of action, we measured markers of oxidative stress (lipid and protein oxidation) and inflammation (cyclooxygenase-2 (COX-2) and TNFalpha protein) in the nerve but treatment with the vitamin B cocktail did not significantly affect any of these parameters. |
| 2150 | 19384082 | In addition, atrial natriuretic peptide and nitric oxide donors are important modulators of the heme-HO system, either through induction of HO-1 or the increased biologic activity of its products. |
| 2151 | 19384082 | Gene therapy and gene transfer, including site- and organ-specific targeted gene transfer have become powerful tools for studying the potential role of the 2 isoforms of HO, HO-1/HO-2, in the treatment of cardiovascular disease, as well as diabetes. |
| 2152 | 19384082 | HO-1 induction by pharmacological agents or the in vitro gene transfer of human HO-1 into ECs increases cell cycle progression and attenuates angiotensin II, tumor necrosis factor-alpha, and heme-mediated DNA damage; administration in vivo corrects blood pressure elevation after angiotensin II exposure. |
| 2153 | 19380603 | We investigated the effect of four distinct AGE subtypes (AGE-modified bovine serum albumin; AGE-2, AGE-3, AGE-4, and AGE-5) at concentrations ranging from 0.1 to 100 microg/ml on the expression of intercellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes and its impact on the production of interferon-gamma and tumor necrosis factor-alpha in human peripheral blood mononuclear cells. |
| 2154 | 19376168 | We co-expressed human vascular endothelial growth factor (hVEGF) and human interleukin-1 receptor antagonist (hIL-1Ra) after transduction of human islets with Adv-hVEGF-hIL-1Ra. |
| 2155 | 19376168 | There was dose and time dependent expression of hVEGF and hIL-1Ra or hHGF and hIL-1Ra by islets, which led to decrease in caspase-3 activity and apoptosis induced by a cocktail of TNF-alpha, IL-1beta and IFN-gamma. |
| 2156 | 19376168 | Immunohistochemical staining of the islet bearing kidney sections was positive for human insulin, growth factor (hVEGF or hHGF) and von Willebrand factor. |
| 2157 | 19375767 | Increased carnitine palmitoyl transferase 1 expression and decreased sterol regulatory element-binding protein 1c expression are associated with reduced intramuscular triglyceride accumulation after insulin therapy in high-fat-diet and streptozotocin-induced diabetic rats. |
| 2158 | 19375767 | Compared with normal rats, untreated diabetic rats had a 30% and 61% increase in lipoprotein lipase protein expression and activity, which were decreased by insulin and gliclazide (P < .05). |
| 2159 | 19375767 | Fatty acid translocase protein was down-regulated by 45% in untreated diabetic rats, which was up-regulated by 31% and 26% with insulin and gliclazide, respectively (P < .05). |
| 2160 | 19375767 | Insulin failed to affect fatty acid transport protein 1 and fatty acid binding protein expressions. |
| 2161 | 19375767 | Moreover, compared with normal rats, untreated diabetic rats had higher expressions of sterol regulatory element-binding protein 1c, tumor necrosis factor alpha, and Tyr(705) phosphorylation of signal transducer and activator of transcription 3 levels, which all were down-regulated after insulin treatment. |
| 2162 | 19375766 | There were only minor or inconsistent effects on adiponectin, leptin, and high-sensitivity C-reactive protein levels during hyperinsulinemia. |
| 2163 | 19375766 | There were only minor or inconsistent effects on adiponectin, leptin, and high-sensitivity C-reactive protein levels during hyperinsulinemia. |
| 2164 | 19375766 | Insulin-induced rise in IL-6 correlated negatively to BMI (P = .001), waist to hip ratio (P = .05), and baseline (fasting) insulin (P = .03) and IL-6 (P = .02) levels and positively to insulin-stimulated glucose uptake in isolated adipocytes (P = .07). |
| 2165 | 19375766 | Insulin-induced rise in IL-6 correlated negatively to BMI (P = .001), waist to hip ratio (P = .05), and baseline (fasting) insulin (P = .03) and IL-6 (P = .02) levels and positively to insulin-stimulated glucose uptake in isolated adipocytes (P = .07). |
| 2166 | 19375766 | Hyperinsulinemia per se can produce an increase in plasma IL-6 and TNFalpha, and this can potentially contribute to the low-grade inflammation seen in obesity and T2DM. |
| 2167 | 19375766 | Hyperinsulinemia per se can produce an increase in plasma IL-6 and TNFalpha, and this can potentially contribute to the low-grade inflammation seen in obesity and T2DM. |
| 2168 | 19375766 | However, obesity seems to attenuate the ability of an acute increase in insulin to further raise circulating levels of IL-6 and possibly TNFalpha. |
| 2169 | 19375766 | However, obesity seems to attenuate the ability of an acute increase in insulin to further raise circulating levels of IL-6 and possibly TNFalpha. |
| 2170 | 19371958 | To evaluate the role of NT-pro-BNP, TNF-alpha and C-reactive protein (CRP) in a population of geriatric patients affected by CHF, and to assess their different plasma levels in diabetics and in normoglycemic patients, we enrolled 57 patients affected by CHF: 29 patients were diabetic and 28 were normoglycemic. |
| 2171 | 19371958 | To evaluate the role of NT-pro-BNP, TNF-alpha and C-reactive protein (CRP) in a population of geriatric patients affected by CHF, and to assess their different plasma levels in diabetics and in normoglycemic patients, we enrolled 57 patients affected by CHF: 29 patients were diabetic and 28 were normoglycemic. |
| 2172 | 19371958 | To evaluate the role of NT-pro-BNP, TNF-alpha and C-reactive protein (CRP) in a population of geriatric patients affected by CHF, and to assess their different plasma levels in diabetics and in normoglycemic patients, we enrolled 57 patients affected by CHF: 29 patients were diabetic and 28 were normoglycemic. |
| 2173 | 19371958 | Plasma NT-pro-BNP, TNF-alpha and CRP levels were measured in each recruited patient. |
| 2174 | 19371958 | Plasma NT-pro-BNP, TNF-alpha and CRP levels were measured in each recruited patient. |
| 2175 | 19371958 | Plasma NT-pro-BNP, TNF-alpha and CRP levels were measured in each recruited patient. |
| 2176 | 19371958 | In the whole population we observed a linear correlation between NT-pro-BNP levels, EF and NYHA-class (p<0.05) but there was no significant correlation between TNF-alpha or CRP and the clinical or echocardiographic data (p=0.588 and p=0.9, respectively). |
| 2177 | 19371958 | In the whole population we observed a linear correlation between NT-pro-BNP levels, EF and NYHA-class (p<0.05) but there was no significant correlation between TNF-alpha or CRP and the clinical or echocardiographic data (p=0.588 and p=0.9, respectively). |
| 2178 | 19371958 | In the whole population we observed a linear correlation between NT-pro-BNP levels, EF and NYHA-class (p<0.05) but there was no significant correlation between TNF-alpha or CRP and the clinical or echocardiographic data (p=0.588 and p=0.9, respectively). |
| 2179 | 19363130 | Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. |
| 2180 | 19363130 | Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. |
| 2181 | 19363130 | Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. |
| 2182 | 19363130 | Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. |
| 2183 | 19363130 | Feed-forward signaling of TNF-alpha and NF-kappaB via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice. |
| 2184 | 19363130 | We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. |
| 2185 | 19363130 | We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. |
| 2186 | 19363130 | We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. |
| 2187 | 19363130 | We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. |
| 2188 | 19363130 | We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. |
| 2189 | 19363130 | The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. |
| 2190 | 19363130 | The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. |
| 2191 | 19363130 | The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. |
| 2192 | 19363130 | The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. |
| 2193 | 19363130 | The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. |
| 2194 | 19363130 | The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. |
| 2195 | 19363130 | The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. |
| 2196 | 19363130 | The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. |
| 2197 | 19363130 | The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. |
| 2198 | 19363130 | The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. |
| 2199 | 19363130 | The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. |
| 2200 | 19363130 | The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. |
| 2201 | 19363130 | The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. |
| 2202 | 19363130 | The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. |
| 2203 | 19363130 | The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. |
| 2204 | 19363130 | The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. |
| 2205 | 19363130 | The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. |
| 2206 | 19363130 | The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. |
| 2207 | 19363130 | The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. |
| 2208 | 19363130 | The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. |
| 2209 | 19363130 | In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes. |
| 2210 | 19363130 | In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes. |
| 2211 | 19363130 | In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes. |
| 2212 | 19363130 | In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes. |
| 2213 | 19363130 | In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes. |
| 2214 | 19362933 | Several cytokines, tumor necrosis factor-alpha and its soluble receptor forms, sTNFR1 and sTNFR2, resistin, retinol-binding protein 4, plasminogen activator inhibitor, lipocain 1 inhibit the signalization of insulin receptor causing insulin resistance in target tissues, mainly in adipose, liver and muscle, brain, endothelial as well as in pancreatic beta-cells. |
| 2215 | 19362933 | However, many other proteins produced by the fat tissue, such as adiponectin, visfatin, vaspin, apelin, omentin and chemerin enhance the signal transmission of the receptor. |
| 2216 | 19362933 | Recently discovered common mechanisms leading to insulin and cytokine resistance in obesity and type 2 diabetes mellitus, e.g. protein family of suppressor of cytokine signaling (SOCS) are also discussed. |
| 2217 | 19360015 | Concentrations of retinol-binding protein 4 (RBP4), adiponectin, tumor necrosis factor-alpha (TNF-alpha), and leptin were determined approximately 1 week prior to surgery and results were related to liver histology. |
| 2218 | 19360015 | Concentrations of retinol-binding protein 4 (RBP4), adiponectin, tumor necrosis factor-alpha (TNF-alpha), and leptin were determined approximately 1 week prior to surgery and results were related to liver histology. |
| 2219 | 19360015 | Concentrations of TNF-alpha, leptin, and RBP4 did not differ among histological groups and thus did not identify NASH; however, there was a trend for adiponectin to be lower in NASH vs. no NAFLD (P = 0.061). |
| 2220 | 19360015 | Concentrations of TNF-alpha, leptin, and RBP4 did not differ among histological groups and thus did not identify NASH; however, there was a trend for adiponectin to be lower in NASH vs. no NAFLD (P = 0.061). |
| 2221 | 19343543 | Inflammation plays a crucial role in the pathogenesis of type 2 diabetes and various lines of evidences suggest an important contribution of type 2 receptor for TNFalpha (TNFR2), a mediator of inflammatory responses. |
| 2222 | 19328014 | This work aimed to study correlation between homeostasis model assessment estimate of insulin resistance (HOMA-IR) with serum levels of inflammatory markers tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), C-reactive protein (CRP), and free fatty acids (FFAs) in experimental model of induced type 2 diabetes in rats, with evaluation of effects of rosiglitazone and aspirin (low or high dose), alone or in combination. |
| 2223 | 19328014 | This work aimed to study correlation between homeostasis model assessment estimate of insulin resistance (HOMA-IR) with serum levels of inflammatory markers tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), C-reactive protein (CRP), and free fatty acids (FFAs) in experimental model of induced type 2 diabetes in rats, with evaluation of effects of rosiglitazone and aspirin (low or high dose), alone or in combination. |
| 2224 | 19328014 | There is significant elevation of insulin resistance and serum levels of fasting glucose, insulin, TNF-alpha, IL-6, CRP, and FFAs in the diabetic group when compared to the normal group, with positive significant correlation between levels of each of TNF-alpha, IL-6, CRP, and FFAs with insulin resistance (HOMA-IR). |
| 2225 | 19328014 | There is significant elevation of insulin resistance and serum levels of fasting glucose, insulin, TNF-alpha, IL-6, CRP, and FFAs in the diabetic group when compared to the normal group, with positive significant correlation between levels of each of TNF-alpha, IL-6, CRP, and FFAs with insulin resistance (HOMA-IR). |
| 2226 | 19321592 | Recently, we identified several flavonoids as inhibitors of the nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 in vitro and in vivo. |
| 2227 | 19321592 | Recently, we identified several flavonoids as inhibitors of the nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 in vitro and in vivo. |
| 2228 | 19321592 | Recently, we identified several flavonoids as inhibitors of the nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 in vitro and in vivo. |
| 2229 | 19321592 | PARP-1 is recognized as coactivator of nuclear factor-kappaB and plays a role in the pathophysiology of diseases with low-grade systemic inflammation, such as chronic obstructive pulmonary disease (COPD) and type 2 diabetes (T2D). |
| 2230 | 19321592 | PARP-1 is recognized as coactivator of nuclear factor-kappaB and plays a role in the pathophysiology of diseases with low-grade systemic inflammation, such as chronic obstructive pulmonary disease (COPD) and type 2 diabetes (T2D). |
| 2231 | 19321592 | PARP-1 is recognized as coactivator of nuclear factor-kappaB and plays a role in the pathophysiology of diseases with low-grade systemic inflammation, such as chronic obstructive pulmonary disease (COPD) and type 2 diabetes (T2D). |
| 2232 | 19321592 | In this study, we assessed the antiinflammatory effects of flavonoids with varying PARP-1-inhibiting effects in whole blood from male patients with COPD or T2D and healthy men. |
| 2233 | 19321592 | In this study, we assessed the antiinflammatory effects of flavonoids with varying PARP-1-inhibiting effects in whole blood from male patients with COPD or T2D and healthy men. |
| 2234 | 19321592 | In this study, we assessed the antiinflammatory effects of flavonoids with varying PARP-1-inhibiting effects in whole blood from male patients with COPD or T2D and healthy men. |
| 2235 | 19321592 | Concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, -8, and -10 were measured in the supernatant. |
| 2236 | 19321592 | Concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, -8, and -10 were measured in the supernatant. |
| 2237 | 19321592 | Concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, -8, and -10 were measured in the supernatant. |
| 2238 | 19321592 | Preincubation with fisetin and tricetin strongly attenuated LPS-induced increases in concentrations of TNFalpha in blood from COPD patients [mean (+/- SEM): -41 +/- 4% (fisetin) and -31 +/- 4% (tricetin); P < 0.001] and IL-6 in blood from T2D patients [-31 +/- 5% (fisetin) and -29 +/- 6% (tricetin); P < or = 0.001]. |
| 2239 | 19321592 | Preincubation with fisetin and tricetin strongly attenuated LPS-induced increases in concentrations of TNFalpha in blood from COPD patients [mean (+/- SEM): -41 +/- 4% (fisetin) and -31 +/- 4% (tricetin); P < 0.001] and IL-6 in blood from T2D patients [-31 +/- 5% (fisetin) and -29 +/- 6% (tricetin); P < or = 0.001]. |
| 2240 | 19321592 | Preincubation with fisetin and tricetin strongly attenuated LPS-induced increases in concentrations of TNFalpha in blood from COPD patients [mean (+/- SEM): -41 +/- 4% (fisetin) and -31 +/- 4% (tricetin); P < 0.001] and IL-6 in blood from T2D patients [-31 +/- 5% (fisetin) and -29 +/- 6% (tricetin); P < or = 0.001]. |
| 2241 | 19321592 | Moreover, LPS-induced changes in TNFalpha and IL-6 concentrations were positively correlated with the extent of reduction by fisetin and tricetin. |
| 2242 | 19321592 | Moreover, LPS-induced changes in TNFalpha and IL-6 concentrations were positively correlated with the extent of reduction by fisetin and tricetin. |
| 2243 | 19321592 | Moreover, LPS-induced changes in TNFalpha and IL-6 concentrations were positively correlated with the extent of reduction by fisetin and tricetin. |
| 2244 | 19321592 | The PARP-1-inhibiting flavonoids fisetin and tricetin were able to attenuate LPS-induced cytokine release from leukocytes of patients with chronic systemic inflammation, indicating a potential application as nutraceutical agents for these patient groups. |
| 2245 | 19321592 | The PARP-1-inhibiting flavonoids fisetin and tricetin were able to attenuate LPS-induced cytokine release from leukocytes of patients with chronic systemic inflammation, indicating a potential application as nutraceutical agents for these patient groups. |
| 2246 | 19321592 | The PARP-1-inhibiting flavonoids fisetin and tricetin were able to attenuate LPS-induced cytokine release from leukocytes of patients with chronic systemic inflammation, indicating a potential application as nutraceutical agents for these patient groups. |
| 2247 | 19318924 | Plasmatic levels of oxidative stress markers (tumor necrosis factor-alpha, nitrotyrosine, oxidized low-density lipoprotein) and coagulation markers (factors VII, VIII, IX, XI, XII, antithrombin III and fibrinogen) of both populations were analyzed following statistic criteria. |
| 2248 | 19318924 | Plasmatic levels of oxidative stress markers (tumor necrosis factor-alpha, nitrotyrosine, oxidized low-density lipoprotein) and coagulation markers (factors VII, VIII, IX, XI, XII, antithrombin III and fibrinogen) of both populations were analyzed following statistic criteria. |
| 2249 | 19318924 | The analyzed data of this study related to oxidative stress and coagulation factors proved that the differences observed between diabetic patients and controls were not statistically significant (P < 0.05) for tumor necrosis factor-alpha, nitrotyrosine, oxidized low-density lipoprotein, factor VII and factor XI; conversely for factor VIII, factor IX, factor XII, antithrombin III and fibrinogen, the results gave a difference statistically significant (P < 0.01). |
| 2250 | 19318924 | The analyzed data of this study related to oxidative stress and coagulation factors proved that the differences observed between diabetic patients and controls were not statistically significant (P < 0.05) for tumor necrosis factor-alpha, nitrotyrosine, oxidized low-density lipoprotein, factor VII and factor XI; conversely for factor VIII, factor IX, factor XII, antithrombin III and fibrinogen, the results gave a difference statistically significant (P < 0.01). |
| 2251 | 19299644 | Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. |
| 2252 | 19299644 | Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. |
| 2253 | 19299644 | Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. |
| 2254 | 19299644 | Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. |
| 2255 | 19299644 | In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. |
| 2256 | 19299644 | In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. |
| 2257 | 19299644 | In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6. |
| 2258 | 19299644 | In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6. |
| 2259 | 19296549 | CO treatment showed reduced diet intake (13%), body weight gain (12%), lipid (29%) and glucose levels (35%). 2-DE results showed differential levels of five proteins namely RBP4, apoE, and apoA-IV by >2-fold down-regulation and by >2-fold of apoA-I and glutathione peroxidase (GPx) up-regulation after CO treatment. |
| 2260 | 19296549 | Immunoblotting studies of adiponectin and resistin showed amelioration in their levels in plasma. |
| 2261 | 19296549 | Furthermore, the results of gene expressions for adipose tissue specific TNF-alpha, and IL-6 secretary molecules were also down-regulated by CO treatment. |
| 2262 | 19296549 | Gene expressions of PPAR gamma in adipose tissue were in good agreement with the ameliorated levels of adipokines, thereby improving the pathological state. |
| 2263 | 19295663 | Role of protein kinase C beta2 activation in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2264 | 19295663 | Role of protein kinase C beta2 activation in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2265 | 19295663 | Role of protein kinase C beta2 activation in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2266 | 19295663 | Role of protein kinase C beta2 activation in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2267 | 19295663 | Protein kinase C (PKC) has been shown to play a critical role in TNF-alpha-induced human endothelial cell apoptosis. |
| 2268 | 19295663 | Protein kinase C (PKC) has been shown to play a critical role in TNF-alpha-induced human endothelial cell apoptosis. |
| 2269 | 19295663 | Protein kinase C (PKC) has been shown to play a critical role in TNF-alpha-induced human endothelial cell apoptosis. |
| 2270 | 19295663 | Protein kinase C (PKC) has been shown to play a critical role in TNF-alpha-induced human endothelial cell apoptosis. |
| 2271 | 19295663 | We investigated the effects of a selective PKCbeta(2) inhibitor (CGP53353) on TNF-alpha-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the production of reactive oxygen species and nitric oxide, and compared its effects with rottlerin, a reagent that has been shown to reduce PKCdelta protein levels. |
| 2272 | 19295663 | We investigated the effects of a selective PKCbeta(2) inhibitor (CGP53353) on TNF-alpha-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the production of reactive oxygen species and nitric oxide, and compared its effects with rottlerin, a reagent that has been shown to reduce PKCdelta protein levels. |
| 2273 | 19295663 | We investigated the effects of a selective PKCbeta(2) inhibitor (CGP53353) on TNF-alpha-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the production of reactive oxygen species and nitric oxide, and compared its effects with rottlerin, a reagent that has been shown to reduce PKCdelta protein levels. |
| 2274 | 19295663 | We investigated the effects of a selective PKCbeta(2) inhibitor (CGP53353) on TNF-alpha-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the production of reactive oxygen species and nitric oxide, and compared its effects with rottlerin, a reagent that has been shown to reduce PKCdelta protein levels. |
| 2275 | 19295663 | We conclude that PKCbeta(2) plays a major role in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2276 | 19295663 | We conclude that PKCbeta(2) plays a major role in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2277 | 19295663 | We conclude that PKCbeta(2) plays a major role in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2278 | 19295663 | We conclude that PKCbeta(2) plays a major role in TNF-alpha-induced human vascular endothelial cell apoptosis. |
| 2279 | 19283894 | In vitro, it inhibited the binding of both human and murine CD154 (CD40L) to their receptor (CD40) even in the presence of protein-containing media and prevented the CD154-induced proliferation of human B cells as well as the corresponding increase in surface expression of CD86, CD80, CD40, and MHC class II in a concentration-dependent manner. |
| 2280 | 19283894 | Furthermore, in isolated human islets, it also decreased the CD154-induced release of inflammatory cytokines such as IFN-g, interleukin-6 (IL-6), and IL-8. |
| 2281 | 19283894 | Suramin was selected for investigation because it has been reported to be an inhibitor of the interaction of TNF-a with its receptor and CD154 is a member of the TNF-family. |
| 2282 | 19281795 | A Jak2 inhibitor, AG490, reverses lipin-1 suppression by TNF-alpha in 3T3-L1 adipocytes. |
| 2283 | 19281795 | A Jak2 inhibitor, AG490, reverses lipin-1 suppression by TNF-alpha in 3T3-L1 adipocytes. |
| 2284 | 19281795 | A Jak2 inhibitor, AG490, reverses lipin-1 suppression by TNF-alpha in 3T3-L1 adipocytes. |
| 2285 | 19281795 | A Jak2 inhibitor, AG490, reverses lipin-1 suppression by TNF-alpha in 3T3-L1 adipocytes. |
| 2286 | 19281795 | Since TNF-alpha is deeply involved in the pathogenesis of obesity, insulin resistance, and diabetes, here we investigated the role of TNF-alpha on lipin-1 expression in adipocytes. |
| 2287 | 19281795 | Since TNF-alpha is deeply involved in the pathogenesis of obesity, insulin resistance, and diabetes, here we investigated the role of TNF-alpha on lipin-1 expression in adipocytes. |
| 2288 | 19281795 | Since TNF-alpha is deeply involved in the pathogenesis of obesity, insulin resistance, and diabetes, here we investigated the role of TNF-alpha on lipin-1 expression in adipocytes. |
| 2289 | 19281795 | Since TNF-alpha is deeply involved in the pathogenesis of obesity, insulin resistance, and diabetes, here we investigated the role of TNF-alpha on lipin-1 expression in adipocytes. |
| 2290 | 19281795 | A Jak2 inhibitor, AG490, reversed the suppressive effect of TNF-alpha on both lipin-1A and -1B. |
| 2291 | 19281795 | A Jak2 inhibitor, AG490, reversed the suppressive effect of TNF-alpha on both lipin-1A and -1B. |
| 2292 | 19281795 | A Jak2 inhibitor, AG490, reversed the suppressive effect of TNF-alpha on both lipin-1A and -1B. |
| 2293 | 19281795 | A Jak2 inhibitor, AG490, reversed the suppressive effect of TNF-alpha on both lipin-1A and -1B. |
| 2294 | 19281795 | In contrast, NF-kappaB, MAPKs, ceramide, and beta-catenin pathway tested were not involved in the mechanism. |
| 2295 | 19281795 | In contrast, NF-kappaB, MAPKs, ceramide, and beta-catenin pathway tested were not involved in the mechanism. |
| 2296 | 19281795 | In contrast, NF-kappaB, MAPKs, ceramide, and beta-catenin pathway tested were not involved in the mechanism. |
| 2297 | 19281795 | In contrast, NF-kappaB, MAPKs, ceramide, and beta-catenin pathway tested were not involved in the mechanism. |
| 2298 | 19281795 | These results suggest that TNF-alpha could be involved in obesity-induced lipin-1 suppression in adipocytes and Jak2 may play an important role in the mechanism. |
| 2299 | 19281795 | These results suggest that TNF-alpha could be involved in obesity-induced lipin-1 suppression in adipocytes and Jak2 may play an important role in the mechanism. |
| 2300 | 19281795 | These results suggest that TNF-alpha could be involved in obesity-induced lipin-1 suppression in adipocytes and Jak2 may play an important role in the mechanism. |
| 2301 | 19281795 | These results suggest that TNF-alpha could be involved in obesity-induced lipin-1 suppression in adipocytes and Jak2 may play an important role in the mechanism. |
| 2302 | 19275676 | Role of resistin in insulin sensitivity in rodents and humans. |
| 2303 | 19275676 | Resistin is a potential link between obesity and insulin resistance or type 2 diabetes. |
| 2304 | 19275676 | This is likely in part due to an up-regulation of suppressor of cytokine signaling (SOCS)-3, which interferes with the activation of insulin receptor substrate (IRS)-1. |
| 2305 | 19275676 | However, in humans resistin is expressed primarily by macrophages and seems to be involved in the recruitment of other immune cells and the secretion of pro-inflammatory factors, including tumor necrosis factor (TNF)alpha. |
| 2306 | 19275676 | Human resistin may interfere with insulin signaling by stimulating the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which dephosphorylates 3-phosphorylated phosphoinositide (PIP(3)). |
| 2307 | 19273093 | As death effector molecules, perforin, Fas ligand, tumor necrosis factor (TNF)-alpha, Interleukin (IL)-1, interferon (IFN)-gamma, and nitric oxide have been claimed. |
| 2308 | 19273093 | As death effector molecules, perforin, Fas ligand, tumor necrosis factor (TNF)-alpha, Interleukin (IL)-1, interferon (IFN)-gamma, and nitric oxide have been claimed. |
| 2309 | 19273093 | As death effector molecules, perforin, Fas ligand, tumor necrosis factor (TNF)-alpha, Interleukin (IL)-1, interferon (IFN)-gamma, and nitric oxide have been claimed. |
| 2310 | 19273093 | Recently, combinations or synergisms between IFN-gamma and TNF-alpha or IL-1beta are being revisited as the death effectors, and signal transduction of such synergisms has been explored to find molecular mechanism of beta -cell death. |
| 2311 | 19273093 | Recently, combinations or synergisms between IFN-gamma and TNF-alpha or IL-1beta are being revisited as the death effectors, and signal transduction of such synergisms has been explored to find molecular mechanism of beta -cell death. |
| 2312 | 19273093 | Recently, combinations or synergisms between IFN-gamma and TNF-alpha or IL-1beta are being revisited as the death effectors, and signal transduction of such synergisms has been explored to find molecular mechanism of beta -cell death. |
| 2313 | 19273093 | By employing TNF-alpha / IFN-gamma synergism model which causes beta -cell apoptosis, we found that the antiapoptotic X-linked inhibitor of apoptosis (XIAP) molecule is upregulated by NF-kappaB in response to TNF-alpha and XIAP induction was inhibited by IFN-gamma-induced signal transducer and activator of transcription-1 (STAT1) activation, which explains the death of beta -cells by TNF-alpha /IFN-gamma synergism. |
| 2314 | 19273093 | By employing TNF-alpha / IFN-gamma synergism model which causes beta -cell apoptosis, we found that the antiapoptotic X-linked inhibitor of apoptosis (XIAP) molecule is upregulated by NF-kappaB in response to TNF-alpha and XIAP induction was inhibited by IFN-gamma-induced signal transducer and activator of transcription-1 (STAT1) activation, which explains the death of beta -cells by TNF-alpha /IFN-gamma synergism. |
| 2315 | 19273093 | By employing TNF-alpha / IFN-gamma synergism model which causes beta -cell apoptosis, we found that the antiapoptotic X-linked inhibitor of apoptosis (XIAP) molecule is upregulated by NF-kappaB in response to TNF-alpha and XIAP induction was inhibited by IFN-gamma-induced signal transducer and activator of transcription-1 (STAT1) activation, which explains the death of beta -cells by TNF-alpha /IFN-gamma synergism. |
| 2316 | 19254713 | ICAM-1 and TNF-alpha, was drastically up-regulated in diabetic retina. |
| 2317 | 19254713 | ICAM-1 and TNF-alpha, was drastically up-regulated in diabetic retina. |
| 2318 | 19254713 | ICAM-1 and TNF-alpha, was drastically up-regulated in diabetic retina. |
| 2319 | 19254713 | In cultured bovine retinal capillary endothelial cells (RCECs) and human ARPE-19 cells, lovastatin attenuated the decrease of tight junction protein (occludin) and adherens junction protein (VE-cadherin) expression-induced by TNF-alpha, a major pro-inflammatory cytokine in diabetic retinopathy. |
| 2320 | 19254713 | In cultured bovine retinal capillary endothelial cells (RCECs) and human ARPE-19 cells, lovastatin attenuated the decrease of tight junction protein (occludin) and adherens junction protein (VE-cadherin) expression-induced by TNF-alpha, a major pro-inflammatory cytokine in diabetic retinopathy. |
| 2321 | 19254713 | In cultured bovine retinal capillary endothelial cells (RCECs) and human ARPE-19 cells, lovastatin attenuated the decrease of tight junction protein (occludin) and adherens junction protein (VE-cadherin) expression-induced by TNF-alpha, a major pro-inflammatory cytokine in diabetic retinopathy. |
| 2322 | 19254713 | Towards the mechanism, we showed that lovastatin ameliorated ICAM-1 expression-induced by hypoxia and TNF-alpha in both RCECs and ARPE-19 cells, in part through inhibition of NF-kappaB activation. |
| 2323 | 19254713 | Towards the mechanism, we showed that lovastatin ameliorated ICAM-1 expression-induced by hypoxia and TNF-alpha in both RCECs and ARPE-19 cells, in part through inhibition of NF-kappaB activation. |
| 2324 | 19254713 | Towards the mechanism, we showed that lovastatin ameliorated ICAM-1 expression-induced by hypoxia and TNF-alpha in both RCECs and ARPE-19 cells, in part through inhibition of NF-kappaB activation. |
| 2325 | 19249901 | Our aim was to assess the reaction of TNFalpha, resistin, leptin and adiponectin to lipid infusion. |
| 2326 | 19249901 | Our aim was to assess the reaction of TNFalpha, resistin, leptin and adiponectin to lipid infusion. |
| 2327 | 19249901 | Plasma concentrations of leptin and adiponectin did not show any significant changes. |
| 2328 | 19249901 | Plasma concentrations of leptin and adiponectin did not show any significant changes. |
| 2329 | 19249901 | Expressions of TNFalpha, leptin and adiponectin were unaffected. |
| 2330 | 19249901 | Expressions of TNFalpha, leptin and adiponectin were unaffected. |
| 2331 | 19249543 | There were significantly lower tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, interferon (IFN)-gamma, IL-6, and MIP-1beta productions from the OptiPrep-based density gradient group. |
| 2332 | 19245657 | AMP-dependent protein kinase (AMPK) is an evolutionarily conserved serine/threonine protein kinase central to the regulation of energy balance at both the cellular and whole-body levels. |
| 2333 | 19245657 | Regulation of AMPK activity at the whole-body level is coordinated by a growing number of hormones and cytokines secreted from adipose tissue, skeletal muscle, pancreas and the gut including leptin, adiponectin, insulin, interluekin-6, resistin, TNF-alpha and ghrelin. |
| 2334 | 19245657 | Understanding how these secreted signalling proteins regulate AMPK activity to control fatty acid oxidation, glucose uptake, gluconeogenesis and appetite may yield therapeutic treatments for metabolic disorders such as diabetes, insulin resistance and obesity. |
| 2335 | 19240767 | TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression. |
| 2336 | 19240767 | Inflammatory cytokines, including MIF via CD74, upregulate TRAIL. |
| 2337 | 19223654 | Here, we examined the role of TxNIP deficiency in vivo in the development of insulin-deficient diabetes and whether it impacted on pancreatic beta-cell mass and/or insulin secretion. |
| 2338 | 19223654 | TxNIP-deficient (Hcb-19/TxNIP(-/-)) mice had lower baseline glycemia, higher circulating insulin concentrations, and higher total pancreatic insulin content and beta-cell mass than control mice (C3H). |
| 2339 | 19223654 | Consistently, cultured pancreatic INS-1 cells transfected with small-interfering RNA against TxNIP were more sensitive to cell death induced by direct exposure to STZ or to the combination of inflammatory cytokines interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha. |
| 2340 | 19223654 | Furthermore, when corrected for insulin content, isolated pancreatic islets from TxNIP(-/-) mice exhibited reduced glucose-induced insulin secretion. |
| 2341 | 19223654 | These data indicate that TxNIP functions as a regulator of beta-cell mass and influences insulin secretion. |
| 2342 | 19221061 | In a previous study, cilostazol promoted differentiation of 3T3-L1 fibroblasts into adipocytes and improved insulin sensitivity by stimulating peroxisome proliferator-activated receptor (PPAR) gamma transcription. |
| 2343 | 19221061 | Elevated plasma insulin and resistin levels were significantly decreased by cilostazol, and decreased adiponectin mRNA expression was elevated along with increased plasma adiponectin. |
| 2344 | 19221061 | Cilostazol significantly increased both adipocyte fatty acid binding protein and fatty acid transport protein-1 mRNA expressions with increased glucose transport 4 in the adipose tissue. |
| 2345 | 19221061 | Cilostazol and rosiglitazone significantly suppressed proinflammatory markers (superoxide, tumor necrosis factor-alpha, and vascular cell adhesion molecule-1) in the carotid artery of db/db mice. |
| 2346 | 19221061 | The transcription activity stimulated by cilostazol was attenuated by KT5720 [(9R,10S,12S)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9, 12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo [3,4-I][1,6]-benzodiazocine-10-carboxylic acid hexyl ester], a cAMP-dependent protein kinase inhibitor, and GW9662 (2-chloro-5-nitrobenzanilide), an antagonist of PPARgamma activity, indicative of implication of the phosphatidylinositol 3-kinase/Akt signal pathway. |
| 2347 | 19221061 | These results suggest that cilostazol may improve insulin sensitivity along with anti-inflammatory effects in type 2 diabetic patients via activation of both cAMP-dependent protein kinase and PPARgamma transcription. |
| 2348 | 19220660 | Effects of probucol on hepatic tumor necrosis factor-alpha, interleukin-6 and adiponectin receptor-2 expression in diabetic rats. |
| 2349 | 19217258 | T cells from recipients transplanted with allogeneic islets +MSC produced low levels of IFN-gamma and TNF-alpha upon ex-vivo activation, and this transplantation protocol promoted the generation of IL-10-secreting CD4(+) T cells. |
| 2350 | 19208906 | Loss-of-function mutation in myostatin reduces tumor necrosis factor alpha production and protects liver against obesity-induced insulin resistance. |
| 2351 | 19208854 | In adipose tissue of obese db/db mice, BBR treatment significantly downregulated the expression of proinflammatory genes such as TNF-alpha, IL-1beta, IL-6, monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). |
| 2352 | 19208854 | Consistently, BBR inhibited LPS-induced expression of proinflammatory genes including IL-1beta, IL-6, iNOS, MCP-1, COX-2, and matrix metalloprotease-9 in peritoneal macrophages and RAW 264.7 cells. |
| 2353 | 19208854 | Upon various proinflammatory signals including LPS, free fatty acids, and hydrogen peroxide, BBR suppressed the phosphorylation of MAPKs, such as p38, ERK, and JNK, and the level of reactive oxygen species in macrophages. |
| 2354 | 19202909 | Increasing evidence indicates that altered secretion of adipocytokines such as adiponectin, tumor necrosis factor alpha, monocyte chemoattractant protein-1 and free fatty acids are contributing factors to insulin resistance in obese states. |
| 2355 | 19202295 | The starch fraction of Japanese millet had no effect on glucose or adiponectin levels, but the prolamin fraction beneficially modulated plasma glucose and insulin concentrations as well as adiponectin and tumor necrosis factor-alpha gene expression. |
| 2356 | 19202295 | Considering the physiological significance of adiponectin and HDL cholesterol levels in type 2 diabetes, insulin resistance, and cardiovascular disease, our findings imply that dietary JMP has the potential to ameliorate these diseases. |
| 2357 | 19201949 | TNFalpha-dependent hepatic steatosis and liver degeneration caused by mutation of zebrafish S-adenosylhomocysteine hydrolase. |
| 2358 | 19196630 | The association between cytokines (IL-1 beta, sIL-4R, IL-6, IL-8, IL-10, IL-12, TNF-alpha) and subcortical white matter lesions, cortical atrophy and lacunar infarctions of the aging brain was investigated among 268 elderly community participants. |
| 2359 | 19196630 | An association between atrophy and the chemokine-cytokine factor (containing sIL-4R, IL-6, IL-8) remained significant after adjustment for age, gender, education, depressive symptoms, diabetes mellitus, cardiovascular diseases (stroke, TIA, myocardial infarction, myocardial insufficiency, arrhythmic heart), hypertension, body-mass index, smoking status and aggregation inhibitors as opposed to single cytokines. |
| 2360 | 19195861 | The expression of intercellular adhesion molecule-1 (ICAM1) and vascular cell adhesion molecule-1 (VCAM1) increased, but that of occludin decreased. |
| 2361 | 19195861 | Apigenin strongly inhibited the expression of VCAM1, IkappaB kinase (IKK) alpha and IKKepsilon/IKKi, and suppressed the adhesion of U937 cells. |
| 2362 | 19195861 | HG and TNFalpha induced the expression of cell adhesion molecules and reduced that of occludin in EC. |
| 2363 | 19188427 | Interleukin-6 attenuates insulin-mediated increases in endothelial cell signaling but augments skeletal muscle insulin action via differential effects on tumor necrosis factor-alpha expression. |
| 2364 | 19181967 | In M. musculus arteries, HG elicited significant upregulation of inflammatory markers (TNF-alpha, IL-6, ICAM-1, VCAM, and monocyte chemoattractant protein-1). |
| 2365 | 19171978 | Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-beta, TNF-alpha, GM-CSF), growth factors, and transcription factors. |
| 2366 | 19171978 | Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion. |
| 2367 | 19165564 | We sought to evaluate the relationship between plasma cytokine levels (sCD14, tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6) and tissue Doppler derived indices of left ventricular systolic and diastolic function in patients with newly diagnosed heart failure. |
| 2368 | 19165564 | We sought to evaluate the relationship between plasma cytokine levels (sCD14, tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6) and tissue Doppler derived indices of left ventricular systolic and diastolic function in patients with newly diagnosed heart failure. |
| 2369 | 19165564 | We sought to evaluate the relationship between plasma cytokine levels (sCD14, tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6) and tissue Doppler derived indices of left ventricular systolic and diastolic function in patients with newly diagnosed heart failure. |
| 2370 | 19165564 | Soluble plasma levels of CD14, TNF-alpha, and IL-6 were measured in all patients during their third day of hospitalization. |
| 2371 | 19165564 | Soluble plasma levels of CD14, TNF-alpha, and IL-6 were measured in all patients during their third day of hospitalization. |
| 2372 | 19165564 | Soluble plasma levels of CD14, TNF-alpha, and IL-6 were measured in all patients during their third day of hospitalization. |
| 2373 | 19165564 | This study reveals that increased plasma levels of CD14, IL-6 and TNF-alpha are associated with impaired left atrial function and more advanced left ventricular diastolic and systolic dysfunction, in patients with newly diagnosed heart failure. |
| 2374 | 19165564 | This study reveals that increased plasma levels of CD14, IL-6 and TNF-alpha are associated with impaired left atrial function and more advanced left ventricular diastolic and systolic dysfunction, in patients with newly diagnosed heart failure. |
| 2375 | 19165564 | This study reveals that increased plasma levels of CD14, IL-6 and TNF-alpha are associated with impaired left atrial function and more advanced left ventricular diastolic and systolic dysfunction, in patients with newly diagnosed heart failure. |
| 2376 | 19164473 | Furthermore, E2 treatment reduced HFD-induced insulin resistance by 50% during hyperinsulinemic euglycemic clamp studies and improved insulin signaling (Akt phosphorylation) in insulin-stimulated skeletal muscles. |
| 2377 | 19164473 | Unexpectedly, we found that E2 treatment enhanced cytokine (IL-6, TNF-alpha) and plasminogen activator inhibitor-1 mRNA expression induced by HFD in the liver and visceral adipose tissue. |
| 2378 | 19151544 | Western blot analysis showed that the expressions of 1 alpha (IV) collagen, intercellular adhesion molecule (ICAM)-1, interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, NF-kappaB p65, and 3-nitrotyrosine (3-NT) protein were increased in the kidneys of diabetic rats; the increases in these proteins were all dose-dependently and significantly inhibited by TGP treatment. |
| 2379 | 19151544 | Western blot analysis showed that the expressions of 1 alpha (IV) collagen, intercellular adhesion molecule (ICAM)-1, interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, NF-kappaB p65, and 3-nitrotyrosine (3-NT) protein were increased in the kidneys of diabetic rats; the increases in these proteins were all dose-dependently and significantly inhibited by TGP treatment. |
| 2380 | 19151544 | Our data suggest that TGP treatment ameliorates early renal injury via the inhibition of expression of ICAM-1, IL-1, TNF-alpha, and 3-NT in the kidneys of diabetic rats. |
| 2381 | 19151544 | Our data suggest that TGP treatment ameliorates early renal injury via the inhibition of expression of ICAM-1, IL-1, TNF-alpha, and 3-NT in the kidneys of diabetic rats. |
| 2382 | 19140212 | TNF-alpha levels higher than the cut-point value were correlated with insulin resistance indices. |
| 2383 | 19136037 | The effect of CTLA-4 allele and haplotype frequencies on the interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta(1) levels and the presence in serum of GAD65 and IA-2 autoantibodies at the onset of T1D was evaluated. |
| 2384 | 19136037 | The effect of CTLA-4 allele and haplotype frequencies on the interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta(1) levels and the presence in serum of GAD65 and IA-2 autoantibodies at the onset of T1D was evaluated. |
| 2385 | 19136037 | On the other hand, higher ketoacidosis at onset, younger age at onset, and higher levels of tumor necrosis factor-alpha and interferon-gamma were observed in T1D patients carriers of G allele in comparison with the carriers of AA genotype. |
| 2386 | 19136037 | On the other hand, higher ketoacidosis at onset, younger age at onset, and higher levels of tumor necrosis factor-alpha and interferon-gamma were observed in T1D patients carriers of G allele in comparison with the carriers of AA genotype. |
| 2387 | 19127455 | Gene polymorphisms of TNF-alpha-308 (G/A), IL-10(-1082) (G/A), IL-6(-174) (G/C) and IL-1Ra (VNTR) in Egyptian cases with type 1 diabetes mellitus. |
| 2388 | 19125180 | Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. |
| 2389 | 19125180 | Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. |
| 2390 | 19125180 | Similarly, mononuclear mRNA levels of the proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6 were all significantly higher in DM2 compared to control women (P < .001). |
| 2391 | 19125180 | Similarly, mononuclear mRNA levels of the proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6 were all significantly higher in DM2 compared to control women (P < .001). |
| 2392 | 19125180 | The corresponding plasma resistin levels were slightly, but not significantly, increased in DM2 women (P = .051), and overall, they correlated significantly with BMI (r = 0.406, P = .010) and waist circumference (r = 0.516, P = .003), but not with fasting insulin levels or HOMA-IR. |
| 2393 | 19125180 | The corresponding plasma resistin levels were slightly, but not significantly, increased in DM2 women (P = .051), and overall, they correlated significantly with BMI (r = 0.406, P = .010) and waist circumference (r = 0.516, P = .003), but not with fasting insulin levels or HOMA-IR. |
| 2394 | 19125180 | Resistin mRNA expression is increased in PBMC from DM2 women, together with increased expression of the inflammatory cytokines IL-1beta, TNF-alpha, and IL-6, independent of obesity. |
| 2395 | 19125180 | Resistin mRNA expression is increased in PBMC from DM2 women, together with increased expression of the inflammatory cytokines IL-1beta, TNF-alpha, and IL-6, independent of obesity. |
| 2396 | 19120317 | Multiple studies have shown that thymus-derived naturally occurring Tregs constitutively express the forkhead/winged helix transcription factor FoxP3 in addition to high levels of CD25, the negative co-stimulatory molecule CTLA-4, and the glucocorticoid-induced TNF receptor-related protein GITR. |
| 2397 | 19120317 | At variance, adaptive or induced Tregs acquire these phenotypic markers as they differentiate in the periphery, following adequate stimulation in the appropriate environment, together with their capacity to produce immunomodulatory cytokines (mainly, IL-4, IL-10 and TGF-beta) and to display regulatory capacities. |
| 2398 | 19120317 | Moreover, data are presented that simultaneous blockade of CTLA4 and TGF-beta further impairs immunoregulatory circuits that control disease progression. |
| 2399 | 19120315 | This study aims to evaluate the production of cytokines, tumor necrosis factor (TNF), and interleukin 10 (IL-10) in peripheral blood mononuclear cells (PBMCs) from type 1 diabetic (T1D) patients by means of intracellular staining, flow cytometry, and ELISA and to correlate it with inadequate (IN) and adequate (A) metabolic controls. |
| 2400 | 19120315 | This study aims to evaluate the production of cytokines, tumor necrosis factor (TNF), and interleukin 10 (IL-10) in peripheral blood mononuclear cells (PBMCs) from type 1 diabetic (T1D) patients by means of intracellular staining, flow cytometry, and ELISA and to correlate it with inadequate (IN) and adequate (A) metabolic controls. |
| 2401 | 19120315 | PBMC cultures were stimulated with LPS to evaluate TNF or were stimulated with PMA/ionomycin or concanavalin A to evaluate IL-10. |
| 2402 | 19120315 | PBMC cultures were stimulated with LPS to evaluate TNF or were stimulated with PMA/ionomycin or concanavalin A to evaluate IL-10. |
| 2403 | 19120272 | Seven SNPs in the TNF genes (TNFA and TNFB) were genotyped in a Korean cohort (398 T1D patients and 1422 nondiabetic controls), along with HLA DRB1, DQB1, and MICA (MHC class I chain-related genes). |
| 2404 | 19120272 | Seven SNPs in the TNF genes (TNFA and TNFB) were genotyped in a Korean cohort (398 T1D patients and 1422 nondiabetic controls), along with HLA DRB1, DQB1, and MICA (MHC class I chain-related genes). |
| 2405 | 19120272 | Among them, three SNPs (TNFB+318, TNFA-857, and TNFA-308) and two common TNF haplotypes showed significant association with the risk of T1D (P= 5 x 10(-3)-10(-5)). |
| 2406 | 19120272 | Among them, three SNPs (TNFB+318, TNFA-857, and TNFA-308) and two common TNF haplotypes showed significant association with the risk of T1D (P= 5 x 10(-3)-10(-5)). |
| 2407 | 19117633 | ONO-1714 significantly reduced cytokine-mediated cytotoxicity and NO production in both MIN6N9a cells and C57BL/6 islets in the presence of IL-1beta, TNF-alpha, and IFN-gamma. |
| 2408 | 19095738 | We found that nuclear factor-kappaB (NF-kappaB) markedly activated GPB5 transcription. |
| 2409 | 19095738 | Disruption of the putative NF-kappaB-binding motifs in the GPB5 5'-flanking region silenced the GPB5 activation by p65. |
| 2410 | 19095738 | Because NF-kappaB is known to associate with acute phase inflammatory cytokines, we examined whether TNFalpha or IL-1beta could regulate GPB5. |
| 2411 | 19095738 | Both these cytokines activated GPB5 transcription by 2- to 3-fold, and their effects were abolished by the addition of MG132, a NF-kappaB inhibitor. |
| 2412 | 19094928 | Peroxisome proliferators activated receptors (PPAR) are ligand-inducible nuclear transacting factors comprising three subtypes, PPARalpha, PPARbeta/delta and PPARgamma, which play a key role in lipids and glucose homeostasis. |
| 2413 | 19094928 | All PPAR subtypes have been identified in joint or inflammatory cells and their activation resulted in a transcriptional repression of pro-inflammatory cytokines (IL-1, TNFalpha), early inflammatory genes (NOS(2), COX-2, mPGES-1) or matrix metalloproteases (MMP-1, MMP-13), at least for the gamma subtype. |
| 2414 | 19094928 | PPAR full agonists were also shown to stimulate IL-1 receptor antagonist (IL-1Ra) production by cytokine-stimulated articular cells in a subtype-dependent manner. |
| 2415 | 19094928 | These anti-inflammatory and anti-catabolic properties were confirmed in animal models of joint diseases where PPAR agonists reduced synovial inflammation while preventing cartilage destruction or inflammatory bone loss, although many effects required much higher doses than needed to restore insulin sensitivity or to lower circulating lipid levels. |
| 2416 | 19094928 | However, these promising effects of PPAR full agonists were hampered by their ability to reduce the growth factor-dependent synthesis of extracellular matrix components or to induce chondrocyte apoptosis, by the possible contribution of immunosuppressive properties to their anti-arthritic effects, by the increased adipocyte differentiation secondary to prolonged stimulation of PPARgamma, and by a variable contribution of PPAR subtypes depending on the system. |
| 2417 | 19084046 | In view of the central role of preadipocyte factor-1, adiponectin and leptin in white adipose tissue function, the aim of the present study was to analyze the mRNA expression of these proteins and of the inflammatory markers interleukin-6 and tumor necrosis factor-alpha in visceral and subcutaneous fat pads of rats with different metabolic disorders. |
| 2418 | 19084046 | In view of the central role of preadipocyte factor-1, adiponectin and leptin in white adipose tissue function, the aim of the present study was to analyze the mRNA expression of these proteins and of the inflammatory markers interleukin-6 and tumor necrosis factor-alpha in visceral and subcutaneous fat pads of rats with different metabolic disorders. |
| 2419 | 19084046 | We demonstrated highly divergent expression of preadipocyte factor-1, upregulated expression of adiponectin, interleukin-6 and TNF-alpha mRNA in adipose tissues of the diabetic Goto Kakizaki rat compared to the obese Zucker rat. |
| 2420 | 19084046 | We demonstrated highly divergent expression of preadipocyte factor-1, upregulated expression of adiponectin, interleukin-6 and TNF-alpha mRNA in adipose tissues of the diabetic Goto Kakizaki rat compared to the obese Zucker rat. |
| 2421 | 19076162 | Angiotensin-converting enzyme inhibitors improve hepatic steatosis by modulating expression of tumour necrosis factor-alpha, interleukin-6 and adiponectin receptor-2 in rats with type 2 diabetes. |
| 2422 | 19076162 | Angiotensin-converting enzyme inhibitors improve hepatic steatosis by modulating expression of tumour necrosis factor-alpha, interleukin-6 and adiponectin receptor-2 in rats with type 2 diabetes. |
| 2423 | 19076162 | Angiotensin-converting enzyme inhibitors improve hepatic steatosis by modulating expression of tumour necrosis factor-alpha, interleukin-6 and adiponectin receptor-2 in rats with type 2 diabetes. |
| 2424 | 19076162 | After six weeks of treatment with 5 mg/kg per day fosinopril, an ACEI, changes in liver histology, serum fasting glucose (FG), insulin, triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, adiponectin were evaluated, as was hepatic TNF-alpha, IL-6 and adiponectin receptor-2 (adipoR2) mRNA expression. 3. |
| 2425 | 19076162 | After six weeks of treatment with 5 mg/kg per day fosinopril, an ACEI, changes in liver histology, serum fasting glucose (FG), insulin, triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, adiponectin were evaluated, as was hepatic TNF-alpha, IL-6 and adiponectin receptor-2 (adipoR2) mRNA expression. 3. |
| 2426 | 19076162 | After six weeks of treatment with 5 mg/kg per day fosinopril, an ACEI, changes in liver histology, serum fasting glucose (FG), insulin, triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, adiponectin were evaluated, as was hepatic TNF-alpha, IL-6 and adiponectin receptor-2 (adipoR2) mRNA expression. 3. |
| 2427 | 19076162 | The degree of hepatic steatosis and inflammation, serum FG, insulin, TG, TC, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression were significantly higher in rats with T2DM than in normal controls. |
| 2428 | 19076162 | The degree of hepatic steatosis and inflammation, serum FG, insulin, TG, TC, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression were significantly higher in rats with T2DM than in normal controls. |
| 2429 | 19076162 | The degree of hepatic steatosis and inflammation, serum FG, insulin, TG, TC, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression were significantly higher in rats with T2DM than in normal controls. |
| 2430 | 19076162 | Serum adiponectin concentrations and hepatic adipoR2 mRNA expression in rats with T2DM were significantly lower than in normal controls. |
| 2431 | 19076162 | Serum adiponectin concentrations and hepatic adipoR2 mRNA expression in rats with T2DM were significantly lower than in normal controls. |
| 2432 | 19076162 | Serum adiponectin concentrations and hepatic adipoR2 mRNA expression in rats with T2DM were significantly lower than in normal controls. |
| 2433 | 19076162 | Fosinopril significantly reduced the degree of hepatic steatosis, serum FG, insulin, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression. |
| 2434 | 19076162 | Fosinopril significantly reduced the degree of hepatic steatosis, serum FG, insulin, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression. |
| 2435 | 19076162 | Fosinopril significantly reduced the degree of hepatic steatosis, serum FG, insulin, ALT, TNF-alpha and IL-6 concentrations and hepatic TNF-alpha and IL-6 mRNA expression. |
| 2436 | 19076162 | Fosinopril significantly increased serum adiponectin concentrations and hepatic adipoR2 mRNA expression. 4. |
| 2437 | 19076162 | Fosinopril significantly increased serum adiponectin concentrations and hepatic adipoR2 mRNA expression. 4. |
| 2438 | 19076162 | Fosinopril significantly increased serum adiponectin concentrations and hepatic adipoR2 mRNA expression. 4. |
| 2439 | 19076162 | In conclusion, the ACEI improved insulin sensitivity and hepatic steatosis in rats with T2DM by increasing circulating adiponectin and hepatic adipoR2 levels, in addition to reducing pro-inflammatory cytokine levels in the circulation and liver. |
| 2440 | 19076162 | In conclusion, the ACEI improved insulin sensitivity and hepatic steatosis in rats with T2DM by increasing circulating adiponectin and hepatic adipoR2 levels, in addition to reducing pro-inflammatory cytokine levels in the circulation and liver. |
| 2441 | 19076162 | In conclusion, the ACEI improved insulin sensitivity and hepatic steatosis in rats with T2DM by increasing circulating adiponectin and hepatic adipoR2 levels, in addition to reducing pro-inflammatory cytokine levels in the circulation and liver. |
| 2442 | 19073595 | The heparan sulfate proteoglycan form of epithelial CD44v3 serves as a CD11b/CD18 counter-receptor during polymorphonuclear leukocyte transepithelial migration. |
| 2443 | 19073595 | Leukocyte beta2-integrin CD11b/CD18 mediates the firm adhesion and subsequent transepithelial migration of polymorphonuclear leukocytes, but the identity of its counter-receptor(s) on epithelia remains elusive. |
| 2444 | 19073595 | Here we identified a monoclonal antibody, clone C3H7, which strongly bound to the basolateral membranes of epithelial cells and inhibited both the adhesion of epithelial cells to immobilized CD11b/CD8 and the transepithelial migration of PMNs in a physiologically relevant basolateral-to-apical direction. |
| 2445 | 19073595 | C3H7 antigen expression in epithelial monolayers was significantly increased by treatment with proinflammatory cytokine interferon-gamma or a combination of interferon-gamma and tumor necrosis factor-alpha. |
| 2446 | 19073595 | Further studies demonstrated that this epithelial CD44v3 specifically binds to CD11b/CD18 through its heparan sulfate moieties. |
| 2447 | 19073595 | In summary, our study demonstrates for the first time that the heparan sulfate proteoglycan form of epithelial CD44v3 plays a critical role in facilitating PMN recruitment during inflammatory episodes via directly binding to CD11b/CD18. |
| 2448 | 19070859 | We previously showed that polymorphisms in the tumor necrosis factor (TNF)-alpha gene, which is regulated by nuclear factor kappa B (NF-kappaB), modify the association between dietary polyunsaturated fatty acid (PUFA) intake and circulating HDL-cholesterol. |
| 2449 | 19070857 | ML treatment also increased the expression of adiponectin, and decreased the expression of TNF-alpha, MCP-1, and macrophage markers in white adipose tissue (WAT). |
| 2450 | 19067524 | Earlier we have shown coexpression of human vascular endothelial growth factor (hVEGF) and human interleukin-1 receptor antagonist (hIL-1Ra) after transfection of plasmid DNA encoding these two genes. |
| 2451 | 19067524 | Coexpression of hVEGF and hIL-1Ra by islets showed decrease in caspase-3 activity and apoptosis induced by a cocktail of inflammatory cytokines such as TNF-alpha, IL-1beta and IFN-gamma. |
| 2452 | 19067524 | Immunohistochemical staining of the islet bearing kidney sections at day 20 after transplantation was positive for human insulin, hVEGF and von Willebrand factor. |
| 2453 | 19060451 | Pulmonary levels of interferon-gamma, tumor necrosis factor-alpha and interleukin-1beta mRNAs were higher in the infected diabetic rats than in WT rats. |
| 2454 | 19050249 | Exposure of APCs of NOD mice to zymosan, a fungal cell wall component that interacts with TLR2 and dectin 1, resulted in the release of significant amounts of IL-10, TGF-beta1, IL-2, and TNF-alpha. |
| 2455 | 19050249 | Zymosan treatment induced suppression of T1D was associated with an increase in the L-selectin(high) T cell frequencies and enhanced suppressor function of CD4(+)CD25(+) T regulatory cells. |
| 2456 | 19050249 | Further, activation by anti-CD3-Ab induced larger amounts of TGF-beta1 and/or IL-10 production by CD4(+)CD25(+) and CD4(+)CD25(-) T cells from zymosan-treated mice. |
| 2457 | 19038972 | TNF-alpha reduces PGC-1alpha expression through NF-kappaB and p38 MAPK leading to increased glucose oxidation in a human cardiac cell model. |
| 2458 | 19029992 | In obesity and insulin-resistant states, adiponectin levels are reduced and loss of its protective effects might contribute to the excess cardiovascular risk observed in these conditions. |
| 2459 | 19029992 | In obesity and insulin-resistant states, adiponectin levels are reduced and loss of its protective effects might contribute to the excess cardiovascular risk observed in these conditions. |
| 2460 | 19029992 | In endothelial cells, adiponectin enhances production of nitric oxide, suppresses production of reactive oxygen species, and protects cells from inflammation that results from exposure to high glucose levels or tumor necrosis factor, through activation of AMP-activated protein kinase and cyclic AMP-dependent protein kinase (also known as protein kinase A) signaling cascades. |
| 2461 | 19029992 | In endothelial cells, adiponectin enhances production of nitric oxide, suppresses production of reactive oxygen species, and protects cells from inflammation that results from exposure to high glucose levels or tumor necrosis factor, through activation of AMP-activated protein kinase and cyclic AMP-dependent protein kinase (also known as protein kinase A) signaling cascades. |
| 2462 | 19029992 | In the myocardium, adiponectin-mediated protection from ischemia-reperfusion injury is linked to cyclo-oxygenase-2-mediated suppression of tumor necrosis factor signaling, inhibition of apoptosis by AMP-activated protein kinase, and inhibition of excess peroxynitrite-induced oxidative and nitrative stress. |
| 2463 | 19029992 | In the myocardium, adiponectin-mediated protection from ischemia-reperfusion injury is linked to cyclo-oxygenase-2-mediated suppression of tumor necrosis factor signaling, inhibition of apoptosis by AMP-activated protein kinase, and inhibition of excess peroxynitrite-induced oxidative and nitrative stress. |
| 2464 | 19026743 | For instance, in AD the accumulation of the amyloid-beta peptide (Abeta), which characterizes the disease and is thought to participate in the neurodegenerative process, may also induce neuronal insulin resistance. |
| 2465 | 19026743 | Conversely, disrupting normal glucose metabolism in transgenic animal models of AD that over-express the human amyloid precursor protein (hAPP) promotes amyloid-peptide aggregation and accelerates the disease progression. |
| 2466 | 19026743 | Studying these processes at a cellular level suggests that insulin resistance and Abeta aggregation may not only be the consequence of excitotoxicity, aberrant Ca(2+) signals, and proinflammatory cytokines such as TNF-alpha, but may also promote these pathological effectors. |
| 2467 | 19026743 | At the molecular level, insulin resistance and Abeta disrupt common signal transduction cascades including the insulin receptor family/PI3 kinase/Akt/GSK3 pathway. |
| 2468 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 2469 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 2470 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 2471 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 2472 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 2473 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 2474 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 2475 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 2476 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 2477 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 2478 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 2479 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 2480 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 2481 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 2482 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 2483 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 2484 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 2485 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 2486 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 2487 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 2488 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 2489 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 2490 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 2491 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 2492 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 2493 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 2494 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 2495 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 2496 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 2497 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 2498 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 2499 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 2500 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 2501 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 2502 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 2503 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 2504 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 2505 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 2506 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 2507 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 2508 | 19022962 | Dietary cod protein reduces plasma C-reactive protein in insulin-resistant men and women. |
| 2509 | 19022962 | Changes in plasma interleukin-6, tumor necrosis factor-alpha, and adiponectin concentrations did not differ between diets. |
| 2510 | 19022947 | Modulation of C-reactive protein, tumor necrosis factor-alpha, and adiponectin by diet, exercise, and weight loss. |
| 2511 | 19022947 | Modulation of C-reactive protein, tumor necrosis factor-alpha, and adiponectin by diet, exercise, and weight loss. |
| 2512 | 19022947 | In contrast to CRP and TNFalpha, adiponectin increases during weight loss and insulin sensitivity. |
| 2513 | 19022947 | In contrast to CRP and TNFalpha, adiponectin increases during weight loss and insulin sensitivity. |
| 2514 | 19013541 | Ursolic acid enhanced IL-2 and IFN-gamma production in response to Con A stimulation, whereas it inhibited TNF-alpha production in response to LPS stimulation. |
| 2515 | 19012034 | Adipose tissue is a massive source of bioactive substances known as adipocytokines, including tumor necrosis factor (TNF)-alpha, resistin, leptin, and adiponectin. |
| 2516 | 19012034 | Adipose tissue is a massive source of bioactive substances known as adipocytokines, including tumor necrosis factor (TNF)-alpha, resistin, leptin, and adiponectin. |
| 2517 | 19012034 | In this review, we discuss the association of adipocytokines, especially leptin, adiponectin, TNF-alpha, and resistin, with liver diseases. |
| 2518 | 19012034 | In this review, we discuss the association of adipocytokines, especially leptin, adiponectin, TNF-alpha, and resistin, with liver diseases. |
| 2519 | 19011089 | The adiponectin-interacting protein contains 2 thioredoxin domains and has very little sequence similarity to other GST isoforms. |
| 2520 | 19011089 | DsbA-L expression in 3T3-L1 adipocytes is stimulated by the insulin sensitizer rosiglitazone and inhibited by the inflammatory cytokine TNFalpha. |
| 2521 | 19011089 | Our results identify DsbA-L as a key regulator for adiponectin biosynthesis and uncover a potential new target for developing therapeutic drugs for the treatment of insulin resistance and its associated metabolic disorders. |
| 2522 | 19010563 | CD14, TLR2 and TLR4 expression were analyzed. |
| 2523 | 19010563 | Monocytes showed significantly higher surface CD14 expression from LADA compared with that from T2DM and controls, and high expression of TLR4 from LADA and T2DM than controls. |
| 2524 | 19010563 | After incubation with LPS or LTA, decreased surface expressions of CD14 were observed on monocytes from T2DM and controls, in contrast to the increased on monocytes from LADA. |
| 2525 | 19010563 | Activation of NF-kappaB and amounts of IL-1beta and TNF-alpha production by stimulation with ligands significantly increased in LADA and T2DM, which was modulated by 1,25(OH)(2)D3 to similar level, as compared to controls. |
| 2526 | 19010456 | These changes were accompanied by diabetes-increased mRNA levels of RANKL, TNF-alpha, and ADAMTS-4 and -5 measured by real-time PCR, which was reversed by insulin treatment. |
| 2527 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 2528 | 19008314 | Tumor necrosis factor-related apoptosis-inducing ligand inhibits experimental autoimmune thyroiditis by the expansion of CD4+CD25+ regulatory T cells. |
| 2529 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 2530 | 19008314 | There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. |
| 2531 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 2532 | 19008314 | In the present study, we specifically examined TRAIL effects on CD4(+)CD25(+) regulatory T cells. |
| 2533 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 2534 | 19008314 | CD4(+)CD25(+) T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. |
| 2535 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 2536 | 19008314 | These CD4(+)CD25(+) T cells included both CD4(+)CD25(+)CD45RB(Low) (regulatory) and CD4(+)CD25(+)CD45RB(High) (effector) T cells. |
| 2537 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 2538 | 19008314 | Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4(+)CD25(+)CD45RB(Low) T cells compared with mice immunized with mTg alone. |
| 2539 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 2540 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFbeta1 than CD4(+)CD25(+)CD45RB(High) T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4(+)CD25(+) T cells. |
| 2541 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 2542 | 19008314 | CD4(+)CD25(+)CD45RB(Low) T cells were more effective at suppressing histological thyroiditis than unfractionated cells. |
| 2543 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 2544 | 19008314 | These results indicated that TRAIL can increase the number of mTg-specific CD4(+)CD25(+)CD45RB(Low) T cells, inhibiting autoimmune responses and preventing the progression of EAT. |
| 2545 | 19003954 | Diabetic rats treated with ethanol or aqueous extracts of CLR at 15 and 30 g/kg dosage for 7 weeks, had decreased body weights, concentration of serum glucose, triglyceride (TG), total cholesterol (TC), and low-density lipoprotein-cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST), while the insulin-sensitivity index (ISI) improved significantly compared with the control group. |
| 2546 | 19003954 | In addition, high contents of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and low adiponectin level were observed in the control group and levels of TNF-alpha and IL-6 in CLR groups showed obvious differences with the control group. |
| 2547 | 18997420 | Effects of dietary Korean proso-millet protein on plasma adiponectin, HDL cholesterol, insulin levels, and gene expression in obese type 2 diabetic mice. |
| 2548 | 18997420 | The findings were that the feeding of PMP clearly elevated plasma high-density lipoprotein cholesterol (HDL cholesterol) and adiponectin levels and brought about effective reduction in the levels of glucose and insulin in mice under high-fat diet conditions as compared with a control diet. |
| 2549 | 18997420 | Gene expression study revealed that the diet up-regulated expression of adiponectin and down-regulated tumor necrosis factor-alpha (TNF-alpha). |
| 2550 | 18988929 | Plasma LDL diameter, interleukin-6 (IL-6), and interleukin-8 (IL-8) showed significant differences among the different degrees of DR severity in analysis of variance (ANOVA) with no definite trend. |
| 2551 | 18988929 | Plasma LDL diameter, interleukin-6 (IL-6), and interleukin-8 (IL-8) showed significant differences among the different degrees of DR severity in analysis of variance (ANOVA) with no definite trend. |
| 2552 | 18988929 | Plasma LDL diameter was smaller and IL-6 and tumor necrosis factor-alpha (TNF-alpha) levels were higher in DM patients with proliferative diabetic retinopathy (PDR) compared to those with non-proliferative diabetic retinopathy (NPDR) (p<0.05). |
| 2553 | 18988929 | Plasma LDL diameter was smaller and IL-6 and tumor necrosis factor-alpha (TNF-alpha) levels were higher in DM patients with proliferative diabetic retinopathy (PDR) compared to those with non-proliferative diabetic retinopathy (NPDR) (p<0.05). |
| 2554 | 18988929 | Levels of IL-6 and TNF-alpha as well as LDL diameter may be helpful in the prediction of PDR in DM patients with DR. |
| 2555 | 18988929 | Levels of IL-6 and TNF-alpha as well as LDL diameter may be helpful in the prediction of PDR in DM patients with DR. |
| 2556 | 18981116 | Furthermore, islet-infiltrating leukocytes in the LTP mice contained Foxp3(+)CD4 T cells. |
| 2557 | 18981116 | The LTP was abolished if mice were treated with either Ab-depleting CD4 T cells or a neutralizing Ab to CTLA-4, in this case, only at a late stage. |
| 2558 | 18981116 | Neutralization of IL-10, TGF-beta, glucocorticoid-induced TNF receptor (GITR), or CD25 had no effect. |
| 2559 | 18981116 | Hence, using monoclonal CD4 T cells, IFN-gamma can have a wide diversity of roles, depending on the setting of the immune process. |
| 2560 | 18979174 | Tumor necrosis factor alpha (TNFalpha)-stimulated gene 6 (TSG-6) is involved in inflammation, extracellular matrix formation, cell migration, and development. |
| 2561 | 18979174 | Pancreata from nondiabetic (8 and 25 weeks old), prediabetic (230-280 mg/dl blood glucose) and diabetic (>300 mg/dl blood glucose) NOD mice were stained for TSG-6, insulin, CD3, CD11c, Mac3 and CD31. |
| 2562 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2563 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2564 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2565 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2566 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2567 | 18972582 | Astragaloside IV attenuates lipolysis and improves insulin resistance induced by TNFalpha in 3T3-L1 adipocytes. |
| 2568 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2569 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2570 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2571 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2572 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2573 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 2574 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2575 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2576 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2577 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2578 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2579 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 2580 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2581 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2582 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2583 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2584 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2585 | 18972582 | Application of AS-IV inhibited TNFalpha-induced accelerated lipolysis in a dose-dependent manner, which was compatible with suppressed phosphorylation of ERK1/2 and reversed the downregulation of perilipin. |
| 2586 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2587 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2588 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2589 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2590 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2591 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 2592 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2593 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2594 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2595 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2596 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2597 | 18972582 | Further studies showed that AS-IV improved TNFalpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 2598 | 18971923 | Inhibition of C-jun N-terminal kinase improves insulin sensitivity but worsens albuminuria in experimental diabetes. |
| 2599 | 18971923 | C-jun N-terminal kinase (JNK) regulates both the development of insulin resistance and inflammation. |
| 2600 | 18971923 | Treatment of podocytes isolated from these two strains of mice with tumor necrosis factor-alpha caused greater phosphorylation of JNK in those obtained from diabetic animals. |
| 2601 | 18971923 | We induced diabetes in JNK1 knockout mice with streptozotocin and found that they had significantly better insulin sensitivity compared to diabetic wild-type or JNK2 knockout mice. |
| 2602 | 18971923 | Albuminuria was, however, worse in all mice treated with the JNK inhibitor and in diabetic JNK2 knockout mice compared to controls. |
| 2603 | 18971923 | Nephrin expression was also reduced in JNK inhibitor-treated mice compared to controls. |
| 2604 | 18971923 | Our study shows that targeting JNK to improve systemic insulin sensitivity does not necessarily prevent diabetic nephropathy. |
| 2605 | 18958647 | TCE administration induced a decrease in CD44(+) splenic T-cells and CD45RB(high), CD54(+) blood and splenic T-cells. |
| 2606 | 18958647 | Interestingly, the progressive increase in serum TNF-alpha and IFN-gamma levels normally seen with age in these mice was inhibited by TCE. |
| 2607 | 18952128 | The zinc finger protein A20 targets TRAF2 to the lysosomes for degradation. |
| 2608 | 18952128 | The zinc finger-containing protein A20 is a negative regulator of TNF-induced JNK (c-Jun-N-terminal kinase) and NFkappaB (nuclear factor kappaB) signaling. |
| 2609 | 18952128 | Although A20 is mostly localized in the cytosol, our recent studies reveal that a fraction of A20 can associate with a lysosome-interacting compartment in a manner that requires its carboxy terminal zinc fingers, but independent of its ubiquitin modifying activities. |
| 2610 | 18952128 | Here, we demonstrate that A20 is capable of targeting an associated signaling molecule such as TRAF2 to the lysosomes for degradation. |
| 2611 | 18952128 | This process is dependent on the membrane tethering zinc finger domains of A20, but does not require A20 ubiquitin modifying activity. |
| 2612 | 18940257 | In particular, the ability of certain cytokines, for example, IL-2, to provide vital survival signals to regulatory cells and to trigger death of effector T cells or impede IL-15 driven expansion of memory cells has spurred several trials. |
| 2613 | 18940257 | The ability of IFNgamma, IL-4, TNFalpha, and lymphotoxin to exert selective effects upon crucial lymphocyte subset populations in vivo may also enable translation into potent therapies. |
| 2614 | 18842989 | The MIF receptor CD74 in diabetic podocyte injury. |
| 2615 | 18842989 | Expression of macrophage migration inhibitory factor (MIF) is increased in experimental diabetic nephropathy, and increased tubulointerstitial mRNA expression of its receptor, CD74, has been observed in human diabetic nephropathy. |
| 2616 | 18842989 | Whether CD74 transduces MIF signals in podocytes, however, is unknown. |
| 2617 | 18842989 | In cultured human podocytes, CD74 was expressed at the cell surface, was upregulated by high concentrations of glucose and TNF-alpha, and was activated by MIF, leading to phosphorylation of extracellular signal-regulated kinase 1/2 and p38. |
| 2618 | 18842989 | In addition, MIF induced the expression of the inflammatory mediators TRAIL and monocyte chemoattractant protein 1 in podocytes and HK2 cells in a p38-dependent manner. |
| 2619 | 18842989 | These data suggest that CD74 acts as a receptor for MIF in podocytes and may play a role in the pathogenesis of diabetic nephropathy. |
| 2620 | 18805489 | Activation of the G(q)-coupled P2Y(6) receptor heterologously expressed in astrocytes significantly attenuates apoptosis induced by tumor necrosis factor alpha (TNFalpha). |
| 2621 | 18805489 | Activation of the G(q)-coupled P2Y(6) receptor heterologously expressed in astrocytes significantly attenuates apoptosis induced by tumor necrosis factor alpha (TNFalpha). |
| 2622 | 18805489 | TNFalpha-induced apoptosis in C2C12 cells correlated with activation of the transcription factor NF-kappaB. |
| 2623 | 18805489 | TNFalpha-induced apoptosis in C2C12 cells correlated with activation of the transcription factor NF-kappaB. |
| 2624 | 18805489 | The NF-kappaB activation was attenuated by 10nM MRS2693, which activated the antiapoptic ERK1/2 pathway. |
| 2625 | 18805489 | The NF-kappaB activation was attenuated by 10nM MRS2693, which activated the antiapoptic ERK1/2 pathway. |
| 2626 | 18805480 | In an effort to exploit these pathways to achieve control of aberrant immune activation we demonstrate that modulation of redox status suppresses cell proliferation and production of IL-2, IFN-gamma, TNF-alpha, and IL-17 in two robust CD8 T-cell-dependent in vitro mouse models: (1) response to alloantigen in an mixed leukocyte reaction and (2) CD8 T cell receptor transgenic OT-1 response to cognate peptide (SIINFEKL). |
| 2627 | 18805480 | To further examine the mechanisms of redox-mediated repression of CTL target cell lysis, we analyzed the expression of the effector molecules IFN-gamma, perforin, and granzyme B and the degranulation marker CD107a (LAMP-1). |
| 2628 | 18797414 | This pattern was also observed in other immunomodulatory factors (notably cortisol and epidermal growth factor), while (interleukin [IL]-1alpha, IL-4, IL-6, IL-9, IL-10, TNF-alpha, Eotaxin) did not change significantly. |
| 2629 | 18790831 | In db(TNF-)/db(TNF-) mice, EDHF-induced vasodilation was greater and comparable with controls, but IL-6 decreased EDHF-mediated vasodilation. |
| 2630 | 18789716 | Relationship of elevated osteoprotegerin with insulin resistance, CRP, and TNF-alpha levels in men with type 2 diabetes. |
| 2631 | 18789669 | Meanwhile, pancreatic mRNA expressions of proinflammatory cytokines interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma; mRNA expression and activity of iNOS and content of nitric oxide were significantly increased by 133.0% (P<.01), 164.0% (P<.001), 111.0% (P<.01), 101.0% (P<.001), 73.2% (P<.001) and 37.6% (P<.01), respectively, in untreated diabetes mellitus group compared with normal control group, and they were decreased by 43.2% (P<.01), 37.5% (P<.01), 33.9 % (P<.05), 35.5% (P<.01), 34.9% (P<.01) and 18.1% (P<.05), respectively, in selenite-treated diabetes mellitus group compared with untreated diabetes mellitus group. |
| 2632 | 18787467 | Interleukin-10 to tumor necrosis factor-alpha ratio is a predictive biomarker in nonalcoholic fatty liver disease: interleukin-10 to tumor necrosis factor-alpha ratio in steatohepatitis. |
| 2633 | 18780776 | Circulating proinflammatory cytokines, tumor necrosis factor-alpha and interleukin-6, were increased in western B6 mice but not 12-LOKO mice, whereas the reported protective adipokine, adiponectin, was decreased only in western B6 mice. 12-LO activity was significantly elevated by western diet in islets from B6 mice. |
| 2634 | 18780773 | In comparison with L subjects, OB subjects exhibited elevated interstitial leptin (P < 0.001), IL-8 (P < 0.05), and IL-18 levels (P = 0.05), as well as higher serum concentrations of leptin (P < 0.0001), IL-6 (P < 0.0001), tumor necrosis factor-alpha (P < 0.001), IL-8 (P = 0.01) and interferon-gamma-inducible protein 10 (P < 0.05). |
| 2635 | 18780773 | In samples from the M1 membranes, leptin decreased and IL-1alpha, IL-18, and RANTES (regulated on activation, normal T-cell expressed and secreted) remained relatively stable, whereas IL-6, IL-8, and monocyte chemoattractant protein-1 significantly increased after the first hour (P < 0.0001 vs. baseline). |
| 2636 | 18773750 | The latter include inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6 and hormones synthesized by adipocytes, such as adiponectin, leptin and resistin. |
| 2637 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2638 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2639 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2640 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2641 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2642 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2643 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2644 | 18772236 | Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. |
| 2645 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2646 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2647 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2648 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2649 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2650 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2651 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2652 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 2653 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2654 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2655 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2656 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2657 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2658 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2659 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2660 | 18772236 | Treatment with HG, but not equimolar mannitol or 3-O-methyl glucose, resulted in phosphorylation and activation of TNF-alpha converting enzyme (TACE) (ADAM17), which were attenuated by sorbinil or AR-specific small interference RNA. |
| 2661 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2662 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2663 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2664 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2665 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2666 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2667 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2668 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 2669 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2670 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2671 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2672 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2673 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2674 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2675 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2676 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 2677 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2678 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2679 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2680 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2681 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2682 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2683 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2684 | 18772236 | Sorbinil treatment also decreased the expression of TNF-alpha, matrix metalloproteinase-2, matrix metalloproteinase-9, and increased tissue inhibitor of metalloproteinase-3 in vascular smooth muscle cells treated with HG and in balloon-injured carotid arteries of diabetic rats. |
| 2685 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2686 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2687 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2688 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2689 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2690 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2691 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2692 | 18772236 | These results indicate that HG-induced TNF-alpha shedding could be attributed to TACE activation, which is regulated, in part, by PKC-delta and AR. |
| 2693 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2694 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2695 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2696 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2697 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2698 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2699 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2700 | 18772236 | Therefore, inhibition of TACE by TNF-alpha protease inhibitor-1, or pharmacological inhibition of PKC-delta or AR may represent useful strategies for treating vascular inflammation associated with diabetes. |
| 2701 | 18771589 | The former pathway proceeds via phosphorylation and degradation of inhibitor of NF-kappaB (IkappaB) and leads most commonly to activation of the heterodimer RelA/NF-kappaB1(p50). |
| 2702 | 18771589 | The latter pathway proceeds via phosphorylation and proteolytic processing of NF-kappaB2 (p100) and leads to activation, most commonly, of the heterodimer RelB/NF-kappaB2 (p52). |
| 2703 | 18771589 | We discuss the involvement of NF-kappaB in self-reactive T and B lymphocyte development, survival and proliferation, and the maintenance of chronic inflammation due to cytokines such as tumor necrosis factor-alpha, IL-1, IL-6, and IL-8. |
| 2704 | 18761006 | PBMC were cultured before and after cryopreservation either with GAD(65) or PHA. |
| 2705 | 18761006 | PBMC were cultured before and after cryopreservation either with GAD(65) or PHA. |
| 2706 | 18761006 | Secretion of cytokines (IL-5, -6, -10, -12, -13 -17, IFN-gamma and TNF-alpha) and chemokines (IP-10, MCP-1, MIP-1alpha, MIP-1beta and RANTES) was analysed in cell supernatants using multiplex fluorochrome technique (Luminex). |
| 2707 | 18761006 | Secretion of cytokines (IL-5, -6, -10, -12, -13 -17, IFN-gamma and TNF-alpha) and chemokines (IP-10, MCP-1, MIP-1alpha, MIP-1beta and RANTES) was analysed in cell supernatants using multiplex fluorochrome technique (Luminex). |
| 2708 | 18761006 | Expression of FOXP3 and TGF-beta mRNA was detected by multiplex real-time RT-PCR. |
| 2709 | 18761006 | Expression of FOXP3 and TGF-beta mRNA was detected by multiplex real-time RT-PCR. |
| 2710 | 18761006 | Increased spontaneous secretion of IL-6, -10, -12, -13, IFN-gamma and MCP-1, and mRNA expression of FOXP3 and TGF-beta, was detected after cryopreservation. |
| 2711 | 18761006 | Increased spontaneous secretion of IL-6, -10, -12, -13, IFN-gamma and MCP-1, and mRNA expression of FOXP3 and TGF-beta, was detected after cryopreservation. |
| 2712 | 18761006 | Stimulation with GAD(65) induced higher levels of IL-6, IFN-gamma, TNF-alpha and MIP-1alpha, whereas lower secretion was found for IL-10 and IL-13 in cryopreserved PBMC. |
| 2713 | 18761006 | Stimulation with GAD(65) induced higher levels of IL-6, IFN-gamma, TNF-alpha and MIP-1alpha, whereas lower secretion was found for IL-10 and IL-13 in cryopreserved PBMC. |
| 2714 | 18761006 | Stimulation with PHA induced lower secretion of IP-10, MCP-1 and RANTES and FOXP3 mRNA expression after cryopreservation. |
| 2715 | 18761006 | Stimulation with PHA induced lower secretion of IP-10, MCP-1 and RANTES and FOXP3 mRNA expression after cryopreservation. |
| 2716 | 18755894 | We isolated highly pure CD4 or CD8 T cells from patients with type 1 diabetes (n = 675), other AI diseases, and healthy controls (n = 512). |
| 2717 | 18755894 | We isolated highly pure CD4 or CD8 T cells from patients with type 1 diabetes (n = 675), other AI diseases, and healthy controls (n = 512). |
| 2718 | 18755894 | Using two cell death assays, we found that a subpopulation of CD8, but not CD4, T cells in patients' blood was vulnerable to TNF or TNF agonist-induced death. |
| 2719 | 18755894 | Using two cell death assays, we found that a subpopulation of CD8, but not CD4, T cells in patients' blood was vulnerable to TNF or TNF agonist-induced death. |
| 2720 | 18755894 | In type 1 diabetes, the subpopulation of T cells susceptible to TNF or TNFR2 agonist-induced death was traced specifically to autoreactive T cells to insulin, a known autoantigen. |
| 2721 | 18755894 | In type 1 diabetes, the subpopulation of T cells susceptible to TNF or TNFR2 agonist-induced death was traced specifically to autoreactive T cells to insulin, a known autoantigen. |
| 2722 | 18716362 | The plasma levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP), adiponectin and tumor necrosis factor-alpha (TNF(alpha)), the urinary excretion of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)) and 8-hydroxydeoxyguanosine (8-OHdG), and the urinary albumin-to-creatinine ratios (ACR) were determined before and after 16-week treatment. |
| 2723 | 18716362 | The plasma levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP), adiponectin and tumor necrosis factor-alpha (TNF(alpha)), the urinary excretion of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)) and 8-hydroxydeoxyguanosine (8-OHdG), and the urinary albumin-to-creatinine ratios (ACR) were determined before and after 16-week treatment. |
| 2724 | 18716362 | However, significant decreases in MCP-1, IL-6, hsCRP, TNF(alpha), 8-epi-PGF(2alpha), 8-OHdG and ACR levels, and a significant increase in the plasma adiponectin level were detected in the AZ group, but not in the NF group. |
| 2725 | 18716362 | However, significant decreases in MCP-1, IL-6, hsCRP, TNF(alpha), 8-epi-PGF(2alpha), 8-OHdG and ACR levels, and a significant increase in the plasma adiponectin level were detected in the AZ group, but not in the NF group. |
| 2726 | 18713984 | The reprogrammed Tregs cease to express IL-10 and TGFbeta, fail to suppress T cell responses, and gain the ability to produce IFN-gamma, IL-17, and TNF-alpha. |
| 2727 | 18708586 | We have now discovered that activation of 5-HT(2A) receptors in primary aortic smooth muscle cells provides a previously unknown and extremely potent inhibition of tumor necrosis factor (TNF)-alpha-mediated inflammation. 5-HT(2A) receptor stimulation with the agonist (R)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(R)-DOI] rapidly inhibits a variety of TNF-alpha-mediated proinflammatory markers, including intracellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 1 (VCAM-1), and interleukin (IL)-6 gene expression, nitric-oxide synthase activity, and nuclear translocation of nuclear factor kappaB, with IC(50) values of only 10 to 20 pM. |
| 2728 | 18708586 | We have now discovered that activation of 5-HT(2A) receptors in primary aortic smooth muscle cells provides a previously unknown and extremely potent inhibition of tumor necrosis factor (TNF)-alpha-mediated inflammation. 5-HT(2A) receptor stimulation with the agonist (R)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(R)-DOI] rapidly inhibits a variety of TNF-alpha-mediated proinflammatory markers, including intracellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 1 (VCAM-1), and interleukin (IL)-6 gene expression, nitric-oxide synthase activity, and nuclear translocation of nuclear factor kappaB, with IC(50) values of only 10 to 20 pM. |
| 2729 | 18708586 | Our results indicate that activation of 5-HT(2A) receptors represents a novel, and extraordinarily potent, potential therapeutic avenue for the treatment of disorders involving TNF-alpha-mediated inflammation. |
| 2730 | 18708586 | Our results indicate that activation of 5-HT(2A) receptors represents a novel, and extraordinarily potent, potential therapeutic avenue for the treatment of disorders involving TNF-alpha-mediated inflammation. |
| 2731 | 18708169 | Th1 response leads to increased IFNgamma and TNFalpha production that in turn stimulates CXCL10 secretion by the target cells, thus perpetuating the immune cascade. |
| 2732 | 18679158 | All the patients had TSH, fT4, fT3, urinary albumin secretion rate, IgA, level of antigliadin antibodies (AGA) IgA and IgG, antitissue transglutaminase IgA antibodies, antiendomysium (EmA) IgA and IgG antibodies and antitireoglobulin antibodies, antithyroid peroxidase antibodies evaluated. |
| 2733 | 18679158 | All the patients had TSH, fT4, fT3, urinary albumin secretion rate, IgA, level of antigliadin antibodies (AGA) IgA and IgG, antitissue transglutaminase IgA antibodies, antiendomysium (EmA) IgA and IgG antibodies and antitireoglobulin antibodies, antithyroid peroxidase antibodies evaluated. |
| 2734 | 18679158 | All the patients had TSH, fT4, fT3, urinary albumin secretion rate, IgA, level of antigliadin antibodies (AGA) IgA and IgG, antitissue transglutaminase IgA antibodies, antiendomysium (EmA) IgA and IgG antibodies and antitireoglobulin antibodies, antithyroid peroxidase antibodies evaluated. |
| 2735 | 18679158 | Serum TNF-alpha, IL-6, and IL-10 levels were also measured. |
| 2736 | 18679158 | Serum TNF-alpha, IL-6, and IL-10 levels were also measured. |
| 2737 | 18679158 | Serum TNF-alpha, IL-6, and IL-10 levels were also measured. |
| 2738 | 18679158 | The group of children with coincident DM1 and celiac disease and without autoimmune thyroiditis was characterized by significantly higher glycosylated hemoglobin, higher serum TNF-alpha, IL-6 but lower serum IL-10 in relation to the remaining diabetic patients. |
| 2739 | 18679158 | The group of children with coincident DM1 and celiac disease and without autoimmune thyroiditis was characterized by significantly higher glycosylated hemoglobin, higher serum TNF-alpha, IL-6 but lower serum IL-10 in relation to the remaining diabetic patients. |
| 2740 | 18679158 | The group of children with coincident DM1 and celiac disease and without autoimmune thyroiditis was characterized by significantly higher glycosylated hemoglobin, higher serum TNF-alpha, IL-6 but lower serum IL-10 in relation to the remaining diabetic patients. |
| 2741 | 18679158 | A statistically significant positive correlation was observed between IgA-anti-tTG and serum TNF-alpha (R = 0.28, p = 0.026); between IgG AGA and serum IL-6 (R = 0.31, p = 0.023); and between glycosylated hemoglobin and IgA-anti-tTG (R = 0.21, p = 0.001) and IgA antiendomysium (R = 0.22, p = 0.001). |
| 2742 | 18679158 | A statistically significant positive correlation was observed between IgA-anti-tTG and serum TNF-alpha (R = 0.28, p = 0.026); between IgG AGA and serum IL-6 (R = 0.31, p = 0.023); and between glycosylated hemoglobin and IgA-anti-tTG (R = 0.21, p = 0.001) and IgA antiendomysium (R = 0.22, p = 0.001). |
| 2743 | 18679158 | A statistically significant positive correlation was observed between IgA-anti-tTG and serum TNF-alpha (R = 0.28, p = 0.026); between IgG AGA and serum IL-6 (R = 0.31, p = 0.023); and between glycosylated hemoglobin and IgA-anti-tTG (R = 0.21, p = 0.001) and IgA antiendomysium (R = 0.22, p = 0.001). |
| 2744 | 18677693 | Advanced glycation end products, inflammatorial cytokines like IL-6 or TNF-alpha are elevated in subjects with metabolic syndrome as well as in frail elderly. |
| 2745 | 18670098 | Inhibition of monocyte chemoattractant protein-1 by Krüppel-like factor 5 small interfering RNA in the tumor necrosis factor- alpha-activated human umbilical vein endothelial cells. |
| 2746 | 18670098 | Inhibition of monocyte chemoattractant protein-1 by Krüppel-like factor 5 small interfering RNA in the tumor necrosis factor- alpha-activated human umbilical vein endothelial cells. |
| 2747 | 18670098 | Inhibition of monocyte chemoattractant protein-1 by Krüppel-like factor 5 small interfering RNA in the tumor necrosis factor- alpha-activated human umbilical vein endothelial cells. |
| 2748 | 18670098 | Inhibition of monocyte chemoattractant protein-1 by Krüppel-like factor 5 small interfering RNA in the tumor necrosis factor- alpha-activated human umbilical vein endothelial cells. |
| 2749 | 18670098 | This study was made to determine whether KLF5 may associate with MCP-1 expression in human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha), in terms of the initial events of damaged vascular cells in diabetes. |
| 2750 | 18670098 | This study was made to determine whether KLF5 may associate with MCP-1 expression in human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha), in terms of the initial events of damaged vascular cells in diabetes. |
| 2751 | 18670098 | This study was made to determine whether KLF5 may associate with MCP-1 expression in human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha), in terms of the initial events of damaged vascular cells in diabetes. |
| 2752 | 18670098 | This study was made to determine whether KLF5 may associate with MCP-1 expression in human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha), in terms of the initial events of damaged vascular cells in diabetes. |
| 2753 | 18670098 | MCP-1 expression was markedly augmented by the treatment of TNF-alpha to HUVECs, but this augmentation was inhibited by KLF5 small interfering RNA, which primarily suppressed the expression of KLF5 at mRNA levels in the cells. |
| 2754 | 18670098 | MCP-1 expression was markedly augmented by the treatment of TNF-alpha to HUVECs, but this augmentation was inhibited by KLF5 small interfering RNA, which primarily suppressed the expression of KLF5 at mRNA levels in the cells. |
| 2755 | 18670098 | MCP-1 expression was markedly augmented by the treatment of TNF-alpha to HUVECs, but this augmentation was inhibited by KLF5 small interfering RNA, which primarily suppressed the expression of KLF5 at mRNA levels in the cells. |
| 2756 | 18670098 | MCP-1 expression was markedly augmented by the treatment of TNF-alpha to HUVECs, but this augmentation was inhibited by KLF5 small interfering RNA, which primarily suppressed the expression of KLF5 at mRNA levels in the cells. |
| 2757 | 18670098 | Though TNF-alpha augmented the levels of endothelin-1 (ET-1) and attenuated those of embryonic form of myosin heavy chain (SMemb) in HUVECs, the inhibition of KLF5 did not affect the levels of these cytokines in the cells. |
| 2758 | 18670098 | Though TNF-alpha augmented the levels of endothelin-1 (ET-1) and attenuated those of embryonic form of myosin heavy chain (SMemb) in HUVECs, the inhibition of KLF5 did not affect the levels of these cytokines in the cells. |
| 2759 | 18670098 | Though TNF-alpha augmented the levels of endothelin-1 (ET-1) and attenuated those of embryonic form of myosin heavy chain (SMemb) in HUVECs, the inhibition of KLF5 did not affect the levels of these cytokines in the cells. |
| 2760 | 18670098 | Though TNF-alpha augmented the levels of endothelin-1 (ET-1) and attenuated those of embryonic form of myosin heavy chain (SMemb) in HUVECs, the inhibition of KLF5 did not affect the levels of these cytokines in the cells. |
| 2761 | 18653783 | Ex vivo expanded CD34(+) human UCB cells have the capacity to generate multiple hematopoietic lineages and a functional human immune system upon transplantation into TNFalpha-treated NOD-scid IL2rgamma(null) mice. |
| 2762 | 18650421 | Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-kappaB-dependent inflammatory genes. |
| 2763 | 18650421 | Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-kappaB-dependent inflammatory genes. |
| 2764 | 18650421 | Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-kappaB-dependent inflammatory genes. |
| 2765 | 18650421 | Role of the histone H3 lysine 4 methyltransferase, SET7/9, in the regulation of NF-kappaB-dependent inflammatory genes. |
| 2766 | 18650421 | Nuclear factor kappa-B (NF-kappaB)-regulated inflammatory genes, such as TNF-alpha (tumor necrosis factor-alpha), play key roles in the pathogenesis of inflammatory diseases, including diabetes and the metabolic syndrome. |
| 2767 | 18650421 | Nuclear factor kappa-B (NF-kappaB)-regulated inflammatory genes, such as TNF-alpha (tumor necrosis factor-alpha), play key roles in the pathogenesis of inflammatory diseases, including diabetes and the metabolic syndrome. |
| 2768 | 18650421 | Nuclear factor kappa-B (NF-kappaB)-regulated inflammatory genes, such as TNF-alpha (tumor necrosis factor-alpha), play key roles in the pathogenesis of inflammatory diseases, including diabetes and the metabolic syndrome. |
| 2769 | 18650421 | Nuclear factor kappa-B (NF-kappaB)-regulated inflammatory genes, such as TNF-alpha (tumor necrosis factor-alpha), play key roles in the pathogenesis of inflammatory diseases, including diabetes and the metabolic syndrome. |
| 2770 | 18650421 | We report here that the chromatin histone H3-lysine 4 methyltransferase, SET7/9, is a novel coactivator of NF-kappaB. |
| 2771 | 18650421 | We report here that the chromatin histone H3-lysine 4 methyltransferase, SET7/9, is a novel coactivator of NF-kappaB. |
| 2772 | 18650421 | We report here that the chromatin histone H3-lysine 4 methyltransferase, SET7/9, is a novel coactivator of NF-kappaB. |
| 2773 | 18650421 | We report here that the chromatin histone H3-lysine 4 methyltransferase, SET7/9, is a novel coactivator of NF-kappaB. |
| 2774 | 18650421 | Gene silencing of SET7/9 with small interfering RNAs in monocytes significantly inhibited TNF-alpha-induced inflammatory genes and histone H3-lysine 4 methylation on these promoters, as well as monocyte adhesion to endothelial or smooth muscle cells. |
| 2775 | 18650421 | Gene silencing of SET7/9 with small interfering RNAs in monocytes significantly inhibited TNF-alpha-induced inflammatory genes and histone H3-lysine 4 methylation on these promoters, as well as monocyte adhesion to endothelial or smooth muscle cells. |
| 2776 | 18650421 | Gene silencing of SET7/9 with small interfering RNAs in monocytes significantly inhibited TNF-alpha-induced inflammatory genes and histone H3-lysine 4 methylation on these promoters, as well as monocyte adhesion to endothelial or smooth muscle cells. |
| 2777 | 18650421 | Gene silencing of SET7/9 with small interfering RNAs in monocytes significantly inhibited TNF-alpha-induced inflammatory genes and histone H3-lysine 4 methylation on these promoters, as well as monocyte adhesion to endothelial or smooth muscle cells. |
| 2778 | 18650421 | Chromatin immunoprecipitation revealed that SET7/9 small interfering RNA could reduce TNF-alpha-induced recruitment of NF-kappaB p65 to inflammatory gene promoters. |
| 2779 | 18650421 | Chromatin immunoprecipitation revealed that SET7/9 small interfering RNA could reduce TNF-alpha-induced recruitment of NF-kappaB p65 to inflammatory gene promoters. |
| 2780 | 18650421 | Chromatin immunoprecipitation revealed that SET7/9 small interfering RNA could reduce TNF-alpha-induced recruitment of NF-kappaB p65 to inflammatory gene promoters. |
| 2781 | 18650421 | Chromatin immunoprecipitation revealed that SET7/9 small interfering RNA could reduce TNF-alpha-induced recruitment of NF-kappaB p65 to inflammatory gene promoters. |
| 2782 | 18650421 | Microarray profiling revealed that, in TNF-alpha-stimulated monocytes, the induction of 25% NF-kappaB downstream genes, including the histone H3-lysine 27 demethylase JMJD3, was attenuated by SET7/9 depletion. |
| 2783 | 18650421 | Microarray profiling revealed that, in TNF-alpha-stimulated monocytes, the induction of 25% NF-kappaB downstream genes, including the histone H3-lysine 27 demethylase JMJD3, was attenuated by SET7/9 depletion. |
| 2784 | 18650421 | Microarray profiling revealed that, in TNF-alpha-stimulated monocytes, the induction of 25% NF-kappaB downstream genes, including the histone H3-lysine 27 demethylase JMJD3, was attenuated by SET7/9 depletion. |
| 2785 | 18650421 | Microarray profiling revealed that, in TNF-alpha-stimulated monocytes, the induction of 25% NF-kappaB downstream genes, including the histone H3-lysine 27 demethylase JMJD3, was attenuated by SET7/9 depletion. |
| 2786 | 18648737 | Emerging lines of studies indicated that insulin resistance, abnormal lipid metabolism, and dysregulation of cytokines/adipokines (e.g., tumor necrosis factor-alpha, adiponectin, and leptin) are profoundly involved in the pathogenesis of NAFLD. |
| 2787 | 18636168 | Inflammatory cytokine signaling in insulin producing beta-cells enhances the colocalization correlation coefficient between L-type voltage-dependent calcium channel and calcium-sensing receptor. |
| 2788 | 18636168 | Inflammatory cytokine signaling in insulin producing beta-cells enhances the colocalization correlation coefficient between L-type voltage-dependent calcium channel and calcium-sensing receptor. |
| 2789 | 18636168 | Inflammatory cytokine signaling in insulin producing beta-cells enhances the colocalization correlation coefficient between L-type voltage-dependent calcium channel and calcium-sensing receptor. |
| 2790 | 18636168 | Inflammatory cytokine signaling in insulin producing beta-cells enhances the colocalization correlation coefficient between L-type voltage-dependent calcium channel and calcium-sensing receptor. |
| 2791 | 18636168 | Tumor necrosis factor-alpha (TNF-alpha), is a cytokine widely known to activate nuclear factor-kappaB (NF-kappaB) transcription in beta-cells. |
| 2792 | 18636168 | Tumor necrosis factor-alpha (TNF-alpha), is a cytokine widely known to activate nuclear factor-kappaB (NF-kappaB) transcription in beta-cells. |
| 2793 | 18636168 | Tumor necrosis factor-alpha (TNF-alpha), is a cytokine widely known to activate nuclear factor-kappaB (NF-kappaB) transcription in beta-cells. |
| 2794 | 18636168 | Tumor necrosis factor-alpha (TNF-alpha), is a cytokine widely known to activate nuclear factor-kappaB (NF-kappaB) transcription in beta-cells. |
| 2795 | 18636168 | To obtain a better understanding of TNF-alpha-induced molecular interactions between CaR and VDCC, confocal fluorescence measurements were performed on insulin-producing beta-cells exposed to varying concentrations of TNF-alpha and the results are discussed in the light of increased colocalization correlation coefficient. |
| 2796 | 18636168 | To obtain a better understanding of TNF-alpha-induced molecular interactions between CaR and VDCC, confocal fluorescence measurements were performed on insulin-producing beta-cells exposed to varying concentrations of TNF-alpha and the results are discussed in the light of increased colocalization correlation coefficient. |
| 2797 | 18636168 | To obtain a better understanding of TNF-alpha-induced molecular interactions between CaR and VDCC, confocal fluorescence measurements were performed on insulin-producing beta-cells exposed to varying concentrations of TNF-alpha and the results are discussed in the light of increased colocalization correlation coefficient. |
| 2798 | 18636168 | To obtain a better understanding of TNF-alpha-induced molecular interactions between CaR and VDCC, confocal fluorescence measurements were performed on insulin-producing beta-cells exposed to varying concentrations of TNF-alpha and the results are discussed in the light of increased colocalization correlation coefficient. |
| 2799 | 18636168 | The insulin producing beta-cells were exposed to 5, 10, 20, 30, and 50 ng/ml TNF-alpha for 24 h at 37 degrees . |
| 2800 | 18636168 | The insulin producing beta-cells were exposed to 5, 10, 20, 30, and 50 ng/ml TNF-alpha for 24 h at 37 degrees . |
| 2801 | 18636168 | The insulin producing beta-cells were exposed to 5, 10, 20, 30, and 50 ng/ml TNF-alpha for 24 h at 37 degrees . |
| 2802 | 18636168 | The insulin producing beta-cells were exposed to 5, 10, 20, 30, and 50 ng/ml TNF-alpha for 24 h at 37 degrees . |
| 2803 | 18636168 | The 3-D confocal fluorescence imaging data also demonstrated that addition of TNF-alpha to RIN cells led to the translocation of NF-kappaB from the cytoplasm to the nucleus. |
| 2804 | 18636168 | The 3-D confocal fluorescence imaging data also demonstrated that addition of TNF-alpha to RIN cells led to the translocation of NF-kappaB from the cytoplasm to the nucleus. |
| 2805 | 18636168 | The 3-D confocal fluorescence imaging data also demonstrated that addition of TNF-alpha to RIN cells led to the translocation of NF-kappaB from the cytoplasm to the nucleus. |
| 2806 | 18636168 | The 3-D confocal fluorescence imaging data also demonstrated that addition of TNF-alpha to RIN cells led to the translocation of NF-kappaB from the cytoplasm to the nucleus. |
| 2807 | 18633186 | This effect of semapimod was well correlated with the reduction in the serum concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-6, and C-reactive protein, as well as with the recovery of AM-induced Akt phosphorylation and cGMP production. |
| 2808 | 18600366 | Incremental increases in TNFalpha/TNFR1 expression induces activation and production of superoxide via NAD(P)H oxidase and/or mitochondria respiratory chain, leading to endothelial dysfunction progressing to the development of type II diabetes. |
| 2809 | 18599066 | Palmitate induced secretion and mRNA expression of TNF-alpha, IL-8 and IL-1 beta, and enhanced lipopolysaccharide (LPS)-induced IL-1 beta secretion. |
| 2810 | 18599066 | Palmitate induced secretion and mRNA expression of TNF-alpha, IL-8 and IL-1 beta, and enhanced lipopolysaccharide (LPS)-induced IL-1 beta secretion. |
| 2811 | 18599066 | Palmitate phosphorylated p38 and JNK kinases, and blocking of these kinases with specific inhibitors diminished the palmitate-induced cytokine secretion. |
| 2812 | 18599066 | Palmitate phosphorylated p38 and JNK kinases, and blocking of these kinases with specific inhibitors diminished the palmitate-induced cytokine secretion. |
| 2813 | 18599066 | Palmitate also activated the AP-1 (c-Jun) transcription factor. |
| 2814 | 18599066 | Palmitate also activated the AP-1 (c-Jun) transcription factor. |
| 2815 | 18599066 | Knockdown of MyD88 reduced the palmitate-induced IL-8, but not TNF-alpha or IL-1 beta secretion. |
| 2816 | 18599066 | Knockdown of MyD88 reduced the palmitate-induced IL-8, but not TNF-alpha or IL-1 beta secretion. |
| 2817 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 2818 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 2819 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 2820 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 2821 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 2822 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 2823 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 2824 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 2825 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 2826 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 2827 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 2828 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 2829 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 2830 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 2831 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 2832 | 18593820 | Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. |
| 2833 | 18593820 | Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. |
| 2834 | 18593820 | Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. |
| 2835 | 18593820 | Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. |
| 2836 | 18593820 | Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. |
| 2837 | 18593820 | The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. |
| 2838 | 18593820 | The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. |
| 2839 | 18593820 | The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. |
| 2840 | 18593820 | The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. |
| 2841 | 18593820 | The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. |
| 2842 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 2843 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 2844 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 2845 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 2846 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 2847 | 18591775 | Biochemical parameters in plasma (glucose, TC, insulin and tumor necrosis factor-alpha (TNF-alpha) level) were significantly suppressed, and abnormal glucose tolerance, elevation of blood pressure and peripheral neuropathy accompanying progression of metabolic disorders were also significantly suppressed. |
| 2848 | 18585970 | Recent research revealed several molecules, including tumor necrosis factor alpha, suppressor of cytokine signaling 1 and 3 proteins, insulin-receptor substrates 1 and 2, and other adipocytokines, potentially are involved in the development of insulin resistance in patients with chronic hepatitis C. |
| 2849 | 18579779 | Furthermore, db/db VSMC were hypersensitive to TNF-alpha inflammatory stimulus, which induced dramatic and sustained decreases in promoter H3K9me3 and Suv39h1 occupancy. |
| 2850 | 18575614 | Association between LTA, TNF and AGER polymorphisms and late diabetic complications. |
| 2851 | 18573564 | Diabetic patients had higher log(CACS+1) (p=0.0089), baPWV (p=0.0293), frequency of elevated urinary albumin excretion (UAE) (p<0.0001) and TNF-alpha (p=0.0029) and similar estimated glomerular filtration rate (eGFR) compared to nondiabetic subjects. |
| 2852 | 18539754 | We also observed in diabetic mice that augmented RAGE signaling augmented expression of TNF-alpha, because this increase was attenuated by sRAGE or NF-kappaB inhibitor MG132. |
| 2853 | 18539754 | Protein and mRNA expression of NAD(P)H oxidase subunits including NOX-2, p22(phox), and p40(phox) increased in diabetic compared with control mice. sRAGE significantly inhibited the expression of NAD(P)H oxidase in diabetic mice. |
| 2854 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 2855 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 2856 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 2857 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 2858 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 2859 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 2860 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 2861 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 2862 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 2863 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 2864 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 2865 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 2866 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 2867 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 2868 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 2869 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 2870 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 2871 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 2872 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 2873 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 2874 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 2875 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 2876 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 2877 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 2878 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 2879 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 2880 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 2881 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 2882 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 2883 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 2884 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 2885 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 2886 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 2887 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 2888 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 2889 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 2890 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 2891 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 2892 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 2893 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 2894 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 2895 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 2896 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 2897 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 2898 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 2899 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 2900 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 2901 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 2902 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 2903 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 2904 | 18511057 | To determine if adiponectin can modulate lipid metabolism in macrophages, we expressed the adiponectin gene in human THP-1 macrophage foam cells using a lentiviral vector expression system and demonstrated that macrophages transduced with the adiponectin gene had decreased lipid accumulation compared with control macrophages transduced with the LacZ gene. |
| 2905 | 18511057 | The second mechanism involves decreased lipid uptake and increased lipid hydrolysis which may result from decreased SR-AI and increased SR-BI and HSL gene activities in the transformed macrophage foam cells. |
| 2906 | 18511057 | We also demonstrated that the expression of two proatherogenic cytokines, MCP-1 and TNFalpha, were decreased in the adiponectin-transduced macrophage foam cells. |
| 2907 | 18502272 | Serum high-sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor levels did not change with time or dietary treatment. |
| 2908 | 18497727 | New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. |
| 2909 | 18497727 | IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. |
| 2910 | 18497727 | The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. |
| 2911 | 18497722 | TNF-alpha, locally produced, induces insulin resistance of adipocytes leading to enhanced lipolysis. |
| 2912 | 18487229 | Anti-proliferative effect of pro-inflammatory cytokines in cultured beta cells is associated with extracellular signal-regulated kinase 1/2 pathway inhibition: protective role of glucagon-like peptide -1. |
| 2913 | 18487229 | Considerable anti-proliferative effects of pro-inflammatory cytokines interleukin (IL)-1beta, interferon (IFN)-gamma, and tumour necrosis factor-alpha (TNF-alpha) were observed. |
| 2914 | 18487229 | The effects were synergistic and independent of glucose concentration, and appeared to be mediated by the inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) activation, the signaling pathway involved in beta-cell replication. |
| 2915 | 18487229 | GLP-1 completely reversed the cytokine-induced inhibition of ERK phosphorylation and increased beta-cell proliferation threefold in cytokine-treated cultures. |
| 2916 | 18487229 | While pro-inflammatory cytokines reduced islet cell ERK1/2 activation and beta-cell proliferation in pancreatic islet culture, GLP-1 was capable of reversing this effect. |
| 2917 | 18481952 | The beta-cell destruction is partially mediated by cytokines, such as IL-1beta (interleukin 1beta), TNFalpha (tumour necrosis factor alpha) and IFN-gamma (interferon gamma). |
| 2918 | 18481952 | The beta-cell destruction is partially mediated by cytokines, such as IL-1beta (interleukin 1beta), TNFalpha (tumour necrosis factor alpha) and IFN-gamma (interferon gamma). |
| 2919 | 18481952 | IL-1beta and TNFalpha mediate activation of the transcription factor NF-kappaB (nuclear factor kappaB) pathway. |
| 2920 | 18481952 | IL-1beta and TNFalpha mediate activation of the transcription factor NF-kappaB (nuclear factor kappaB) pathway. |
| 2921 | 18481952 | Use of a degradation-resistant NF-kappaB protein inhibitor (DeltaNIkappaBalpha), specifically expressed in beta-cells, significantly reduced IL-1beta+IFN-gamma-induced apoptosis. |
| 2922 | 18481952 | Use of a degradation-resistant NF-kappaB protein inhibitor (DeltaNIkappaBalpha), specifically expressed in beta-cells, significantly reduced IL-1beta+IFN-gamma-induced apoptosis. |
| 2923 | 18481951 | IFNgamma (interferon gamma), a cytokine typically secreted by infiltrating immune cells in insulitis in Type 1 diabetes, is by itself not detrimental to beta-cells, but, together with other cytokines, such as IL-1beta (interleukin 1beta) and TNFalpha (tumour necrosis factor alpha), or dsRNA (double-stranded RNA), it induces beta-cell apoptosis. |
| 2924 | 18481951 | IFNgamma acts mostly via JAK (Janus kinase) activation, with the transcription factors STAT-1 (signal transducer and activator of transcription-1) and IRF-1 (IFNgamma regulatory factor-1) playing a central role in the downstream pathway. |
| 2925 | 18481951 | We demonstrated that the absence of STAT-1 from beta-cells completely protects against IFNgamma+IL-1beta- and IFNgamma+dsRNA-mediated beta-cell death in vitro, whereas absence of IRF-1 does not prevent cytokine-induced beta-cell apoptosis. |
| 2926 | 18481951 | In vivo, a lack of the IRF-1 gene in pancreatic islets even promotes low-dose streptozotocin-induced diabetes, whereas lack of STAT-1 confers resistance against beta-cell death following low-dose streptozotocin-induced diabetes. |
| 2927 | 18481951 | Additionally, IRF-1(-/-) islets are more sensitive to PNF (primary islet non-function) after transplantation in spontaneously diabetic NOD (non-obese diabetic) mice, whereas STAT-1(-/-) islets are fully protected. |
| 2928 | 18481951 | Moreover, proteomic analysis of beta-cells exposed to IFNgamma or IFNgamma+IL-1beta confirms that very different pathways are activated by IFNgamma alone compared with the combination. |
| 2929 | 18481951 | Transcription factors drive this dual role, with STAT-1 driving beta-cell destruction and IRF-1 possibly playing a role in up-regulation of protective pathways induced by IFNgamma. |
| 2930 | 18475052 | Suppressive effects of glucagon-like peptide-1 on interferon-gamma-induced nitric oxide production in insulin-producing cells is mediated by inhibition of tumor necrosis factor-alpha production. |
| 2931 | 18475052 | Suppressive effects of glucagon-like peptide-1 on interferon-gamma-induced nitric oxide production in insulin-producing cells is mediated by inhibition of tumor necrosis factor-alpha production. |
| 2932 | 18475052 | Suppressive effects of glucagon-like peptide-1 on interferon-gamma-induced nitric oxide production in insulin-producing cells is mediated by inhibition of tumor necrosis factor-alpha production. |
| 2933 | 18475052 | Suppressive effects of glucagon-like peptide-1 on interferon-gamma-induced nitric oxide production in insulin-producing cells is mediated by inhibition of tumor necrosis factor-alpha production. |
| 2934 | 18475052 | We treated MIN6N8a mouse beta cells with interferon (IFN)-gamma in the presence or absence of GLP-1 and found that IFN-gamma treatment induced iNOS mRNA expression and NO production, which was significantly inhibited by treatment with GLP-1. |
| 2935 | 18475052 | We treated MIN6N8a mouse beta cells with interferon (IFN)-gamma in the presence or absence of GLP-1 and found that IFN-gamma treatment induced iNOS mRNA expression and NO production, which was significantly inhibited by treatment with GLP-1. |
| 2936 | 18475052 | We treated MIN6N8a mouse beta cells with interferon (IFN)-gamma in the presence or absence of GLP-1 and found that IFN-gamma treatment induced iNOS mRNA expression and NO production, which was significantly inhibited by treatment with GLP-1. |
| 2937 | 18475052 | We treated MIN6N8a mouse beta cells with interferon (IFN)-gamma in the presence or absence of GLP-1 and found that IFN-gamma treatment induced iNOS mRNA expression and NO production, which was significantly inhibited by treatment with GLP-1. |
| 2938 | 18475052 | Blocking of GLP-1 receptor signaling via the cyclic AMP and phosphatidylinositol 3-kinase pathway did not directly affect the suppressive effect of GLP-1 on IFN- gamma-induced iNOS mRNA expression. |
| 2939 | 18475052 | Blocking of GLP-1 receptor signaling via the cyclic AMP and phosphatidylinositol 3-kinase pathway did not directly affect the suppressive effect of GLP-1 on IFN- gamma-induced iNOS mRNA expression. |
| 2940 | 18475052 | Blocking of GLP-1 receptor signaling via the cyclic AMP and phosphatidylinositol 3-kinase pathway did not directly affect the suppressive effect of GLP-1 on IFN- gamma-induced iNOS mRNA expression. |
| 2941 | 18475052 | Blocking of GLP-1 receptor signaling via the cyclic AMP and phosphatidylinositol 3-kinase pathway did not directly affect the suppressive effect of GLP-1 on IFN- gamma-induced iNOS mRNA expression. |
| 2942 | 18475052 | Further studies revealed that IFN-gamma induced the expression of TNF-alpha mRNA and protein, which synergistically induced NO production, and GLP-1 treatment inhibited this induction of TNF-alpha. |
| 2943 | 18475052 | Further studies revealed that IFN-gamma induced the expression of TNF-alpha mRNA and protein, which synergistically induced NO production, and GLP-1 treatment inhibited this induction of TNF-alpha. |
| 2944 | 18475052 | Further studies revealed that IFN-gamma induced the expression of TNF-alpha mRNA and protein, which synergistically induced NO production, and GLP-1 treatment inhibited this induction of TNF-alpha. |
| 2945 | 18475052 | Further studies revealed that IFN-gamma induced the expression of TNF-alpha mRNA and protein, which synergistically induced NO production, and GLP-1 treatment inhibited this induction of TNF-alpha. |
| 2946 | 18475052 | To examine whether the reduction of TNF-alpha by GLP-1 treatment plays a role in suppressing NO production, we treated MIN6N8a cells with IFN-gamma in the presence of anti-TNF-alpha neutralizing antibody and found that NO production was reduced. |
| 2947 | 18475052 | To examine whether the reduction of TNF-alpha by GLP-1 treatment plays a role in suppressing NO production, we treated MIN6N8a cells with IFN-gamma in the presence of anti-TNF-alpha neutralizing antibody and found that NO production was reduced. |
| 2948 | 18475052 | To examine whether the reduction of TNF-alpha by GLP-1 treatment plays a role in suppressing NO production, we treated MIN6N8a cells with IFN-gamma in the presence of anti-TNF-alpha neutralizing antibody and found that NO production was reduced. |
| 2949 | 18475052 | To examine whether the reduction of TNF-alpha by GLP-1 treatment plays a role in suppressing NO production, we treated MIN6N8a cells with IFN-gamma in the presence of anti-TNF-alpha neutralizing antibody and found that NO production was reduced. |
| 2950 | 18475052 | In addition, treatment of mouse islets with GLP-1 inhibited the expression of iNOS and TNFmRNA. |
| 2951 | 18475052 | In addition, treatment of mouse islets with GLP-1 inhibited the expression of iNOS and TNFmRNA. |
| 2952 | 18475052 | In addition, treatment of mouse islets with GLP-1 inhibited the expression of iNOS and TNFmRNA. |
| 2953 | 18475052 | In addition, treatment of mouse islets with GLP-1 inhibited the expression of iNOS and TNFmRNA. |
| 2954 | 18475052 | These results suggest that GLP-1 inhibits IFN-gamma-induced NO production by suppression of TNF-alpha production. |
| 2955 | 18475052 | These results suggest that GLP-1 inhibits IFN-gamma-induced NO production by suppression of TNF-alpha production. |
| 2956 | 18475052 | These results suggest that GLP-1 inhibits IFN-gamma-induced NO production by suppression of TNF-alpha production. |
| 2957 | 18475052 | These results suggest that GLP-1 inhibits IFN-gamma-induced NO production by suppression of TNF-alpha production. |
| 2958 | 18463842 | Induction of nuclear factor-kappaB and its downstream genes by TNF-alpha and IL-1beta has a pro-apoptotic role in pancreatic beta cells. |
| 2959 | 18457636 | Drugs as angiotensin converting enzyme inhibitors (ACEI), thiazolidinediones (glitazones) or angiotensin-II receptor antagonists, generally associated with the adequate hypolipidemic (statins, fibrates) or antiobesity (orlistat, sibutramine, rimonabant) medication, would increase those adipocytokines with anti-inflammatory and insulin-sensitizing properties (i.e. adiponectin or visfatin), while reducing pro-inflammatory and thrombogenic cytokines (as leptin, tumor necrosis factor [TNF]-alpha, plasminogen activator inhibitor 1 [PAI-1]). |
| 2960 | 18457011 | In this regard, expression of apelin gene in adipose tissue is increased by insulin and TNFalpha. |
| 2961 | 18457008 | Through inflammatory cytokines production, adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promote adipocyte insulin resistance by a paracrine way. |
| 2962 | 18457008 | Through inflammatory cytokines production, adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promote adipocyte insulin resistance by a paracrine way. |
| 2963 | 18457008 | Through inflammatory cytokines production, adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promote adipocyte insulin resistance by a paracrine way. |
| 2964 | 18457008 | Since xanthine family compounds such as caffeine were shown to decrease inflammatory production by human blood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factor alpha (TNFalpha) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture. |
| 2965 | 18457008 | Since xanthine family compounds such as caffeine were shown to decrease inflammatory production by human blood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factor alpha (TNFalpha) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture. |
| 2966 | 18457008 | Since xanthine family compounds such as caffeine were shown to decrease inflammatory production by human blood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factor alpha (TNFalpha) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture. |
| 2967 | 18457008 | Then, TNFalpha and IL-6 mRNA were analysed by real-time PCR alternatively in adipocytes and SVF cells. |
| 2968 | 18457008 | Then, TNFalpha and IL-6 mRNA were analysed by real-time PCR alternatively in adipocytes and SVF cells. |
| 2969 | 18457008 | Then, TNFalpha and IL-6 mRNA were analysed by real-time PCR alternatively in adipocytes and SVF cells. |
| 2970 | 18457008 | Our findings show a strong and dose dependent down-regulation of TNF-alpha gene expression in both adipocyte and SVF cells whereas IL-6 was only down regulated in SVF cells. |
| 2971 | 18457008 | Our findings show a strong and dose dependent down-regulation of TNF-alpha gene expression in both adipocyte and SVF cells whereas IL-6 was only down regulated in SVF cells. |
| 2972 | 18457008 | Our findings show a strong and dose dependent down-regulation of TNF-alpha gene expression in both adipocyte and SVF cells whereas IL-6 was only down regulated in SVF cells. |
| 2973 | 18455422 | TNFalpha and IFNgamma secretion was decreased by high glucose. |
| 2974 | 18455422 | TNFalpha and IFNgamma secretion was decreased by high glucose. |
| 2975 | 18455422 | This effect was counteracted by an elevated glucose concentration for TNFalpha and IFNgamma, but not IL-10. |
| 2976 | 18455422 | This effect was counteracted by an elevated glucose concentration for TNFalpha and IFNgamma, but not IL-10. |
| 2977 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2978 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2979 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2980 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2981 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2982 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2983 | 18446810 | Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. |
| 2984 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2985 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2986 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2987 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2988 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2989 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2990 | 18446810 | We have previously shown that the angiogenic growth factor fibroblast growth factor-2 (FGF-2), which is generally protective against endothelial cell death, is similarly elevated in high glucose conditions. |
| 2991 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2992 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2993 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2994 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2995 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2996 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2997 | 18446810 | We therefore investigated the effect of TNFalpha on endothelial cell death under normal and elevated glucose conditions, with a particular focus on FGF-2. |
| 2998 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 2999 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3000 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3001 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3002 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3003 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3004 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 3005 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3006 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3007 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3008 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3009 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3010 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3011 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 3012 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3013 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3014 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3015 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3016 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3017 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3018 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 3019 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3020 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3021 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3022 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3023 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3024 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3025 | 18446810 | The FGF-2 associated increase in TNFalpha-induced cell death was negated by blocking cell entry into S phase. |
| 3026 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3027 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3028 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3029 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3030 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3031 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3032 | 18446810 | Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. |
| 3033 | 18445887 | Bone mineral metabolism and bone remodeling involve a variety of molecules, for instance, bone morphogenetic proteins (BMPs) , fibroblast growth factors (FGFs) , insulin growth factors (IGFs) , interleukin-1 (IL-1) , prostagrandin E(2) (PGE(2)) , and tumor necrosis factor-alpha (TNF-alpha) . |
| 3034 | 18443205 | siRNA-mediated reduction of inhibitor of nuclear factor-kappaB kinase prevents tumor necrosis factor-alpha-induced insulin resistance in human skeletal muscle. |
| 3035 | 18442814 | The study objective is to prove an association among plasma concentration of big endothelin and endothelin-1, other clinical parameters and two frequent polymorphisms - G8002A and -3A/-4A - in the endothelin-1 (EDN-1) coding gene (6p21-23), and among plasma concentration of TNF alpha and gene polymorphisms TNF alpha -308 A/G, -238 A/G, TNF beta Ncol and 3'TACE (tumour necrosis factor alpha converting enzyme) in patients with chronic heart failure (CHF). |
| 3036 | 18442814 | The study objective is to prove an association among plasma concentration of big endothelin and endothelin-1, other clinical parameters and two frequent polymorphisms - G8002A and -3A/-4A - in the endothelin-1 (EDN-1) coding gene (6p21-23), and among plasma concentration of TNF alpha and gene polymorphisms TNF alpha -308 A/G, -238 A/G, TNF beta Ncol and 3'TACE (tumour necrosis factor alpha converting enzyme) in patients with chronic heart failure (CHF). |
| 3037 | 18442814 | The study objective is to prove an association among plasma concentration of big endothelin and endothelin-1, other clinical parameters and two frequent polymorphisms - G8002A and -3A/-4A - in the endothelin-1 (EDN-1) coding gene (6p21-23), and among plasma concentration of TNF alpha and gene polymorphisms TNF alpha -308 A/G, -238 A/G, TNF beta Ncol and 3'TACE (tumour necrosis factor alpha converting enzyme) in patients with chronic heart failure (CHF). |
| 3038 | 18442814 | No associations were observed between plasma concentration of TNF alpha and genotypes in four polymorphisms in TNF alpha, beta and TACE genes. |
| 3039 | 18442814 | No associations were observed between plasma concentration of TNF alpha and genotypes in four polymorphisms in TNF alpha, beta and TACE genes. |
| 3040 | 18442814 | No associations were observed between plasma concentration of TNF alpha and genotypes in four polymorphisms in TNF alpha, beta and TACE genes. |
| 3041 | 18442814 | It might be speculated that in the case of endothelin-1 and TNF alpha in CHF the genetic determination is not important, and plasma concentrations are influenced more by the disease severity. |
| 3042 | 18442814 | It might be speculated that in the case of endothelin-1 and TNF alpha in CHF the genetic determination is not important, and plasma concentrations are influenced more by the disease severity. |
| 3043 | 18442814 | It might be speculated that in the case of endothelin-1 and TNF alpha in CHF the genetic determination is not important, and plasma concentrations are influenced more by the disease severity. |
| 3044 | 18442781 | In the present study, serum and pancreatic islets were isolated to investigate the relationship between IL-1beta, IFN-gamma, IL-12 and TNF-alpha expression and diabetes onset, morphological aspects, and diacerhein dose dependence in animals treated with different doses (5, 10 and 50 mg/kg/day) and the control group (saline solution). |
| 3045 | 18442781 | In the present study, serum and pancreatic islets were isolated to investigate the relationship between IL-1beta, IFN-gamma, IL-12 and TNF-alpha expression and diabetes onset, morphological aspects, and diacerhein dose dependence in animals treated with different doses (5, 10 and 50 mg/kg/day) and the control group (saline solution). |
| 3046 | 18442781 | In the present study, serum and pancreatic islets were isolated to investigate the relationship between IL-1beta, IFN-gamma, IL-12 and TNF-alpha expression and diabetes onset, morphological aspects, and diacerhein dose dependence in animals treated with different doses (5, 10 and 50 mg/kg/day) and the control group (saline solution). |
| 3047 | 18442781 | The results demonstrated upregulation of mRNA islets and downregulation of the serum concentration of IL-1beta, IL-12 and TNF-alpha in the group treated with 5 and 10 mg/kg/day diacerhein, when compared with the saline group, and increased IFN-gamma serum concentration in the group treated with 50 mg/kg/day. |
| 3048 | 18442781 | The results demonstrated upregulation of mRNA islets and downregulation of the serum concentration of IL-1beta, IL-12 and TNF-alpha in the group treated with 5 and 10 mg/kg/day diacerhein, when compared with the saline group, and increased IFN-gamma serum concentration in the group treated with 50 mg/kg/day. |
| 3049 | 18442781 | The results demonstrated upregulation of mRNA islets and downregulation of the serum concentration of IL-1beta, IL-12 and TNF-alpha in the group treated with 5 and 10 mg/kg/day diacerhein, when compared with the saline group, and increased IFN-gamma serum concentration in the group treated with 50 mg/kg/day. |
| 3050 | 18442781 | These results suggest that diacerhein in NOD mice, decreases, in a dose-dependent manner, the diabetes frequency downregulating proinflammatory cytokines, such as IL-1beta, TNF-alpha, IFN-gamma and IL-12 at posttranscriptional or posttranslational level. |
| 3051 | 18442781 | These results suggest that diacerhein in NOD mice, decreases, in a dose-dependent manner, the diabetes frequency downregulating proinflammatory cytokines, such as IL-1beta, TNF-alpha, IFN-gamma and IL-12 at posttranscriptional or posttranslational level. |
| 3052 | 18442781 | These results suggest that diacerhein in NOD mice, decreases, in a dose-dependent manner, the diabetes frequency downregulating proinflammatory cytokines, such as IL-1beta, TNF-alpha, IFN-gamma and IL-12 at posttranscriptional or posttranslational level. |
| 3053 | 18440241 | Additional metabolic variables including plasma cholesterol (total-C, HDL-C, LDL-C), triglyceride, and inflammatory markers (IL-6, TNF-alpha, and CRP) were also measured. |
| 3054 | 18440241 | Additional metabolic variables including plasma cholesterol (total-C, HDL-C, LDL-C), triglyceride, and inflammatory markers (IL-6, TNF-alpha, and CRP) were also measured. |
| 3055 | 18440241 | However, levels of IL-6, TNF-alpha, and CRP were all significantly reduced. |
| 3056 | 18440241 | However, levels of IL-6, TNF-alpha, and CRP were all significantly reduced. |
| 3057 | 18433704 | TNF-alpha induces the osteogenic bone morphogenetic protein-2 (BMP-2), Msx2, Wnt3a, and Wnt7a mRNAs and leads to increased aortic calcium accumulation. |
| 3058 | 18433704 | TNF-alpha induces the osteogenic bone morphogenetic protein-2 (BMP-2), Msx2, Wnt3a, and Wnt7a mRNAs and leads to increased aortic calcium accumulation. |
| 3059 | 18433704 | TNF-alpha induces the osteogenic bone morphogenetic protein-2 (BMP-2), Msx2, Wnt3a, and Wnt7a mRNAs and leads to increased aortic calcium accumulation. |
| 3060 | 18433704 | Treatment with the TNF-alpha neutralizing antibody infliximab abrogates aortic BMP-2-Msx2-Wnt3a and Wnt7a signaling and attenuates aortic calcium accumulation significantly. |
| 3061 | 18433704 | Treatment with the TNF-alpha neutralizing antibody infliximab abrogates aortic BMP-2-Msx2-Wnt3a and Wnt7a signaling and attenuates aortic calcium accumulation significantly. |
| 3062 | 18433704 | Treatment with the TNF-alpha neutralizing antibody infliximab abrogates aortic BMP-2-Msx2-Wnt3a and Wnt7a signaling and attenuates aortic calcium accumulation significantly. |
| 3063 | 18433704 | Mice with vascular TNF-alpha augmented by the SM22-TNF-alpha transgene upregulate the aortic Msx2-Wnt3a/Wnt7a axis. |
| 3064 | 18433704 | Mice with vascular TNF-alpha augmented by the SM22-TNF-alpha transgene upregulate the aortic Msx2-Wnt3a/Wnt7a axis. |
| 3065 | 18433704 | Mice with vascular TNF-alpha augmented by the SM22-TNF-alpha transgene upregulate the aortic Msx2-Wnt3a/Wnt7a axis. |
| 3066 | 18414053 | Resveratrol has also been shown to activate various transcription factor (e.g; NFkappaB, STAT3, HIF-1alpha, beta-catenin and PPAR-gamma), suppress the expression of antiapoptotic gene products (e.g; Bcl-2, Bcl-X(L), XIAP and survivin), inhibit protein kinases (e.g; src, PI3K, JNK, and AKT), induce antioxidant enzymes (e,g; catalase, superoxide dismutase and hemoxygenase-1), suppress the expression of inflammatory biomarkers (e.g., TNF, COX-2, iNOS, and CRP), inhibit the expression of angiogenic and metastatic gene products (e.g., MMPs, VEGF, cathepsin D, and ICAM-1), and modulate cell cycle regulatory genes (e.g., p53, Rb, PTEN, cyclins and CDKs). |
| 3067 | 18400329 | First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice. |
| 3068 | 18400329 | First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice. |
| 3069 | 18400329 | First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice. |
| 3070 | 18400329 | First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice. |
| 3071 | 18400329 | Transplantation of IL-12p40, TNF-alpha, and CTLA4-Ig but not TGF-beta-secreting islets displayed enhanced survival and delayed diabetes recurrence in recent-onset diabetic recipients. |
| 3072 | 18400329 | Transplantation of IL-12p40, TNF-alpha, and CTLA4-Ig but not TGF-beta-secreting islets displayed enhanced survival and delayed diabetes recurrence in recent-onset diabetic recipients. |
| 3073 | 18400329 | Transplantation of IL-12p40, TNF-alpha, and CTLA4-Ig but not TGF-beta-secreting islets displayed enhanced survival and delayed diabetes recurrence in recent-onset diabetic recipients. |
| 3074 | 18400329 | Transplantation of IL-12p40, TNF-alpha, and CTLA4-Ig but not TGF-beta-secreting islets displayed enhanced survival and delayed diabetes recurrence in recent-onset diabetic recipients. |
| 3075 | 18400329 | In addition, local production of TNF-alpha and CTLA4-Ig significantly prolonged islet graft survival. |
| 3076 | 18400329 | In addition, local production of TNF-alpha and CTLA4-Ig significantly prolonged islet graft survival. |
| 3077 | 18400329 | In addition, local production of TNF-alpha and CTLA4-Ig significantly prolonged islet graft survival. |
| 3078 | 18400329 | In addition, local production of TNF-alpha and CTLA4-Ig significantly prolonged islet graft survival. |
| 3079 | 18400329 | In conclusion, this study showed comparisons of the immunomodulating effects of 4 different adenoviral vectors in the same transplantation model and local production of IL-12p40, TNF-alpha and CTLA4-Ig significantly prevented recurrent diabetes in NOD mice. |
| 3080 | 18400329 | In conclusion, this study showed comparisons of the immunomodulating effects of 4 different adenoviral vectors in the same transplantation model and local production of IL-12p40, TNF-alpha and CTLA4-Ig significantly prevented recurrent diabetes in NOD mice. |
| 3081 | 18400329 | In conclusion, this study showed comparisons of the immunomodulating effects of 4 different adenoviral vectors in the same transplantation model and local production of IL-12p40, TNF-alpha and CTLA4-Ig significantly prevented recurrent diabetes in NOD mice. |
| 3082 | 18400329 | In conclusion, this study showed comparisons of the immunomodulating effects of 4 different adenoviral vectors in the same transplantation model and local production of IL-12p40, TNF-alpha and CTLA4-Ig significantly prevented recurrent diabetes in NOD mice. |
| 3083 | 18393827 | Vitamin D ligands are designed to target the local immune response in vitiligo, acting on specific T cell activation, mainly by inhibiting the transition of T cells from early to late G1 phase and by inhibiting the expression of several pro-inflammatory cytokines genes, such as those encoding tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). |
| 3084 | 18385666 | In vitro, insulin phosphorylated AKT solely in podocytes from db/+ mice. |
| 3085 | 18385666 | Serum deprivation and exposure to tumor necrosis factor-alpha significantly compromised cell viability in podocytes from db/db but not from db/+ mice, and this was associated with a significant decrease in AKT phosphorylation. |
| 3086 | 18370642 | Adiponectin and leptin in relation to insulin sensitivity. |
| 3087 | 18370642 | The most important products of adipose tissue collectively referred to as adipocytokines, include adiponectin, leptin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), resistin, plasminogen-activating inhibitor-I (PAI-1), and angiotensinogen. |
| 3088 | 18370642 | This review describes the metabolic role of two of these proteins, adiponectin and leptin, in relation to insulin sensitivity. |
| 3089 | 18370640 | Inflammatory markers that have been associated with MS include hs-CRP, TNF-alpha, fibrinogen, and IL-6, among others. |
| 3090 | 18369459 | We replicated the previously reported association with interleukin 23 receptor and interleukin 12B (IL12B) polymorphisms in PS and PSA cohorts (IL23R: rs11209026, U.S. |
| 3091 | 18369459 | PSA, P = 1.3x10(-3)) and detected an independent association in the IL23R region with a SNP 4 kb upstream from IL12RB2 (P = 0.001). |
| 3092 | 18369459 | PS cohort included the region harboring lipoma HMGIC fusion partner (LHFP) and conserved oligomeric golgi complex component 6 (COG6) genes on chromosome 13q13 (combined P = 2x10(-6) for rs7993214; OR = 0.71), the late cornified envelope gene cluster (LCE) from the Epidermal Differentiation Complex (PSORS4) (combined P = 6.2x10(-5) for rs6701216; OR 1.45) and a region of LD at 15q21 (combined P = 2.9x10(-5) for rs3803369; OR = 1.43). |
| 3093 | 18369459 | This region is of interest because it harbors ubiquitin-specific protease-8 whose processed pseudogene lies upstream from HLA-C. |
| 3094 | 18369459 | This region of 15q21 also harbors the gene for SPPL2A (signal peptide peptidase like 2a) which activates tumor necrosis factor alpha by cleavage, triggering the expression of IL12 in human dendritic cells. |
| 3095 | 18369459 | This region harbors the interleukin 2 (IL2) and interleukin 21 (IL21) genes and was recently shown to be associated with four autoimmune diseases (Celiac disease, Type 1 diabetes, Grave's disease and Rheumatoid Arthritis). |
| 3096 | 18368274 | A number of studies have established that a relationship exists between depression and inflammation, with alterations in the levels of inflammatory markers (IL-1, IL-6, TNF-alpha and others). |
| 3097 | 18361930 | ICAM-1-mediated adhesion of peripheral blood mononuclear cells (PBMC) to GE-Cos7 cells or TNF-treated GEGE HUVEC was significantly increased. |
| 3098 | 18354376 | AP214 reduced serum TNF-alpha and IL-10 levels with a bell-shaped dose-response curve. |
| 3099 | 18348311 | It has recently been reported that tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) plays various roles in such autoimmune diseases as diabetes, multiple sclerosis (MS), and systemic lupus erythematosus (SLE). |
| 3100 | 18348311 | It has recently been reported that tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) plays various roles in such autoimmune diseases as diabetes, multiple sclerosis (MS), and systemic lupus erythematosus (SLE). |
| 3101 | 18348311 | It has recently been reported that tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) plays various roles in such autoimmune diseases as diabetes, multiple sclerosis (MS), and systemic lupus erythematosus (SLE). |
| 3102 | 18348311 | The specific messenger ribonucleic acid (mRNA) levels of TRAIL in peripheral blood mononuclear cells (PBMCs), serum sTRAIL, and TNF-alpha concentrations from 60 AS patients, 20 rheumatoid arthritis (RA) patients, and 30 healthy controls were determined by real-time fluorescent quantitative polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). |
| 3103 | 18348311 | The specific messenger ribonucleic acid (mRNA) levels of TRAIL in peripheral blood mononuclear cells (PBMCs), serum sTRAIL, and TNF-alpha concentrations from 60 AS patients, 20 rheumatoid arthritis (RA) patients, and 30 healthy controls were determined by real-time fluorescent quantitative polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). |
| 3104 | 18348311 | The specific messenger ribonucleic acid (mRNA) levels of TRAIL in peripheral blood mononuclear cells (PBMCs), serum sTRAIL, and TNF-alpha concentrations from 60 AS patients, 20 rheumatoid arthritis (RA) patients, and 30 healthy controls were determined by real-time fluorescent quantitative polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). |
| 3105 | 18348311 | In HLA-B27-positive patients, TRAIL mRNA and sTRAIL closely correlated with serum TNF-alpha and C-reactive protein (CRP), but did not correlate in HLA-B27-negative patients. |
| 3106 | 18348311 | In HLA-B27-positive patients, TRAIL mRNA and sTRAIL closely correlated with serum TNF-alpha and C-reactive protein (CRP), but did not correlate in HLA-B27-negative patients. |
| 3107 | 18348311 | In HLA-B27-positive patients, TRAIL mRNA and sTRAIL closely correlated with serum TNF-alpha and C-reactive protein (CRP), but did not correlate in HLA-B27-negative patients. |
| 3108 | 18346651 | We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. |
| 3109 | 18346651 | We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. |
| 3110 | 18346651 | We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. |
| 3111 | 18346651 | IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. |
| 3112 | 18346651 | IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. |
| 3113 | 18346651 | IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. |
| 3114 | 18346651 | In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. |
| 3115 | 18346651 | In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. |
| 3116 | 18346651 | In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. |
| 3117 | 18343625 | Our results also demonstrate that the tumor necrosis factor (TNF)alpha increases porcine visfatin gene expression in stromal-vascular (SV) cell cultures, thus suggesting an intermediary role for TNFalpha in visfatin response. |
| 3118 | 18338073 | It also appears that TNFalpha fulfills these functions via interaction with leukemia inhibitory factor (LIF) and the transcription factor NF-kappaB. |
| 3119 | 18333370 | The adipokines-leptin, adiponectin, TNF-alpha-, which are modified in obesity, have been proposed as determinant factors of non-responsiveness to the IFN-alpha/Ribavirin treatment and of liver fibrosis extension in patients with CHC and obesity. |
| 3120 | 18329889 | Ganglioside GM1 effects on the expression of nerve growth factor (NGF), Trk-A receptor, proinflammatory cytokines and on autoimmune diabetes onset in non-obese diabetic (NOD) mice. |
| 3121 | 18329889 | Ganglioside GM1 effects on the expression of nerve growth factor (NGF), Trk-A receptor, proinflammatory cytokines and on autoimmune diabetes onset in non-obese diabetic (NOD) mice. |
| 3122 | 18329889 | In the present study, serum, pancreas islets and spleen mononuclear cells from NOD mice treated with monosialic ganglioside GM1 (100 mg/kg/day) and the group control which received saline solution were isolated to investigate the proinflammatory cytokines (IL-1beta, IFN-gamma, IL-12, TNF-alpha), NGF and its high-affinity receptor TrkA, peri-islet Schwann cells components (GFAP, S100-beta) expression and the relationship with diabetes onset and morphological aspects. |
| 3123 | 18329889 | In the present study, serum, pancreas islets and spleen mononuclear cells from NOD mice treated with monosialic ganglioside GM1 (100 mg/kg/day) and the group control which received saline solution were isolated to investigate the proinflammatory cytokines (IL-1beta, IFN-gamma, IL-12, TNF-alpha), NGF and its high-affinity receptor TrkA, peri-islet Schwann cells components (GFAP, S100-beta) expression and the relationship with diabetes onset and morphological aspects. |
| 3124 | 18329889 | Our results suggest that GM1 administration to female NOD mice beginning at the 4th week of life is able to reduce the index of inflammatory infiltrate and consequently the expression of diabetes, modulating the expression of proinflammatory cytokines (IL-12, IFN-gamma, TNF-alpha and IL-1beta). |
| 3125 | 18329889 | Our results suggest that GM1 administration to female NOD mice beginning at the 4th week of life is able to reduce the index of inflammatory infiltrate and consequently the expression of diabetes, modulating the expression of proinflammatory cytokines (IL-12, IFN-gamma, TNF-alpha and IL-1beta). |
| 3126 | 18329889 | Furthermore, GM1 increases GFAP, S-100beta and NGF in pancreas islets, factors involved in beta cell survival. |
| 3127 | 18329889 | Furthermore, GM1 increases GFAP, S-100beta and NGF in pancreas islets, factors involved in beta cell survival. |
| 3128 | 18329387 | A20 is a tumor necrosis factor (TNF)-inducible zinc finger protein that contains both ubiquitinating and deubiquitinating activities. |
| 3129 | 18329387 | A20 is a tumor necrosis factor (TNF)-inducible zinc finger protein that contains both ubiquitinating and deubiquitinating activities. |
| 3130 | 18329387 | A20 negatively regulates NFkappaB (nuclear factor kappaB) signaling induced by TNF receptor family and Toll-like receptors, but the mechanism of A20 action is poorly defined. |
| 3131 | 18329387 | A20 negatively regulates NFkappaB (nuclear factor kappaB) signaling induced by TNF receptor family and Toll-like receptors, but the mechanism of A20 action is poorly defined. |
| 3132 | 18329387 | The lysosomal association of A20 requires its carboxy terminal zinc finger domains, but is independent of its ubiquitin-modifying activities. |
| 3133 | 18329387 | The lysosomal association of A20 requires its carboxy terminal zinc finger domains, but is independent of its ubiquitin-modifying activities. |
| 3134 | 18328265 | Association of high sensitivity C-reactive protein (hsCRP) and tumour necrosis factor-alpha (TNF-alpha) with carotid intimal medial thickness in subjects with different grades of glucose intolerance--the Chennai Urban Rural Epidemiology Study (CURES-31). |
| 3135 | 18323732 | IL-1beta, TNF-alpha, cytokine-induced neutrophil chemoattractant-2alpha/beta, and IL-10 measurements were performed in elicited peritoneal cells from control, diabetic, and insulin-treated diabetic rats. |
| 3136 | 18322021 | Previously, we have reported that pigment epithelium-derived factor (PEDF) ameliorates albuminuria and inhibits matrix protein deposition in the kidney of streptozotocin (STZ)-induced diabetic rats, suggesting a renoprotective effect of PEDF in early stages of diabetic nephropathy. |
| 3137 | 18322021 | Three wk after the injection, diabetic rats treated with the control virus showed significantly elevated renal levels of proinflammatory factors such as ICAM-1, MCP-1, TNF-alpha, and VEGF compared with age-matched nondiabetic controls. |
| 3138 | 18322021 | In cultured primary human renal mesangial cells (HMC), the high-glucose medium-induced upregulation of VEGF and MCP-1 was largely blocked by PEDF. |
| 3139 | 18322021 | Furthermore, PEDF inhibited high glucose-induced activation of NF-kappaB, a key transcription factor mediating inflammatory responses, and hypoxia-inducible factor-1, a major activator of VEGF expression in HMC. |
| 3140 | 18322021 | These results suggest that the renoprotective effect of PEDF against diabetic nephropathy may be partially through its anti-inflammatory activity, likely by blocking the NF-kappaB and HIF-1 pathways. |
| 3141 | 18313835 | We found that, among the factors examined, adipocyte-derived cytokines (adipokines), like TNFalpha and IL-1beta, potently stimulated the transcriptional activity of 11beta-HSD1 gene in human HuH7 cells. |
| 3142 | 18313835 | We found that, among the factors examined, adipocyte-derived cytokines (adipokines), like TNFalpha and IL-1beta, potently stimulated the transcriptional activity of 11beta-HSD1 gene in human HuH7 cells. |
| 3143 | 18313835 | Glucocorticoid receptor (GR)-dependent transcription was indeed increased even with an inactive glucocorticoid cortisone following TNFalpha pretreatment, indicating the enhanced intracellular conversion. |
| 3144 | 18313835 | Glucocorticoid receptor (GR)-dependent transcription was indeed increased even with an inactive glucocorticoid cortisone following TNFalpha pretreatment, indicating the enhanced intracellular conversion. |
| 3145 | 18313835 | Finally, PPARgamma/PPARalpha agonists, clinically used as anti-diabetic drugs, significantly inhibited the transcriptional activity of 11beta-HSD1. |
| 3146 | 18313835 | Finally, PPARgamma/PPARalpha agonists, clinically used as anti-diabetic drugs, significantly inhibited the transcriptional activity of 11beta-HSD1. |
| 3147 | 18303564 | These effects were replicated by treatment of SY5Y cells with Fas ligand, tumor necrosis factor alpha and an agonist anti-Fas antibody. |
| 3148 | 18297990 | Serum values of IL1alpha, IL-1beta, IL-6, TNF-alpha were assessed in 22 patients with TED before and after treatment (aged 46.82 +/- 12.47, M:F=16:6). |
| 3149 | 18297990 | No stimulatory effect of IL-1beta on IL-6 was observed: IL-1beta was unchanged while IL-6 levels were increased after treatment. |
| 3150 | 18296638 | Overexpression of the dual-specificity phosphatase MKP-4/DUSP-9 protects against stress-induced insulin resistance. |
| 3151 | 18296638 | Insulin resistance, a hallmark of type 2 diabetes and obesity, is associated with increased activity of MAP and stress-activated protein (SAP) kinases, which results in decreased insulin signaling. |
| 3152 | 18296638 | Our goal was to investigate the role of MAP kinase phosphatase-4 (MKP-4) in modulating this process. |
| 3153 | 18296638 | We found that MKP-4 expression is up-regulated during adipocyte and myocyte differentiation in vitro and up-regulated during fasting in white adipose tissue in vivo. |
| 3154 | 18296638 | Overexpression of MKP-4 in 3T3-L1 cells inhibited ERK and JNK phosphorylation and, to a lesser extent, p38MAPK phosphorylation. |
| 3155 | 18296638 | As a result, the phosphorylation of IRS-1 serine 307 induced by anisomycin was abolished, leading to a sensitization of insulin signaling with recovery of insulin-stimulated IRS-1 tyrosine phosphorylation, IRS-1 docking with phosphatidylinositol 3-kinase, and Akt phosphorylation. |
| 3156 | 18296638 | MKP-4 also reversed the effect of TNF-alpha to inhibit insulin signaling; alter IL-6, Glut1 and Glut4 expression; and inhibit insulin-stimulated glucose uptake in 3T3-L1 adipocytes. |
| 3157 | 18296638 | Overexpression of MKP-4 in the liver of ob/ob mice decreased ERK and JNK phosphorylation, leading to a reduction in fed and fasted glycemia, improved glucose intolerance, decreased expression of gluconeogenic and lipogenic genes, and reduced hepatic steatosis. |
| 3158 | 18296638 | Thus, MKP-4 has a protective effect against the development of insulin resistance through its ability to dephosphorylate and inactivate crucial mediators of stress-induced insulin resistance, such as ERK and JNK, and increasing MKP-4 activity might provide a therapy for insulin-resistant disorders. |
| 3159 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 3160 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 3161 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 3162 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 3163 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 3164 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 3165 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 3166 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 3167 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 3168 | 18292388 | Adiponectin protects against angiotensin II or tumor necrosis factor alpha-induced endothelial cell monolayer hyperpermeability: role of cAMP/PKA signaling. |
| 3169 | 18291098 | Anti-inflammatory effect of resveratrol on TNF-alpha-induced MCP-1 expression in adipocytes. |
| 3170 | 18291098 | Anti-inflammatory effect of resveratrol on TNF-alpha-induced MCP-1 expression in adipocytes. |
| 3171 | 18291098 | Anti-inflammatory effect of resveratrol on TNF-alpha-induced MCP-1 expression in adipocytes. |
| 3172 | 18291098 | Anti-inflammatory effect of resveratrol on TNF-alpha-induced MCP-1 expression in adipocytes. |
| 3173 | 18291098 | Anti-inflammatory effect of resveratrol on TNF-alpha-induced MCP-1 expression in adipocytes. |
| 3174 | 18291098 | In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipocytes. |
| 3175 | 18291098 | In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipocytes. |
| 3176 | 18291098 | In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipocytes. |
| 3177 | 18291098 | In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipocytes. |
| 3178 | 18291098 | In this study we investigated the effects of resveratrol upon both tumor necrosis factor (TNF)-alpha-induced MCP-1 gene expression and its underlying signaling pathways in 3T3-L1 adipocytes. |
| 3179 | 18291098 | Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription, as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. |
| 3180 | 18291098 | Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription, as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. |
| 3181 | 18291098 | Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription, as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. |
| 3182 | 18291098 | Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription, as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. |
| 3183 | 18291098 | Resveratrol was found to inhibit TNF-alpha-induced MCP-1 secretion and gene transcription, as well as promoter activity, which based on down-regulation of TNF-alpha-induced MCP-1 transcription. |
| 3184 | 18291098 | Nuclear factor (NF)-kappaB was determined to play a major role in the TNF-alpha-induced MCP-1 expression. |
| 3185 | 18291098 | Nuclear factor (NF)-kappaB was determined to play a major role in the TNF-alpha-induced MCP-1 expression. |
| 3186 | 18291098 | Nuclear factor (NF)-kappaB was determined to play a major role in the TNF-alpha-induced MCP-1 expression. |
| 3187 | 18291098 | Nuclear factor (NF)-kappaB was determined to play a major role in the TNF-alpha-induced MCP-1 expression. |
| 3188 | 18291098 | Nuclear factor (NF)-kappaB was determined to play a major role in the TNF-alpha-induced MCP-1 expression. |
| 3189 | 18291098 | Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in TNF-alpha-stimulated cells. |
| 3190 | 18291098 | Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in TNF-alpha-stimulated cells. |
| 3191 | 18291098 | Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in TNF-alpha-stimulated cells. |
| 3192 | 18291098 | Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in TNF-alpha-stimulated cells. |
| 3193 | 18291098 | Further analysis showed that resveratrol inhibited DNA binding activity of the NF-kappaB complex and subsequently suppressed NF-kappaB transcriptional activity in TNF-alpha-stimulated cells. |
| 3194 | 18287017 | CD4 T cells, lymphopenia, and IL-7 in a multistep pathway to autoimmunity. |
| 3195 | 18287017 | We show in a model of beta-islet cell self-reactivity that the transfer of activated autoreactive CD4 T cells can prime and expand endogenous autoreactive CD8 T cells in a CD28- and CD40-dependent manner through the licensing of dendritic cells. |
| 3196 | 18287017 | Autoimmune diabetes rapidly ensued with CD4 help and the subsequent activation of CD8 T cells, which contributed to disease progression. |
| 3197 | 18287017 | With the advent of many biologicals targeting TNFalpha, IL-6, and IL-1 and their effective use in the treatment of autoimmune diseases, we propose that IL-7 and its receptor may be promising targets for biological agents in the treatment of autoimmunity. |
| 3198 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3199 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3200 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3201 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3202 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3203 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3204 | 18281274 | Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. |
| 3205 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3206 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3207 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3208 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3209 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3210 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3211 | 18281274 | PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. |
| 3212 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3213 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3214 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3215 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3216 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3217 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3218 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 3219 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3220 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3221 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3222 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3223 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3224 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3225 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 3226 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3227 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3228 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3229 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3230 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3231 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3232 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 3233 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3234 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3235 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3236 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3237 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3238 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3239 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 3240 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3241 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3242 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3243 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3244 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3245 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3246 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 3247 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3248 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3249 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3250 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3251 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3252 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3253 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 3254 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3255 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3256 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3257 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3258 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3259 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3260 | 18281274 | In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. |
| 3261 | 18278435 | The imidazoline RX871024 induces death of proliferating insulin-secreting cells by activation of c-jun N-terminal kinase. |
| 3262 | 18278435 | Our data demonstrate that RX871024, but not efaroxan, triggered MIN6 cell death and potentiated death induced by a combination of the pro-inflammatory cytokines interleukin-1beta, interferon- gamma and tumor necrosis factor-alpha. |
| 3263 | 18278435 | These effects did not involve changes in nitric oxide production but correlated with stimulation of c-jun N-terminal kinase (JNK) activity and activation of caspases-1, -3, -8 and -9. |
| 3264 | 18278435 | Our results suggest that the imidazoline RX871024 causes death of highly proliferating insulin-secreting cells, putatively via augmentation of JNK activity, a finding that may impact on the possibility of using compounds of similar activity in the treatment of diabetes. |
| 3265 | 18267303 | We analyzed the genes expressed (transcriptomes) and the proteins translated (pro- teomes) in muscle tissues and activated CD4(+) and CD8(+) T-lymphocytes (T-cells) of five Type 2 diabetes (T2DM) subjects using Affymetrix microarrays and mass spectrometry, and compared them with matched non-diabetic controls. |
| 3266 | 18267303 | Gene expressions of insulin receptor (INSR), vitamin D receptor, insulin degrading enzyme, Akt, insulin receptor substrate-1 (IRS-1), IRS-2, glucose transporter 4 (GLUT4), and enzymes of the glycolytic pathway were decreased at least 50% in T2DM than in controls. |
| 3267 | 18267303 | The gene silencing for INSR or TNFalpha resulted in the inhibition or stimulation of GLUT4, respectively. |
| 3268 | 18267111 | DAA significantly suppressed the production of proinflammatory mediators such as MCP-1, TNF-alpha, and NO in stimulated RAW 264 macrophages and in the coculture of RAW 264 macrophages and 3T3-L1 adipocytes. |
| 3269 | 18265948 | Here, we demonstrate that CAPE significantly decreased the levels of nitric oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase in the brain. |
| 3270 | 18265948 | Here, we demonstrate that CAPE significantly decreased the levels of nitric oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase in the brain. |
| 3271 | 18265948 | Here, we demonstrate that CAPE significantly decreased the levels of nitric oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase in the brain. |
| 3272 | 18265948 | The mRNA expressions of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. |
| 3273 | 18265948 | The mRNA expressions of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. |
| 3274 | 18265948 | The mRNA expressions of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. |
| 3275 | 18265948 | CAPE treatments significantly suppressed these inflammatory cytokines (about 70% for TNF-alpha, 26% for IFN-gamma) and NOS (completely). |
| 3276 | 18265948 | CAPE treatments significantly suppressed these inflammatory cytokines (about 70% for TNF-alpha, 26% for IFN-gamma) and NOS (completely). |
| 3277 | 18265948 | CAPE treatments significantly suppressed these inflammatory cytokines (about 70% for TNF-alpha, 26% for IFN-gamma) and NOS (completely). |
| 3278 | 18265948 | Moreover, CAPE reduces the mRNA expressions of TNF-alpha and IFN-gamma in diabetic brain; suggesting CAPE suppresses inflammation as well as oxidative stress occurred in the brain of diabetic patients. |
| 3279 | 18265948 | Moreover, CAPE reduces the mRNA expressions of TNF-alpha and IFN-gamma in diabetic brain; suggesting CAPE suppresses inflammation as well as oxidative stress occurred in the brain of diabetic patients. |
| 3280 | 18265948 | Moreover, CAPE reduces the mRNA expressions of TNF-alpha and IFN-gamma in diabetic brain; suggesting CAPE suppresses inflammation as well as oxidative stress occurred in the brain of diabetic patients. |
| 3281 | 18265478 | Obesity has been shown to be associated with a state of low-grade chronic inflammation, and insulin resistance and the metabolic syndrome are associated with adverse metabolic profiles and with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor-, many of which have been shown to enhance tumor growth. |
| 3282 | 18256353 | Inflammatory cytokines, mainly IL-1, IL-6, and IL-18, as well as TNF-alpha, are involved in the development and progression of diabetic nephropathy. |
| 3283 | 18253705 | Some of the beneficial changes by n-3 FA include enhancing antioxidant enzymes and lowering Th-1/Th-2 cytokines, adhesion molecules, COX-2/PGE(2) levels, pro-inflammatory cytokines (IL-1beta, IL-6 and TNF-alpha etc. |
| 3284 | 18253705 | Further, Fat-1 transgenic mice (which make n-3 FA endogenously in vivo from n-6 FA) when fed CR revealed decreased NF-kappaB and AP-1 activity and increased expression of life-prolonging gene SIRT1. |
| 3285 | 18249219 | Interaction of single nucleotide polymorphisms in ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL with physical activity on the risk of type 2 diabetes mellitus and changes in characteristics of the metabolic syndrome: The Finnish Diabetes Prevention Study. |
| 3286 | 18249219 | Interaction of single nucleotide polymorphisms in ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL with physical activity on the risk of type 2 diabetes mellitus and changes in characteristics of the metabolic syndrome: The Finnish Diabetes Prevention Study. |
| 3287 | 18249219 | Single nucleotide polymorphisms (SNPs) in the ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL genes were associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2D) in the Finnish Diabetes Prevention Study (DPS). |
| 3288 | 18249219 | Single nucleotide polymorphisms (SNPs) in the ADRB2, ADRB3, TNF, IL6, IGF1R, LIPC, LEPR, and GHRL genes were associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2D) in the Finnish Diabetes Prevention Study (DPS). |
| 3289 | 18247339 | Various death ligands of the TNF family such as FasL, TNF, and TNF-Related Apoptosis-Inducing Ligand (TRAIL) have been studied for this purpose. |
| 3290 | 18247339 | Various death ligands of the TNF family such as FasL, TNF, and TNF-Related Apoptosis-Inducing Ligand (TRAIL) have been studied for this purpose. |
| 3291 | 18247339 | Various death ligands of the TNF family such as FasL, TNF, and TNF-Related Apoptosis-Inducing Ligand (TRAIL) have been studied for this purpose. |
| 3292 | 18247339 | The over-expression of TNF or FasL in pancreatic islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation. |
| 3293 | 18247339 | The over-expression of TNF or FasL in pancreatic islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation. |
| 3294 | 18247339 | The over-expression of TNF or FasL in pancreatic islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation. |
| 3295 | 18247339 | These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into pancreatic islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes. |
| 3296 | 18247339 | These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into pancreatic islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes. |
| 3297 | 18247339 | These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into pancreatic islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes. |
| 3298 | 18247160 | In order to characterize the potential causative effects of interleukin-18 (IL-18) on insulin resistance, we measured glucose uptake in 3T3-L1 adipocytes treated with mouse recombinant IL-18. |
| 3299 | 18247160 | IL-18 surprisingly enhanced, rather than reduced insulin-mediated glucose uptake in adipocytes. |
| 3300 | 18247160 | Moreover IL-18 could counteract the glucose uptake suppression caused by tumor necrosis factor alpha in 3T3-L1 adipocytes. |
| 3301 | 18247160 | The mechanism dissection showed that the IL-18 upregulated phosphorylated Akt and downregulated phosphorylated P38 MAPK. |
| 3302 | 18247160 | These findings indicated that the elevated serum IL-18 levels in obesity and diabetes might be a compensatory response to insulin resistance. |
| 3303 | 18235842 | Among those are several pro-inflammatory cytokines such as tumor necrosis factor-alpha(TNF-alpha), interleukin (IL)-1, IL-6, and various adipocytokines. |
| 3304 | 18235842 | Furthermore, several transcription factors and kinases such as c-Jun N-terminal kinase (JNK) and inhibitor of kappa B kinase-beta (IKKbeta), a kinase located proximal of nuclear factor-kappaB (NF-kappaB), participate in this process. |
| 3305 | 18224429 | Metabolic parameters and serum high-sensitivity C-reactive protein, interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha levels were determined in 20 patients with type 1 DM and 21 patients with type 2 DM and compared to 34 healthy subjects. |
| 3306 | 18223156 | HSP72 protects against obesity-induced insulin resistance. |
| 3307 | 18223156 | Patients with type 2 diabetes have reduced gene expression of heat shock protein (HSP) 72, which correlates with reduced insulin sensitivity. |
| 3308 | 18223156 | Activation of several inflammatory signaling proteins such as c-jun amino terminal kinase (JNK), inhibitor of kappaB kinase, and tumor necrosis factor-alpha, can induce insulin resistance, but HSP 72 can block the induction of these molecules in vitro. |
| 3309 | 18223156 | Accordingly, we examined whether activation of HSP72 can protect against the development of insulin resistance. |
| 3310 | 18223156 | First, we show that obese, insulin resistant humans have reduced HSP72 protein expression and increased JNK phosphorylation in skeletal muscle. |
| 3311 | 18223156 | Herein, we show that regardless of the means used to achieve an elevation in HSP72 protein, protection against diet- or obesity-induced hyperglycemia, hyperinsulinemia, glucose intolerance, and insulin resistance was observed. |
| 3312 | 18223156 | These findings identify an essential role for HSP72 in blocking inflammation and preventing insulin resistance in the context of genetic obesity or high-fat feeding. |
| 3313 | 18221086 | Three PPAR subtypes, encoded by distinct genes, are designated as PPAR-alpha, PPAR-delta (also know as beta) and PPAR-gamma. |
| 3314 | 18221086 | PPAR-alpha is the main metabolic regulator for catabolism whereas PPAR-gamma regulates anabolism or storage. |
| 3315 | 18221086 | In 1997, a Glaxo patent described that Troglitazone (first PPAR-gamma ligand to reach market) reduced TNF-induced VCAM1 expression in HUVECs indicating the potential benefit in atherosclerosis. |
| 3316 | 18221086 | Patents from Metabolex and Tularik in 2001 and 2002 described the beneficial effects of SPPARM molecules for insulin resistance and diabetes, without showing concern on PPAR-gamma related side effects such as edema and body weight. |
| 3317 | 18220690 | Inflammatory markers such as Interleukin-18 and Tumor Necrosis Factor (TNF)-alpha are increased in the serum of patients with diabetes and DN. |
| 3318 | 18220690 | Inflammatory markers such as Interleukin-18 and Tumor Necrosis Factor (TNF)-alpha are increased in the serum of patients with diabetes and DN. |
| 3319 | 18220690 | Experimental animal models have recently provided evidence that some acute phase markers of inflammation such as intracellular cell adhesion molecule-1 (ICAM-1), TNF-alpha and Monocytes Chemoattractant Protein-1 (MCP-1) may have a causative role in the development of DN. |
| 3320 | 18220690 | Experimental animal models have recently provided evidence that some acute phase markers of inflammation such as intracellular cell adhesion molecule-1 (ICAM-1), TNF-alpha and Monocytes Chemoattractant Protein-1 (MCP-1) may have a causative role in the development of DN. |
| 3321 | 18220644 | In this review, we summarize the possible links between insulin and various hormones (growth hormones (GH), catecholamines, glucocorticoids and sex hormones), partly mediated through visceral adiposity and adipocytokines (notably adiponectin, leptin, resistin, visfatin, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6)) in the pathogenesis of this syndrome. |
| 3322 | 18220642 | Visceral adipose tissue and its adipose-tissue resident macrophages produce more proinflamatory cytokines like tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) and less adiponectin. |
| 3323 | 18220615 | Weight loss reduces subcutaneous adipose tissue production of pro-inflammatory cytokines (i.e. interleukin 6, tumor necrosis factor alpha) and increases adipose expression of anti-inflammatory cytokines (i.e. interleukin 10, interleukin 1 receptor antagonist). |
| 3324 | 18220614 | Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area. |
| 3325 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3326 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3327 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3328 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3329 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3330 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3331 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3332 | 18201373 | The objective of the study was to analyse levels of IL-12 and TNF-alpha and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). |
| 3333 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3334 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3335 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3336 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3337 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3338 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3339 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3340 | 18201373 | Serum levels of IL-12 and TNF-alpha were measured by an immunoenzymatic ELISA technique. |
| 3341 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3342 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3343 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3344 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3345 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3346 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3347 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3348 | 18201373 | TNF-alpha and IL-12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine's equilibrium. |
| 3349 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3350 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3351 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3352 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3353 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3354 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3355 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3356 | 18201373 | Among the patients with an established retinopathy, two IL-12/TNF-alpha combinations were visible. |
| 3357 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3358 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3359 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3360 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3361 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3362 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3363 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3364 | 18201373 | Either a lack of detectable TNF-alpha was accompanied by measurable IL-12 serum concentrations or TNF-alpha incidence was associated with undetectable IL-12 values. |
| 3365 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3366 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3367 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3368 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3369 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3370 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3371 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3372 | 18201373 | Simultaneous lack of TNF-alpha and presence of IL-12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. |
| 3373 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3374 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3375 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3376 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3377 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3378 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3379 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3380 | 18201373 | The state of equilibrium between TNF-alpha and IL-12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. |
| 3381 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3382 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3383 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3384 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3385 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3386 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3387 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3388 | 18201373 | It may suggest that a disharmony between pro- and anti-angiogenic function of these cytokines underlie the mechanism by which TNF-alpha and IL-12 shape the disease course. |
| 3389 | 18195475 | However, in pathological states such as obesity, hypertension, diabetes metabolic syndrome and other cardiovascular disorders perivascular tissue becomes dysfunctional and production of protective factors diminishes while detrimental adipocytokines such as leptin, resistin, IL-6, TNF-alpha or IL-17 increases. |
| 3390 | 18195475 | Adipokines also regulate immune system as chemokines (such as MIP-1 or RANTES) and induce inflammation with infiltration of T cells and macrophages to the vessel wall. |
| 3391 | 18191048 | Weight reduction resulted in a decrease in the mRNA expression of IL-1beta (IL1B), IL-1 receptor antagonist, and tumor necrosis factor alpha (P < .001) and an increase in expression of IL-6 (IL6) and IL-8 (P < .01). |
| 3392 | 18191048 | Interestingly, the decrease in IL1B expression was correlated with an increase in insulin sensitivity index (r = -0.68, P < .01). |
| 3393 | 18191048 | The decrease in IL-1 receptor antagonist expression after weight loss and the strong correlation between the decrease in IL1B expression and the increase in insulin sensitivity suggest a contribution of these genes to insulin-resistant states found in obesity and the metabolic syndrome. |
| 3394 | 18188531 | Advanced oxidation protein products in obese women: its relation to insulin resistance and resistin. |
| 3395 | 18188531 | Advanced oxidation protein products in obese women: its relation to insulin resistance and resistin. |
| 3396 | 18188531 | Advanced oxidation protein products in obese women: its relation to insulin resistance and resistin. |
| 3397 | 18188531 | Advanced oxidation protein products in obese women: its relation to insulin resistance and resistin. |
| 3398 | 18188531 | Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. |
| 3399 | 18188531 | Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. |
| 3400 | 18188531 | Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. |
| 3401 | 18188531 | Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. |
| 3402 | 18188531 | The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. |
| 3403 | 18188531 | The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. |
| 3404 | 18188531 | The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. |
| 3405 | 18188531 | The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. |
| 3406 | 18188531 | Serum levels of TNF-a, IL-6, resistin, glucose, insulin and AOPPs were measured. |
| 3407 | 18188531 | Serum levels of TNF-a, IL-6, resistin, glucose, insulin and AOPPs were measured. |
| 3408 | 18188531 | Serum levels of TNF-a, IL-6, resistin, glucose, insulin and AOPPs were measured. |
| 3409 | 18188531 | Serum levels of TNF-a, IL-6, resistin, glucose, insulin and AOPPs were measured. |
| 3410 | 18188531 | Diabetic and prediabetic obese patients had increases in serum resistin and TNF-alpha levels (P<0.01 and P<0.001, respectively). |
| 3411 | 18188531 | Diabetic and prediabetic obese patients had increases in serum resistin and TNF-alpha levels (P<0.01 and P<0.001, respectively). |
| 3412 | 18188531 | Diabetic and prediabetic obese patients had increases in serum resistin and TNF-alpha levels (P<0.01 and P<0.001, respectively). |
| 3413 | 18188531 | Diabetic and prediabetic obese patients had increases in serum resistin and TNF-alpha levels (P<0.01 and P<0.001, respectively). |
| 3414 | 18188531 | Insulin was significantly associated with circulating resistin and TNF-alpha. |
| 3415 | 18188531 | Insulin was significantly associated with circulating resistin and TNF-alpha. |
| 3416 | 18188531 | Insulin was significantly associated with circulating resistin and TNF-alpha. |
| 3417 | 18188531 | Insulin was significantly associated with circulating resistin and TNF-alpha. |
| 3418 | 18188531 | The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. |
| 3419 | 18188531 | The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. |
| 3420 | 18188531 | The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. |
| 3421 | 18188531 | The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. |
| 3422 | 18188414 | Leptin-deficient ob/ob mice are a murine model for obesity, insulin resistance, and diabetes. |
| 3423 | 18188414 | Gene expression of the radiation-inducible cdk-inhibitor, p21, and the adipocytokines, tumor necrosis factor alpha and interleukin-1beta, were induced as expected; but genes involved in adipogenesis such as peroxisome proliferator-activated receptor gamma and adipsin were not affected in the irradiated adipose tissue. |
| 3424 | 18188414 | Inversely, hepatic lipid content was elevated with concomitant increases in the expression of lipogenic enzymes such as fatty acid synthase (FAS), and sterol regulatory element-binding protein 1c. |
| 3425 | 18187553 | Trauma and hemorrhage-induced acute hepatic insulin resistance: dominant role of tumor necrosis factor-alpha. |
| 3426 | 18187553 | Trauma and hemorrhage-induced acute hepatic insulin resistance: dominant role of tumor necrosis factor-alpha. |
| 3427 | 18187553 | Trauma and hemorrhage-induced acute hepatic insulin resistance: dominant role of tumor necrosis factor-alpha. |
| 3428 | 18187553 | Trauma and hemorrhage-induced acute hepatic insulin resistance: dominant role of tumor necrosis factor-alpha. |
| 3429 | 18187553 | With increasing extent of blood loss, there were increases in serum TNF-alpha levels, phosphorylation of liver insulin receptor substrate-1 on serine 307, and liver c-Jun N-terminal kinase activation/phosphorylation. |
| 3430 | 18187553 | With increasing extent of blood loss, there were increases in serum TNF-alpha levels, phosphorylation of liver insulin receptor substrate-1 on serine 307, and liver c-Jun N-terminal kinase activation/phosphorylation. |
| 3431 | 18187553 | With increasing extent of blood loss, there were increases in serum TNF-alpha levels, phosphorylation of liver insulin receptor substrate-1 on serine 307, and liver c-Jun N-terminal kinase activation/phosphorylation. |
| 3432 | 18187553 | With increasing extent of blood loss, there were increases in serum TNF-alpha levels, phosphorylation of liver insulin receptor substrate-1 on serine 307, and liver c-Jun N-terminal kinase activation/phosphorylation. |
| 3433 | 18187553 | Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. |
| 3434 | 18187553 | Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. |
| 3435 | 18187553 | Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. |
| 3436 | 18187553 | Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. |
| 3437 | 18187553 | Conversely, neutralizing TNF-alpha antibody treatment reversed many of the hemorrhage-induced changes in hepatic insulin signaling. |
| 3438 | 18187553 | Conversely, neutralizing TNF-alpha antibody treatment reversed many of the hemorrhage-induced changes in hepatic insulin signaling. |
| 3439 | 18187553 | Conversely, neutralizing TNF-alpha antibody treatment reversed many of the hemorrhage-induced changes in hepatic insulin signaling. |
| 3440 | 18187553 | Conversely, neutralizing TNF-alpha antibody treatment reversed many of the hemorrhage-induced changes in hepatic insulin signaling. |
| 3441 | 18180317 | Glucagon-like peptide-1 attenuates tumour necrosis factor-alpha-mediated induction of plasminogen [corrected] activator inhibitor-1 expression. |
| 3442 | 18180317 | Glucagon-like peptide-1 attenuates tumour necrosis factor-alpha-mediated induction of plasminogen [corrected] activator inhibitor-1 expression. |
| 3443 | 18180317 | Glucagon-like peptide-1 attenuates tumour necrosis factor-alpha-mediated induction of plasminogen [corrected] activator inhibitor-1 expression. |
| 3444 | 18180317 | Glucagon-like peptide-1 attenuates tumour necrosis factor-alpha-mediated induction of plasminogen [corrected] activator inhibitor-1 expression. |
| 3445 | 18180317 | Glucagon-like peptide-1 attenuates tumour necrosis factor-alpha-mediated induction of plasminogen [corrected] activator inhibitor-1 expression. |
| 3446 | 18180317 | Elevated plasminogen activator inhibitor type-1 [corrected] (PAI-1) levels have been implicated in endothelial cell dysfunction. |
| 3447 | 18180317 | Elevated plasminogen activator inhibitor type-1 [corrected] (PAI-1) levels have been implicated in endothelial cell dysfunction. |
| 3448 | 18180317 | Elevated plasminogen activator inhibitor type-1 [corrected] (PAI-1) levels have been implicated in endothelial cell dysfunction. |
| 3449 | 18180317 | Elevated plasminogen activator inhibitor type-1 [corrected] (PAI-1) levels have been implicated in endothelial cell dysfunction. |
| 3450 | 18180317 | Elevated plasminogen activator inhibitor type-1 [corrected] (PAI-1) levels have been implicated in endothelial cell dysfunction. |
| 3451 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 3452 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 3453 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 3454 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 3455 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 3456 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 3457 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 3458 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 3459 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 3460 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 3461 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 3462 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 3463 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 3464 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 3465 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 3466 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 3467 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 3468 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 3469 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 3470 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 3471 | 18180317 | GLP-1 treatment also inhibited TNF-alpha-mediated induction of Akt phosphorylation. |
| 3472 | 18180317 | GLP-1 treatment also inhibited TNF-alpha-mediated induction of Akt phosphorylation. |
| 3473 | 18180317 | GLP-1 treatment also inhibited TNF-alpha-mediated induction of Akt phosphorylation. |
| 3474 | 18180317 | GLP-1 treatment also inhibited TNF-alpha-mediated induction of Akt phosphorylation. |
| 3475 | 18180317 | GLP-1 treatment also inhibited TNF-alpha-mediated induction of Akt phosphorylation. |
| 3476 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 3477 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 3478 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 3479 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 3480 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 3481 | 18171911 | HIV-protease inhibitors induce expression of suppressor of cytokine signaling-1 in insulin-sensitive tissues and promote insulin resistance and type 2 diabetes mellitus. |
| 3482 | 18171911 | Oligonucleotide gene array analyses revealed upregulation of suppressor of cytokine signaling-1 (SOCS-1) expression in insulin-sensitive tissues of IDV rats. |
| 3483 | 18171911 | SOCS-1 is a known inducer of insulin resistance and diabetes, and immunoblotting analyses revealed increases in SOCS-1 protein expression in adipose, skeletal muscle, and liver tissues of IDV-administered ZDF rats. |
| 3484 | 18171911 | This was associated with increases in the upstream regulator TNF-alpha and downstream effector sterol regulatory element-binding protein-1 and a decrease in IRS-2. |
| 3485 | 18171433 | RNAi screens reveal novel metabolic regulators: RIP140, MAP4k4 and the lipid droplet associated fat specific protein (FSP) 27. |
| 3486 | 18171433 | These short interfering RNA (siRNA)-based screens identified the transcriptional corepressor receptor interacting protein 140 (RIP140) (J Clin Invest 116: 125, 2006) and the mitogen-activated protein kinase (MAP4k4) (Proc Natl Acad Sci USA 103: 2087, 2006) as negative regulators of insulin-responsive hexose uptake and oxidative metabolism. |
| 3487 | 18171433 | MAP4k4 depletion in adipocytes increases many of the RIP140-sensitive genes, increases adipogenesis and mediates some actions of tumour necrosis factor-alpha (TNF-alpha). |
| 3488 | 18171433 | We conclude that RIP140, MAP4k4 and the novel lipid droplet protein FSP27 are powerful regulators of adipose tissue metabolism and are potential therapeutic targets for controlling metabolic disease. |
| 3489 | 19378424 | C-reactive protein and tumor necrosis factor-alpha in relation to insulin-mediated glucose uptake, smoking and atherosclerosis. |
| 3490 | 19284081 | Leptin, adiponectin, TNF alfa, the hepatic expression of suppressor of cytokine signalling 3 (SOCS3), and hyperinsulinemia have been considered as heavily influencing fibrosis extension and nonresponsiveness to the IFN-alpha. |
| 3491 | 19284081 | The adipokines increased hepatic expression of SOCS3, and hyperinsulinemia has been proposed as heavily influencing non-responsiveness to the IFN-alpha and fibrosis extension by maintaining the hepatic stellate cells activated phenotype in patients with chronic hepatitis C and insulin resistance-related obesity. |
| 3492 | 19284081 | We shall review the mechanisms by which obesity-related insulin resistance may be associated with fibrosis extension and decreased efficacy of IFN-alpha based therapies in obese individuals with chronic hepatitis C and the therapeutic strategies that may increase the effectiveness of these therapies. |
| 3493 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3494 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3495 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3496 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3497 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3498 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3499 | 18162526 | The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. |
| 3500 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3501 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3502 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3503 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3504 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3505 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3506 | 18162526 | TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. |
| 3507 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3508 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3509 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3510 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3511 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3512 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3513 | 18162526 | Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. |
| 3514 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3515 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3516 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3517 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3518 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3519 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3520 | 18162526 | Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. |
| 3521 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3522 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3523 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3524 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3525 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3526 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3527 | 18162526 | The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. |
| 3528 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3529 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3530 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3531 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3532 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3533 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3534 | 18162526 | Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. |
| 3535 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3536 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3537 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3538 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3539 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3540 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3541 | 18162526 | The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. |
| 3542 | 18095312 | The levels of Fatty acid synthase (FAS) and SREBP-2 expressions in placenta are significantly increased in the HC group while expression of both sterol regulatory element-binding proteins-1 (SREBP-1) and HMG-CoA reductase (HMGR) are not modified. |
| 3543 | 18095312 | GDM is not associated with modification in the maternal lipid profile but it increases the concentration of inflammatory cytokines (IL-1beta and TNF-alpha) in placenta which correlates with a dramatic induction of FAS expression without affecting the expression of mature SREBPs proteins. |
| 3544 | 18093861 | Adipose tissue is known to express and secrete a variety of products known as 'adipokines', including leptin, adiponectin, resistin and visfatin, as well as cytokines and chemokines such as tumor necrosis factor-alpha, interleukin-6 and monocyte chemoattractant protein-1. |
| 3545 | 18091354 | We tested the hypothesis that formula feeding during the neonatal period accelerates the development of T1D in diabetes-prone BioBreeding (BBDP) rats through regulation of CD4+CD25+ regulatory T lymphocytes (T(reg)) and anti-inflammatory cytokines. |
| 3546 | 18091354 | We tested the hypothesis that formula feeding during the neonatal period accelerates the development of T1D in diabetes-prone BioBreeding (BBDP) rats through regulation of CD4+CD25+ regulatory T lymphocytes (T(reg)) and anti-inflammatory cytokines. |
| 3547 | 18091354 | The spleen and thymus were analyzed for Foxp3-expressing CD4+/CD25+ T cells. |
| 3548 | 18091354 | The spleen and thymus were analyzed for Foxp3-expressing CD4+/CD25+ T cells. |
| 3549 | 18091354 | Multiplex enzyme-linked immunosorbent assays (ELISAs) were performed to measure cytokine-induced neutrophil chemoattractant (CINC), tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin (IL)-4, IL-10, and IL-18. |
| 3550 | 18091354 | Multiplex enzyme-linked immunosorbent assays (ELISAs) were performed to measure cytokine-induced neutrophil chemoattractant (CINC), tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin (IL)-4, IL-10, and IL-18. |
| 3551 | 18091354 | There were no differences in ileal cytokine concentrations of 75-d-old rats, but the formula-fed rats had greater liver TNF-alpha (p < 0.001), IFN-gamma, and IL-4 (p < 0.01) and lower IL-10 (p = 0.002) compared with MF animals. |
| 3552 | 18091354 | There were no differences in ileal cytokine concentrations of 75-d-old rats, but the formula-fed rats had greater liver TNF-alpha (p < 0.001), IFN-gamma, and IL-4 (p < 0.01) and lower IL-10 (p = 0.002) compared with MF animals. |
| 3553 | 18083784 | Increased skeletal muscle tumor necrosis factor-alpha and impaired insulin signaling persist in obese women with gestational diabetes mellitus 1 year postpartum. |
| 3554 | 18081694 | This study examined the effects of interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumour necrosis factor alpha (TNFalpha) on a rat insulinoma cell line (RIN-r) in order to identify the core mechanism of cytokine-induced beta-cell death. |
| 3555 | 18081694 | This study examined the effects of interleukin-1beta (IL-1beta), interferon-gamma (IFNgamma) and tumour necrosis factor alpha (TNFalpha) on a rat insulinoma cell line (RIN-r) in order to identify the core mechanism of cytokine-induced beta-cell death. |
| 3556 | 18081694 | Treatment of cells with a combination of IL-1beta and IFNgamma (IL-1beta/IFNgamma)induced apoptotic cell death. |
| 3557 | 18081694 | Treatment of cells with a combination of IL-1beta and IFNgamma (IL-1beta/IFNgamma)induced apoptotic cell death. |
| 3558 | 18081694 | TNFalpha neither induced beta-cell death nor did it potentiate the effects of IL-1beta, IFNgamma or IL-1beta/IFNgamma . |
| 3559 | 18081694 | TNFalpha neither induced beta-cell death nor did it potentiate the effects of IL-1beta, IFNgamma or IL-1beta/IFNgamma . |
| 3560 | 18081694 | The cytotoxic effect of IL-1beta/IFNgamma was associated with the expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide. |
| 3561 | 18081694 | The cytotoxic effect of IL-1beta/IFNgamma was associated with the expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide. |
| 3562 | 18081694 | The broad range caspase inhibitor, Boc-D-fmk, blocked IL-1beta/IFNgamma -induced caspase activity, but not nitric oxide production nor cell death. |
| 3563 | 18081694 | The broad range caspase inhibitor, Boc-D-fmk, blocked IL-1beta/IFNgamma -induced caspase activity, but not nitric oxide production nor cell death. |
| 3564 | 18081694 | IL-1beta/IFNgamma -induced apoptosis was accompanied by loss of mitochondrial membrane potential, release of cytochrome c and cleavage of pro-caspase-9, -7 and -3. |
| 3565 | 18081694 | IL-1beta/IFNgamma -induced apoptosis was accompanied by loss of mitochondrial membrane potential, release of cytochrome c and cleavage of pro-caspase-9, -7 and -3. |
| 3566 | 18081694 | Transduction of cells with Ad-Bcl-X(L) blocked both iNOS and cytokine-mediated mitochondrial changes and subsequent apoptosis, downstream of nitric oxide. |
| 3567 | 18081694 | Transduction of cells with Ad-Bcl-X(L) blocked both iNOS and cytokine-mediated mitochondrial changes and subsequent apoptosis, downstream of nitric oxide. |
| 3568 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3569 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3570 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3571 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3572 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3573 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3574 | 18078928 | Cross talk of tumor necrosis factor-alpha and the renin-angiotensin system in tumor necrosis factor-alpha-induced plasminogen activator inhibitor-1 production from hepatocytes. |
| 3575 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3576 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3577 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3578 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3579 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3580 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3581 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 3582 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3583 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3584 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3585 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3586 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3587 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3588 | 18078928 | We found that the gene expression of renin-angiotensin system components, together with that of plasminogen activator inhibitor (PAI)-1, is upregulated in the liver of patients with obesity and type 2 diabetes. |
| 3589 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3590 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3591 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3592 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3593 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3594 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3595 | 18078928 | We next examined the role of the renin-angiotensin system on TNF-alpha-induced PAI-1 production in the nonmalignant human hepatocyte cell line THLE-5b. |
| 3596 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3597 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3598 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3599 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3600 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3601 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3602 | 18078928 | THLE-5b cells expressed genes encoding renin-angiotensin system components including angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin type 1 (AT(1)) receptor. |
| 3603 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3604 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3605 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3606 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3607 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3608 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3609 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 3610 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3611 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3612 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3613 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3614 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3615 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3616 | 18078928 | Moreover, angiotensin AT(1) receptor antagonist dose-dependently inhibited TNF-alpha-induced PAI-1 production. |
| 3617 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3618 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3619 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3620 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3621 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3622 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3623 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 3624 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3625 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3626 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3627 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3628 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3629 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3630 | 18078928 | Selective angiotensin AT(1) receptor antagonists inhibit both TNF-alpha- and angiotensin II-induced PAI-1 production in hepatocytes, suggesting a cross talk between both systems. |
| 3631 | 18075292 | MEDLINE was searched for articles relating GDM and the adipokines (tumor necrosis factor-alpha and adiponectin) as well as the acute-phase inflammatory biomarker C-reactive protein that contribute to the development of diabetic pregnancy and vascular complications. |
| 3632 | 18070989 | We confirm previously reported inverse associations of coffee consumption with inflammatory markers, C-reactive protein, and tumor necrosis factor-alpha receptor II. |
| 3633 | 18064633 | MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1beta. |
| 3634 | 18064633 | MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1beta. |
| 3635 | 18064633 | Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, and iNOS in the islets of Langerhans. |
| 3636 | 18064633 | Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, and iNOS in the islets of Langerhans. |
| 3637 | 18064633 | These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-/-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. |
| 3638 | 18064633 | These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-/-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. |
| 3639 | 18064475 | Paraffin sections of sural nerves from 19 patients with DLRPN, 13 patients with LRPN, and 20 disease control patients were immunostained for intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nuclear factor kappaB (NF-kappaB). |
| 3640 | 18064475 | Paraffin sections of sural nerves from 19 patients with DLRPN, 13 patients with LRPN, and 20 disease control patients were immunostained for intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nuclear factor kappaB (NF-kappaB). |
| 3641 | 18064475 | Paraffin sections of sural nerves from 19 patients with DLRPN, 13 patients with LRPN, and 20 disease control patients were immunostained for intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nuclear factor kappaB (NF-kappaB). |
| 3642 | 18064475 | TNF-alpha expression was seen in Schwann cells and some macrophages of DLRPN and LRPN nerves, whereas IL-6 expression was minimal. |
| 3643 | 18064475 | TNF-alpha expression was seen in Schwann cells and some macrophages of DLRPN and LRPN nerves, whereas IL-6 expression was minimal. |
| 3644 | 18064475 | TNF-alpha expression was seen in Schwann cells and some macrophages of DLRPN and LRPN nerves, whereas IL-6 expression was minimal. |
| 3645 | 18064475 | NF-kappaB expression correlated with the number of empty nerve strands (P < 0.01) and the frequency of axonal degeneration (P < 0.05), whereas TNF-alpha expression correlated inversely with the number of empty nerve strands of teased fibers (P < 0.05). |
| 3646 | 18064475 | NF-kappaB expression correlated with the number of empty nerve strands (P < 0.01) and the frequency of axonal degeneration (P < 0.05), whereas TNF-alpha expression correlated inversely with the number of empty nerve strands of teased fibers (P < 0.05). |
| 3647 | 18064475 | NF-kappaB expression correlated with the number of empty nerve strands (P < 0.01) and the frequency of axonal degeneration (P < 0.05), whereas TNF-alpha expression correlated inversely with the number of empty nerve strands of teased fibers (P < 0.05). |
| 3648 | 18063842 | TNF binds to two specific receptors, TNF-receptor type I (TNF-R1, CD120a, p55/60) and TNF-receptor type II (TNF-R2, CD120b, p75/80). |
| 3649 | 18063842 | TNF binds to two specific receptors, TNF-receptor type I (TNF-R1, CD120a, p55/60) and TNF-receptor type II (TNF-R2, CD120b, p75/80). |
| 3650 | 18063842 | Role of TNF-R2 phosphorylation on its signaling properties is understood less than TNF-R1. |
| 3651 | 18063842 | Role of TNF-R2 phosphorylation on its signaling properties is understood less than TNF-R1. |
| 3652 | 18063842 | Other cellular substrates as TRADD adaptor protein, TRAF protein family and RIP kinases are reviewed in relation to TNF receptor-mediated apoptosis or survival pathways and regulation of their actions by phosphorylation. |
| 3653 | 18063842 | Other cellular substrates as TRADD adaptor protein, TRAF protein family and RIP kinases are reviewed in relation to TNF receptor-mediated apoptosis or survival pathways and regulation of their actions by phosphorylation. |
| 3654 | 18060853 | Selective activation of PKA type I, but not PKA type II or Epac, with chemical analogs of cAMP was sufficient to inhibit LPS-induced TNF-alpha mRNA levels. |
| 3655 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3656 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3657 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3658 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3659 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3660 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3661 | 18060802 | LPS induces interleukin-6 and interleukin-8 but not tumor necrosis factor-alpha in human adipocytes. |
| 3662 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3663 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3664 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3665 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3666 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3667 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3668 | 18060802 | Here we studied the lipopolysaccharide (LPS)-induced expression dynamics of tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and IL-10 in human adipose tissue biopsies, in preadipocyte-derived adipocytes, and in mesenchymal stem cell (MSC)-derived adipocytes. |
| 3669 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3670 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3671 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3672 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3673 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3674 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3675 | 18060802 | TNFalpha, IL-6, IL-8 and IL-10 secretions by adipose tissue explants were increased 5.5-, 19.5-, 3.5- and 12.5-fold, respectively, by LPS (1 microg/mL) administration. |
| 3676 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3677 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3678 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3679 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3680 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3681 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3682 | 18060802 | Concordantly, IL-6 and IL-8 release was dose-dependently induced in MSC-derived adipocytes by LPS (>10 pg/mL). |
| 3683 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3684 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3685 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3686 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3687 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3688 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3689 | 18060802 | In contrast, TNFalpha and IL-10 remained undetectable even at the highest LPS dose (1 microg/mL) after 24h. |
| 3690 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3691 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3692 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3693 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3694 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3695 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3696 | 18060802 | In MSC- and preadipocyte-derived adipocytes, respectively, exposure to LPS evoked a weak and transient induction of TNFalpha mRNA whereas induction of IL-6 and IL-8 mRNA were pronounced and sustained for at least 24h. |
| 3697 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3698 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3699 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3700 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3701 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3702 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3703 | 18060802 | Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). |
| 3704 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3705 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3706 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3707 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3708 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3709 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3710 | 18060802 | In this adipocyte model TNFalpha induces well known metabolic effects, but together with previous reports these data suggest that inflammation-induced TNFalpha may derive from non-adipocyte sources in adipose tissue, likely to be macrophages. |
| 3711 | 17991133 | In addition, the serum levels of adipocytokines, such as adiponectin, leptin, tumor necrosis factor-alpha, resistin, interleukin-6, plasminogen activator inhibitor-1, and their correlation with childhood obesity have been extensively investigated. |
| 3712 | 18049445 | Acetylcholinesterase and butyrylcholinesterase as possible markers of low-grade systemic inflammation. |
| 3713 | 18049445 | Acetylcholinesterase and butyrylcholinesterase as possible markers of low-grade systemic inflammation. |
| 3714 | 18049445 | Plasma levels of C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and lipid peroxides are high whereas those of endothelial nitric oxide are low in insulin resistance, obesity, type 2 diabetes mellitus, hypertension, hyperlipidemias, metabolic syndrome X, and Alzheimer's disease suggesting that these diseases are characterized by low-grade systemic inflammation. |
| 3715 | 18049445 | Plasma levels of C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and lipid peroxides are high whereas those of endothelial nitric oxide are low in insulin resistance, obesity, type 2 diabetes mellitus, hypertension, hyperlipidemias, metabolic syndrome X, and Alzheimer's disease suggesting that these diseases are characterized by low-grade systemic inflammation. |
| 3716 | 18049445 | Recent studies showed that the plasma and tissue activities of enzymes butyrylcholinesterase and acetylcholinesterase are elevated in patients with Alzheimer's disease, and diabetes mellitus, hypertension, insulin resistance, and hyperlipidemia. |
| 3717 | 18049445 | Recent studies showed that the plasma and tissue activities of enzymes butyrylcholinesterase and acetylcholinesterase are elevated in patients with Alzheimer's disease, and diabetes mellitus, hypertension, insulin resistance, and hyperlipidemia. |
| 3718 | 18049445 | As a result of this increase in the activities of enzymes acetylcholinesterase and butyrylcholinesterase, the plasma and tissue levels of acetylcholine (ACh) will be low. |
| 3719 | 18049445 | As a result of this increase in the activities of enzymes acetylcholinesterase and butyrylcholinesterase, the plasma and tissue levels of acetylcholine (ACh) will be low. |
| 3720 | 18049445 | The "cholinergic anti-inflammatory pathway" mediated by acetylcholine acts by inhibiting the production of tumor necrosis factor, interleukin-1, macrophage migration inhibitory factor, and high mobility group box-1 and suppresses the activation of nuclear factor-kappa B expression. |
| 3721 | 18049445 | The "cholinergic anti-inflammatory pathway" mediated by acetylcholine acts by inhibiting the production of tumor necrosis factor, interleukin-1, macrophage migration inhibitory factor, and high mobility group box-1 and suppresses the activation of nuclear factor-kappa B expression. |
| 3722 | 18049445 | Hence, both acetylcholinesterase and butyrylcholinesterase by inactivating acetylcholine may enhance inflammation. |
| 3723 | 18049445 | Hence, both acetylcholinesterase and butyrylcholinesterase by inactivating acetylcholine may enhance inflammation. |
| 3724 | 18049445 | This suggests that increased plasma and tissue activities of acetylcholinesterase and butyrylcholinesterase seen in various clinical conditions could serve as a marker of low-grade systemic inflammation. |
| 3725 | 18049445 | This suggests that increased plasma and tissue activities of acetylcholinesterase and butyrylcholinesterase seen in various clinical conditions could serve as a marker of low-grade systemic inflammation. |
| 3726 | 18046434 | At the start of the study and after 6 months' therapy blood samples were taken to evaluate total peroxides (TP), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha), and the patients underwent a (123)I-metaiodobenzylguanidine myocardial scintigraphy study. |
| 3727 | 18046434 | At the start of the study and after 6 months' therapy blood samples were taken to evaluate total peroxides (TP), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha), and the patients underwent a (123)I-metaiodobenzylguanidine myocardial scintigraphy study. |
| 3728 | 18046434 | ACE-i caused a significant reduction in levels of cytokines and TP (P<0.001 for IL-6 and TNF-alpha, P=0.001 for TP). |
| 3729 | 18046434 | ACE-i caused a significant reduction in levels of cytokines and TP (P<0.001 for IL-6 and TNF-alpha, P=0.001 for TP). |
| 3730 | 18037376 | TNF-alpha and adipocyte biology. |
| 3731 | 18036359 | After 8 months of follow-up, only the telmisartan group showed significant decreases in interleukin-6 and tumor necrosis factor-alpha. |
| 3732 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 3733 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 3734 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 3735 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 3736 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 3737 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 3738 | 17989340 | Modulation of type 1 diabetes susceptibility by tumor necrosis factor alpha -308 G/A and lymphotoxin alpha +249 A/G haplotypes and lack of linkage disequilibrium with predisposing DQB1-DRB1 haplotypes in Bahraini patients. |
| 3739 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 3740 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 3741 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 3742 | 17989340 | Tumor necrosis factor alpha (TNF-alpha) -308 G/A and lymphotoxin alpha (LTalpha) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. |
| 3743 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 3744 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 3745 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 3746 | 17989340 | Only LTalpha +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-alpha/LTalpha alleles and susceptible/protective DRB1-DQB1 haplotypes. |
| 3747 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 3748 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 3749 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 3750 | 17989340 | TNF-alpha/LTalpha T1DM-susceptible (-308G/+249G) and protective (-308G/+249A) haplotypes were identified. |
| 3751 | 17985235 | Interactions between TNF and GnRH. |
| 3752 | 17985235 | Interactions between TNF and GnRH. |
| 3753 | 17985235 | Interactions between TNF and GnRH. |
| 3754 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 3755 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 3756 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 3757 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 3758 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 3759 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 3760 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 3761 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 3762 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 3763 | 17983440 | Intracellular staining revealed that these Th2 T-cell clones produce low levels of tumour necrosis factor-alpha (TNF-alpha) in vitro, and after adoptive transfer, they migrate to the pancreas where they produce TNF-alpha as well as Th2 cytokines (interleukin (IL)-4, IL-10). |
| 3764 | 17981625 | Each of these can lead to aberrant cell signalling that affects innate immunity for example, by activating the MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. |
| 3765 | 17981625 | These complications are frequently associated with increased expression of inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species. |
| 3766 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 3767 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 3768 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 3769 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 3770 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 3771 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 3772 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 3773 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 3774 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 3775 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 3776 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 3777 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 3778 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 3779 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 3780 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 3781 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 3782 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 3783 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 3784 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 3785 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 3786 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 3787 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 3788 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 3789 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 3790 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 3791 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 3792 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 3793 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 3794 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 3795 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 3796 | 17966038 | Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. |
| 3797 | 17966038 | We describe how CD4+ or CD8+T cells can contribute differentially to the pathogenesis of T1D using the HLA-DQ8 transgenic mouse models. |
| 3798 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 3799 | 17966038 | In the RIP-B7.RIP-TNF double transgenic mouse model, either CD4+ or CD8+T cells were sufficient to precipitate diabetes in 100% of the animals. |
| 3800 | 17966038 | Thus, the relative roles of CD4+ or CD8+T cells in the pathogenesis of T1D are possibly determined by the local inflammatory stimuli. |
| 3801 | 17952840 | Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. |
| 3802 | 17952840 | Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. |
| 3803 | 17952840 | Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. |
| 3804 | 17952840 | Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. |
| 3805 | 17952840 | Visfatin, TNF-alpha and IL-6 mRNA expression is increased in mononuclear cells from type 2 diabetic women. |
| 3806 | 17952840 | Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. |
| 3807 | 17952840 | Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. |
| 3808 | 17952840 | Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. |
| 3809 | 17952840 | Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. |
| 3810 | 17952840 | Mononuclear TNF-alpha and IL-6 mRNA expression was also elevated in DM2 compared to control women (p=0.001 and p=0.004, respectively), an increase observed in both lean and overweight DM2 women. |
| 3811 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 3812 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 3813 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 3814 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 3815 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 3816 | 17952840 | Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. |
| 3817 | 17952840 | Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. |
| 3818 | 17952840 | Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. |
| 3819 | 17952840 | Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. |
| 3820 | 17952840 | Circulating visfatin and TNF-alpha levels did not differ either between the lean and the overweight subgroups of DM2 and control women, while IL-6 plasma levels were significantly higher in both overweight subgroups compared to their lean counterparts. |
| 3821 | 17952840 | In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients. |
| 3822 | 17952840 | In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients. |
| 3823 | 17952840 | In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients. |
| 3824 | 17952840 | In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients. |
| 3825 | 17952840 | In conclusion, visfatin, TNF-alpha, and IL-6 mRNA expressions are increased in peripheral mononuclear-monocytic cells from women with type 2 diabetes, independent of their BMI, which may enhance the effects of their adipose-derived levels and may contribute to the increased insulin resistance and atherogenic risk of these patients. |
| 3826 | 17950103 | The aim of this study was to analyze LPIN1 adipose tissue gene expression levels in 3 clinical insulin-resistant conditions-obesity, type 2 diabetes mellitus, and human immunodeficiency virus (HIV)-associated lipodystrophy-and its relationship with adipogenic and inflammatory markers. |
| 3827 | 17950103 | Real-time polymerase chain reaction was used to measure gene expression of LPIN1 and adipogenic (PPARgamma, SREBP1c) and inflammatory markers (IL6, TNFalpha, TNFR1, and TNFR2). |
| 3828 | 17950103 | LPIN1 messenger RNA levels positively correlated with insulin sensitivity in all subjects. |
| 3829 | 17949947 | The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded to an immunodominant epitope of the human islet protein GAD65, an epitope shared with both GAD65 and GAD67 in the mouse. |
| 3830 | 17949947 | The resulting HLA-DR4/GAD-TcR transgenic mice on a Rag2(o/o)/I-Ab(o/o)/B6 background exhibited a CD4(+) infiltrate into pancreatic islets that correlated with a loss of insulin in infiltrated islets. |
| 3831 | 17949947 | T cells containing the GAD65/67 (555-567) responsive TcR undergo strong negative selection as evidenced by a 10-fold lower thymocyte cellularity compared to non-TcR transgenic mice, and clonotype peripheral T cells represented approximately 1% of CD4(+) T cells in Rag2 sufficient mice. |
| 3832 | 17949947 | Upon in vitro stimulation, GAD65/67 555-567 responsive T cells secrete interferon-gamma, minimal interleukin (IL)-2 and tumor necrosis factor-alpha, and no IL-4, IL-5, IL-10, or IL-17, consistent with a T(H)1 profile. |
| 3833 | 17949947 | These data demonstrate that CD4(+) T cells specific for a naturally processed epitope within GAD can specifically home to pancreatic islets and lead to impaired islet beta-cell function in diabetes-associated HLA-DR4 transgenic mice on the relatively non-autoimmune C57BL/6 background. |
| 3834 | 17947648 | Recruitment and activation of macrophages by pathogenic CD4 T cells in type 1 diabetes: evidence for involvement of CCR8 and CCL1. |
| 3835 | 17947648 | Adoptive transfer of diabetogenic CD4 Th1 T cell clones into young NOD or NOD.scid recipients rapidly induces onset of diabetes and also provides a system for analysis of the pancreatic infiltrate. |
| 3836 | 17947648 | Analysis of infiltrating cells after adoptive transfer by the diabetogenic T cell clone BDC-2.5 indicates that large numbers of cells staining for both F4/80 and CD11b are recruited into the pancreas where they are activated to make IL-1beta, TNF-alpha, and NO, and express the chemokine receptors CCR5, CXCR3, and CCR8. |
| 3837 | 17947648 | Diabetogenic CD4 T cell clones produce several inflammatory chemokines in vitro, but after adoptive transfer we found that the only chemokine that could be detected ex vivo was CCL1. |
| 3838 | 17947648 | These results provide the first evidence that CCR8/CCL1 interaction may play a role in type 1 diabetes through macrophage recruitment and activation. |
| 3839 | 17943458 | Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control. |
| 3840 | 17939209 | Data showed that LOX-1 expression is enhanced by proatherogenic factors relevant to human diabetes, including high glucose, oxLDL, advance glycation end products, and C-reactive protein. |
| 3841 | 17939209 | LOX-1 expression increased also through oxygen species (ROS), endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-alpha), shear stress, activation of protein kinase-C (PKC), angiotensin-II (ANG-II), and through inflammatory pathways. |
| 3842 | 17936398 | Resistin was initially identified as a protein, secreted by adipocytes, which inhibits insulin action and adipose differentiation. |
| 3843 | 17936398 | Resistin was initially identified as a protein, secreted by adipocytes, which inhibits insulin action and adipose differentiation. |
| 3844 | 17936398 | Resistin and RELMalpha are abundantly expressed in adipose, but RELMbeta and RELMgamma are secreted mainly from the gut. |
| 3845 | 17936398 | Resistin and RELMalpha are abundantly expressed in adipose, but RELMbeta and RELMgamma are secreted mainly from the gut. |
| 3846 | 17936398 | Since nutrient composition greatly affects insulin sensitivity, we investigated the regulatory effects of various nutritional factors in food on the expressions of resistin family proteins. |
| 3847 | 17936398 | Since nutrient composition greatly affects insulin sensitivity, we investigated the regulatory effects of various nutritional factors in food on the expressions of resistin family proteins. |
| 3848 | 17936398 | Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. |
| 3849 | 17936398 | Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. |
| 3850 | 17936398 | These results suggest RELMbeta expression to be regulated directly by nutrients such as glucose and saturated free fatty acids including stearic acid, as well as by hormones including insulin and TNFalpha. |
| 3851 | 17936398 | These results suggest RELMbeta expression to be regulated directly by nutrients such as glucose and saturated free fatty acids including stearic acid, as well as by hormones including insulin and TNFalpha. |
| 3852 | 17928988 | Associations between insulin resistance and TNF-alpha in plasma, skeletal muscle and adipose tissue in humans with and without type 2 diabetes. |
| 3853 | 17927013 | Insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), macrophage migration inhibitory factor (MIF) and other pro-inflammatory cytokines and reactive oxygen species (ROS), enhances the synthesis of endothelial nitric oxide (eNO), and anti-inflammatory cytokines interleukins-4 (IL-4) and interleukin-10 (IL-10). |
| 3854 | 17927013 | Insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), macrophage migration inhibitory factor (MIF) and other pro-inflammatory cytokines and reactive oxygen species (ROS), enhances the synthesis of endothelial nitric oxide (eNO), and anti-inflammatory cytokines interleukins-4 (IL-4) and interleukin-10 (IL-10). |
| 3855 | 17927013 | In subjects who are critically ill, monocyte HLA-DR expression was significantly decreased with a concomitant increase in plasma IL-10 and IL-4 concentrations. |
| 3856 | 17927013 | In subjects who are critically ill, monocyte HLA-DR expression was significantly decreased with a concomitant increase in plasma IL-10 and IL-4 concentrations. |
| 3857 | 17927013 | Large increases in the plasma concentrations of TNF-alpha, IL-6, sustained increase in the expression of leukocyte CD11b/CD18, and ROS generation following surgery and infections were found to be associated with increased mortality. |
| 3858 | 17927013 | Large increases in the plasma concentrations of TNF-alpha, IL-6, sustained increase in the expression of leukocyte CD11b/CD18, and ROS generation following surgery and infections were found to be associated with increased mortality. |
| 3859 | 17912155 | In contrast, leptin, tumor necrosis factor a, interleukin-6, monocyte chemoattractant protein-1, and plasminogen activator inhibitor-1 are upregulated in obesity and contribute to the development of diabetes and vascular disease. |
| 3860 | 17909696 | Intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1, beta2-lymphocyte-integrins(+) (CD18(+), CD11a(+), CD11b(+)), ED1/CD68(+) and cytokine (TNF-alpha, interleukin (IL)-1beta)- expressing infiltrates, total collagen content and stainings of collagen I and III were quantified by digital image analysis. |
| 3861 | 17909696 | Intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1, beta2-lymphocyte-integrins(+) (CD18(+), CD11a(+), CD11b(+)), ED1/CD68(+) and cytokine (TNF-alpha, interleukin (IL)-1beta)- expressing infiltrates, total collagen content and stainings of collagen I and III were quantified by digital image analysis. |
| 3862 | 17909696 | TNFalpha-antagonism reduced ICAM-1- and VCAM-1 expression and leukocyte infiltration to levels of non-diabetics and decreased macrophage residence by 3.3-fold compared with untreated diabetics. |
| 3863 | 17909696 | TNFalpha-antagonism reduced ICAM-1- and VCAM-1 expression and leukocyte infiltration to levels of non-diabetics and decreased macrophage residence by 3.3-fold compared with untreated diabetics. |
| 3864 | 17909696 | In addition, anti-TNF-alpha mAb-treatment decreased diabetes-induced cardiac TNF-alpha and IL-1beta expression by 2.0-fold and 1.8- fold, respectively, and reduced the ratio of phosphorylated to total ERK by 2.7-fold. |
| 3865 | 17909696 | In addition, anti-TNF-alpha mAb-treatment decreased diabetes-induced cardiac TNF-alpha and IL-1beta expression by 2.0-fold and 1.8- fold, respectively, and reduced the ratio of phosphorylated to total ERK by 2.7-fold. |
| 3866 | 17909696 | The reduction in intramyocardial inflammation was associated with a 5.4-fold and 3.6-fold reduction in cardiac collagen I and III content, respectively. |
| 3867 | 17909696 | The reduction in intramyocardial inflammation was associated with a 5.4-fold and 3.6-fold reduction in cardiac collagen I and III content, respectively. |
| 3868 | 17906687 | PPAR-gamma receptor activation by TZDs improves insulin sensitivity by promoting fatty acid uptake into adipose tissue, increasing production of adiponectin and reducing levels of inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor-1(PAI-1) and interleukin-6 (IL-6). |
| 3869 | 17906687 | Dual PPAR-alpha/gamma agonists may offer superior treatment of insulin resistance and cardioprotection, but their safety has not yet been assured. |
| 3870 | 17905606 | Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. |
| 3871 | 17905606 | Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. |
| 3872 | 17905606 | The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. |
| 3873 | 17905606 | The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. |
| 3874 | 17890950 | The prothrombotic effect of hyperglycemia was assessed in a separate experiment, showing that collagen/thrombin-induced platelet procoagulant activity was increased in hyperglycemic mice. |
| 3875 | 17890950 | The effect of inflammation was studied by injecting a low dose of endotoxin that caused a systemic inflammatory state after 24 h (increased plasma levels of tumor necrosis factor alpha, interleukin-6 and monocyte chemotactic protein 1 in diabetic and nondiabetic mice) associated with a mild delay in thrombus formation. |
| 3876 | 17884446 | Adiponectin can improve both glucose metabolism and insulin resistance via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. |
| 3877 | 17884446 | Adiponectin can improve both glucose metabolism and insulin resistance via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. |
| 3878 | 17884446 | Adiponectin can improve both glucose metabolism and insulin resistance via the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. |
| 3879 | 17884446 | Activated AMPK phosphorylates a variety of intracellular proteins, including acetyl coenzyme A carboxylase (ACC) that is involved in fatty acid oxidation. |
| 3880 | 17884446 | Activated AMPK phosphorylates a variety of intracellular proteins, including acetyl coenzyme A carboxylase (ACC) that is involved in fatty acid oxidation. |
| 3881 | 17884446 | Activated AMPK phosphorylates a variety of intracellular proteins, including acetyl coenzyme A carboxylase (ACC) that is involved in fatty acid oxidation. |
| 3882 | 17884446 | We also explored whether the levels of AMPK, ACC, and GLUT4 will be altered with the changed adiponectin and its receptors in STZ diabetic rat hearts. |
| 3883 | 17884446 | We also explored whether the levels of AMPK, ACC, and GLUT4 will be altered with the changed adiponectin and its receptors in STZ diabetic rat hearts. |
| 3884 | 17884446 | We also explored whether the levels of AMPK, ACC, and GLUT4 will be altered with the changed adiponectin and its receptors in STZ diabetic rat hearts. |
| 3885 | 17884446 | Plasma and cardiac interleukin 6 and plasma tumor necrosis factor alpha (TNF-alpha) were assayed by enzyme-linked immunosorbent assay. |
| 3886 | 17884446 | Plasma and cardiac interleukin 6 and plasma tumor necrosis factor alpha (TNF-alpha) were assayed by enzyme-linked immunosorbent assay. |
| 3887 | 17884446 | Plasma and cardiac interleukin 6 and plasma tumor necrosis factor alpha (TNF-alpha) were assayed by enzyme-linked immunosorbent assay. |
| 3888 | 17884446 | Cardiac adiponectin receptors, AMPK-alpha, ACC, GLUT4, and TNF-alpha were analyzed by Western blot in control and STZ diabetic rats. |
| 3889 | 17884446 | Cardiac adiponectin receptors, AMPK-alpha, ACC, GLUT4, and TNF-alpha were analyzed by Western blot in control and STZ diabetic rats. |
| 3890 | 17884446 | Cardiac adiponectin receptors, AMPK-alpha, ACC, GLUT4, and TNF-alpha were analyzed by Western blot in control and STZ diabetic rats. |
| 3891 | 17884446 | The plasma adiponectin level was decreased, but the cardiac protein expression of adiponectin receptor 1 was increased in diabetic rats. |
| 3892 | 17884446 | The plasma adiponectin level was decreased, but the cardiac protein expression of adiponectin receptor 1 was increased in diabetic rats. |
| 3893 | 17884446 | The plasma adiponectin level was decreased, but the cardiac protein expression of adiponectin receptor 1 was increased in diabetic rats. |
| 3894 | 17884446 | There was no difference in the cardiac adiponectin level and the cardiac adiponectin receptor 2 protein expression between control and diabetic rats. |
| 3895 | 17884446 | There was no difference in the cardiac adiponectin level and the cardiac adiponectin receptor 2 protein expression between control and diabetic rats. |
| 3896 | 17884446 | There was no difference in the cardiac adiponectin level and the cardiac adiponectin receptor 2 protein expression between control and diabetic rats. |
| 3897 | 17884446 | The phosphorylation of AMPK-alpha and protein expression of GLUT4 were decreased, but the phosphorylation of ACC was unchanged in diabetic rat hearts. |
| 3898 | 17884446 | The phosphorylation of AMPK-alpha and protein expression of GLUT4 were decreased, but the phosphorylation of ACC was unchanged in diabetic rat hearts. |
| 3899 | 17884446 | The phosphorylation of AMPK-alpha and protein expression of GLUT4 were decreased, but the phosphorylation of ACC was unchanged in diabetic rat hearts. |
| 3900 | 17884446 | Plasma and cardiac levels of interleukin 6 and TNF-alpha were increased in diabetic rats. |
| 3901 | 17884446 | Plasma and cardiac levels of interleukin 6 and TNF-alpha were increased in diabetic rats. |
| 3902 | 17884446 | Plasma and cardiac levels of interleukin 6 and TNF-alpha were increased in diabetic rats. |
| 3903 | 17884446 | Despite an increase in cardiac adiponectin receptor 1 expression, there is an increased cardiac inflammatory response and a decreased GLUT4 protein expression associated with a reduction in circulating adiponectin. |
| 3904 | 17884446 | Despite an increase in cardiac adiponectin receptor 1 expression, there is an increased cardiac inflammatory response and a decreased GLUT4 protein expression associated with a reduction in circulating adiponectin. |
| 3905 | 17884446 | Despite an increase in cardiac adiponectin receptor 1 expression, there is an increased cardiac inflammatory response and a decreased GLUT4 protein expression associated with a reduction in circulating adiponectin. |
| 3906 | 17882804 | Fat issue secretes leptin, tumor necrosis factor alpha, resistin, adiponectin, interleukin-6, free fatty acids, visfatin, omentin, perilipin, and other substances that influence the condition of insulinoresistance, one of the main factors responsible for DM2. |
| 3907 | 17882804 | Fat issue secretes leptin, tumor necrosis factor alpha, resistin, adiponectin, interleukin-6, free fatty acids, visfatin, omentin, perilipin, and other substances that influence the condition of insulinoresistance, one of the main factors responsible for DM2. |
| 3908 | 17882804 | The article also cover the participation of other mechanisms - insulin secretion defect, oxidation stress, low secretion of glucagon-like peptide 1, apoptosis, an increased quantity of amyloid and the fl-cell pull in the pancreatic island--in DM2 pathogenesis. |
| 3909 | 17882804 | The article also cover the participation of other mechanisms - insulin secretion defect, oxidation stress, low secretion of glucagon-like peptide 1, apoptosis, an increased quantity of amyloid and the fl-cell pull in the pancreatic island--in DM2 pathogenesis. |
| 3910 | 17882804 | The authors present data on the secretion of leptin, resistin, adiponectin, and tumor necrosis factor a, as well as the condition of the functional activity of beta-cells and the degree of insulinoresistance in 30 DM2 patients receiving dietotherapy. |
| 3911 | 17882804 | The authors present data on the secretion of leptin, resistin, adiponectin, and tumor necrosis factor a, as well as the condition of the functional activity of beta-cells and the degree of insulinoresistance in 30 DM2 patients receiving dietotherapy. |
| 3912 | 17881007 | Changes in pro-inflammatory target genes, such as tumor necrotic factor (TNF)-alpha, intracellular adhesion molecule (ICAM)-1, and vascular endothelial growth factor (VEGF) were assessed by immunoblottings, immunostaining, and ELISA analyses. |
| 3913 | 17869225 | Cyanidin 3-glucoside ameliorates hyperglycemia and insulin sensitivity due to downregulation of retinol binding protein 4 expression in diabetic mice. |
| 3914 | 17869225 | In this study, we have demonstrated that anthocyanin (cyanidin 3-glucoside; C3G) which is a pigment widespread in the plant kingdom, ameliorates hyperglycemia and insulin sensitivity due to the reduction of retinol binding protein 4 (RBP4) expression in type 2 diabetic mice. |
| 3915 | 17869225 | C3G significantly upregulated the glucose transporter 4 (Glut4) and downregulated RBP4 in the white adipose tissue, which is accompanied by downregulation of the inflammatory adipocytokines (monocyte chemoattractant protein-1 and tumor necrosis factor-alpha) in the white adipose tissue of the C3G group. |
| 3916 | 17823503 | Although the majority of mechanisms of beta cell destruction remain unclear, many molecules, including proinflammatory cytokines and chemokines such as tumor necrosis factor alpha and monocyte chemoattractant protein-1, are implicated in the development of beta cell damage. |
| 3917 | 17823503 | Although the majority of mechanisms of beta cell destruction remain unclear, many molecules, including proinflammatory cytokines and chemokines such as tumor necrosis factor alpha and monocyte chemoattractant protein-1, are implicated in the development of beta cell damage. |
| 3918 | 17823503 | Development and progression of renal injuries in patients with diabetic nephropathy are also associated with several growth factors and proinflammatory cytokines, including tumor necrosis factor alpha, insulin-like growth factor-1, monocyte chemoattractant protein-1, vascular endothelial growth factor, and transforming growth factor beta. |
| 3919 | 17823503 | Development and progression of renal injuries in patients with diabetic nephropathy are also associated with several growth factors and proinflammatory cytokines, including tumor necrosis factor alpha, insulin-like growth factor-1, monocyte chemoattractant protein-1, vascular endothelial growth factor, and transforming growth factor beta. |
| 3920 | 17823366 | Adipose cell enlargement leads to a proinflammatory state in the cells with reduced secretion of adiponectin and with increased secretion of several cytokines and chemokines including interleukin (IL)-6, IL-8, and MCP-1. |
| 3921 | 17823366 | In particular tumor necrosis factor (TNF) alpha, but also IL-6, has been shown to induce these effects in preadipocytes and this is associated with an increased Wnt signaling maintaining the cells in an undifferentiated and proinflammatory state. |
| 3922 | 17805239 | After 3 months, the urinary albumin to creatinine ratio was significantly decreased, while the glucose metabolic clearance rate, during insulin clamp, was significantly increased by rosiglitazone compared to the placebo group. |
| 3923 | 17805239 | After 3 months, the urinary albumin to creatinine ratio was significantly decreased, while the glucose metabolic clearance rate, during insulin clamp, was significantly increased by rosiglitazone compared to the placebo group. |
| 3924 | 17805239 | After 3 months, the urinary albumin to creatinine ratio was significantly decreased, while the glucose metabolic clearance rate, during insulin clamp, was significantly increased by rosiglitazone compared to the placebo group. |
| 3925 | 17805239 | Fasting free fatty acid and tumor necrosis factor-alpha (TNF-alpha) levels were significantly decreased, while the adiponectin concentration was significantly increased by rosiglitazone treatment. |
| 3926 | 17805239 | Fasting free fatty acid and tumor necrosis factor-alpha (TNF-alpha) levels were significantly decreased, while the adiponectin concentration was significantly increased by rosiglitazone treatment. |
| 3927 | 17805239 | Fasting free fatty acid and tumor necrosis factor-alpha (TNF-alpha) levels were significantly decreased, while the adiponectin concentration was significantly increased by rosiglitazone treatment. |
| 3928 | 17805239 | The percentage decrease in albuminuria correlated with the decrease in fasting plasma glucose, free fatty acids TNF-alpha and the increase in fat mass, plasma adiponectin, and glucose metabolic clearance rate. |
| 3929 | 17805239 | The percentage decrease in albuminuria correlated with the decrease in fasting plasma glucose, free fatty acids TNF-alpha and the increase in fat mass, plasma adiponectin, and glucose metabolic clearance rate. |
| 3930 | 17805239 | The percentage decrease in albuminuria correlated with the decrease in fasting plasma glucose, free fatty acids TNF-alpha and the increase in fat mass, plasma adiponectin, and glucose metabolic clearance rate. |
| 3931 | 17805239 | Stepwise linear regression analysis showed the decrease in TNF-alpha and the increase in adiponectin were independently associated with decreased albuminuria. |
| 3932 | 17805239 | Stepwise linear regression analysis showed the decrease in TNF-alpha and the increase in adiponectin were independently associated with decreased albuminuria. |
| 3933 | 17805239 | Stepwise linear regression analysis showed the decrease in TNF-alpha and the increase in adiponectin were independently associated with decreased albuminuria. |
| 3934 | 17785827 | The Idd6 locus on mouse chromosome 6, which controls the development of type 1 diabetes in the NOD mouse, affects proliferation rates of T cells and the activity of regulatory CD4+CD25+ T cells. |
| 3935 | 17785827 | This phenotype correlates with a diminished proliferation capacity of both CD4+CD25- effector and CD4+CD25+ regulatory T cells upon in vitro stimulation of the TLR1/TLR2 pathway by the ligand palmitoyl-3-cysteine-serine-lysine 4, and with the constitutive down-regulation of Tnf-alpha and IL-6 in macrophages of Idd6- congenic mice. |
| 3936 | 17785501 | Our objective was to examine NPY's role in AT, specifically addressing NPY protein expression, the effect of NPY on adipokine secretion, and the influence of insulin and rosiglitazone (RSG) on adipocyte-derived NPY in vitro. |
| 3937 | 17785501 | Abdominal subcutaneous (AbSc) adipocytes were isolated and treated with recombinant (rh) NPY, insulin, and RSG. |
| 3938 | 17785501 | Insulin increased NPY secretion (control: 0.22 +/- 0.024 ng/ml; 1 nM insulin: 0.26 +/- 0.05 ng/ml; 100 nM insulin: 0.29 +/- 0.04 ng/ml; 1,000 nM insulin: 0.3 +/- 0.04 ng/ml; P < 0.05, n = 13), but cotreatment of RSG (10 nM) with insulin (100 nM) had no effect on NPY secretion. |
| 3939 | 17785501 | Furthermore, adipocyte treatment with rh-NPY downregulated leptin secretion (control: 6.99 +/- 0.89 ng/ml; 1 nmol/l rh-NPY: 4.4 +/- 0.64 ng/ml; 10 nmol/l rh-NPY: 4.3 +/- 0.61 ng/ml, 100 nmol/l rh-NPY: 4.2 +/- 0.67 ng/ml; P < 0.05, n = 10) but had no effect on adiponectin or TNF-alpha secretion. |
| 3940 | 17785501 | NPY secretion is stimulated by insulin, but this increment was limited by cotreatment with RSG. |
| 3941 | 17785501 | Adipose-derived NPY mediates reduction of leptin secretion and may have implications for central feedback of adiposity signals. |
| 3942 | 17767370 | Effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3943 | 17767370 | Effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3944 | 17767370 | Effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3945 | 17767370 | Effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3946 | 17767370 | Effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3947 | 17767370 | The objective is to assess the effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3948 | 17767370 | The objective is to assess the effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3949 | 17767370 | The objective is to assess the effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3950 | 17767370 | The objective is to assess the effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3951 | 17767370 | The objective is to assess the effect of TNF-alpha inhibition on urinary albumin excretion in experimental diabetic rats. |
| 3952 | 17767370 | Body weight, blood sugar, 24-h urinary TNF-alpha, and 24-h urinary albumin/creatinine ratio (Ualb/Ucr) levels were determined at 1, 4, 8, and 12 weeks after the STZ-injection. |
| 3953 | 17767370 | Body weight, blood sugar, 24-h urinary TNF-alpha, and 24-h urinary albumin/creatinine ratio (Ualb/Ucr) levels were determined at 1, 4, 8, and 12 weeks after the STZ-injection. |
| 3954 | 17767370 | Body weight, blood sugar, 24-h urinary TNF-alpha, and 24-h urinary albumin/creatinine ratio (Ualb/Ucr) levels were determined at 1, 4, 8, and 12 weeks after the STZ-injection. |
| 3955 | 17767370 | Body weight, blood sugar, 24-h urinary TNF-alpha, and 24-h urinary albumin/creatinine ratio (Ualb/Ucr) levels were determined at 1, 4, 8, and 12 weeks after the STZ-injection. |
| 3956 | 17767370 | Body weight, blood sugar, 24-h urinary TNF-alpha, and 24-h urinary albumin/creatinine ratio (Ualb/Ucr) levels were determined at 1, 4, 8, and 12 weeks after the STZ-injection. |
| 3957 | 17767370 | Treatment of rats with STZ caused a significant loss of body weight, as well as polyuria and hyperglycemia within 1 week, while the urinary excretions of albumin and TNF-alpha were increased. |
| 3958 | 17767370 | Treatment of rats with STZ caused a significant loss of body weight, as well as polyuria and hyperglycemia within 1 week, while the urinary excretions of albumin and TNF-alpha were increased. |
| 3959 | 17767370 | Treatment of rats with STZ caused a significant loss of body weight, as well as polyuria and hyperglycemia within 1 week, while the urinary excretions of albumin and TNF-alpha were increased. |
| 3960 | 17767370 | Treatment of rats with STZ caused a significant loss of body weight, as well as polyuria and hyperglycemia within 1 week, while the urinary excretions of albumin and TNF-alpha were increased. |
| 3961 | 17767370 | Treatment of rats with STZ caused a significant loss of body weight, as well as polyuria and hyperglycemia within 1 week, while the urinary excretions of albumin and TNF-alpha were increased. |
| 3962 | 17767370 | Neither infliximab nor FR167653 affected body weight or blood sugar levels, whereas both decreased urinary albumin excretion, together with a modest decrease in the urinary excretion of TNF-alpha. |
| 3963 | 17767370 | Neither infliximab nor FR167653 affected body weight or blood sugar levels, whereas both decreased urinary albumin excretion, together with a modest decrease in the urinary excretion of TNF-alpha. |
| 3964 | 17767370 | Neither infliximab nor FR167653 affected body weight or blood sugar levels, whereas both decreased urinary albumin excretion, together with a modest decrease in the urinary excretion of TNF-alpha. |
| 3965 | 17767370 | Neither infliximab nor FR167653 affected body weight or blood sugar levels, whereas both decreased urinary albumin excretion, together with a modest decrease in the urinary excretion of TNF-alpha. |
| 3966 | 17767370 | Neither infliximab nor FR167653 affected body weight or blood sugar levels, whereas both decreased urinary albumin excretion, together with a modest decrease in the urinary excretion of TNF-alpha. |
| 3967 | 17761768 | TNF-alpha plays an important role in obesity-linked insulin resistance and diabetes mellitus by activating at least two serine kinases capable of promoting negative regulation of key elements of the insulin signaling pathway. |
| 3968 | 17761768 | TNF-alpha plays an important role in obesity-linked insulin resistance and diabetes mellitus by activating at least two serine kinases capable of promoting negative regulation of key elements of the insulin signaling pathway. |
| 3969 | 17761768 | In addition, the clinical outcomes were accompanied by improved insulin signal transduction in muscle, liver, and hypothalamus, as determined by the evaluation of insulin-induced insulin receptor, insulin receptor substrate-1, and receptor substrate-2 tyrosine phosphorylation and Akt and forkhead box protein O1 serine phosphorylation. |
| 3970 | 17761768 | In addition, the clinical outcomes were accompanied by improved insulin signal transduction in muscle, liver, and hypothalamus, as determined by the evaluation of insulin-induced insulin receptor, insulin receptor substrate-1, and receptor substrate-2 tyrosine phosphorylation and Akt and forkhead box protein O1 serine phosphorylation. |
| 3971 | 17761768 | Thus, pharmacological inhibition of TNF-alpha may be an attractive approach to treat severely insulin-resistant patients with type 2 diabetes mellitus. |
| 3972 | 17761768 | Thus, pharmacological inhibition of TNF-alpha may be an attractive approach to treat severely insulin-resistant patients with type 2 diabetes mellitus. |
| 3973 | 17761767 | Palmitate activated the E3 ubiquitin ligases by suppressing insulin receptor substrate-1/Akt signaling in the C2C12 muscle cells, whereas adiponectin attenuated the E3 ubiquitin ligase activation by increasing both insulin receptor substrate-1 tyrosine phosphorylation and Akt Ser473 phosphorylation. |
| 3974 | 17761767 | In related experiments, adiponectin overexpression decreased TNFalpha and IL-6 expression in 3T3-L1 adipocytes, whereas exposure to free fatty acids had the opposite effect. |
| 3975 | 17761767 | We conclude that the balance between free fatty acids and adiponectin impacts muscle proteolysis in insulin-resistant conditions and suggest a role for adipose tissue-muscle cross talk in diabetes and obesity. |
| 3976 | 17726611 | Tumor necrosis factor-alpha (TNF-alpha) inhibitors have been used in the treatment of psoriasis, which is associated with the insulin resistance syndrome. |
| 3977 | 17726611 | Tumor necrosis factor-alpha (TNF-alpha) inhibitors have been used in the treatment of psoriasis, which is associated with the insulin resistance syndrome. |
| 3978 | 17726611 | The purpose of this study was to determine the effect of etanercept, a TNF-alpha inhibitor, on insulin secretion and insulin sensitivity in psoriatic patients with high risk factors to develop type 2 diabetes mellitus. |
| 3979 | 17726611 | The purpose of this study was to determine the effect of etanercept, a TNF-alpha inhibitor, on insulin secretion and insulin sensitivity in psoriatic patients with high risk factors to develop type 2 diabetes mellitus. |
| 3980 | 17725706 | Factors such as tumour necrosis factor-alpha (TNF-alpha) and adiponectin, released from adipose tissue, can also modulate insulin resistance. |
| 3981 | 17725706 | Recent study results suggest that peroxisome proliferator-activated receptor (PPAR)gamma agonists have an effect on the development of Type 2 diabetes. |
| 3982 | 17725275 | [Interleukin-12, vascular endothelial growth factor and tumor necrosis factor-alpha in the process of neoangiogenesis of diabetic retinopathy in children]. |
| 3983 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3984 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3985 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3986 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3987 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3988 | 17725274 | [The assessment of the correlation between vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-alpha), interleukin 6 (IL-6), glycaemic control (HbA1c) and the development of the diabetic retinopathy in children with diabetes mellitus type 1]. |
| 3989 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3990 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3991 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3992 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3993 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3994 | 17725274 | The aim of the work is to assess the correlation between HbA1c, VEGF, TNF-alpha, IL-6 and the development of diabetic retinopathy in children diagnosed with diabetes mellitus type 1. |
| 3995 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 3996 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 3997 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 3998 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 3999 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 4000 | 17725274 | All the examined children had VEGF, TNF-alpha and IL-6 measured in the blood serum using highly sensitive ELISA tests. |
| 4001 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4002 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4003 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4004 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4005 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4006 | 17725274 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the group 1 in comparison with the group 2. |
| 4007 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4008 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4009 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4010 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4011 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4012 | 17725274 | Children of the group 2 in relation to healthy controls showed statistically significant higher blood serum levels of VEGF, TNF-alpha and IL-6. |
| 4013 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4014 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4015 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4016 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4017 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4018 | 17725274 | Elevated levels of VEGF, TNF-alpha, IL-6, HbA1c in blood serum of children with diabetes mellitus type 1 detected before development of overt signs of diabetic retinopathy might indicate the possibility of the occurrence of changes in the eye shortly. |
| 4019 | 17716860 | Our data indicate that NOD derived FTOC produce a smaller percentage of double negative (CD4(-)/CD8(-)) thymocytes expressing TNF receptors compared to non-diabetic C57BL/6 (B6) derived FTOC. |
| 4020 | 17716860 | Our data indicate that NOD derived FTOC produce a smaller percentage of double negative (CD4(-)/CD8(-)) thymocytes expressing TNF receptors compared to non-diabetic C57BL/6 (B6) derived FTOC. |
| 4021 | 17716860 | Neutralization of this endogenous TNF-alpha production in NOD derived FTOC with soluble TNF receptor (sTNF R1) rescued insulin production in our in vitro T1DM model. |
| 4022 | 17716860 | Neutralization of this endogenous TNF-alpha production in NOD derived FTOC with soluble TNF receptor (sTNF R1) rescued insulin production in our in vitro T1DM model. |
| 4023 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4024 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4025 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4026 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4027 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4028 | 17716775 | The role of vascular endothelial growth factor, tumor necrosis factor alpha and interleukin-6 in pathogenesis of diabetic retinopathy. |
| 4029 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4030 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4031 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4032 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4033 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4034 | 17716775 | The aim of the study was to analyze the relation between early diabetic retinopathy and the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) in children with diabetes mellitus type 1. |
| 4035 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4036 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4037 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4038 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4039 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4040 | 17716775 | All the children had 24h urine albumin secretion rate, glycosylated hemoglobin HbA1c level, and C-reactive protein level measured, underwent 24h blood pressure monitoring and had ophthalmologic examination performed. |
| 4041 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4042 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4043 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4044 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4045 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4046 | 17716775 | Additionally, all the children had serum TNF-alpha, IL-6 and VEGF level measured using an ELISA test (Quantikine High Sensitivity Human). |
| 4047 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4048 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4049 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4050 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4051 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4052 | 17716775 | Statistically significant higher blood serum levels of HbA1c, VEGF, TNF-alpha and IL-6 were found in the Group 1 in comparison with the Group 2. |
| 4053 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4054 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4055 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4056 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4057 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4058 | 17716775 | Additionally, the children of the Group 1 showed statistically significant correlation between serum VEGF and serum TNF-alpha (R=0.35, p=0.000), CRP level (R=0.23, p=0.006), 24h albumin urine secretion rate (R=0.45, p=0.000) and duration of the disease (R=0.26, p=0.002). |
| 4059 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4060 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4061 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4062 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4063 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4064 | 17716775 | The results of the current study suggest that there is a relationship between VEGF, TNF-alpha, IL-6 and the development of the diabetic retinopathy in children with diabetes mellitus type 1. |
| 4065 | 17715888 | Leptin and tumor necrosis factor (TNFalpha) mRNA expression in WAT were significantly down-regulated by 0.2% fucoxanthin. |
| 4066 | 17715888 | Leptin and tumor necrosis factor (TNFalpha) mRNA expression in WAT were significantly down-regulated by 0.2% fucoxanthin. |
| 4067 | 17715888 | These results suggest that dietary fucoxanthin decreases the blood glucose and plasma insulin concentration of KK- A(y) along with down-regulating TNFalpha mRNA. |
| 4068 | 17715888 | These results suggest that dietary fucoxanthin decreases the blood glucose and plasma insulin concentration of KK- A(y) along with down-regulating TNFalpha mRNA. |
| 4069 | 17712725 | Therefore, expression of fatty acid amide hydrolase (FAAH), cannabinoid receptor 1 (Cb1), adiponectin, and tumor necrosis factor (TNF)-alpha was compared in visceral adipose tissue from 10 normal-weight (BMI 24.4+/-1.1 kg/m2) and 11 obese subjects (BMI 37.6+/-13.6 kg/m2) using quantitative RT-PCR, and gene expression changes were analyzed after in vitro stimulation of visceral adipose tissue with TNF-alpha. |
| 4070 | 17712725 | The data demonstrate that the ECS is activated in obese visceral adipose tissue as shown by decreased FAAH, Cb1, and adiponectin expression. |
| 4071 | 17708341 | The expression of IL-1beta, TNF-alpha, IFN-gamma, IL-6, IL-10, and IL-4 genes was determined by real-time PCR in freshly isolated islets, in 24-h cultured islets and in islet grafts on days 1, 3, and 7 after transplantation. |
| 4072 | 17708341 | IL-6 and IL-10 were not detected in freshly isolated islets, but their expression was clearly enhanced in 24-h cultured islets and islet grafts. |
| 4073 | 17708341 | IFN-gamma mRNA was barely detected in a few grafts, and IL-4 mRNA was never detected. |
| 4074 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 4075 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 4076 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 4077 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 4078 | 17707941 | Studies indicate that both CD4(+) and CD8(+) T lymphocytes and their cytokines play a critical role in different clinical stages of type 1 diabetes (T1D). |
| 4079 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 4080 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 4081 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 4082 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 4083 | 17707941 | Intracytoplasmic interleukin (IL)-2, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels of isolated CD4(+) and CD8(+) T cells, and neutrophil functions were determined by flow cytometry. |
| 4084 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 4085 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 4086 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 4087 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 4088 | 17707941 | Intracellular TNF-alpha level of CD4(+) T lymphocytes was significantly decreased in Group 1 compared to Group 2 and healthy subjects. |
| 4089 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 4090 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 4091 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 4092 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 4093 | 17707941 | In contrast, TNF-alpha in CD8(+) T lymphocytes was higher in Group 1 compared to Group 2. |
| 4094 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 4095 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 4096 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 4097 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 4098 | 17707941 | Increased TNF-alpha content of CD8(+) T lymphocytes was also obtained in Groups 1 and 2 compared to healthy subjects. |
| 4099 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 4100 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 4101 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 4102 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 4103 | 17707941 | Increased TNF-alpha secretion of CD8(+) T cells might reflect the role of CD8(+) T cells in beta cell destruction. |
| 4104 | 17705672 | Adiponectin and resistin gene polymorphisms in patients with anorexia nervosa and obesity and its influence on metabolic phenotype. |
| 4105 | 17705672 | Genes for adiponectin and resistin are candidate genes of insulin resistance and type 2 diabetes mellitus. |
| 4106 | 17705672 | The aim of our study was to determine the frequency of single nucleotide polymorphisms (SNP) 45T>G and 276G>T of the adiponectin gene and 62G>A and -180C>G of the resistin gene in patients with obesity (OB), anorexia nervosa (AN) and in control healthy normal-weight women (NW) and to study the influence of particular genotypes on serum concentrations of these hormones and on insulin sensitivity. |
| 4107 | 17705672 | Serum adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), insulin, cholesterol, glycated hemoglobin (HbA1c) and blood glucose levels were measured in 77 patients with OB, 28 with AN and 38 NW. |
| 4108 | 17705672 | We conclude that polymorphisms in adiponectin and resistin genes can contribute to metabolic phenotype of patients with obesity and anorexia nervosa. |
| 4109 | 17699218 | Statin treatment and diabetes affect myeloperoxidase activity in maintenance hemodialysis patients. |
| 4110 | 17699218 | In a cross-sectional evaluation of 115 prevalent (vintage 25 mo) HD patients (62 men; 63 +/- 1 yr), data on comorbidity (Davies score), diabetes, medication (statins and antihypertensive drugs), nutritional status (subjective global assessment), blood lipids (cholesterol, HDL cholesterol, and triglycerides), inflammatory biomarkers (serum albumin, C-reactive protein, TNF-alpha, and IL-6), oxidative stress biomarkers (pentosidine, 8-hydroxydeoxyguanosine, and MPO activity) were recorded. |
| 4111 | 17699218 | Patients with MPO activity greater than the median had significantly (P < 0.05) lower serum albumin levels (33.2 +/- 0.7 versus 35.0 +/- 0.5 g/L), higher 8-hydroxydeoxyguanosine levels (1.26 +/- 0.08 versus 1.05 +/- 0.06 ng/ml), and a lower prevalence of statin treatment (18 versus 36%). |
| 4112 | 17699218 | Therefore, the median MPO activity was significantly (P < 0.05) lower (17.7 versus 26.6 deltaOD630/min per mg protein) in the subgroup of 31 HD patients with ongoing statin treatment. |
| 4113 | 17699218 | In a multiple regression model, correction for the impact of age, gender, vintage, serum cholesterol, serum albumin, comorbidity, diabetes, and statin use, only diabetes (P < 0.01) and statin use (P < 0.01) were significantly associated to MPO activity. |
| 4114 | 17699218 | Fourteen patients who had diabetes and were receiving statin treatment had markedly (P = 0.001) lower median (19.9 versus 41.2 deltaOD630/min per mg protein) MPO activity compared with 18 who had diabetes and were not taking statins. |
| 4115 | 17699218 | This cross-sectional study suggests that both diabetes and statin treatment affect MPO activity in prevalent HD patients. |
| 4116 | 17702846 | We have used U937 cells stably transfected to express luciferase under the control of NF-kappaB to examine if adiponectin may modulate NF-kappaB activity. |
| 4117 | 17702846 | We have used U937 cells stably transfected to express luciferase under the control of NF-kappaB to examine if adiponectin may modulate NF-kappaB activity. |
| 4118 | 17702846 | Physiological concentrations of native adiponectin induced NF-kappaB activity. |
| 4119 | 17702846 | Physiological concentrations of native adiponectin induced NF-kappaB activity. |
| 4120 | 17702846 | This effect was relatively strong compared with proinflammatory adipokines like leptin, resistin, and IL-6. |
| 4121 | 17702846 | This effect was relatively strong compared with proinflammatory adipokines like leptin, resistin, and IL-6. |
| 4122 | 17702846 | The enhanced NF-kappaB activity was attributed to the high molecular weight adiponectin isoforms. |
| 4123 | 17702846 | The enhanced NF-kappaB activity was attributed to the high molecular weight adiponectin isoforms. |
| 4124 | 17702846 | NF-kappaB was not activated by mutated adiponectin that is unable to form high molecular weight complexes. |
| 4125 | 17702846 | NF-kappaB was not activated by mutated adiponectin that is unable to form high molecular weight complexes. |
| 4126 | 17702846 | Furthermore, the C-terminal fragment, globular adiponectin, markedly increased NF-kappaB reporter activity, cytokine release, and mRNA expression of inflammation marker genes, at higher levels than stimulation with TNF-alpha and lipopolysaccharide. |
| 4127 | 17702846 | Furthermore, the C-terminal fragment, globular adiponectin, markedly increased NF-kappaB reporter activity, cytokine release, and mRNA expression of inflammation marker genes, at higher levels than stimulation with TNF-alpha and lipopolysaccharide. |
| 4128 | 17702846 | NF-kappaB activation by globular adiponectin was not affected by antibody inhibition of toll-like receptor 4 or TNF receptors 1 and 2 but was attenuated by inhibitors of p38 MAPK, phosphatidylinositol 3-kinase, and protein kinase C. |
| 4129 | 17702846 | NF-kappaB activation by globular adiponectin was not affected by antibody inhibition of toll-like receptor 4 or TNF receptors 1 and 2 but was attenuated by inhibitors of p38 MAPK, phosphatidylinositol 3-kinase, and protein kinase C. |
| 4130 | 17702846 | Analyses of the p65 subunit of NF-kappaB in different leukocyte cell lines showed activation of two monocytic cell lines (U937 and THP-1) by native and globular adiponectin. |
| 4131 | 17702846 | Analyses of the p65 subunit of NF-kappaB in different leukocyte cell lines showed activation of two monocytic cell lines (U937 and THP-1) by native and globular adiponectin. |
| 4132 | 17679816 | That adipose tissue releases a wide range of adipokines, growth factors, enzymes, and enzyme substrates linked to vascular injury provides a plausible explanation for the role of fat in vascular disease: tumor necrosis factor-alpha, leptin, resistin, interleukin-1, -6, -8, and -18, serum amyloid A, monocyte chemoattractant protein I, macrophage inhibitory factor, aortic carboxypeptidase, hepa-rin-binding epidermal growth factor-like growth factor, vascular endothelial growth factor, transforming growth factor beta, angiotensinogen, cathepsin S, estradiol, cortisol, mineralocorticoid releasing factor, and calcitonin peptides are probable fat-derived prothrombotic, proinflammatory, and proatherosclerotic agents acting in a paracrine and/or endocrine manner. |
| 4133 | 17679816 | Other adipocyte products such as adiponectin, transforming growth factor beta, and interleukin-10 exert some antiatherogenic effects. |
| 4134 | 17678725 | To determine the contribution of the tumor necrosis factor alpha gene (TNFA) to the immunogenetic risk prediction of type 1 diabetes (T1D) in the Belgian population, well-characterized antibody-positive patients with type 1 diabetes (T1D), nondiabetic control subjects, and nuclear families were analyzed for HLA-DQA1-DQB1, TNFA -308 G/A promoter single nucleotide polymorphism (SNP) and TNFa microsatellite markers in both case-control and transmission studies. |
| 4135 | 17670746 | Methylglyoxal modification of mSin3A results in increased recruitment of O-GlcNAc-transferase, with consequent increased modification of Sp3 by O-linked N-acetylglucosamine. |
| 4136 | 17670746 | This modification of Sp3 causes decreased binding to a glucose-responsive GC-box in the angiopoietin-2 (Ang-2) promoter, resulting in increased Ang-2 expression. |
| 4137 | 17670746 | Increased Ang-2 expression induced by high glucose increased expression of intracellular adhesion molecule 1 and vascular cell adhesion molecule 1 in cells and in kidneys from diabetic mice and sensitized microvascular endothelial cells to the proinflammatory effects of tumor necrosis factor alpha. |
| 4138 | 17669395 | NAD(P)H activity, protein expression nuclear factor-kappaBp65 (NF-kappaBp65) and phosphorylation of the extracellular signal-regulated kinase (ERK1/2) were assessed in the quadriceps muscle. |
| 4139 | 17669395 | Protein and mRNA levels of intracellular and vascular adhesion molecules (ICAM-1, VCAM-1) and cytokines were measured by Taqman or immunohistochemistry staining, respectively. |
| 4140 | 17669395 | Low-dose therapy by atorvastatin did not alter the lipid profile but led to a reduction of NAD(P)H activity (-28%, P<0.05) associated with reduced protein expression of NF-kappaBp65 (-53%, P<0.05) and phosphorylation of its regulator mitogen-activated protein kinase (MAPK) ERK1/2 in diabetic rats. |
| 4141 | 17669395 | Also inflammatory markers were reduced after atorvastatin treatment indexed by reduced mRNA expression of VCAM-1 (-24%), tumor necrosis factor alpha (-59%) and interleukin 1beta (-50%) and reduced ICAM-1 (-81%) and VCAM-1 (-74%) positive staining. |
| 4142 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4143 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4144 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4145 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4146 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4147 | 17664271 | Tumor necrosis factor receptor-1 can function through a G alpha q/11-beta-arrestin-1 signaling complex. |
| 4148 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4149 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4150 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4151 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4152 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4153 | 17664271 | It is well known that chronic TNFalpha exposure can lead to insulin resistance both in vitro and in vivo and that elevated blood levels of TNFalpha are observed in obese and/or diabetic individuals. |
| 4154 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4155 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4156 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4157 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4158 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4159 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 4160 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4161 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4162 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4163 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4164 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4165 | 17664271 | Small interfering RNA-mediated knockdown of beta-arrestin-1 inhibits TNFalpha-induced tyrosine phosphorylation of G alpha(q/11) by interruption of Src kinase activation. |
| 4166 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4167 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4168 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4169 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4170 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4171 | 17664271 | TNFalpha stimulates lipolysis in 3T3-L1 adipocytes, and beta-arrestin-1 knockdown blocks the effects of TNFalpha to stimulate ERK activation and glycerol release. |
| 4172 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4173 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4174 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4175 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4176 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4177 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 4178 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4179 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4180 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4181 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4182 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4183 | 17664271 | Taken together these results reveal novel elements of TNFalpha action; 1) the trimeric G-protein component G alpha(q/11) and the adapter protein beta-arrestin-1 can function as signaling molecules in the TNFalpha action cascade; 2) beta-arrestin-1 can couple TNFalpha stimulation to ERK activation and lipolysis; 3) beta-arrestin-1 and G alpha(q/11) can mediate TNFalpha-induced phosphatidylinositol 3-kinase activation and inflammatory gene expression. |
| 4184 | 17661007 | Regulation of retinol binding protein 4 production in primary human adipocytes by adiponectin, troglitazone and TNF-alpha. |
| 4185 | 17659259 | The contribution of nutrient overload and associated inflammation to insulin resistance has highlighted several therapeutic targets including c-Jun N-terminal kinase (JNK) and S6 kinase (S6K). |
| 4186 | 17659259 | Administration of 0.06-4 mg/kg LPS to C57BL/6 mice stimulated increases in plasma levels of TNFalpha, IL-12p40, IL-6 and MCP-1 and in JNK activity as measured by phosphorylated c-Jun in fat. |
| 4187 | 17659259 | For the first time, we show that LPS induces S6K activity by up to 6.1-fold, as measured by the phosphorylation of S6 ribosomal protein in liver, and increases by up to 1.8-fold, plasma levels of the novel pro-inflammatory cytokine osteopontin which is implicated in the pathogenesis of insulin resistance. |
| 4188 | 17642242 | For evaluation of treatment with TNF inhibitors, RA patients should be determined for the ACR core set of measures, including tender joint count, swollen joint count, pain score, patient global assessment, physician global assessment, patient-reported functional disability, and acute phase reactants (ESR and CRP), and more practically for the 28-joint Disease Activity Score (DAS28) within the first 3-6 months, and the efficacy could be assessed using the ACR preliminary criteria and the EULAR criteria. |
| 4189 | 17642242 | For evaluation of treatment with TNF inhibitors, RA patients should be determined for the ACR core set of measures, including tender joint count, swollen joint count, pain score, patient global assessment, physician global assessment, patient-reported functional disability, and acute phase reactants (ESR and CRP), and more practically for the 28-joint Disease Activity Score (DAS28) within the first 3-6 months, and the efficacy could be assessed using the ACR preliminary criteria and the EULAR criteria. |
| 4190 | 17642242 | Post-marketing surveillance of INF and ETA in Japan indicated that the most serious adverse effects were bacterial pneumonia, pneumocytosis, and interstitial pneumonia, as well as tuberculosis. |
| 4191 | 17642242 | Post-marketing surveillance of INF and ETA in Japan indicated that the most serious adverse effects were bacterial pneumonia, pneumocytosis, and interstitial pneumonia, as well as tuberculosis. |
| 4192 | 17642242 | So far no clinical predictors of response to TNF inhibitors have been identified, but genetic variation in the HLA-DRB1 and the LTA-TNF regions was shown to influence the response. |
| 4193 | 17642242 | So far no clinical predictors of response to TNF inhibitors have been identified, but genetic variation in the HLA-DRB1 and the LTA-TNF regions was shown to influence the response. |
| 4194 | 17641733 | Levels of TNF-alpha, IL-6, and IL-12 in serum were measured by ELISA tests (Quantikine High Sensitivity Human by R&D Systems, Minneapolis, Minn, USA). |
| 4195 | 17641733 | Levels of TNF-alpha, IL-6, and IL-12 in serum were measured by ELISA tests (Quantikine High Sensitivity Human by R&D Systems, Minneapolis, Minn, USA). |
| 4196 | 17641733 | The NPDR children demonstrated a significantly longer duration of the disease in addition to higher HbA1c, albumin excretion rate, C-reactive protein, systolic blood pressure, as well as TNF-alpha and IL-6 levels than those without retinopathy. |
| 4197 | 17641733 | The NPDR children demonstrated a significantly longer duration of the disease in addition to higher HbA1c, albumin excretion rate, C-reactive protein, systolic blood pressure, as well as TNF-alpha and IL-6 levels than those without retinopathy. |
| 4198 | 17618956 | The patients with metabolic syndrome had significantly higher levels of waist circumference, insulin, insulin resistance index of homeostasis model assessment, systolic and diastolic blood pressures, and serum triglycerides, and lower concentrations of adiponectin. |
| 4199 | 17618956 | However, there was no significant difference in age, sex, glycosylated hemoglobin (hemoglobin A1c), fasting glucose, leptin, and tumor necrosis factor system activities including tumor necrosis factor alpha between the 2 groups. |
| 4200 | 17614271 | After 12 weeks, weight, body mass index, waist circumference, hip circumference, waist-to-hip ratio, total body fat, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-alpha), IL-6, resistin and leptin had significantly decreased, while adiponectin and IL-10 had significantly increased. |
| 4201 | 17614271 | After 12 weeks, weight, body mass index, waist circumference, hip circumference, waist-to-hip ratio, total body fat, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-alpha), IL-6, resistin and leptin had significantly decreased, while adiponectin and IL-10 had significantly increased. |
| 4202 | 17614271 | A bivariate correlation analysis found that increment in IL-10 and baseline IL-10 levels significantly correlated with decrement in TNF-alpha (P<.01) and baseline adiponectin (r=.52, P<.001), respectively. |
| 4203 | 17614271 | A bivariate correlation analysis found that increment in IL-10 and baseline IL-10 levels significantly correlated with decrement in TNF-alpha (P<.01) and baseline adiponectin (r=.52, P<.001), respectively. |
| 4204 | 17611256 | It results in insulin deficiency as a consequence of autoimmune destruction of islet beta-cells in the pancreas and is believed to be mediated by Th1 cytokines (IFNgamma, TNFalpha, and IL-2). |
| 4205 | 17611256 | It results in insulin deficiency as a consequence of autoimmune destruction of islet beta-cells in the pancreas and is believed to be mediated by Th1 cytokines (IFNgamma, TNFalpha, and IL-2). |
| 4206 | 17611256 | It results in insulin deficiency as a consequence of autoimmune destruction of islet beta-cells in the pancreas and is believed to be mediated by Th1 cytokines (IFNgamma, TNFalpha, and IL-2). |
| 4207 | 17611256 | A number of genes have been associated with type 1 diabetes in humans, including the human leukocyte antigen region, the insulin variable number tandem repeat, PTPN22, CTLA4, IL-4, and IL-13. |
| 4208 | 17611256 | A number of genes have been associated with type 1 diabetes in humans, including the human leukocyte antigen region, the insulin variable number tandem repeat, PTPN22, CTLA4, IL-4, and IL-13. |
| 4209 | 17611256 | A number of genes have been associated with type 1 diabetes in humans, including the human leukocyte antigen region, the insulin variable number tandem repeat, PTPN22, CTLA4, IL-4, and IL-13. |
| 4210 | 17611256 | In this study, 483 cases of canine diabetes and 869 controls of known breed were analyzed for association with IFNgamma, IGF2, IL-10, IL-12beta, IL-6, insulin, PTPN22, RANTES, IL-4, IL-1alpha and TNFalpha. |
| 4211 | 17611256 | In this study, 483 cases of canine diabetes and 869 controls of known breed were analyzed for association with IFNgamma, IGF2, IL-10, IL-12beta, IL-6, insulin, PTPN22, RANTES, IL-4, IL-1alpha and TNFalpha. |
| 4212 | 17611256 | In this study, 483 cases of canine diabetes and 869 controls of known breed were analyzed for association with IFNgamma, IGF2, IL-10, IL-12beta, IL-6, insulin, PTPN22, RANTES, IL-4, IL-1alpha and TNFalpha. |
| 4213 | 17611256 | Some associations were with increased susceptibility to the disease (IFNgamma, IL-10, IL-12beta, IL-6, insulin, PTPN22, IL-4, and TNFalpha), whereas others were protective (IL-4, PTPN22, IL-6, insulin, IGF2, TNFalpha). |
| 4214 | 17611256 | Some associations were with increased susceptibility to the disease (IFNgamma, IL-10, IL-12beta, IL-6, insulin, PTPN22, IL-4, and TNFalpha), whereas others were protective (IL-4, PTPN22, IL-6, insulin, IGF2, TNFalpha). |
| 4215 | 17611256 | Some associations were with increased susceptibility to the disease (IFNgamma, IL-10, IL-12beta, IL-6, insulin, PTPN22, IL-4, and TNFalpha), whereas others were protective (IL-4, PTPN22, IL-6, insulin, IGF2, TNFalpha). |
| 4216 | 17594598 | To elucidate the impact of immunological factors in development of these neuropathies the expression of some cytokines in serum was studied: tumour necrosis factor a (TNF-a), monocyte chemotactic protein-1 (MCP-1) and growth-regulated oncogene alpha (GRO-alpha; CXCL1). 29 patients with type 2 diabetes, 31 with chronic alcohol abuse and 20 healthy controls were included in the study. |
| 4217 | 17584970 | Aldose reductase-regulated tumor necrosis factor-alpha production is essential for high glucose-induced vascular smooth muscle cell growth. |
| 4218 | 17584970 | Aldose reductase-regulated tumor necrosis factor-alpha production is essential for high glucose-induced vascular smooth muscle cell growth. |
| 4219 | 17584970 | Aldose reductase-regulated tumor necrosis factor-alpha production is essential for high glucose-induced vascular smooth muscle cell growth. |
| 4220 | 17584970 | High glucose (HG)-induced TNF-alpha release was specifically inhibited by protein kinase C (PKC)-delta inhibitor (Rottlerin; EMD Biosciences, San Diego, CA), but not PKC-beta2 inhibitor (CGP53353; Tocris Cookson Inc., Ellisville, MO), indicating the possible involvement of PKC-delta in HG signaling. |
| 4221 | 17584970 | High glucose (HG)-induced TNF-alpha release was specifically inhibited by protein kinase C (PKC)-delta inhibitor (Rottlerin; EMD Biosciences, San Diego, CA), but not PKC-beta2 inhibitor (CGP53353; Tocris Cookson Inc., Ellisville, MO), indicating the possible involvement of PKC-delta in HG signaling. |
| 4222 | 17584970 | High glucose (HG)-induced TNF-alpha release was specifically inhibited by protein kinase C (PKC)-delta inhibitor (Rottlerin; EMD Biosciences, San Diego, CA), but not PKC-beta2 inhibitor (CGP53353; Tocris Cookson Inc., Ellisville, MO), indicating the possible involvement of PKC-delta in HG signaling. |
| 4223 | 17584970 | TNF-alpha secretion was also prevented by pretreating cells with aldose reductase (AR) inhibitors, sorbinil or tolrestat and in cells treated with antisense AR mRNA. |
| 4224 | 17584970 | TNF-alpha secretion was also prevented by pretreating cells with aldose reductase (AR) inhibitors, sorbinil or tolrestat and in cells treated with antisense AR mRNA. |
| 4225 | 17584970 | TNF-alpha secretion was also prevented by pretreating cells with aldose reductase (AR) inhibitors, sorbinil or tolrestat and in cells treated with antisense AR mRNA. |
| 4226 | 17579087 | Suppression of pleckstrin expression with RNA interference silencing revealed that phosphorylation of pleckstrin is an important intermediate in the secretion and activation pathways of proinflammatory cytokines (TNF-alpha and IL-1beta) induced by RAGE activation. |
| 4227 | 17578890 | SAT probe effluents were analyzed for IL-1beta, IL-6, CXCL8 (IL-8), and TNF-alpha. |
| 4228 | 17578890 | Local administration of insulin exerted a stimulatory effect on the inflammatory response of IL-6. |
| 4229 | 17572841 | Adipose tissue, which classically has been considered as an energy-storing organ, is now viewed as a massive source of bioactive substances such as leptin, tumor necrosis factor (TNF)-alpha, and adiponectin. |
| 4230 | 17572841 | In addition, adiponectin was inversely related to cardiovascular risk factors, such as insulin resistance, blood pressure, and low-density lipoprotein (LDL) cholesterol and triglyceride levels, and was positively related to high-density lipoprotein (HDL) cholesterol levels. |
| 4231 | 17569223 | Curcumin inhibits these autoimmune diseases by regulating inflammatory cytokines such as IL-1beta, IL-6, IL-12, TNF-alpha and IFN-gamma and associated JAK-STAT, AP-1, and NF-kappaB signaling pathways in immune cells. |
| 4232 | 17569205 | Curcumin exhibits activities similar to recently discovered tumor necrosis factor blockers (e.g., HUMIRA, REMICADE, and ENBREL), a vascular endothelial cell growth factor blocker (e.g., AVASTIN), human epidermal growth factor receptor blockers (e.g., ERBITUX, ERLOTINIB, and GEFTINIB), and a HER2 blocker (e.g., HERCEPTIN). |
| 4233 | 17558713 | The HLA-DQ2, HLA-DR3(17), RAGE -429C allele, the mono-S-C4B genotype, the HSP70-2 1267G allele and the TNF -308A (TNF2) allele were used as markers of the AH8.1. |
| 4234 | 17558713 | The HLA-DQ2, HLA-DR3(17), RAGE -429C allele, the mono-S-C4B genotype, the HSP70-2 1267G allele and the TNF -308A (TNF2) allele were used as markers of the AH8.1. |
| 4235 | 17558713 | In both populations, 29%, 50-59%, 52-56% and 76-96%, respectively of the carriers of HSP70-2 1267G, RAGE-429C, TNF2, and mono-S carriers carried the whole 8.1 haplotype. |
| 4236 | 17558713 | In both populations, 29%, 50-59%, 52-56% and 76-96%, respectively of the carriers of HSP70-2 1267G, RAGE-429C, TNF2, and mono-S carriers carried the whole 8.1 haplotype. |
| 4237 | 17553629 | Elevated butyrylcholinesterase and acetylcholinesterase may predict the development of type 2 diabetes mellitus and Alzheimer's disease. |
| 4238 | 17553629 | Plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and lipid peroxides are elevated and concentrations of endothelial nitric oxide (eNO) decreased in type 2 diabetes mellitus and Alzheimer's disease. |
| 4239 | 17553629 | Recent studies revealed that plasma and tissue concentrations of enzymes butyrylcholinesterase and acetylcholinesterase are elevated in type 2 diabetes and Alzheimer's disease. |
| 4240 | 17553629 | Hence, elevated butyrylcholinesterase and acetylcholinesterase concentrations will lead to a decrease in the levels of acetylcholine that could trigger the onset of low-grade systemic inflammation seen in type 2 diabetes and Alzheimer's disease. |
| 4241 | 17553629 | In view of this, we propose that butyrylcholinesterase and acetylcholinesterase will not only serve as therapeutic targets but also may serve as markers to predict the development of type 2 diabetes mellitus and Alzheimer's disease. |
| 4242 | 17542672 | The aim of this review is to summarize our current knowledge on the role of basic peptides of adipose tissue, such as adiponectin, interleukin-6, tumor necrosis factor-alpha, and resistin, in states of altered thyroid function. |
| 4243 | 17533199 | NADPH oxidase contributes to vascular inflammation, insulin resistance, and remodeling in the transgenic (mRen2) rat. |
| 4244 | 17533199 | NADPH oxidase contributes to vascular inflammation, insulin resistance, and remodeling in the transgenic (mRen2) rat. |
| 4245 | 17533199 | Angiotensin II, acting through its angiotensin type 1 receptor, inhibits the actions of insulin in the vasculature which may lead to deleterious effects such as vascular inflammation, remodeling, endothelial dysfunction, and insulin resistance. |
| 4246 | 17533199 | Angiotensin II, acting through its angiotensin type 1 receptor, inhibits the actions of insulin in the vasculature which may lead to deleterious effects such as vascular inflammation, remodeling, endothelial dysfunction, and insulin resistance. |
| 4247 | 17533199 | To explore the impact of angiotensin II on insulin signaling, NADPH oxidase-derived reactive oxygen species formation, vascular inflammation, apoptosis, and remodeling, we used transgenic TG(mRen2)27 (Ren2) rats, which harbor the mouse renin transgene and exhibits elevated tissue angiotensin II levels. |
| 4248 | 17533199 | To explore the impact of angiotensin II on insulin signaling, NADPH oxidase-derived reactive oxygen species formation, vascular inflammation, apoptosis, and remodeling, we used transgenic TG(mRen2)27 (Ren2) rats, which harbor the mouse renin transgene and exhibits elevated tissue angiotensin II levels. |
| 4249 | 17533199 | Compared with Sprague-Dawley controls, Ren2 aortas exhibited greater NADPH oxidase activity, reactive oxygen species levels, C-reactive protein, tumor necrosis factor-alpha expression, apoptosis, and wall thickness, which were significantly attenuated by in vivo treatment with angiotensin type 1 receptor blockade (valsartan) or the superoxide dismutase/catalase mimetic (tempol). |
| 4250 | 17533199 | Compared with Sprague-Dawley controls, Ren2 aortas exhibited greater NADPH oxidase activity, reactive oxygen species levels, C-reactive protein, tumor necrosis factor-alpha expression, apoptosis, and wall thickness, which were significantly attenuated by in vivo treatment with angiotensin type 1 receptor blockade (valsartan) or the superoxide dismutase/catalase mimetic (tempol). |
| 4251 | 17533199 | There was substantially diminished Akt and endothelial NO synthase activation in Ren2 aortas in response to in vivo insulin stimulation, and this was significantly improved by in vivo treatment with valsartan or tempol. |
| 4252 | 17533199 | There was substantially diminished Akt and endothelial NO synthase activation in Ren2 aortas in response to in vivo insulin stimulation, and this was significantly improved by in vivo treatment with valsartan or tempol. |
| 4253 | 17533199 | Further, there was reduced insulin induced Akt activation and increased tumor necrosis factor-alpha levels in vascular smooth muscle cells from Ren2 and Sprague-Dawley rats treated with angiotensin II, abnormalities that were abrogated by angiotensin type 1 receptor blockade with valsartan or antioxidant N-acetylcysteine. |
| 4254 | 17533199 | Further, there was reduced insulin induced Akt activation and increased tumor necrosis factor-alpha levels in vascular smooth muscle cells from Ren2 and Sprague-Dawley rats treated with angiotensin II, abnormalities that were abrogated by angiotensin type 1 receptor blockade with valsartan or antioxidant N-acetylcysteine. |
| 4255 | 17533199 | Collectively, these data suggest that increased angiotensin type 1 receptor/NADPH oxidase activation/reactive oxygen species contribute to vascular insulin resistance, endothelial dysfunction, apoptosis, and inflammation. |
| 4256 | 17533199 | Collectively, these data suggest that increased angiotensin type 1 receptor/NADPH oxidase activation/reactive oxygen species contribute to vascular insulin resistance, endothelial dysfunction, apoptosis, and inflammation. |
| 4257 | 17530468 | Insulin-dependent diabetes mellitus (IDDM) is an organ-specific autoimmune disorder triggered by autoreactive T cells directed to pancreas beta-cell antigens. |
| 4258 | 17530468 | One of these ligands may be tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF-alpha superfamily. |
| 4259 | 17525801 | Hypothalamic resistin induces hepatic insulin resistance. |
| 4260 | 17525801 | We also report that centrally mediated mechanisms partially control resistin-induced expression of TNF-alpha, IL-6, and SOCS-3 in the liver. |
| 4261 | 17512085 | They are also effector cells that may exacerbate insulin resistance in hepatocytes by increasing oxidative stress and by secreting cytokines such as TNF and IL-6. |
| 4262 | 17510266 | The influence of these agents on the plasma levels of fibronectin, C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and tumour necrosis factor-alpha (TNF-alpha), and on the activity of plasminogen activator inhibitor-1 (PAI-1), antithrombin III (AT-III) and protein C, in MRSA-infected diabetic mice was examined. |
| 4263 | 17510266 | The influence of these agents on the plasma levels of fibronectin, C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and tumour necrosis factor-alpha (TNF-alpha), and on the activity of plasminogen activator inhibitor-1 (PAI-1), antithrombin III (AT-III) and protein C, in MRSA-infected diabetic mice was examined. |
| 4264 | 17510266 | The influence of these agents on the plasma levels of fibronectin, C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and tumour necrosis factor-alpha (TNF-alpha), and on the activity of plasminogen activator inhibitor-1 (PAI-1), antithrombin III (AT-III) and protein C, in MRSA-infected diabetic mice was examined. |
| 4265 | 17510266 | MRSA infection in diabetic mice significantly elevated the plasma levels of IL-6 and TNF-alpha (P<0.05). |
| 4266 | 17510266 | MRSA infection in diabetic mice significantly elevated the plasma levels of IL-6 and TNF-alpha (P<0.05). |
| 4267 | 17510266 | MRSA infection in diabetic mice significantly elevated the plasma levels of IL-6 and TNF-alpha (P<0.05). |
| 4268 | 17510266 | DAS or DADS given once did not affect the plasma levels of IL-6 and TNF-alpha (P>0.05); however, DAS or DADS given twice significantly decreased the plasma levels of both IL-6 and TNF-alpha (P<0.05). |
| 4269 | 17510266 | DAS or DADS given once did not affect the plasma levels of IL-6 and TNF-alpha (P>0.05); however, DAS or DADS given twice significantly decreased the plasma levels of both IL-6 and TNF-alpha (P<0.05). |
| 4270 | 17510266 | DAS or DADS given once did not affect the plasma levels of IL-6 and TNF-alpha (P>0.05); however, DAS or DADS given twice significantly decreased the plasma levels of both IL-6 and TNF-alpha (P<0.05). |
| 4271 | 17510266 | DAS or DADS treatment did not affect PAI-1 activity (P>0.05), but DAS or DADS given twice significantly increased AT-III activity (P<0.05). |
| 4272 | 17510266 | DAS or DADS treatment did not affect PAI-1 activity (P>0.05), but DAS or DADS given twice significantly increased AT-III activity (P<0.05). |
| 4273 | 17510266 | DAS or DADS treatment did not affect PAI-1 activity (P>0.05), but DAS or DADS given twice significantly increased AT-III activity (P<0.05). |
| 4274 | 17505154 | The correlation between adiposity and adiponectin, tumor necrosis factor alpha, interleukin-6 and high sensitivity C-reactive protein levels. |
| 4275 | 17499233 | Association of serum levels of glycated albumin, C-reactive protein and tumor necrosis factor-alpha with the severity of coronary artery disease and renal impairment in patients with type 2 diabetes mellitus. |
| 4276 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 4277 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 4278 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 4279 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 4280 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 4281 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 4282 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 4283 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 4284 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 4285 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 4286 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 4287 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 4288 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 4289 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 4290 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 4291 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 4292 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 4293 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 4294 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 4295 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 4296 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 4297 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 4298 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 4299 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 4300 | 17496212 | In this report, evidence is provided demonstrating that treatment with TNF-alpha (10 ng/ml) suppresses not only eNOS expression but also the availability of arginine via the coordinate suppression of argininosuccinate synthase (AS) expression in aortic endothelial cells. |
| 4301 | 17496212 | In this report, evidence is provided demonstrating that treatment with TNF-alpha (10 ng/ml) suppresses not only eNOS expression but also the availability of arginine via the coordinate suppression of argininosuccinate synthase (AS) expression in aortic endothelial cells. |
| 4302 | 17496212 | In this report, evidence is provided demonstrating that treatment with TNF-alpha (10 ng/ml) suppresses not only eNOS expression but also the availability of arginine via the coordinate suppression of argininosuccinate synthase (AS) expression in aortic endothelial cells. |
| 4303 | 17496212 | In this report, evidence is provided demonstrating that treatment with TNF-alpha (10 ng/ml) suppresses not only eNOS expression but also the availability of arginine via the coordinate suppression of argininosuccinate synthase (AS) expression in aortic endothelial cells. |
| 4304 | 17496212 | Reporter gene analysis demonstrated that TNF-alpha suppresses the AS proximal promoter, and EMSA analysis showed reduced binding to three essential Sp1 elements. |
| 4305 | 17496212 | Reporter gene analysis demonstrated that TNF-alpha suppresses the AS proximal promoter, and EMSA analysis showed reduced binding to three essential Sp1 elements. |
| 4306 | 17496212 | Reporter gene analysis demonstrated that TNF-alpha suppresses the AS proximal promoter, and EMSA analysis showed reduced binding to three essential Sp1 elements. |
| 4307 | 17496212 | Reporter gene analysis demonstrated that TNF-alpha suppresses the AS proximal promoter, and EMSA analysis showed reduced binding to three essential Sp1 elements. |
| 4308 | 17496212 | Inhibitor studies suggested that the repression of AS expression by TNF-alpha may be mediated, in part, via the NF-kappaB signaling pathway. |
| 4309 | 17496212 | Inhibitor studies suggested that the repression of AS expression by TNF-alpha may be mediated, in part, via the NF-kappaB signaling pathway. |
| 4310 | 17496212 | Inhibitor studies suggested that the repression of AS expression by TNF-alpha may be mediated, in part, via the NF-kappaB signaling pathway. |
| 4311 | 17496212 | Inhibitor studies suggested that the repression of AS expression by TNF-alpha may be mediated, in part, via the NF-kappaB signaling pathway. |
| 4312 | 17496212 | These findings demonstrate that TNF-alpha coordinately downregulates eNOS and AS expression, resulting in a severely impaired citrulline-NO cycle. |
| 4313 | 17496212 | These findings demonstrate that TNF-alpha coordinately downregulates eNOS and AS expression, resulting in a severely impaired citrulline-NO cycle. |
| 4314 | 17496212 | These findings demonstrate that TNF-alpha coordinately downregulates eNOS and AS expression, resulting in a severely impaired citrulline-NO cycle. |
| 4315 | 17496212 | These findings demonstrate that TNF-alpha coordinately downregulates eNOS and AS expression, resulting in a severely impaired citrulline-NO cycle. |
| 4316 | 17495249 | Thymosin beta-4 and the eye: I can see clearly now the pain is gone. |
| 4317 | 17495249 | Thymosin beta-4 and the eye: I can see clearly now the pain is gone. |
| 4318 | 17495249 | Evidence is mounting to support the idea that thymosin beta-4 (Tbeta-4) has multiple, seemingly diverse, cellular functions. |
| 4319 | 17495249 | Evidence is mounting to support the idea that thymosin beta-4 (Tbeta-4) has multiple, seemingly diverse, cellular functions. |
| 4320 | 17495249 | Recently, we demonstrated that Tbeta-4 suppresses the activation of the transcription factor, nuclear factor-kappa b (NF-kappaB) in TNF-alpha-stimulated cells. |
| 4321 | 17495249 | Recently, we demonstrated that Tbeta-4 suppresses the activation of the transcription factor, nuclear factor-kappa b (NF-kappaB) in TNF-alpha-stimulated cells. |
| 4322 | 17495249 | TNF-alpha initiates cell signaling pathways that converge on the activation of NF-kappaB, thus both are known mediators of the inflammatory process. |
| 4323 | 17495249 | TNF-alpha initiates cell signaling pathways that converge on the activation of NF-kappaB, thus both are known mediators of the inflammatory process. |
| 4324 | 17491689 | Rosiglitazone is an insulin-sensitizing drug that is a ligand for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). |
| 4325 | 17491689 | Rosiglitazone is an insulin-sensitizing drug that is a ligand for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). |
| 4326 | 17491689 | Blood glucose level (BGL), serum insulin level and pancreatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and NO were measured. |
| 4327 | 17491689 | Blood glucose level (BGL), serum insulin level and pancreatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and NO were measured. |
| 4328 | 17491689 | Histopathological examination and immunohistochemical determination of CD4 and CD8 T lymphocytes in the pancreatic islets were performed. |
| 4329 | 17491689 | Histopathological examination and immunohistochemical determination of CD4 and CD8 T lymphocytes in the pancreatic islets were performed. |
| 4330 | 17491689 | The results showed that rosiglitazone treatment resulted in a significant decrease in the BGL and the pancreatic levels of TNF-alpha, IFN-gamma and NO compared to diabetic mice. |
| 4331 | 17491689 | The results showed that rosiglitazone treatment resulted in a significant decrease in the BGL and the pancreatic levels of TNF-alpha, IFN-gamma and NO compared to diabetic mice. |
| 4332 | 17491689 | The destroyed pancreatic islets were regenerated and became free from both CD4 and CD8 T cells after treatment. |
| 4333 | 17491689 | The destroyed pancreatic islets were regenerated and became free from both CD4 and CD8 T cells after treatment. |
| 4334 | 17482403 | These include a very low level of inflammation as evidenced by low circulating levels of c-reactive protein and TNFalpha, serum triiodothyronine levels at the low end of the normal range, and a more elastic "younger" left ventricle (LV), as evaluated by echo-doppler measures of LV stiffness. |
| 4335 | 17465340 | A new member of the family namely Tumor necrosis factor alpha-Related Apoptosis-Inducing Ligand (TRAIL) is involved not only in apoptosis and immune regulation, but also it has a provocative role in vascular biology as reported recently. |
| 4336 | 17462956 | The decrease in MDC and PDC counts was less evident in patients with a combination of T1D and coeliac disease (CD) or CD alone. |
| 4337 | 17462956 | The age-dependent decline in blood DC numbers, found in control children, was not evident in ND patients, such that 2-10 years old ND children had similar MDC and PDC numbers to 15-17 years old controls. |
| 4338 | 17462956 | In ED patients the t-score of MDC and PDC numbers related to the age of diagnosis but not to disease duration. |
| 4339 | 17462956 | Blood DC in T1D patients were not distinguished from those of controls by the levels of HLA-DR, CD40 and CD86 expression or the percentage of DC expressing cytokines, IL-12, IL-10, IL-6 and TNF-alpha, in responses to poly I:C. |
| 4340 | 17460730 | Systemic administration of neutralizing monoclonal antibodies against tumor necrosis factor (TNF)alpha (V1q) or monocyte/macrophage-expressed EGF-like module-containing mucin-like hormone receptor-like (Emr)-1 (F4/80) into wounded ob/ob mice at the end of acute wound inflammation initiated a rapid and complete neo-epidermal coverage of impaired wound tissue in the presence of a persisting diabetic phenotype. |
| 4341 | 17460169 | On the other hand, plasma zinc concentration is influenced by proinflammatory cytokines (IL-6 and TNF-alpha) and by metallothioneins (MT) homeostasis, which is in turn affected by proinflammatory cytokines. |
| 4342 | 17458222 | [Resistin and TNFalpha]. |
| 4343 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4344 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4345 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4346 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4347 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4348 | 17454170 | Circulating concentrations of adiponectin and tumor necrosis factor-alpha in gestational diabetes mellitus. |
| 4349 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4350 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4351 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4352 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4353 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4354 | 17454170 | Adiponectin and tumor necrosis factor-alpha (TNF-alpha) have been implicated in insulin resistance and diabetes mellitus (DM). |
| 4355 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4356 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4357 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4358 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4359 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4360 | 17454170 | In the present study we investigated levels of adiponectin and TNF-alpha and their relationships with each other and metabolic factors in women with gestational DM (GDM). |
| 4361 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4362 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4363 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4364 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4365 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4366 | 17454170 | After adjustment for pre-pregnancy and current body mass index (BMI), adiponectin levels correlated negatively with insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) and 0-h and 1-h glucose both at glucose challenge test and oral glucose tolerance test in GDM. |
| 4367 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4368 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4369 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4370 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4371 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4372 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 4373 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4374 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4375 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4376 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4377 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4378 | 17454170 | HOMA-IR for adiponectin and pre-pregnancy BMI for TNF-alpha remained as significant determinants in multiple regression analyses. |
| 4379 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4380 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4381 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4382 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4383 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4384 | 17454170 | In conclusion, these data suggest that reduced adiponectin and increased TNF-alpha may be involved in the pathogenesis of GDM. |
| 4385 | 17451548 | Effects of periodontal therapy on serum C-reactive protein, sE-selectin, and tumor necrosis factor-alpha secretion by peripheral blood-derived macrophages in diabetes. |
| 4386 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4387 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4388 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4389 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4390 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4391 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4392 | 17447161 | TNF-alpha alters visfatin and adiponectin levels in human fat. |
| 4393 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4394 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4395 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4396 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4397 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4398 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4399 | 17447161 | Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. |
| 4400 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4401 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4402 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4403 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4404 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4405 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4406 | 17447161 | To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. |
| 4407 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4408 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4409 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4410 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4411 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4412 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4413 | 17447161 | The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. |
| 4414 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4415 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4416 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4417 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4418 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4419 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4420 | 17447161 | A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. |
| 4421 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4422 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4423 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4424 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4425 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4426 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4427 | 17447161 | The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. |
| 4428 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4429 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4430 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4431 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4432 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4433 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4434 | 17447161 | The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). |
| 4435 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4436 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4437 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4438 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4439 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4440 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4441 | 17447161 | We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. |
| 4442 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4443 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4444 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4445 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4446 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4447 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4448 | 17447161 | TNF levels are elevated in states of obesity and insulin resistance. |
| 4449 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4450 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4451 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4452 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4453 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4454 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4455 | 17447161 | Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance. |
| 4456 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4457 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4458 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4459 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4460 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4461 | 17447160 | Differentiated skeletal muscle cells were incubated for 24-72 hours with high concentrations of glucose and insulin (GI) or TNFalpha. |
| 4462 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4463 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4464 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4465 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4466 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4467 | 17447160 | In addition, myocytes were co-stimulated with monocyte chemotactic protein (MCP)-1 or adipocyte-conditioned medium (CM) and TNFalpha for 24 and 48 hours. |
| 4468 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4469 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4470 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4471 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4472 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4473 | 17447160 | Treatment with GI rapidly induced insulin resistance whereas TNFalpha impaired insulin signaling in a more chronic fashion (48-72 h). |
| 4474 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4475 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4476 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4477 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4478 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4479 | 17447160 | CM and MCP-1 also induced insulin resistance that was, however, not increased by co-stimulation with TNFalpha. |
| 4480 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4481 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4482 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4483 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4484 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4485 | 17447160 | Expression of CCR2 was decreased during differentiation but up-regulated in insulin-resistant myocytes after treatment with GI (24-72 h) and TNFalpha (72 h). |
| 4486 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4487 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4488 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4489 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4490 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4491 | 17447160 | Expression of CCR4 and CCR10 was down-regulated after treatment with TNFalpha, MCP-1, and CM. |
| 4492 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4493 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4494 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4495 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4496 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4497 | 17447160 | Our data show that the expression of CCR2, CCR4, and CCR10 is differentially regulated by different insulin resistance-inducing treatments in myotubes. |
| 4498 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4499 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4500 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4501 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4502 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4503 | 17447160 | In conclusion, we propose that upregulation of CCR2 in skeletal muscle does not represent a major step leading to muscle insulin resistance. |
| 4504 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4505 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4506 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4507 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4508 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4509 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4510 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4511 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4512 | 17446186 | Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. |
| 4513 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4514 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4515 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4516 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4517 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4518 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4519 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4520 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4521 | 17446186 | Systemic infusion of TNF-alpha abrogates insulin's action to enhance skeletal muscle microvascular perfusion. |
| 4522 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4523 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4524 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4525 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4526 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4527 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4528 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4529 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4530 | 17446186 | In skeletal muscle TNF-alpha induces insulin resistance via the p38 MAPK pathway. |
| 4531 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4532 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4533 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4534 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4535 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4536 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4537 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4538 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4539 | 17446186 | To examine whether p38 MAPK also regulates TNF-alpha-induced vascular insulin resistance, bovine aortic endothelial cells (bAECs) were incubated+/-TNF-alpha (5 ng/ml) for 6 h in the presence or absence of SB203580 (p38 MAPK specific inhibitor, 10 microM) after serum starvation for 10 h. |
| 4540 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4541 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4542 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4543 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4544 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4545 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4546 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4547 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4548 | 17446186 | For the last 30 min, cells were treated+/-1 nM insulin, and insulin receptor substrate (IRS)-1, Akt, endothelial nitric oxide synthase (eNOS), p38 MAPK, ERK1/2, c-Jun N-terminal kinase, and AMP-activated protein kinase (AMPK) phosphorylation, and eNOS activity were measured. |
| 4549 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4550 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4551 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4552 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4553 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4554 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4555 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4556 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4557 | 17446186 | TNF-alpha increased p38 MAPK phosphorylation, potently stimulated IRS-1 serine phosphorylation, and blunted insulin-stimulated IRS-1 tyrosine and Akt phosphorylation and eNOS activity. |
| 4558 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4559 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4560 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4561 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4562 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4563 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4564 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4565 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4566 | 17446186 | TNF-alpha also potently stimulated the phosphorylation of ERK1/2 and AMPK. |
| 4567 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4568 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4569 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4570 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4571 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4572 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4573 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4574 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4575 | 17446186 | Treatment with SB203580 decreased p38 MAPK phosphorylation back to the baseline and restored insulin sensitivity of IRS-1 tyrosine and Akt phosphorylation and eNOS activity in TNF-alpha-treated bAECs without affecting TNF-alpha-induced ERK1/2 and AMPK phosphorylation. |
| 4576 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4577 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4578 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4579 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4580 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4581 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4582 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4583 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4584 | 17446186 | We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK-dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway. |
| 4585 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4586 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4587 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4588 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4589 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4590 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4591 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4592 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4593 | 17446186 | This differential modulation of TNF-alpha's actions by p38 MAPK suggests that p38 MAPK plays a key role in TNF-alpha-mediated vascular insulin resistance and may contribute to the generalized endothelial dysfunction seen in type 2 diabetes mellitus and the cardiometabolic syndrome. |
| 4594 | 17445545 | The aim of the present study was to evaluate plasma interleukin 6 (IL-6), adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1 (MCP-1) levels in patients with AI. |
| 4595 | 17445545 | The aim of the present study was to evaluate plasma interleukin 6 (IL-6), adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1 (MCP-1) levels in patients with AI. |
| 4596 | 17445545 | The aim of the present study was to evaluate plasma interleukin 6 (IL-6), adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1 (MCP-1) levels in patients with AI. |
| 4597 | 17445545 | The aim of the present study was to evaluate plasma interleukin 6 (IL-6), adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), and monocyte chemoattractant protein 1 (MCP-1) levels in patients with AI. |
| 4598 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were measured in 20 healthy subjects (6 males; 14 females; age, 58.5 +/- 2.2 years; body mass index, 28.1 +/- 0.9 kg/m(2)) and in 20 patients (5 males; 15 females; age, 57.9 +/- 2.0 years; body mass index, 28.0 +/- 0.8 kg/m(2)) with AI and typical computed tomographic features of cortical adenoma, who were not affected by diabetes mellitus, hypertension, or other relevant diseases. |
| 4599 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were measured in 20 healthy subjects (6 males; 14 females; age, 58.5 +/- 2.2 years; body mass index, 28.1 +/- 0.9 kg/m(2)) and in 20 patients (5 males; 15 females; age, 57.9 +/- 2.0 years; body mass index, 28.0 +/- 0.8 kg/m(2)) with AI and typical computed tomographic features of cortical adenoma, who were not affected by diabetes mellitus, hypertension, or other relevant diseases. |
| 4600 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were measured in 20 healthy subjects (6 males; 14 females; age, 58.5 +/- 2.2 years; body mass index, 28.1 +/- 0.9 kg/m(2)) and in 20 patients (5 males; 15 females; age, 57.9 +/- 2.0 years; body mass index, 28.0 +/- 0.8 kg/m(2)) with AI and typical computed tomographic features of cortical adenoma, who were not affected by diabetes mellitus, hypertension, or other relevant diseases. |
| 4601 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were measured in 20 healthy subjects (6 males; 14 females; age, 58.5 +/- 2.2 years; body mass index, 28.1 +/- 0.9 kg/m(2)) and in 20 patients (5 males; 15 females; age, 57.9 +/- 2.0 years; body mass index, 28.0 +/- 0.8 kg/m(2)) with AI and typical computed tomographic features of cortical adenoma, who were not affected by diabetes mellitus, hypertension, or other relevant diseases. |
| 4602 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were higher in patients than in controls (64.4 +/- 2.8 vs 5.5 +/- 0.6 pg/mL, 13.7 +/- 1.3 vs 3.6 +/- 0.5 microg/mL, 12.5 +/- 1.9 vs 5.1 +/- 0.2 ng/mL, 27.0 +/- 1.5 vs 22.2 +/- 1.5 pg/mL, 172.5 +/- 20.0 vs 104.4 +/- 19.5 pg/mL, respectively; P < .05) and apparently not affected by the presence of visceral obesity. |
| 4603 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were higher in patients than in controls (64.4 +/- 2.8 vs 5.5 +/- 0.6 pg/mL, 13.7 +/- 1.3 vs 3.6 +/- 0.5 microg/mL, 12.5 +/- 1.9 vs 5.1 +/- 0.2 ng/mL, 27.0 +/- 1.5 vs 22.2 +/- 1.5 pg/mL, 172.5 +/- 20.0 vs 104.4 +/- 19.5 pg/mL, respectively; P < .05) and apparently not affected by the presence of visceral obesity. |
| 4604 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were higher in patients than in controls (64.4 +/- 2.8 vs 5.5 +/- 0.6 pg/mL, 13.7 +/- 1.3 vs 3.6 +/- 0.5 microg/mL, 12.5 +/- 1.9 vs 5.1 +/- 0.2 ng/mL, 27.0 +/- 1.5 vs 22.2 +/- 1.5 pg/mL, 172.5 +/- 20.0 vs 104.4 +/- 19.5 pg/mL, respectively; P < .05) and apparently not affected by the presence of visceral obesity. |
| 4605 | 17445545 | Plasma IL-6, adiponectin, resistin, TNF-alpha, and MCP-1 levels were higher in patients than in controls (64.4 +/- 2.8 vs 5.5 +/- 0.6 pg/mL, 13.7 +/- 1.3 vs 3.6 +/- 0.5 microg/mL, 12.5 +/- 1.9 vs 5.1 +/- 0.2 ng/mL, 27.0 +/- 1.5 vs 22.2 +/- 1.5 pg/mL, 172.5 +/- 20.0 vs 104.4 +/- 19.5 pg/mL, respectively; P < .05) and apparently not affected by the presence of visceral obesity. |
| 4606 | 17445545 | Plasma IL-6 levels were negatively correlated with urinary free cortisol (r = -0.461, P < .05), and TNF-alpha levels were positively correlated with cortisol after the administration of 1 mg dexamethasone (r = 0.636, P < .01). |
| 4607 | 17445545 | Plasma IL-6 levels were negatively correlated with urinary free cortisol (r = -0.461, P < .05), and TNF-alpha levels were positively correlated with cortisol after the administration of 1 mg dexamethasone (r = 0.636, P < .01). |
| 4608 | 17445545 | Plasma IL-6 levels were negatively correlated with urinary free cortisol (r = -0.461, P < .05), and TNF-alpha levels were positively correlated with cortisol after the administration of 1 mg dexamethasone (r = 0.636, P < .01). |
| 4609 | 17445545 | Plasma IL-6 levels were negatively correlated with urinary free cortisol (r = -0.461, P < .05), and TNF-alpha levels were positively correlated with cortisol after the administration of 1 mg dexamethasone (r = 0.636, P < .01). |
| 4610 | 17445540 | Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that impairs insulin action and alters lipid metabolism. |
| 4611 | 17445540 | Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that impairs insulin action and alters lipid metabolism. |
| 4612 | 17445540 | Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that impairs insulin action and alters lipid metabolism. |
| 4613 | 17445540 | We investigated the effects of genetic polymorphisms of TNF-alpha on circulating biomarkers of insulin resistance and lipid metabolism during an 8-hour metabolic profile test and a 2-hour oral glucose tolerance test in subjects with type 2 diabetes mellitus. |
| 4614 | 17445540 | We investigated the effects of genetic polymorphisms of TNF-alpha on circulating biomarkers of insulin resistance and lipid metabolism during an 8-hour metabolic profile test and a 2-hour oral glucose tolerance test in subjects with type 2 diabetes mellitus. |
| 4615 | 17445540 | We investigated the effects of genetic polymorphisms of TNF-alpha on circulating biomarkers of insulin resistance and lipid metabolism during an 8-hour metabolic profile test and a 2-hour oral glucose tolerance test in subjects with type 2 diabetes mellitus. |
| 4616 | 17445540 | Our findings suggest that the -238G>A and -308G>A polymorphisms of TNF-alpha alter circulating free fatty acids and insulin resistance in obese subjects with type 2 diabetes mellitus. |
| 4617 | 17445540 | Our findings suggest that the -238G>A and -308G>A polymorphisms of TNF-alpha alter circulating free fatty acids and insulin resistance in obese subjects with type 2 diabetes mellitus. |
| 4618 | 17445540 | Our findings suggest that the -238G>A and -308G>A polymorphisms of TNF-alpha alter circulating free fatty acids and insulin resistance in obese subjects with type 2 diabetes mellitus. |
| 4619 | 17442272 | Wnt-signaling is maintained and adipogenesis inhibited by TNFalpha but not MCP-1 and resistin. |
| 4620 | 17442272 | Wnt-signaling is maintained and adipogenesis inhibited by TNFalpha but not MCP-1 and resistin. |
| 4621 | 17442272 | Wnt-signaling is maintained and adipogenesis inhibited by TNFalpha but not MCP-1 and resistin. |
| 4622 | 17442272 | Cytokines like TNFalpha and IL-6 are secreted by the inflammatory cells and have been shown to impair normal adipocyte differentiation. |
| 4623 | 17442272 | Cytokines like TNFalpha and IL-6 are secreted by the inflammatory cells and have been shown to impair normal adipocyte differentiation. |
| 4624 | 17442272 | Cytokines like TNFalpha and IL-6 are secreted by the inflammatory cells and have been shown to impair normal adipocyte differentiation. |
| 4625 | 17442272 | Also other cytokines like MCP-1 and resistin are involved in the inflammatory process and are secreted by macrophages. |
| 4626 | 17442272 | Also other cytokines like MCP-1 and resistin are involved in the inflammatory process and are secreted by macrophages. |
| 4627 | 17442272 | Also other cytokines like MCP-1 and resistin are involved in the inflammatory process and are secreted by macrophages. |
| 4628 | 17442272 | In the present study, we show that while TNFalpha is able to maintain an active Wnt-signaling, induce inflammation and completely block adipose cell differentiation, no effect was found by either MCP-1 or resistin on these processes. |
| 4629 | 17442272 | In the present study, we show that while TNFalpha is able to maintain an active Wnt-signaling, induce inflammation and completely block adipose cell differentiation, no effect was found by either MCP-1 or resistin on these processes. |
| 4630 | 17442272 | In the present study, we show that while TNFalpha is able to maintain an active Wnt-signaling, induce inflammation and completely block adipose cell differentiation, no effect was found by either MCP-1 or resistin on these processes. |
| 4631 | 17440992 | The intake of SEC caused significantly dose-dependent increase in insulin and decrease in blood glucose, urinary albumin and type IV collagen (P < 0.05). |
| 4632 | 17440992 | The intake of SEC caused significantly dose-dependent increase in insulin and decrease in blood glucose, urinary albumin and type IV collagen (P < 0.05). |
| 4633 | 17440992 | SEC treatments dose-dependently decreased IL-6 and TNF-alpha levels, increased IL-4 and IL-10 levels, as well as upregulated IL-10 mRNA expression (P < 0.05). |
| 4634 | 17440992 | SEC treatments dose-dependently decreased IL-6 and TNF-alpha levels, increased IL-4 and IL-10 levels, as well as upregulated IL-10 mRNA expression (P < 0.05). |
| 4635 | 17440992 | SMC treatments significantly suppressed renal IL-6 and TNF-alpha levels (P < 0.05), but did not affect IL-4 and IL-10 levels (P < 0.05). |
| 4636 | 17440992 | SMC treatments significantly suppressed renal IL-6 and TNF-alpha levels (P < 0.05), but did not affect IL-4 and IL-10 levels (P < 0.05). |
| 4637 | 17439741 | Elevation of tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 levels in aortic intima of Chinese Guizhou minipigs with streptozotocin-induced diabetes. |
| 4638 | 17438370 | The factors contributing to defects in fatty acid metabolism are not understood but new data demonstrates that increased TNFalpha in obesity increases protein phosphatase 2C (PP2C), which in turn suppresses the activity of AMP-activated protein kinase (AMPK), a critical regulator of energy metabolism.(1) These data identify a novel mechanism by which inflammation in obesity is a precursor to defects in skeletal muscle fatty acid oxidation that generates a vicious cycle exacerbating the development of insulin resistance. |
| 4639 | 17431229 | This dual effect of TNF on hepatocytes reflects its ability to induce both nuclear factor kappaB (NF-kappaB)-dependent gene expression and cell death. |
| 4640 | 17431229 | This dual effect of TNF on hepatocytes reflects its ability to induce both nuclear factor kappaB (NF-kappaB)-dependent gene expression and cell death. |
| 4641 | 17431229 | This dual effect of TNF on hepatocytes reflects its ability to induce both nuclear factor kappaB (NF-kappaB)-dependent gene expression and cell death. |
| 4642 | 17431229 | Although many studies confirmed this crucial cytoprotective role of NF-kappaB in adult liver, a number of genetic studies recently obtained conflicting results on the exact role of NF-kappaB in different mouse models of TNF hepatotoxicity, demonstrating that caution should be taken when interpreting studies using different NF-kappaB-deficient mice in distinct models of liver injury. |
| 4643 | 17431229 | Although many studies confirmed this crucial cytoprotective role of NF-kappaB in adult liver, a number of genetic studies recently obtained conflicting results on the exact role of NF-kappaB in different mouse models of TNF hepatotoxicity, demonstrating that caution should be taken when interpreting studies using different NF-kappaB-deficient mice in distinct models of liver injury. |
| 4644 | 17431229 | Although many studies confirmed this crucial cytoprotective role of NF-kappaB in adult liver, a number of genetic studies recently obtained conflicting results on the exact role of NF-kappaB in different mouse models of TNF hepatotoxicity, demonstrating that caution should be taken when interpreting studies using different NF-kappaB-deficient mice in distinct models of liver injury. |
| 4645 | 17431229 | Recent reports showing a role for hepatic NF-kappaB activation in the proliferation of malignant cells during hepatocarcinogenesis, and in the progression of fatty liver diseases to insulin resistance and type 2 diabetes mellitus demonstrate that NF-kappaB can also have more detrimental effects in the liver. |
| 4646 | 17431229 | Recent reports showing a role for hepatic NF-kappaB activation in the proliferation of malignant cells during hepatocarcinogenesis, and in the progression of fatty liver diseases to insulin resistance and type 2 diabetes mellitus demonstrate that NF-kappaB can also have more detrimental effects in the liver. |
| 4647 | 17431229 | Recent reports showing a role for hepatic NF-kappaB activation in the proliferation of malignant cells during hepatocarcinogenesis, and in the progression of fatty liver diseases to insulin resistance and type 2 diabetes mellitus demonstrate that NF-kappaB can also have more detrimental effects in the liver. |
| 4648 | 17431229 | Therefore, understanding the regulation of hepatic TNF signaling and NF-kappaB activation is of critical therapeutic importance. |
| 4649 | 17431229 | Therefore, understanding the regulation of hepatic TNF signaling and NF-kappaB activation is of critical therapeutic importance. |
| 4650 | 17431229 | Therefore, understanding the regulation of hepatic TNF signaling and NF-kappaB activation is of critical therapeutic importance. |
| 4651 | 17430113 | Immunomodulatory factors including IFNgamma, TNFalpha, IL-1, and LPS use IDO induction in responsive antigen presenting cells (APCs) also to transmit tolerogenic signals to T cells. |
| 4652 | 17430113 | Immunomodulatory factors including IFNgamma, TNFalpha, IL-1, and LPS use IDO induction in responsive antigen presenting cells (APCs) also to transmit tolerogenic signals to T cells. |
| 4653 | 17430113 | The importance of IDO dysregulation manifest as autoimmune pellagric dementia is genetically illustrated for Nasu-Hakola Disease (or PLOSL), which is caused by a mutation in the IDO antagonizing genes TYROBP/DAP12 or TREM2. |
| 4654 | 17430113 | The importance of IDO dysregulation manifest as autoimmune pellagric dementia is genetically illustrated for Nasu-Hakola Disease (or PLOSL), which is caused by a mutation in the IDO antagonizing genes TYROBP/DAP12 or TREM2. |
| 4655 | 17430113 | Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD. |
| 4656 | 17430113 | Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD. |
| 4657 | 17430113 | Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the IDO-inducing tolerogenic prostaglandins PGE(2) and PGD(2). |
| 4658 | 17430113 | Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the IDO-inducing tolerogenic prostaglandins PGE(2) and PGD(2). |
| 4659 | 17430113 | Next, PGD(2) is converted to the anti-inflammatory prostaglandin, 15d-PGJ(2). |
| 4660 | 17430113 | Next, PGD(2) is converted to the anti-inflammatory prostaglandin, 15d-PGJ(2). |
| 4661 | 17430113 | These prostaglandins exert potent anti-inflammatory activities through endogenous signaling mechanisms involving the GPCRs EP2, EP4, and DP1 along with PPARgamma respectively. |
| 4662 | 17430113 | These prostaglandins exert potent anti-inflammatory activities through endogenous signaling mechanisms involving the GPCRs EP2, EP4, and DP1 along with PPARgamma respectively. |
| 4663 | 17430113 | Alternatively the direct targeting of the non-redox NAD-dependent proteins using resveratrol to activate SIRT1 or PJ34 in order to inhibit PARP1 and prevent autoimmune pathogenesis are also given consideration. |
| 4664 | 17430113 | Alternatively the direct targeting of the non-redox NAD-dependent proteins using resveratrol to activate SIRT1 or PJ34 in order to inhibit PARP1 and prevent autoimmune pathogenesis are also given consideration. |
| 4665 | 17428349 | Association of TGFbeta1, TNFalpha, CCR2 and CCR5 gene polymorphisms in type-2 diabetes and renal insufficiency among Asian Indians. |
| 4666 | 17425653 | Plasma concentrations of inflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-18 and chemokine CCL2 in patients with diabetic nephropathy (DN) were significantly higher than control subjects, while IL-10, CXCL8, CXCL9, CXCL10 and adiponectin concentrations of DN were significantly higher than patients without diabetic nephropathy (NDN) and control subjects (all P < 0.05). |
| 4667 | 17425653 | Plasma concentrations of inflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-18 and chemokine CCL2 in patients with diabetic nephropathy (DN) were significantly higher than control subjects, while IL-10, CXCL8, CXCL9, CXCL10 and adiponectin concentrations of DN were significantly higher than patients without diabetic nephropathy (NDN) and control subjects (all P < 0.05). |
| 4668 | 17425653 | Plasma concentrations of inflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-18 and chemokine CCL2 in patients with diabetic nephropathy (DN) were significantly higher than control subjects, while IL-10, CXCL8, CXCL9, CXCL10 and adiponectin concentrations of DN were significantly higher than patients without diabetic nephropathy (NDN) and control subjects (all P < 0.05). |
| 4669 | 17425653 | Plasma concentrations of inflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-18 and chemokine CCL2 in patients with diabetic nephropathy (DN) were significantly higher than control subjects, while IL-10, CXCL8, CXCL9, CXCL10 and adiponectin concentrations of DN were significantly higher than patients without diabetic nephropathy (NDN) and control subjects (all P < 0.05). |
| 4670 | 17425653 | Plasma concentrations of TNF-alpha, IL-6, IL-10, IL-18, CCL2, CXCL8, CXCL9, CXCL10 and adiponectin exhibited significant positive correlation with urine albumin : creatinine ratio in DN patients. |
| 4671 | 17425653 | Plasma concentrations of TNF-alpha, IL-6, IL-10, IL-18, CCL2, CXCL8, CXCL9, CXCL10 and adiponectin exhibited significant positive correlation with urine albumin : creatinine ratio in DN patients. |
| 4672 | 17425653 | Plasma concentrations of TNF-alpha, IL-6, IL-10, IL-18, CCL2, CXCL8, CXCL9, CXCL10 and adiponectin exhibited significant positive correlation with urine albumin : creatinine ratio in DN patients. |
| 4673 | 17425653 | Plasma concentrations of TNF-alpha, IL-6, IL-10, IL-18, CCL2, CXCL8, CXCL9, CXCL10 and adiponectin exhibited significant positive correlation with urine albumin : creatinine ratio in DN patients. |
| 4674 | 17425653 | The percentage increases of ex vivo production of IL-6, CXCL8, CXCL10, CCL2 and CCL5 upon TNF-alpha activation were significantly higher in both NDN and DN patients than controls (all P < 0.05). |
| 4675 | 17425653 | The percentage increases of ex vivo production of IL-6, CXCL8, CXCL10, CCL2 and CCL5 upon TNF-alpha activation were significantly higher in both NDN and DN patients than controls (all P < 0.05). |
| 4676 | 17425653 | The percentage increases of ex vivo production of IL-6, CXCL8, CXCL10, CCL2 and CCL5 upon TNF-alpha activation were significantly higher in both NDN and DN patients than controls (all P < 0.05). |
| 4677 | 17425653 | The percentage increases of ex vivo production of IL-6, CXCL8, CXCL10, CCL2 and CCL5 upon TNF-alpha activation were significantly higher in both NDN and DN patients than controls (all P < 0.05). |
| 4678 | 17425653 | The percentage increases in IL-18-induced phosphorylation of extracellular signal-regulated kinase (ERK) in Th cells of NDN and DN were significantly higher than controls (P < 0.05), while the percentage increase in TNF-alpha-induced phosphorylation of p38 MAPK in monocytes and IL-18-induced phosphorylation of p38 MAPK in Th cells and monocytes were significantly higher in NDN patients than controls. |
| 4679 | 17425653 | The percentage increases in IL-18-induced phosphorylation of extracellular signal-regulated kinase (ERK) in Th cells of NDN and DN were significantly higher than controls (P < 0.05), while the percentage increase in TNF-alpha-induced phosphorylation of p38 MAPK in monocytes and IL-18-induced phosphorylation of p38 MAPK in Th cells and monocytes were significantly higher in NDN patients than controls. |
| 4680 | 17425653 | The percentage increases in IL-18-induced phosphorylation of extracellular signal-regulated kinase (ERK) in Th cells of NDN and DN were significantly higher than controls (P < 0.05), while the percentage increase in TNF-alpha-induced phosphorylation of p38 MAPK in monocytes and IL-18-induced phosphorylation of p38 MAPK in Th cells and monocytes were significantly higher in NDN patients than controls. |
| 4681 | 17425653 | The percentage increases in IL-18-induced phosphorylation of extracellular signal-regulated kinase (ERK) in Th cells of NDN and DN were significantly higher than controls (P < 0.05), while the percentage increase in TNF-alpha-induced phosphorylation of p38 MAPK in monocytes and IL-18-induced phosphorylation of p38 MAPK in Th cells and monocytes were significantly higher in NDN patients than controls. |
| 4682 | 17409686 | TNFalpha induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 4683 | 17407763 | We used oligonucleotide microarray and quantitative RT-PCR to identify molecular markers of physiological and immunological stress in porcine islets cultured under stress conditions of elevated glucose (16.7 mM), inflammatory cytokine addition (IL-1beta, TNF-alpha, and IFN-gamma), or both, for 48 h. |
| 4684 | 17406657 | We hypothesized that the enhanced brain injury in GK rats could be caused by differential regulation of the heme degrading enzyme heme oxygenase (HO)-1, known to interact with the expression of other target genes implicated in antioxidant defense, inflammation and neurodegeneration, such as superoxide dismutase (SOD)-1, -2, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNFalpha). |
| 4685 | 17406657 | We hypothesized that the enhanced brain injury in GK rats could be caused by differential regulation of the heme degrading enzyme heme oxygenase (HO)-1, known to interact with the expression of other target genes implicated in antioxidant defense, inflammation and neurodegeneration, such as superoxide dismutase (SOD)-1, -2, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNFalpha). |
| 4686 | 17406657 | Baseline expression of HO-1, iNOS, and TNFalpha mRNA was increased in the cortex of sham GK rats. |
| 4687 | 17406657 | Baseline expression of HO-1, iNOS, and TNFalpha mRNA was increased in the cortex of sham GK rats. |
| 4688 | 17405852 | NECA failed to prevent cytokine-induced beta-cell death in vitro, but NECA strongly suppressed expression of the proinflammatory cytokines TNF-alpha, MIP-1alpha, IL-12, and IFN-gamma in pancreata, endotoxin, or anti-CD3-stimulated splenic cells, and T helper 1 lymphocytes, indicating that the beneficial effect of NECA was due to immunomodulation. |
| 4689 | 17398176 | Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). |
| 4690 | 17398176 | Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). |
| 4691 | 17398176 | Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). |
| 4692 | 17398176 | Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). |
| 4693 | 17398176 | Serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been shown to be predictors of adverse outcomes in patients with coronary artery disease (CAD). |
| 4694 | 17398176 | We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. |
| 4695 | 17398176 | We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. |
| 4696 | 17398176 | We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. |
| 4697 | 17398176 | We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. |
| 4698 | 17398176 | We prospectively measured hs-CRP, IL-6, and TNF-alpha in 249 patients who were admitted with acute chest pain and underwent coronary angiography. |
| 4699 | 17398176 | After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. |
| 4700 | 17398176 | After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. |
| 4701 | 17398176 | After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. |
| 4702 | 17398176 | After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. |
| 4703 | 17398176 | After adjusting for conventional CAD risk factors (age, gender, diabetes, hypertension, smoking, and hypercholesterolemia), there was no association between inflammatory markers (hs-CRP, IL-6, and TNF-alpha) and angiographic severity of CAD. |
| 4704 | 17398176 | There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. |
| 4705 | 17398176 | There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. |
| 4706 | 17398176 | There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. |
| 4707 | 17398176 | There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. |
| 4708 | 17398176 | There was no significant positive association between MACEs and hs-CRP, IL-6, or TNF-alpha level in unadjusted and adjusted models. |
| 4709 | 17398176 | In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors. |
| 4710 | 17398176 | In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors. |
| 4711 | 17398176 | In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors. |
| 4712 | 17398176 | In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors. |
| 4713 | 17398176 | In conclusion, in patients hospitalized with chest pain, we found no association of serum levels of hs-CRP, IL-6, or TNF-alpha with coronary atherosclerotic burden or MACEs at 6 months after adjustment for traditional CAD risk factors. |
| 4714 | 17392582 | Adipokines and ghrelin play role in insulin resistance, the key pathophysiological abnormality in patients with nonalcoholic fatty liver diseases. |
| 4715 | 17392582 | Adipokines and ghrelin play role in insulin resistance, the key pathophysiological abnormality in patients with nonalcoholic fatty liver diseases. |
| 4716 | 17392582 | Serum adiponectin, leptin, TNF-alpha, and ghrelin were determined. |
| 4717 | 17392582 | Serum adiponectin, leptin, TNF-alpha, and ghrelin were determined. |
| 4718 | 17392582 | Serum leptin (15.49 +/- 4.84 vs 10.31 +/- 2.53) and TNF-alpha (12.1 +/- 2.7 vs 10.31 +/- 2.56) levels were significantly higher in the NASH group compared to in the control group (P < .001 for each). |
| 4719 | 17392582 | Serum leptin (15.49 +/- 4.84 vs 10.31 +/- 2.53) and TNF-alpha (12.1 +/- 2.7 vs 10.31 +/- 2.56) levels were significantly higher in the NASH group compared to in the control group (P < .001 for each). |
| 4720 | 17392582 | Nevertheless, adiponectin (11.1 +/- 2.1 vs 17.3 +/- 2.8) and ghrelin (6.46 +/- 1.1 vs 7.8 +/- 1.1) levels were lower in the NASH group than in the control group (P < .001 for each). |
| 4721 | 17392582 | Nevertheless, adiponectin (11.1 +/- 2.1 vs 17.3 +/- 2.8) and ghrelin (6.46 +/- 1.1 vs 7.8 +/- 1.1) levels were lower in the NASH group than in the control group (P < .001 for each). |
| 4722 | 17390149 | In multivariate adjusted models, the strongest associations observed were between higher European ancestry and interleukin-6 soluble receptor (IL-6 SR), C-reactive protein (CRP), and adiponectin levels, with interleukin-2 soluble receptor (IL-2 SR) and soluble tumor necrosis factor receptor II (TNF-alpha SR II) also showing more modest but significant associations. |
| 4723 | 17390149 | These novel findings suggest that admixture mapping may identify genetic factors influencing the levels of IL-6 SR, CRP, IL-2 SR, and adiponectin. |
| 4724 | 17389595 | Ad-GPAT1-treated rats had 50% lower hepatic NF-kappaB activity and no difference in expression of tumor necrosis factor-alpha and interleukin-beta, consistent with hepatic insulin resistance in the absence of increased hepatic inflammation. |
| 4725 | 17375405 | Glucose, glucose metabolites and AGEs alter endothelial cell functions, induce adhesion molecule overexpression (ICAM-1, VCAM), cytokine release (IL-6, MCP-1) and tissue factor production. |
| 4726 | 17375405 | Tumor necrosis factor alpha systemic level is increased during the postprandial phase as are augmented C reactive protein and fibrinogen level. |
| 4727 | 17373637 | Association of free fatty acids (FFA) and tumor necrosis factor-alpha (TNF-alpha) and insulin-resistant metabolic disorder. |
| 4728 | 17373637 | Association of free fatty acids (FFA) and tumor necrosis factor-alpha (TNF-alpha) and insulin-resistant metabolic disorder. |
| 4729 | 17373637 | Association of free fatty acids (FFA) and tumor necrosis factor-alpha (TNF-alpha) and insulin-resistant metabolic disorder. |
| 4730 | 17373637 | The roles of free fatty acids (FFA), tumor necrosis factor-alpha (TNF-alpha), and adiponectin in the development of the insulin-resistant metabolic disorder in several subjects have been studied. |
| 4731 | 17373637 | The roles of free fatty acids (FFA), tumor necrosis factor-alpha (TNF-alpha), and adiponectin in the development of the insulin-resistant metabolic disorder in several subjects have been studied. |
| 4732 | 17373637 | The roles of free fatty acids (FFA), tumor necrosis factor-alpha (TNF-alpha), and adiponectin in the development of the insulin-resistant metabolic disorder in several subjects have been studied. |
| 4733 | 17373637 | The results suggest that FFA and possibly TNF-alpha levels are closely related to the development of insulin resistance in subjects with metabolic disorders. |
| 4734 | 17373637 | The results suggest that FFA and possibly TNF-alpha levels are closely related to the development of insulin resistance in subjects with metabolic disorders. |
| 4735 | 17373637 | The results suggest that FFA and possibly TNF-alpha levels are closely related to the development of insulin resistance in subjects with metabolic disorders. |
| 4736 | 17373119 | [Evaluation of adiponectin and TNFalpha genes expression in women with gestational diabetes. |
| 4737 | 17367566 | The present study examined the effects of a 6-week supplementation with two trans-18 : 1 isomers (trans-11 and trans-12) in human subjects on immune cells, several inflammatory and immunological biomarkers (for example, IL, TNFalpha, C-reactive protein, adiponectin, intercellular adhesion molecule-1, prostacyclin, phagocytic process). |
| 4738 | 17367566 | The present study examined the effects of a 6-week supplementation with two trans-18 : 1 isomers (trans-11 and trans-12) in human subjects on immune cells, several inflammatory and immunological biomarkers (for example, IL, TNFalpha, C-reactive protein, adiponectin, intercellular adhesion molecule-1, prostacyclin, phagocytic process). |
| 4739 | 17367566 | Generally, trans-isomer supplementation did not affect either inflammatory biomarkers (for example, IL-6, IL-8, TNFalpha) or immune function (for example, phagocytosis) during the present study. |
| 4740 | 17367566 | Generally, trans-isomer supplementation did not affect either inflammatory biomarkers (for example, IL-6, IL-8, TNFalpha) or immune function (for example, phagocytosis) during the present study. |
| 4741 | 17362204 | IL-6 (interleukin-6), IL-1beta (interleukin-1beta) and TNF-alpha (tumour necrosis factor-alpha) were measured before and after 24 h of incubation of whole blood with LPS (lipopolysaccharide) or saline. |
| 4742 | 17362204 | IL-6 (interleukin-6), IL-1beta (interleukin-1beta) and TNF-alpha (tumour necrosis factor-alpha) were measured before and after 24 h of incubation of whole blood with LPS (lipopolysaccharide) or saline. |
| 4743 | 17362204 | IL-6 (interleukin-6), IL-1beta (interleukin-1beta) and TNF-alpha (tumour necrosis factor-alpha) were measured before and after 24 h of incubation of whole blood with LPS (lipopolysaccharide) or saline. |
| 4744 | 17362204 | The basal values of IL-1beta, IL-6 and TNF-alpha were low and were not significantly related to hs-CRP levels. |
| 4745 | 17362204 | The basal values of IL-1beta, IL-6 and TNF-alpha were low and were not significantly related to hs-CRP levels. |
| 4746 | 17362204 | The basal values of IL-1beta, IL-6 and TNF-alpha were low and were not significantly related to hs-CRP levels. |
| 4747 | 17362204 | A univariate analysis showed that the level of IL-1beta and IL-6, obtained after 24 h of incubation of whole blood with LPS, increased significantly with increasing levels of hs-CRP and, after adjusting for potential confounders, IL-1beta still remained statistically significant. |
| 4748 | 17362204 | A univariate analysis showed that the level of IL-1beta and IL-6, obtained after 24 h of incubation of whole blood with LPS, increased significantly with increasing levels of hs-CRP and, after adjusting for potential confounders, IL-1beta still remained statistically significant. |
| 4749 | 17362204 | A univariate analysis showed that the level of IL-1beta and IL-6, obtained after 24 h of incubation of whole blood with LPS, increased significantly with increasing levels of hs-CRP and, after adjusting for potential confounders, IL-1beta still remained statistically significant. |
| 4750 | 17362204 | In our sample of patients with Type 2 diabetes, there was no association between serum hs-CRP levels and basal levels of IL-6, IL-1beta and TNF-alpha. |
| 4751 | 17362204 | In our sample of patients with Type 2 diabetes, there was no association between serum hs-CRP levels and basal levels of IL-6, IL-1beta and TNF-alpha. |
| 4752 | 17362204 | In our sample of patients with Type 2 diabetes, there was no association between serum hs-CRP levels and basal levels of IL-6, IL-1beta and TNF-alpha. |
| 4753 | 17362204 | Conversely, a significant association was observed between serum hs-CRP levels and IL-1beta and IL-6 production after 24 h of incubation of whole blood with LPS. |
| 4754 | 17362204 | Conversely, a significant association was observed between serum hs-CRP levels and IL-1beta and IL-6 production after 24 h of incubation of whole blood with LPS. |
| 4755 | 17362204 | Conversely, a significant association was observed between serum hs-CRP levels and IL-1beta and IL-6 production after 24 h of incubation of whole blood with LPS. |
| 4756 | 17360983 | Specifically, strong antiapoptotic activities for AAT (Prolastin, human) were observed when murine insulinoma cells (MIN6) were exposed to tumor necrosis factor-alpha. |
| 4757 | 17360983 | Importantly, in both model systems, treatment with AAT completely abolished induced caspase-3 activity. |
| 4758 | 17352408 | Insulin down-regulates TRAIL expression in vascular smooth muscle cells both in vivo and in vitro. |
| 4759 | 17352408 | To dissect the effect of hyperinsulinemia versus hyperglycemia on TNF-related apoptosis inducing ligand (TRAIL) expression in the macrovascular district, we measured TRAIL mRNA and protein in four groups of animals: streptozotocin (SZT)-induced diabetic rats, vehicle-treated control animals, diabetic rats treated with insulin and non-diabetic rats treated with insulin. |
| 4760 | 17352408 | While the aortas of diabetic rats did not show significant differences in TRAIL expression with respect to vehicle-treated control animals, the aortas of both diabetic and non-diabetic rats treated in vivo for 16 days with insulin showed a significant decrease in TRAIL expression with respect to either diabetic and control rats. |
| 4761 | 17352408 | Moreover, in vitro treatment of both rat and human vascular smooth muscle cells (VSMC) with insulin induced the down-regulation of TRAIL protein. |
| 4762 | 17352408 | These findings suggest that TRAIL might act as an endogenous regulator of the vascular tone and that chronic elevation of insulin might contribute to the vascular abnormalities characterizing type-2 diabetes mellitus by down-regulating TRAIL expression and activity. |
| 4763 | 17347312 | We then assayed the plasma adipocytokines levels related to insulin sensitivity, plasma lipid levels, and tissue triglycerides accumulation and examined adipocyte morphology. |
| 4764 | 17347312 | Our results suggest that decreased plasma adiponectin, increased plasma resistin and cholesterol, and elevated levels of TNF-alpha and IL-6 in adipocytes may all contribute to the insulin resistance observed in GH-Tg mice. |
| 4765 | 17347312 | An increase in plasma adiponectin and decrease in plasma IL-6, triglycerides, and cholesterol levels in response to CR may improve insulin sensitivity. |
| 4766 | 17346751 | Induction of reactive oxygen species from isolated rat glomeruli by protein kinase C activation and TNF-alpha stimulation, and effects of a phosphodiesterase inhibitor. |
| 4767 | 17346751 | Induction of reactive oxygen species from isolated rat glomeruli by protein kinase C activation and TNF-alpha stimulation, and effects of a phosphodiesterase inhibitor. |
| 4768 | 17346751 | Constituent cells of the renal glomeruli have the capacity to release reactive oxygen species (ROS) upon stimulation of NADPH oxidase activated by protein kinase C (PKC). |
| 4769 | 17346751 | Constituent cells of the renal glomeruli have the capacity to release reactive oxygen species (ROS) upon stimulation of NADPH oxidase activated by protein kinase C (PKC). |
| 4770 | 17346751 | Hyperglycemia and insulin resistance in the diabetic state are often associated with activation of PKC and tumor necrosis factor (TNF)-alpha, respectively. |
| 4771 | 17346751 | Hyperglycemia and insulin resistance in the diabetic state are often associated with activation of PKC and tumor necrosis factor (TNF)-alpha, respectively. |
| 4772 | 17346751 | The PKC inhibitor H-7, the NADPH oxidase inhibitor diphenylene iodonium and the phosphatidylinositol-3 (PI-3) kinase inhibitor wortmannin inhibited PMA-induced ROS production by 100%, 100% and 80%, respectively. |
| 4773 | 17346751 | The PKC inhibitor H-7, the NADPH oxidase inhibitor diphenylene iodonium and the phosphatidylinositol-3 (PI-3) kinase inhibitor wortmannin inhibited PMA-induced ROS production by 100%, 100% and 80%, respectively. |
| 4774 | 17346438 | Through its effects on endothelial function, coagulation, insulin resistance and lipid metabolism, the proinflammatory cytokine TNF could be involved in cardiovascular pathophysiology. |
| 4775 | 17345784 | Telmisartan and irbesartan therapy in type 2 diabetic patients treated with rosiglitazone: effects on insulin-resistance, leptin and tumor necrosis factor-alpha. |
| 4776 | 17345784 | Telmisartan and irbesartan therapy in type 2 diabetic patients treated with rosiglitazone: effects on insulin-resistance, leptin and tumor necrosis factor-alpha. |
| 4777 | 17345784 | Telmisartan and irbesartan therapy in type 2 diabetic patients treated with rosiglitazone: effects on insulin-resistance, leptin and tumor necrosis factor-alpha. |
| 4778 | 17345784 | We evaluated body mass index (BMI), glycemic control (HbA1c fasting plasma glucose and insulin levels [FPG, and FPI, respectively], and homeostasis model assessment [HOMA] index), lipid profile (total cholesterol [TC], low density lipoprotein-cholesterol [LDL-C], high density lipoprotein-cholesterol [HDL-C], and triglycerides [TG]), systolic and diastolic blood pressure (SBP and DBP), tumor necrosis factor-alpha (TNF-alpha), and leptin during the 12 months of this treatment. |
| 4779 | 17345784 | We evaluated body mass index (BMI), glycemic control (HbA1c fasting plasma glucose and insulin levels [FPG, and FPI, respectively], and homeostasis model assessment [HOMA] index), lipid profile (total cholesterol [TC], low density lipoprotein-cholesterol [LDL-C], high density lipoprotein-cholesterol [HDL-C], and triglycerides [TG]), systolic and diastolic blood pressure (SBP and DBP), tumor necrosis factor-alpha (TNF-alpha), and leptin during the 12 months of this treatment. |
| 4780 | 17345784 | We evaluated body mass index (BMI), glycemic control (HbA1c fasting plasma glucose and insulin levels [FPG, and FPI, respectively], and homeostasis model assessment [HOMA] index), lipid profile (total cholesterol [TC], low density lipoprotein-cholesterol [LDL-C], high density lipoprotein-cholesterol [HDL-C], and triglycerides [TG]), systolic and diastolic blood pressure (SBP and DBP), tumor necrosis factor-alpha (TNF-alpha), and leptin during the 12 months of this treatment. |
| 4781 | 17345784 | Significant decreases in TNF-alpha and leptin levels were observed after 6 months in the telmisartan group, and after 12 months in both groups. |
| 4782 | 17345784 | Significant decreases in TNF-alpha and leptin levels were observed after 6 months in the telmisartan group, and after 12 months in both groups. |
| 4783 | 17345784 | Significant decreases in TNF-alpha and leptin levels were observed after 6 months in the telmisartan group, and after 12 months in both groups. |
| 4784 | 17335802 | IL-1beta, TNF-alpha and C5b-9 are components of SIR and have been speculated to be involved in the clinical brain edema (BE) of DKA. |
| 4785 | 17335802 | IL-1beta, TNF-alpha and C5b-9 are components of SIR and have been speculated to be involved in the clinical brain edema (BE) of DKA. |
| 4786 | 17335802 | IL-1beta, TNF-alpha and C5b-9 are components of SIR and have been speculated to be involved in the clinical brain edema (BE) of DKA. |
| 4787 | 17335802 | We studied IL-1beta, TNF-alpha, C5b-9, inducible nitric oxide (iNOS), ICAM-1, IL-10 and Hsp70 expression in the brains of two patients who died as the result of clinical BE during the treatment of DKA. |
| 4788 | 17335802 | We studied IL-1beta, TNF-alpha, C5b-9, inducible nitric oxide (iNOS), ICAM-1, IL-10 and Hsp70 expression in the brains of two patients who died as the result of clinical BE during the treatment of DKA. |
| 4789 | 17335802 | We studied IL-1beta, TNF-alpha, C5b-9, inducible nitric oxide (iNOS), ICAM-1, IL-10 and Hsp70 expression in the brains of two patients who died as the result of clinical BE during the treatment of DKA. |
| 4790 | 17335802 | TNF-alpha was expressed to a lesser extent than IL-1beta, and only in the CP. |
| 4791 | 17335802 | TNF-alpha was expressed to a lesser extent than IL-1beta, and only in the CP. |
| 4792 | 17335802 | TNF-alpha was expressed to a lesser extent than IL-1beta, and only in the CP. |
| 4793 | 17335802 | C5b-9, previously shown to be deposited on neurons and oligodendrocytes, was found on CPE and ependymal cells. iNOS and ICAM-1 had increased expression in the CPE and ependyma. |
| 4794 | 17335802 | C5b-9, previously shown to be deposited on neurons and oligodendrocytes, was found on CPE and ependymal cells. iNOS and ICAM-1 had increased expression in the CPE and ependyma. |
| 4795 | 17335802 | C5b-9, previously shown to be deposited on neurons and oligodendrocytes, was found on CPE and ependymal cells. iNOS and ICAM-1 had increased expression in the CPE and ependyma. |
| 4796 | 17335802 | Hsp70 and IL-10 were also expressed in the CPE of the case with the shorter duration of treatment. |
| 4797 | 17335802 | Hsp70 and IL-10 were also expressed in the CPE of the case with the shorter duration of treatment. |
| 4798 | 17335802 | Hsp70 and IL-10 were also expressed in the CPE of the case with the shorter duration of treatment. |
| 4799 | 17327451 | Globular adiponectin activates nuclear factor-kappaB and activating protein-1 and enhances angiotensin II-induced proliferation in cardiac fibroblasts. |
| 4800 | 17327451 | Nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1) activation were examined using cardiac fibroblasts prepared from the ventricles of 1- to 2-day-old Wistar rats and grown in culture. gAd activated NF-kappaB and enhanced tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB activity. gAd also activated AP-1 and enhanced angiotensin II (Ang II)-induced AP-1 activity. gAd induced mRNA expression of c-fos and c-jun and activated extracellular signal-regulated kinase. |
| 4801 | 17327451 | Thus, gAd enhanced Ang II-induced DNA and collagen synthesis. |
| 4802 | 17327451 | Antibodies against adiponectin receptor (AdipoR)1 and AdipoR2 elicit activation of NF-kappaB or AP-1, two redox-sensitive transcription factors. |
| 4803 | 17327450 | Effects of pioglitazone on suppressor of cytokine signaling 3 expression: potential mechanisms for its effects on insulin sensitivity and adiponectin expression. |
| 4804 | 17327450 | Effects of pioglitazone on suppressor of cytokine signaling 3 expression: potential mechanisms for its effects on insulin sensitivity and adiponectin expression. |
| 4805 | 17327450 | Recent studies have shown that the induction of suppressor of cytokine signaling 3 (SOCS3) is related to the development of insulin resistance. |
| 4806 | 17327450 | Recent studies have shown that the induction of suppressor of cytokine signaling 3 (SOCS3) is related to the development of insulin resistance. |
| 4807 | 17327450 | Here, we examined whether the insulin-sensitizing effect of pioglitazone affects the SOCS induction. |
| 4808 | 17327450 | Here, we examined whether the insulin-sensitizing effect of pioglitazone affects the SOCS induction. |
| 4809 | 17327450 | In 3T3-L1 adipocytes, mediators of insulin resistance such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6, growth hormone, and insulin increased SOCS3 expression, which was partially inhibited by pioglitazone. |
| 4810 | 17327450 | In 3T3-L1 adipocytes, mediators of insulin resistance such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6, growth hormone, and insulin increased SOCS3 expression, which was partially inhibited by pioglitazone. |
| 4811 | 17327450 | The ability of pioglitazone to suppress SOCS3 induction by TNF-alpha was greatly augmented by peroxisome proliferator-activated receptor gamma overexpression. |
| 4812 | 17327450 | The ability of pioglitazone to suppress SOCS3 induction by TNF-alpha was greatly augmented by peroxisome proliferator-activated receptor gamma overexpression. |
| 4813 | 17327450 | SOCS3 overexpression and tyrphostin AG490, a Janus kinase 2 inhibitor, or dominant-negative STAT3 expression partially inhibited adiponectin secretion and was accompanied by decreased STAT3 phosphorylation. |
| 4814 | 17327450 | SOCS3 overexpression and tyrphostin AG490, a Janus kinase 2 inhibitor, or dominant-negative STAT3 expression partially inhibited adiponectin secretion and was accompanied by decreased STAT3 phosphorylation. |
| 4815 | 17327450 | Conversely, pioglitazone increased adiponectin secretion and STAT3 phosphorylation in fat tissue of db/db mice and in 3T3-L1 adipocytes. |
| 4816 | 17327450 | Conversely, pioglitazone increased adiponectin secretion and STAT3 phosphorylation in fat tissue of db/db mice and in 3T3-L1 adipocytes. |
| 4817 | 17327450 | These results suggest that pioglitazone exerts its effect to improve whole-body insulin sensitivity in part through the suppression of SOCS3, which is associated with the increase in STAT3 phosphorylation and adiponectin production in fat tissue. |
| 4818 | 17327450 | These results suggest that pioglitazone exerts its effect to improve whole-body insulin sensitivity in part through the suppression of SOCS3, which is associated with the increase in STAT3 phosphorylation and adiponectin production in fat tissue. |
| 4819 | 17327444 | Increases in adiponectin predict improved liver, but not peripheral, insulin sensitivity in severely obese women during weight loss. |
| 4820 | 17327444 | Plasma concentrations of leptin decreased and adiponectin increased significantly by 1 month, and decreases in interleukin-6, C-reactive protein (CRP), and tumor necrosis factor-alpha were observed at 6 months of weight loss. |
| 4821 | 17327444 | Longitudinal decreases in CRP (r = -0.53, P < 0.05) were associated with increases in S(i), and decreases in HOMA-IR were related to increases in adiponectin (r = -0.37, P < 0.05). |
| 4822 | 17327444 | Decreases in VAT were more strongly related to increases in adiponectin and decreases in CRP than were changes in general adiposity or SAT. |
| 4823 | 17327444 | Thus, in severely obese women, specific loss of VAT leads to acute improvements in hepatic insulin sensitivity mediated by increases in adiponectin and in peripheral insulin sensitivity mediated by decreases in CRP. |
| 4824 | 17327432 | LR-90 significantly inhibited S100b-induced expression of RAGE and other proinflammatory genes including monocyte chemoattractant protein-1, interferon-gamma-inducible protein-10, and cyclooxygenase-2 in a dose-dependent manner. |
| 4825 | 17327432 | These inhibitory effects may be exerted via inhibition of nuclear factor-kappaB (NF-kappaB) activation, as LR-90 suppressed both S100b-and tumor necrosis factor-alpha-induced IkappaB-alpha degradation as well as NF-kappaB promoter transcriptional activity. |
| 4826 | 17327424 | Feeding a c9,t11-CLA-enriched diet reduced fasting glucose (P < 0.05), insulin (P < 0.05), and triacylglycerol concentrations (P < 0.01) and increased adipose tissue plasma membrane GLUT4 (P < 0.05) and insulin receptor (P < 0.05) expression compared with the control linoleic acid-enriched diet. |
| 4827 | 17327424 | Feeding a c9,t11-CLA-enriched diet reduced fasting glucose (P < 0.05), insulin (P < 0.05), and triacylglycerol concentrations (P < 0.01) and increased adipose tissue plasma membrane GLUT4 (P < 0.05) and insulin receptor (P < 0.05) expression compared with the control linoleic acid-enriched diet. |
| 4828 | 17327424 | Interestingly, after the c9,t11-CLA diet, adipose tissue macrophage infiltration was less, with marked downregulation of several inflammatory markers in adipose tissue, including reduced tumor necrosis factor-alpha and CD68 mRNA (P < 0.05), nuclear factor-kappaB (NF-kappaB) p65 expression (P < 0.01), NF-kappaB DNA binding (P < 0.01), and NF-kappaB p65, p50, c-Rel, p52, and RelB transcriptional activity (P < 0.01). |
| 4829 | 17327424 | Interestingly, after the c9,t11-CLA diet, adipose tissue macrophage infiltration was less, with marked downregulation of several inflammatory markers in adipose tissue, including reduced tumor necrosis factor-alpha and CD68 mRNA (P < 0.05), nuclear factor-kappaB (NF-kappaB) p65 expression (P < 0.01), NF-kappaB DNA binding (P < 0.01), and NF-kappaB p65, p50, c-Rel, p52, and RelB transcriptional activity (P < 0.01). |
| 4830 | 17327424 | To define whether these observations were direct effects of the nutrient intervention, complimentary cell culture studies showed that c9,t11-CLA inhibited tumor necrosis factor-alpha-induced downregulation of insulin receptor substrate 1 and GLUT4 mRNA expression and promoted insulin-stimulated glucose transport in 3T3-L1 adipocytes compared with linoleic acid. |
| 4831 | 17327424 | To define whether these observations were direct effects of the nutrient intervention, complimentary cell culture studies showed that c9,t11-CLA inhibited tumor necrosis factor-alpha-induced downregulation of insulin receptor substrate 1 and GLUT4 mRNA expression and promoted insulin-stimulated glucose transport in 3T3-L1 adipocytes compared with linoleic acid. |
| 4832 | 17322487 | Tumour necrosis factor alpha (TNFalpha) is a pro-inflammatory cytokine which has been closely linked to obesity and insulin resistance. |
| 4833 | 17322487 | Tumour necrosis factor alpha (TNFalpha) is a pro-inflammatory cytokine which has been closely linked to obesity and insulin resistance. |
| 4834 | 17322487 | This finding may implicate that TNFalpha blockade causes better glycaemic control in RA patients with concomitant diabetes, possibly by improving insulin resistance. |
| 4835 | 17322487 | This finding may implicate that TNFalpha blockade causes better glycaemic control in RA patients with concomitant diabetes, possibly by improving insulin resistance. |
| 4836 | 17321107 | Examination of peritoneal proinflammatory cytokine levels 2h after LPS administration showed that diabetic mice had 4-, 2.5- and 3.6-fold greater concentrations of IL-1beta, IL-6 and TNF-alpha, respectively, when compared to non-diabetic mice. |
| 4837 | 17295835 | The dual function of hepatic SOCS3 in insulin resistance in vivo. |
| 4838 | 17295835 | The suppressor of cytokine signaling 3 (SOCS3), which is induced by pro-inflammatory cytokines, such as TNFalpha and IL-6, has been implicated in inflammation-mediated insulin resistance in the liver and adipocytes. |
| 4839 | 17295835 | However, no genetic evidence has been provided for the involvement of SOCS3 on insulin resistance. |
| 4840 | 17295835 | Here, we generated hepatocyte-specific SOCS3-deficient (L-SOCS3 cKO) mice and examined insulin sensitivity. |
| 4841 | 17295835 | Being consistent with a previous idea, the loss of SOCS3 in the liver apparently improved insulin sensitivity. |
| 4842 | 17295835 | However, unexpectedly, L-SOCS3 cKO mice exhibited obesity and systemic insulin resistance with age. |
| 4843 | 17295835 | Insulin signaling was rather suppressed in muscles, suggesting that deletion of the SOCS3 gene in the liver modulates insulin sensitivity in other organs. |
| 4844 | 17295835 | Anti-inflammatory reagent, sodium salicylate, partial improved insulin resistance of aged L-SOCS3 cKO mice, suggesting that enhanced inflammatory status is associated with the phenotype of these mice. |
| 4845 | 17295835 | STAT3 was hyperactivated and acute-phase proteins were elevated in L-SOCS3 cKO mice liver, which were reduced by sodium salicylate treatment. |
| 4846 | 17295835 | We conclude that hepatic SOCS3 is a mediator of insulin resistance in the liver; however, lack of SOCS3 in the liver promotes systemic insulin resistance by mimicking chronic inflammation. |
| 4847 | 17292732 | Fasting levels of plasma adiponectin and circulating markers of inflammation (high-sensitivity C-reactive protein, CD40 ligand, interleukin 1beta, tumor necrosis factor alpha, vascular cell adhesion molecule 1, and intracellular adhesion molecule) were measured. |
| 4848 | 17287468 | Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). |
| 4849 | 17287468 | Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. |
| 4850 | 17287460 | Pharmacological inhibition of glucosylceramide synthase enhances insulin sensitivity. |
| 4851 | 17287460 | In cultured 3T3-L1 adipocytes, the iminosugar derivative N-(5'-adamantane-1'-yl-methoxy)-pentyl-1-deoxynojirimycin (AMP-DNM) counteracted tumor necrosis factor-alpha-induced abnormalities in glycosphingolipid concentrations and concomitantly reversed abnormalities in insulin signal transduction. |
| 4852 | 17275415 | Tumor necrosis factor-alpha and insulin resistance play central roles in the pathogenesis of abnormal hepatocellular function. |
| 4853 | 17275415 | Serum ALT, AST and GGT, insulin resistance, adiponectin and DS-TNFR2 isoform concentrations were measured in 492 subjects from two different Caucasian Spanish populations. |
| 4854 | 17272875 | Several factors associated with diabetes have been shown to be related to the development and deterioration of diabetic periodontitis, i.e., glycated hemoglobin (HbA(1C)), advanced glycation endproducts (AGEs), C-reactive protein (CRP), and glucose tolerance, as well as inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. |
| 4855 | 17267600 | To investigate the role of beta cell NF-kappaB in autoimmune diabetes, we produced transgenic mice expressing a nondegradable form of IkappaBalpha in pancreatic beta cells (RIP-mIkappaBalpha mice). beta cells of these mice were more susceptible to killing by TNF-alpha plus IFN-gamma but more resistant to IL-1beta plus IFN-gamma than normal beta cells. |
| 4856 | 17267600 | To investigate the role of beta cell NF-kappaB in autoimmune diabetes, we produced transgenic mice expressing a nondegradable form of IkappaBalpha in pancreatic beta cells (RIP-mIkappaBalpha mice). beta cells of these mice were more susceptible to killing by TNF-alpha plus IFN-gamma but more resistant to IL-1beta plus IFN-gamma than normal beta cells. |
| 4857 | 17267600 | Inhibition of beta cell NF-kappaB accelerated the development of autoimmune diabetes in nonobese diabetic mice but had no effect on glucose tolerance or serum insulin in C57BL/6 mice, precluding a nonphysiological effect of transgene expression. |
| 4858 | 17267600 | Inhibition of beta cell NF-kappaB accelerated the development of autoimmune diabetes in nonobese diabetic mice but had no effect on glucose tolerance or serum insulin in C57BL/6 mice, precluding a nonphysiological effect of transgene expression. |
| 4859 | 17267600 | These results suggest that under conditions that resemble autoimmune type 1 diabetes, the dominant effect of NF-kappaB is prevention of TNF-induced apoptosis. |
| 4860 | 17267600 | These results suggest that under conditions that resemble autoimmune type 1 diabetes, the dominant effect of NF-kappaB is prevention of TNF-induced apoptosis. |
| 4861 | 17267050 | Serum amyloid A (SAA), a HDL apolipoprotein is a risk marker for cardiovascular disease. |
| 4862 | 17267050 | Serum amyloid A (SAA), a HDL apolipoprotein is a risk marker for cardiovascular disease. |
| 4863 | 17267050 | TNF-alpha, IL-1beta, IL-8 and IL-1ra levels were measured by ELISA in the culture supernatants and in serum of subjects. |
| 4864 | 17267050 | TNF-alpha, IL-1beta, IL-8 and IL-1ra levels were measured by ELISA in the culture supernatants and in serum of subjects. |
| 4865 | 17267050 | We make the novel observation that neutrophils and monocytes of diabetics are more responsive to SAA for the induction of the proinflammatory cytokine IL-1beta and the proangiogenic and chemotactic protein IL-8. |
| 4866 | 17267050 | We make the novel observation that neutrophils and monocytes of diabetics are more responsive to SAA for the induction of the proinflammatory cytokine IL-1beta and the proangiogenic and chemotactic protein IL-8. |
| 4867 | 17267050 | Incremental TNF-alpha production was also found to occur when monocytes were stimulated with SAA. |
| 4868 | 17267050 | Incremental TNF-alpha production was also found to occur when monocytes were stimulated with SAA. |
| 4869 | 17261957 | Brachial artery flow-mediated vasodilation (FMD), lipopolysaccharide-induced release of interleukin-6 and TNF-alpha from peripheral blood leukocytes ex vivo, and circulating proinflammatory cytokines were determined before and during the clamp. |
| 4870 | 17261957 | Brachial artery flow-mediated vasodilation (FMD), lipopolysaccharide-induced release of interleukin-6 and TNF-alpha from peripheral blood leukocytes ex vivo, and circulating proinflammatory cytokines were determined before and during the clamp. |
| 4871 | 17261957 | Valsartan attenuated endothelial dysfunction [FMD 7.0 +/- 0.7 (t = 2 hr), 6.1 +/- 0.7 (t = 4 hr), 6.2 +/- 0.6% (t = 22 hr); P < 0.005] and decreased the release of interleukin-6 and TNF-alpha from leukocytes both before and during the clamp (P < 0.05). |
| 4872 | 17261957 | Valsartan attenuated endothelial dysfunction [FMD 7.0 +/- 0.7 (t = 2 hr), 6.1 +/- 0.7 (t = 4 hr), 6.2 +/- 0.6% (t = 22 hr); P < 0.005] and decreased the release of interleukin-6 and TNF-alpha from leukocytes both before and during the clamp (P < 0.05). |
| 4873 | 17259397 | A20 or tumor necrosis factor (TNF)-induced protein 3 (TNFAIP3) is a negative regulator of nuclear factor-kappaB (NF-kappaB). |
| 4874 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4875 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4876 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4877 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4878 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4879 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4880 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4881 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4882 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4883 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4884 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 4885 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4886 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4887 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4888 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4889 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4890 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4891 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4892 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4893 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4894 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4895 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 4896 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4897 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4898 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4899 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4900 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4901 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4902 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4903 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4904 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4905 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4906 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 4907 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4908 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4909 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4910 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4911 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4912 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4913 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4914 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4915 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4916 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4917 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 4918 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4919 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4920 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4921 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4922 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4923 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4924 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4925 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4926 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4927 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4928 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 4929 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4930 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4931 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4932 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4933 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4934 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4935 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4936 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4937 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4938 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4939 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 4940 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4941 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4942 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4943 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4944 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4945 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4946 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4947 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4948 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4949 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4950 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 4951 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4952 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4953 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4954 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4955 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4956 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4957 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4958 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4959 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4960 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4961 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 4962 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4963 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4964 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4965 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4966 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4967 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4968 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4969 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4970 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4971 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4972 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 4973 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4974 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4975 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4976 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4977 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4978 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4979 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4980 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4981 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4982 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4983 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 4984 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4985 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4986 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4987 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4988 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4989 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4990 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4991 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4992 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4993 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4994 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 4995 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 4996 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 4997 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 4998 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 4999 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5000 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5001 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5002 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5003 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5004 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5005 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 5006 | 17259385 | Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. |
| 5007 | 17259385 | Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. |
| 5008 | 17259385 | Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. |
| 5009 | 17259385 | Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. |
| 5010 | 17259385 | Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. |
| 5011 | 17259385 | Protein-tyrosine phosphatase (PTP)1B is a negative regulator of insulin signaling and a therapeutic target for type 2 diabetes. |
| 5012 | 17259385 | Protein-tyrosine phosphatase (PTP)1B is a negative regulator of insulin signaling and a therapeutic target for type 2 diabetes. |
| 5013 | 17259385 | Protein-tyrosine phosphatase (PTP)1B is a negative regulator of insulin signaling and a therapeutic target for type 2 diabetes. |
| 5014 | 17259385 | Protein-tyrosine phosphatase (PTP)1B is a negative regulator of insulin signaling and a therapeutic target for type 2 diabetes. |
| 5015 | 17259385 | Protein-tyrosine phosphatase (PTP)1B is a negative regulator of insulin signaling and a therapeutic target for type 2 diabetes. |
| 5016 | 17259385 | In this study, we have assessed the role of PTP1B in the insulin sensitivity of skeletal muscle under physiological and insulin-resistant conditions. |
| 5017 | 17259385 | In this study, we have assessed the role of PTP1B in the insulin sensitivity of skeletal muscle under physiological and insulin-resistant conditions. |
| 5018 | 17259385 | In this study, we have assessed the role of PTP1B in the insulin sensitivity of skeletal muscle under physiological and insulin-resistant conditions. |
| 5019 | 17259385 | In this study, we have assessed the role of PTP1B in the insulin sensitivity of skeletal muscle under physiological and insulin-resistant conditions. |
| 5020 | 17259385 | In this study, we have assessed the role of PTP1B in the insulin sensitivity of skeletal muscle under physiological and insulin-resistant conditions. |
| 5021 | 17259385 | PTP1B(-/-) myocytes showed enhanced insulin-dependent activation of insulin receptor autophosphorylation and downstream signaling (tyrosine phosphorylation of insulin receptor substrate [IRS]-1 and IRS-2, activation of phosphatidylinositol 3-kinase, and serine phosphorylation of AKT), compared with wild-type cells. |
| 5022 | 17259385 | PTP1B(-/-) myocytes showed enhanced insulin-dependent activation of insulin receptor autophosphorylation and downstream signaling (tyrosine phosphorylation of insulin receptor substrate [IRS]-1 and IRS-2, activation of phosphatidylinositol 3-kinase, and serine phosphorylation of AKT), compared with wild-type cells. |
| 5023 | 17259385 | PTP1B(-/-) myocytes showed enhanced insulin-dependent activation of insulin receptor autophosphorylation and downstream signaling (tyrosine phosphorylation of insulin receptor substrate [IRS]-1 and IRS-2, activation of phosphatidylinositol 3-kinase, and serine phosphorylation of AKT), compared with wild-type cells. |
| 5024 | 17259385 | PTP1B(-/-) myocytes showed enhanced insulin-dependent activation of insulin receptor autophosphorylation and downstream signaling (tyrosine phosphorylation of insulin receptor substrate [IRS]-1 and IRS-2, activation of phosphatidylinositol 3-kinase, and serine phosphorylation of AKT), compared with wild-type cells. |
| 5025 | 17259385 | PTP1B(-/-) myocytes showed enhanced insulin-dependent activation of insulin receptor autophosphorylation and downstream signaling (tyrosine phosphorylation of insulin receptor substrate [IRS]-1 and IRS-2, activation of phosphatidylinositol 3-kinase, and serine phosphorylation of AKT), compared with wild-type cells. |
| 5026 | 17259385 | Accordingly, PTP1B(-/-) myocytes displayed higher insulin-dependent stimulation of glucose uptake and GLUT4 translocation to the plasma membrane than wild-type cells. |
| 5027 | 17259385 | Accordingly, PTP1B(-/-) myocytes displayed higher insulin-dependent stimulation of glucose uptake and GLUT4 translocation to the plasma membrane than wild-type cells. |
| 5028 | 17259385 | Accordingly, PTP1B(-/-) myocytes displayed higher insulin-dependent stimulation of glucose uptake and GLUT4 translocation to the plasma membrane than wild-type cells. |
| 5029 | 17259385 | Accordingly, PTP1B(-/-) myocytes displayed higher insulin-dependent stimulation of glucose uptake and GLUT4 translocation to the plasma membrane than wild-type cells. |
| 5030 | 17259385 | Accordingly, PTP1B(-/-) myocytes displayed higher insulin-dependent stimulation of glucose uptake and GLUT4 translocation to the plasma membrane than wild-type cells. |
| 5031 | 17259385 | Treatment with tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance on glucose uptake, impaired insulin signaling, and increased PTP1B activity in wild-type cells. |
| 5032 | 17259385 | Treatment with tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance on glucose uptake, impaired insulin signaling, and increased PTP1B activity in wild-type cells. |
| 5033 | 17259385 | Treatment with tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance on glucose uptake, impaired insulin signaling, and increased PTP1B activity in wild-type cells. |
| 5034 | 17259385 | Treatment with tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance on glucose uptake, impaired insulin signaling, and increased PTP1B activity in wild-type cells. |
| 5035 | 17259385 | Treatment with tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance on glucose uptake, impaired insulin signaling, and increased PTP1B activity in wild-type cells. |
| 5036 | 17259385 | Conversely, the lack of PTP1B confers protection against insulin resistance by TNF-alpha in myocyte cell lines and in adult male mice. |
| 5037 | 17259385 | Conversely, the lack of PTP1B confers protection against insulin resistance by TNF-alpha in myocyte cell lines and in adult male mice. |
| 5038 | 17259385 | Conversely, the lack of PTP1B confers protection against insulin resistance by TNF-alpha in myocyte cell lines and in adult male mice. |
| 5039 | 17259385 | Conversely, the lack of PTP1B confers protection against insulin resistance by TNF-alpha in myocyte cell lines and in adult male mice. |
| 5040 | 17259385 | Conversely, the lack of PTP1B confers protection against insulin resistance by TNF-alpha in myocyte cell lines and in adult male mice. |
| 5041 | 17259385 | Wild-type mice treated with TNF-alpha developed a pronounced hyperglycemia along the glucose tolerance test, accompanied by an impaired insulin signaling and increased PTP1B activity in muscle. |
| 5042 | 17259385 | Wild-type mice treated with TNF-alpha developed a pronounced hyperglycemia along the glucose tolerance test, accompanied by an impaired insulin signaling and increased PTP1B activity in muscle. |
| 5043 | 17259385 | Wild-type mice treated with TNF-alpha developed a pronounced hyperglycemia along the glucose tolerance test, accompanied by an impaired insulin signaling and increased PTP1B activity in muscle. |
| 5044 | 17259385 | Wild-type mice treated with TNF-alpha developed a pronounced hyperglycemia along the glucose tolerance test, accompanied by an impaired insulin signaling and increased PTP1B activity in muscle. |
| 5045 | 17259385 | Wild-type mice treated with TNF-alpha developed a pronounced hyperglycemia along the glucose tolerance test, accompanied by an impaired insulin signaling and increased PTP1B activity in muscle. |
| 5046 | 17259385 | However, mice lacking PTP1B maintained a rapid clearance of glucose and insulin sensitivity and displayed normal muscle insulin signaling regardless the presence of TNF-alpha. |
| 5047 | 17259385 | However, mice lacking PTP1B maintained a rapid clearance of glucose and insulin sensitivity and displayed normal muscle insulin signaling regardless the presence of TNF-alpha. |
| 5048 | 17259385 | However, mice lacking PTP1B maintained a rapid clearance of glucose and insulin sensitivity and displayed normal muscle insulin signaling regardless the presence of TNF-alpha. |
| 5049 | 17259385 | However, mice lacking PTP1B maintained a rapid clearance of glucose and insulin sensitivity and displayed normal muscle insulin signaling regardless the presence of TNF-alpha. |
| 5050 | 17259385 | However, mice lacking PTP1B maintained a rapid clearance of glucose and insulin sensitivity and displayed normal muscle insulin signaling regardless the presence of TNF-alpha. |
| 5051 | 17256873 | Coexpression of vascular endothelial growth factor and interleukin-1 receptor antagonist for improved human islet survival and function. |
| 5052 | 17256873 | We have recently shown improvement in islet survival and function following ex vivo infection of islets with a mixture of adenoviral vectors encoding human vascular endothelial growth factor (Adv-hVEGF) and human interleukin-1 receptor antagonist (Adv-hIL-1Ra). |
| 5053 | 17256873 | Coexpression of hVEGF and hIL-1Ra suppressed nitric oxide production, total caspases, apoptosis, and necrosis in the presence of inflammatory cytokine cocktail consisting of IL-1beta, TNFalpha, and IFNgamma. |
| 5054 | 17243079 | Besides release of free fatty acids, adipocytes secrete substances that contribute to peripheral insulin resistance, including adiponectin, resistin, TNF-alpha and interleukin 6. |
| 5055 | 17243079 | A new class of anti-diabetic drugs (thiazolidinediones, or glitazones) bind to peroxisome proliferator activated receptor (PPAR-gamma) and lower thereby plasma free fatty acids and cytokine production in adipocytes, in addition to a decrease of resistin and an increase in adiponectin observed in animals, resulting in an overall increase in insulin sensitivity and in an improvement of glucose homeostasis. |
| 5056 | 17242490 | Thereby, exercise offers protection against TNF-alpha-induced insulin resistance. |
| 5057 | 17237715 | Insulin-like growth factor binding protein-3 induces insulin resistance in adipocytes in vitro and in rats in vivo. |
| 5058 | 17237715 | Insulin-like growth factor binding protein-3 induces insulin resistance in adipocytes in vitro and in rats in vivo. |
| 5059 | 17237715 | Insulin-like growth factor binding protein (IGFBP)-3 binds to IGF and modulates their actions and also possesses intrinsic activities. |
| 5060 | 17237715 | Insulin-like growth factor binding protein (IGFBP)-3 binds to IGF and modulates their actions and also possesses intrinsic activities. |
| 5061 | 17237715 | We investigated its effects on insulin action and found that when IGFBP-3 was added to fully differentiated 3T3-L1 adipocytes in culture, insulin-stimulated glucose transport was significantly inhibited to 60% of control in a time- and dose-dependent manner. |
| 5062 | 17237715 | We investigated its effects on insulin action and found that when IGFBP-3 was added to fully differentiated 3T3-L1 adipocytes in culture, insulin-stimulated glucose transport was significantly inhibited to 60% of control in a time- and dose-dependent manner. |
| 5063 | 17237715 | Tumor necrosis factor (TNF)-alpha treatment also inhibited glucose transport to the same degree as IGFBP-3 and, in addition, increased IGFBP-3 levels 3-fold. |
| 5064 | 17237715 | Tumor necrosis factor (TNF)-alpha treatment also inhibited glucose transport to the same degree as IGFBP-3 and, in addition, increased IGFBP-3 levels 3-fold. |
| 5065 | 17237715 | Co-treatment with TNF-alpha and IGFBP-3 antisense partially prevented the inhibitory effect of TNF-alpha on glucose transport, indicating a role for IGFBP-3 in cytokine-induced insulin resistance. |
| 5066 | 17237715 | Co-treatment with TNF-alpha and IGFBP-3 antisense partially prevented the inhibitory effect of TNF-alpha on glucose transport, indicating a role for IGFBP-3 in cytokine-induced insulin resistance. |
| 5067 | 17237715 | Insulin-stimulated phosphorylation of the insulin receptor was markedly decreased by IGFBP-3 treatment. |
| 5068 | 17237715 | Insulin-stimulated phosphorylation of the insulin receptor was markedly decreased by IGFBP-3 treatment. |
| 5069 | 17237715 | IGFBP-3 treatment suppressed adiponectin expression in 3T3-L1 adipocytes. |
| 5070 | 17237715 | IGFBP-3 treatment suppressed adiponectin expression in 3T3-L1 adipocytes. |
| 5071 | 17237715 | These in vitro and in vivo findings demonstrate that IGFBP-3 has potent insulin-antagonizing capability and suggest a role for IGFBP-3 in cytokine-induced insulin resistance and other mechanisms involved in the development of type-2 diabetes. |
| 5072 | 17237715 | These in vitro and in vivo findings demonstrate that IGFBP-3 has potent insulin-antagonizing capability and suggest a role for IGFBP-3 in cytokine-induced insulin resistance and other mechanisms involved in the development of type-2 diabetes. |
| 5073 | 17229978 | These are achieved predominantly through release of adipocytokines, which include several novel and highly active molecules released abundantly by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells infiltrating fat, like TNF-alpha, IL-6, MCP-1 (CCL-2), IL-1. |
| 5074 | 17229978 | Present review, in a concise form, focuses on the effects of major adipocytokines, characteristic for adipose tissue like leptin, adiponectin, resistin and visfatin on the immune system, particularly innate and adaptive immunity as well as on blood vessels. |
| 5075 | 17229078 | Our objectives were (1) to confirm that low levels of pre-transplant adiponectin are an independent risk factor for the development of NODAT in a larger transplanted population; (2) to analyze whether adiponectin is a better predictor of NODAT than other inflammatory markers (C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and pregnancy-associated plasma protein A (PAPP-A)) and (3) to assess the relationship between obesity, inflammatory markers and NODAT. |
| 5076 | 17229078 | Our objectives were (1) to confirm that low levels of pre-transplant adiponectin are an independent risk factor for the development of NODAT in a larger transplanted population; (2) to analyze whether adiponectin is a better predictor of NODAT than other inflammatory markers (C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and pregnancy-associated plasma protein A (PAPP-A)) and (3) to assess the relationship between obesity, inflammatory markers and NODAT. |
| 5077 | 17229078 | Pre-transplant plasma glucose, insulin, adiponectin, CRP, TNF-alpha, IL-6 and PAPP-A were measured. |
| 5078 | 17229078 | Pre-transplant plasma glucose, insulin, adiponectin, CRP, TNF-alpha, IL-6 and PAPP-A were measured. |
| 5079 | 17229078 | Adiponectin was lower (p < 0.001) and CRP higher (p = 0.032) in patients with NODAT. |
| 5080 | 17229078 | Adiponectin was lower (p < 0.001) and CRP higher (p = 0.032) in patients with NODAT. |
| 5081 | 17213612 | Diabetes or obesity often causes systemic and cardiac increases in tumor necrosis factor-alpha, interleukin-18 and plasminogen activator inhibitor-1. |
| 5082 | 17213232 | We investigated the relationship of nine common single-nucleotide polymorphisms (SNPs) in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, IL-4 and transforming growth factor (TGF)-beta1 with the atherosclerotic severity in 10 different arteries based on 1503 consecutive autopsies of elderly Japanese subjects registered in the Japanese SNPs for geriatric research (JG-SNP) study. |
| 5083 | 17213232 | We investigated the relationship of nine common single-nucleotide polymorphisms (SNPs) in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, IL-4 and transforming growth factor (TGF)-beta1 with the atherosclerotic severity in 10 different arteries based on 1503 consecutive autopsies of elderly Japanese subjects registered in the Japanese SNPs for geriatric research (JG-SNP) study. |
| 5084 | 17213232 | The -511T of IL-1beta and the +29T of TGF-beta1 were significant risk factors for atherogenesis in the subclavian and intracranial arteries (OR: 1.35 and 1.48, respectively). |
| 5085 | 17213232 | The -511T of IL-1beta and the +29T of TGF-beta1 were significant risk factors for atherogenesis in the subclavian and intracranial arteries (OR: 1.35 and 1.48, respectively). |
| 5086 | 17213232 | Functional SNPs in TNF-alpha, IL-1beta and TGF-beta1 genes play a role in atherogenesis, although their influences are less pronounced than those of conventional risk factors and appear to be limited to specific arteries in the Japanese elderly. |
| 5087 | 17213232 | Functional SNPs in TNF-alpha, IL-1beta and TGF-beta1 genes play a role in atherogenesis, although their influences are less pronounced than those of conventional risk factors and appear to be limited to specific arteries in the Japanese elderly. |
| 5088 | 17212015 | Association of adipocytokines (leptin, adiponectin TNF-alpha), insulin and proinsulin with diabetes--the Mumbai Obesity Project [MOP]. |
| 5089 | 17212015 | Association of adipocytokines (leptin, adiponectin TNF-alpha), insulin and proinsulin with diabetes--the Mumbai Obesity Project [MOP]. |
| 5090 | 17212015 | In this study we looked at adipocytokines--leptin, adiponectin and tumour necrosis factor-a [TNF-alpha] and insulin and proinsulin in subjects with diabetes and obesity. |
| 5091 | 17212015 | In this study we looked at adipocytokines--leptin, adiponectin and tumour necrosis factor-a [TNF-alpha] and insulin and proinsulin in subjects with diabetes and obesity. |
| 5092 | 17212015 | Leptin [p=0.002J and adiponectin levels [p=0.011] were lower and proinsulin values higher [p<0.001] in diabetic subjects compared to non-diabetic subjects. |
| 5093 | 17212015 | Leptin [p=0.002J and adiponectin levels [p=0.011] were lower and proinsulin values higher [p<0.001] in diabetic subjects compared to non-diabetic subjects. |
| 5094 | 17212015 | In addition, leptin [p<0.001] and proinsulin [p<0.001] were higher and adiponectin [p<0.001] lower, in obese subjects compared to non-obese subjects. |
| 5095 | 17212015 | In addition, leptin [p<0.001] and proinsulin [p<0.001] were higher and adiponectin [p<0.001] lower, in obese subjects compared to non-obese subjects. |
| 5096 | 17212015 | Leptin and proinsulin showed a significant and positive correlation with BMI [p<0.001] and waist circumference [p<0.001]. |
| 5097 | 17212015 | Leptin and proinsulin showed a significant and positive correlation with BMI [p<0.001] and waist circumference [p<0.001]. |
| 5098 | 17212015 | Proinsulin showed a significant negative association with adiponectin [p=0.002]. |
| 5099 | 17212015 | Proinsulin showed a significant negative association with adiponectin [p=0.002]. |
| 5100 | 17212015 | Logistic regression analysis revealed leptin to be negatively associated [Odds ratio [OR]: 0.864, 95% confidence interval [95% CI]: 0.775 -0.963, p=0.008] and proinsulin [OR: 1.567, 95% CI: 1.246-1.971, p<0.001] to be positively associated with diabetes even after adjusting for age, gender and BMI. |
| 5101 | 17212015 | Logistic regression analysis revealed leptin to be negatively associated [Odds ratio [OR]: 0.864, 95% confidence interval [95% CI]: 0.775 -0.963, p=0.008] and proinsulin [OR: 1.567, 95% CI: 1.246-1.971, p<0.001] to be positively associated with diabetes even after adjusting for age, gender and BMI. |
| 5102 | 17212015 | Leptin [OR: 1.365, 95% CI: 1.170-1.592, p<0.001] and proinsulin [OR: 1.617, 95% CI: 1.218 -2.147, p=0.001] showed a significant positive association with obesity, while adiponectin [OR: 0.927, 95% CI: 0.865 - 0.995, p=0.035] had a significant inverse association. |
| 5103 | 17212015 | Leptin [OR: 1.365, 95% CI: 1.170-1.592, p<0.001] and proinsulin [OR: 1.617, 95% CI: 1.218 -2.147, p=0.001] showed a significant positive association with obesity, while adiponectin [OR: 0.927, 95% CI: 0.865 - 0.995, p=0.035] had a significant inverse association. |
| 5104 | 17212015 | Linear regression analysis revealed that adiponectin is inversely associated with proinsulin even after the addition of age, gender and diabetes status [beta= -0.61, p=0.033] into the model. |
| 5105 | 17212015 | Linear regression analysis revealed that adiponectin is inversely associated with proinsulin even after the addition of age, gender and diabetes status [beta= -0.61, p=0.033] into the model. |
| 5106 | 17212015 | In conclusion, in urban Asian Indians in western India, proinsulin levels showed a positive association, while leptin and adiponectin showed a negative association with diabetes. |
| 5107 | 17212015 | In conclusion, in urban Asian Indians in western India, proinsulin levels showed a positive association, while leptin and adiponectin showed a negative association with diabetes. |
| 5108 | 17212015 | With regard to obesity, leptin and proinsulin had a positive association, while adiponectin had a negative association. |
| 5109 | 17212015 | With regard to obesity, leptin and proinsulin had a positive association, while adiponectin had a negative association. |
| 5110 | 17212015 | Proinsulin levels showed an inverse association with adiponectin indicating a possible link between insulin secretion and insulin resistance. |
| 5111 | 17212015 | Proinsulin levels showed an inverse association with adiponectin indicating a possible link between insulin secretion and insulin resistance. |
| 5112 | 17211725 | Curcumin can also downregulate the expression of various proinflammatory cytokines including TNF, IL-1, IL-2, IL-6, IL-8, IL-12, and chemokines, most likely through inactivation of the transcription factor NF-kappaB. |
| 5113 | 17208662 | Central obesity, one of the components of metabolic syndrome, is a cardiometabolic risk factor associated with a state of chronic inflammation and coagulation, one in which the expression of certain adipocytokines, including tumor necrosis factor-alpha (TNF-(alpha), interleukin (IL)-6, and plasminogen activator inhibitor-1 (PAI-1) is more abundantly increased, while adiponectin expression is decreased. |
| 5114 | 17208662 | Weight loss drugs, such as orlistat, a lipase inhibitor, and sibutramine, a serotonin and norepinephrine reuptake inhibitor, have both been shown to produce a decrease in C-reactive protein levels and an increase in serum adiponectin. |
| 5115 | 17202352 | Successful Ag activation of naive T helper cells requires at least two signals consisting of TCR and CD28 on the T cell interacting with MHC II and CD80/CD86, respectively, on APCs. |
| 5116 | 17202352 | Successful Ag activation of naive T helper cells requires at least two signals consisting of TCR and CD28 on the T cell interacting with MHC II and CD80/CD86, respectively, on APCs. |
| 5117 | 17202352 | We have reported that modulation of redox balance with a catalytic antioxidant effectively inhibited the generation of third signal components from the innate immune response (TNF-alpha, IL-1beta, ROS). |
| 5118 | 17202352 | We have reported that modulation of redox balance with a catalytic antioxidant effectively inhibited the generation of third signal components from the innate immune response (TNF-alpha, IL-1beta, ROS). |
| 5119 | 17202352 | Modulating redox balance led to decreased Ag-specific T cell proliferation and IFN-gamma synthesis by diminishing ROS production in the APC, which affected TNF-alpha levels produced by CD4(+) T cells and impairing effector function. |
| 5120 | 17202352 | Modulating redox balance led to decreased Ag-specific T cell proliferation and IFN-gamma synthesis by diminishing ROS production in the APC, which affected TNF-alpha levels produced by CD4(+) T cells and impairing effector function. |
| 5121 | 17202329 | We show that KRV infection strongly stimulates BBDR splenocytes to produce the proinflammatory cytokines IL-6 and IL-12p40 but not TNF-alpha. |
| 5122 | 17202329 | KRV infection induces high levels of IL-12p40 by splenic B cells and Flt-3-ligand-induced bone marrow-derived dendritic cells (DCs) but only low levels of IL-12p40 production by thioglycolate-elicited peritoneal macrophages or GM-CSF plus IL-4-induced bone marrow-derived DCs. |
| 5123 | 17202326 | Augmented lipopolysaccharide-induced TNF-alpha production by peritoneal macrophages in type 2 diabetic mice is dependent on elevated glucose and requires p38 MAPK. |
| 5124 | 17202326 | Augmented lipopolysaccharide-induced TNF-alpha production by peritoneal macrophages in type 2 diabetic mice is dependent on elevated glucose and requires p38 MAPK. |
| 5125 | 17202326 | Augmented lipopolysaccharide-induced TNF-alpha production by peritoneal macrophages in type 2 diabetic mice is dependent on elevated glucose and requires p38 MAPK. |
| 5126 | 17202326 | Augmented lipopolysaccharide-induced TNF-alpha production by peritoneal macrophages in type 2 diabetic mice is dependent on elevated glucose and requires p38 MAPK. |
| 5127 | 17202326 | In this study, we show that augmented LPS-induced TNF-alpha production by resident peritoneal macrophages (PerMphi) in type 2 diabetic (db/db) mice is dependent on elevated glucose and requires p38 MAPK. |
| 5128 | 17202326 | In this study, we show that augmented LPS-induced TNF-alpha production by resident peritoneal macrophages (PerMphi) in type 2 diabetic (db/db) mice is dependent on elevated glucose and requires p38 MAPK. |
| 5129 | 17202326 | In this study, we show that augmented LPS-induced TNF-alpha production by resident peritoneal macrophages (PerMphi) in type 2 diabetic (db/db) mice is dependent on elevated glucose and requires p38 MAPK. |
| 5130 | 17202326 | In this study, we show that augmented LPS-induced TNF-alpha production by resident peritoneal macrophages (PerMphi) in type 2 diabetic (db/db) mice is dependent on elevated glucose and requires p38 MAPK. |
| 5131 | 17202326 | Examination of the TLR-4/MD2 complex and CD14 expression showed no difference between db/db and db/+ PerMphi. |
| 5132 | 17202326 | Examination of the TLR-4/MD2 complex and CD14 expression showed no difference between db/db and db/+ PerMphi. |
| 5133 | 17202326 | Examination of the TLR-4/MD2 complex and CD14 expression showed no difference between db/db and db/+ PerMphi. |
| 5134 | 17202326 | Examination of the TLR-4/MD2 complex and CD14 expression showed no difference between db/db and db/+ PerMphi. |
| 5135 | 17202326 | LPS-dependent stimulation of PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice. |
| 5136 | 17202326 | LPS-dependent stimulation of PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice. |
| 5137 | 17202326 | LPS-dependent stimulation of PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice. |
| 5138 | 17202326 | LPS-dependent stimulation of PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice. |
| 5139 | 17202326 | Only inhibition of p38 kinase blocked LPS-induced TNF-alpha production in PerMphi from db/db mice. |
| 5140 | 17202326 | Only inhibition of p38 kinase blocked LPS-induced TNF-alpha production in PerMphi from db/db mice. |
| 5141 | 17202326 | Only inhibition of p38 kinase blocked LPS-induced TNF-alpha production in PerMphi from db/db mice. |
| 5142 | 17202326 | Only inhibition of p38 kinase blocked LPS-induced TNF-alpha production in PerMphi from db/db mice. |
| 5143 | 17202326 | Taken together, these data indicate that augmented TNF-alpha production induced by LPS in macrophages during diabetes is due to hyperglycemia and increased LPS-dependent activation of p38 kinase. |
| 5144 | 17202326 | Taken together, these data indicate that augmented TNF-alpha production induced by LPS in macrophages during diabetes is due to hyperglycemia and increased LPS-dependent activation of p38 kinase. |
| 5145 | 17202326 | Taken together, these data indicate that augmented TNF-alpha production induced by LPS in macrophages during diabetes is due to hyperglycemia and increased LPS-dependent activation of p38 kinase. |
| 5146 | 17202326 | Taken together, these data indicate that augmented TNF-alpha production induced by LPS in macrophages during diabetes is due to hyperglycemia and increased LPS-dependent activation of p38 kinase. |
| 5147 | 17202130 | Current investigations assessing the impact of anti-TNF agents on intermediary metabolism suggest that TNF-alpha blockade may improve insulin resistance and lipid profiles in patients with chronic inflammatory diseases. |
| 5148 | 17199240 | Effect of insulin and its combination with resveratrol or curcumin in attenuation of diabetic neuropathic pain: participation of nitric oxide and TNF-alpha. |
| 5149 | 17199240 | Effect of insulin and its combination with resveratrol or curcumin in attenuation of diabetic neuropathic pain: participation of nitric oxide and TNF-alpha. |
| 5150 | 17199240 | These results indicate an antinociceptive activity of resveratrol and curcumin and point towards the beneficial effect of these combinations with insulin in attenuating diabetic neuropathic pain, possibly through the participation of NO and TNF-alpha. |
| 5151 | 17199240 | These results indicate an antinociceptive activity of resveratrol and curcumin and point towards the beneficial effect of these combinations with insulin in attenuating diabetic neuropathic pain, possibly through the participation of NO and TNF-alpha. |
| 5152 | 17196622 | Macrophage activation was estimated by measuring tumor necrosis factor-alpha (TNF-alpha), nitric oxide, and monocyte chemoattractant protein-1 (MCP-1) concentrations. |
| 5153 | 17196622 | Macrophage activation was estimated by measuring tumor necrosis factor-alpha (TNF-alpha), nitric oxide, and monocyte chemoattractant protein-1 (MCP-1) concentrations. |
| 5154 | 17196622 | Among the active spice-derived components studied, allyl isothiocyanate, zingerone, and curcumin significantly inhibited the cellular production of proinflammatory mediators such as TNF-alpha and nitric oxide, and significantly inhibited the release of MCP-1 from 3T3-L1 adipocytes. |
| 5155 | 17196622 | Among the active spice-derived components studied, allyl isothiocyanate, zingerone, and curcumin significantly inhibited the cellular production of proinflammatory mediators such as TNF-alpha and nitric oxide, and significantly inhibited the release of MCP-1 from 3T3-L1 adipocytes. |
| 5156 | 20476950 | Among adipocytokines, tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs and may contribute to the development of vascular diseases. |
| 5157 | 20476950 | Among adipocytokines, tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs and may contribute to the development of vascular diseases. |
| 5158 | 20476950 | In contrast to these adipocytokines, adiponectin, an adipose tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein or as an anti-inflammatory protein. |
| 5159 | 20476950 | In contrast to these adipocytokines, adiponectin, an adipose tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein or as an anti-inflammatory protein. |
| 5160 | 20476950 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor necrosis factor-alpha, plasminogen activator inhibitor type 1, heparin-binding epidermal growth factor-like growth factor and visfatin and hyposecretion of adiponectin simultaneously, which results in the development of a variety of metabolic and circulatory diseases. |
| 5161 | 20476950 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor necrosis factor-alpha, plasminogen activator inhibitor type 1, heparin-binding epidermal growth factor-like growth factor and visfatin and hyposecretion of adiponectin simultaneously, which results in the development of a variety of metabolic and circulatory diseases. |
| 5162 | 17194640 | TNF-alpha, soluble TNF receptor and interleukin-6 plasma levels in the general population. |
| 5163 | 17194640 | TNF-alpha, soluble TNF receptor and interleukin-6 plasma levels in the general population. |
| 5164 | 17194640 | TNF-alpha, soluble TNF receptor and interleukin-6 plasma levels in the general population. |
| 5165 | 17194640 | TNF-alpha, soluble TNF receptor and interleukin-6 plasma levels in the general population. |
| 5166 | 17194640 | The cytokines tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptors p55 and p75, and interleukin 6 (IL-6) are involved in host defense against several microbiological agents, in the process of inflammation and also in body weight regulation. |
| 5167 | 17194640 | The cytokines tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptors p55 and p75, and interleukin 6 (IL-6) are involved in host defense against several microbiological agents, in the process of inflammation and also in body weight regulation. |
| 5168 | 17194640 | The cytokines tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptors p55 and p75, and interleukin 6 (IL-6) are involved in host defense against several microbiological agents, in the process of inflammation and also in body weight regulation. |
| 5169 | 17194640 | The cytokines tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptors p55 and p75, and interleukin 6 (IL-6) are involved in host defense against several microbiological agents, in the process of inflammation and also in body weight regulation. |
| 5170 | 17194640 | In the present study, we sought to assess the influence of age, gender, smoking, and body mass index on plasma levels of TNF-alpha, TNF receptors, and IL-6 in more than 550 adult subjects randomly selected from the Bavarian population. |
| 5171 | 17194640 | In the present study, we sought to assess the influence of age, gender, smoking, and body mass index on plasma levels of TNF-alpha, TNF receptors, and IL-6 in more than 550 adult subjects randomly selected from the Bavarian population. |
| 5172 | 17194640 | In the present study, we sought to assess the influence of age, gender, smoking, and body mass index on plasma levels of TNF-alpha, TNF receptors, and IL-6 in more than 550 adult subjects randomly selected from the Bavarian population. |
| 5173 | 17194640 | In the present study, we sought to assess the influence of age, gender, smoking, and body mass index on plasma levels of TNF-alpha, TNF receptors, and IL-6 in more than 550 adult subjects randomly selected from the Bavarian population. |
| 5174 | 17194640 | Plasma levels of TNF-alpha, TNF receptors, and IL-6 correlated significantly with the BMI. |
| 5175 | 17194640 | Plasma levels of TNF-alpha, TNF receptors, and IL-6 correlated significantly with the BMI. |
| 5176 | 17194640 | Plasma levels of TNF-alpha, TNF receptors, and IL-6 correlated significantly with the BMI. |
| 5177 | 17194640 | Plasma levels of TNF-alpha, TNF receptors, and IL-6 correlated significantly with the BMI. |
| 5178 | 17192490 | In the combined data, we replicated association (P < 0.05) for 12 SNPs: PPARG Pro12Ala and His447, KCNJ11 Glu23Lys and rs5210, TNF -857, SLC2A2 Ile110Thr, HNF1A/TCF1 rs2701175 and GE117881_360, PCK1 -232, NEUROD1 Thr45Ala, IL6 -598, and ENPP1 Lys121Gln. |
| 5179 | 17192481 | Modulating protective and pathogenic CD4+ subsets via CD137 in type 1 diabetes. |
| 5180 | 17192481 | CD137 (TNFRSF9) is an activation-inducible T-cell costimulatory molecule and a member of the tumor necrosis factor (TNF) receptor superfamily. |
| 5181 | 17192481 | Transfer of CD4(+), but not CD8(+), cells from anti-CD137-treated pre-diabetic NOD mice into NOD-scid mice delayed diabetes onset. |
| 5182 | 17192481 | Anti-CD137 treatment significantly increased the number of CD4(+)CD25(+) cells, which demonstrated intracellular Foxp3 expression and in vitro suppressive activity. |
| 5183 | 17192481 | The CD4(+)CD25(+) cell subset from anti-CD137-treated mice transferred complete protection from diabetes, whereas the CD4(+)CD25(-) cell subset offered no significant protection. |
| 5184 | 17189875 | Proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) also stimulated NF-kappaB-dependent transcription and showed an additive effect with high glucose. |
| 5185 | 17189875 | Similar effects were obtained on acute-phase or coagulation/fibrinolysis-related gene promoters such as fibrinogen or plasminogen activator inhibitor-1, all of which are shown to have NF-kappaB-mediated transcription. |
| 5186 | 17189873 | We compared the number of circulating monocyte and dendritic cell (DC) subsets as well as their capacity to produce inflammatory cytokines IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) in type 2 diabetic men with (n=11) and without (n=44) chronic atherosclerotic complications. |
| 5187 | 17189873 | We compared the number of circulating monocyte and dendritic cell (DC) subsets as well as their capacity to produce inflammatory cytokines IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) in type 2 diabetic men with (n=11) and without (n=44) chronic atherosclerotic complications. |
| 5188 | 17189873 | We compared the number of circulating monocyte and dendritic cell (DC) subsets as well as their capacity to produce inflammatory cytokines IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) in type 2 diabetic men with (n=11) and without (n=44) chronic atherosclerotic complications. |
| 5189 | 17189873 | Identification and enumeration of peripheral blood (PB) lymphoid subsets, monocytes, myeloid (CD33strong+), CD16+, and plasmacytoid (CD33-/dim+) DCs as well as of their spontaneous and stimulated production of IL-1beta, IL-6, and TNF-alpha were performed at the single-cell level by flow cytometry. |
| 5190 | 17189873 | Identification and enumeration of peripheral blood (PB) lymphoid subsets, monocytes, myeloid (CD33strong+), CD16+, and plasmacytoid (CD33-/dim+) DCs as well as of their spontaneous and stimulated production of IL-1beta, IL-6, and TNF-alpha were performed at the single-cell level by flow cytometry. |
| 5191 | 17189873 | Identification and enumeration of peripheral blood (PB) lymphoid subsets, monocytes, myeloid (CD33strong+), CD16+, and plasmacytoid (CD33-/dim+) DCs as well as of their spontaneous and stimulated production of IL-1beta, IL-6, and TNF-alpha were performed at the single-cell level by flow cytometry. |
| 5192 | 17189873 | Our results show that type 2 diabetic men with atherosclerotic complications display a significantly reduced spontaneous secretion of IL-6 by monocytes and CD16+ DCs and of TNF-alpha by CD16+ DCs as compared to patients without atherosclerotic complications. |
| 5193 | 17189873 | Our results show that type 2 diabetic men with atherosclerotic complications display a significantly reduced spontaneous secretion of IL-6 by monocytes and CD16+ DCs and of TNF-alpha by CD16+ DCs as compared to patients without atherosclerotic complications. |
| 5194 | 17189873 | Our results show that type 2 diabetic men with atherosclerotic complications display a significantly reduced spontaneous secretion of IL-6 by monocytes and CD16+ DCs and of TNF-alpha by CD16+ DCs as compared to patients without atherosclerotic complications. |
| 5195 | 17189873 | Spontaneous secretion of IL-1beta by monocytes and CD16 DCs and of IL-6 by CD33+ and plasmacytoid DCs was detected in patients without atherosclerotic complications but not in the other patients with complications. |
| 5196 | 17189873 | Spontaneous secretion of IL-1beta by monocytes and CD16 DCs and of IL-6 by CD33+ and plasmacytoid DCs was detected in patients without atherosclerotic complications but not in the other patients with complications. |
| 5197 | 17189873 | Spontaneous secretion of IL-1beta by monocytes and CD16 DCs and of IL-6 by CD33+ and plasmacytoid DCs was detected in patients without atherosclerotic complications but not in the other patients with complications. |
| 5198 | 17184177 | In endothelial cells, high-glucose treatment increases mitochondrial ROS and normalization of the ROS production by inhibitors of mitochondrial metabolism, or by overexpression of UCP-1 or MnSOD, prevents glucose-induced activation of PKC, formation of AGE, and accumulation of sorbitol, all of which are believed to be the main molecular mechanisms of diabetic complications. |
| 5199 | 17184177 | In pancreatic beta cells, hyperglycemia also increases mitochondrial ROS, which suppresses the first phase of glucose-induced insulin secretion, at least in part, through the suppression of GAPDH activity. |
| 5200 | 17184177 | In liver cells, similar to that in hyperglycemia, TNF-alpha increases mitochondrial ROS, which in turn activates apoptosis signal-regulating kinase 1 (ASK1) and c-jun NH2-terminal kinases (JNK), increases serine phosphorylation of IRS-1, and decreases insulin-stimulated tyrosine phosphorylation of IRS-1, leading to insulin resistance. |
| 5201 | 17183659 | Its transcriptional and functional similarity with the murine myeloid-specific and CCAAT/enhancer binding protein epsilon (Cebpe)-dependent gene, resistin-like gamma (Retnlg), is unexplored. |
| 5202 | 17183659 | Its transcriptional and functional similarity with the murine myeloid-specific and CCAAT/enhancer binding protein epsilon (Cebpe)-dependent gene, resistin-like gamma (Retnlg), is unexplored. |
| 5203 | 17183659 | Real-time RT-PCR analysis demonstrated lack of both the transcriptional factor CEBPE and RETN expression in adipose and muscle cells. |
| 5204 | 17183659 | Real-time RT-PCR analysis demonstrated lack of both the transcriptional factor CEBPE and RETN expression in adipose and muscle cells. |
| 5205 | 17183659 | Mouse Cebpe and Retnlg were predictably expressed in macrophages, whereas Retn was abundant in adipocytes. |
| 5206 | 17183659 | Mouse Cebpe and Retnlg were predictably expressed in macrophages, whereas Retn was abundant in adipocytes. |
| 5207 | 17183659 | Quite the opposite, a low and inconsistent RETN transcription was seen in some human white adipose tissue (WAT) biopsies without any relationship to body mass index, insulin sensitivity, or fat depot. |
| 5208 | 17183659 | Quite the opposite, a low and inconsistent RETN transcription was seen in some human white adipose tissue (WAT) biopsies without any relationship to body mass index, insulin sensitivity, or fat depot. |
| 5209 | 17183659 | However, in these cases, RETN was co-detected with CEBPE and the leukocyte-specific marker, EMR1, indicating the presence of inflammatory cells and their possible resistin-mediated effect on adipocytes. |
| 5210 | 17183659 | However, in these cases, RETN was co-detected with CEBPE and the leukocyte-specific marker, EMR1, indicating the presence of inflammatory cells and their possible resistin-mediated effect on adipocytes. |
| 5211 | 17183659 | Indeed, addition of human resistin to WAT in culture induced, like in PBMC, the inflammatory cytokines IL6, IL8 and TNF. |
| 5212 | 17183659 | Indeed, addition of human resistin to WAT in culture induced, like in PBMC, the inflammatory cytokines IL6, IL8 and TNF. |
| 5213 | 17183659 | Importantly, the expression of the adipose-specific markers CEBPA, FABP4 and SLC2A4 was unchanged, while the expected inhibitory effect was seen with TNF. |
| 5214 | 17183659 | Importantly, the expression of the adipose-specific markers CEBPA, FABP4 and SLC2A4 was unchanged, while the expected inhibitory effect was seen with TNF. |
| 5215 | 17183659 | Both cytokines increased the mRNA level of CCL2 and MMP3, which may further promote inflammation in WAT. |
| 5216 | 17183659 | Both cytokines increased the mRNA level of CCL2 and MMP3, which may further promote inflammation in WAT. |
| 5217 | 17183659 | Thus, the myeloid-restricted nature of CEBPE precludes the expression of RETN in human adipocytes which, however, are targeted by this innate immune-derived proinflammatory cytokine. |
| 5218 | 17183659 | Thus, the myeloid-restricted nature of CEBPE precludes the expression of RETN in human adipocytes which, however, are targeted by this innate immune-derived proinflammatory cytokine. |
| 5219 | 17181562 | Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. |
| 5220 | 17181562 | Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. |
| 5221 | 17181562 | Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. |
| 5222 | 17181562 | In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. |
| 5223 | 17181562 | In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. |
| 5224 | 17181562 | In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. |
| 5225 | 17181562 | This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. |
| 5226 | 17181562 | This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. |
| 5227 | 17181562 | This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. |
| 5228 | 17181562 | The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. |
| 5229 | 17181562 | The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. |
| 5230 | 17181562 | The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. |
| 5231 | 17181562 | In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. |
| 5232 | 17181562 | In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. |
| 5233 | 17181562 | In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-alpha concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. |
| 5234 | 17177137 | Histological studies evaluated insulitis development and Western blot analysis was employed to evaluate the expression levels of Th1 cytokines (TNF-alpha and IFN-gamma) and Th2 cytokines (IL-10 and IL-4). |
| 5235 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5236 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5237 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5238 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5239 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5240 | 17174749 | Linkage disequilibrium with predisposing DR3 haplotypes accounts for apparent effects of tumor necrosis factor and lymphotoxin-alpha polymorphisms on type 1 diabetes susceptibility. |
| 5241 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5242 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5243 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5244 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5245 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5246 | 17174749 | Tumor necrosis factor (TNF) and lymphotoxin alpha (LT-alpha) are immunomodulators that have been hypothesized to contribute to susceptibility to type 1 diabetes (T1D). |
| 5247 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5248 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5249 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5250 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5251 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5252 | 17174749 | Several polymorphisms in the TNF and LT-alpha loci have been extensively studied for T1D association, with conflicting reports. |
| 5253 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5254 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5255 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5256 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5257 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5258 | 17174749 | In this study, we examined two TNF variants and one LT-alpha variant for T1D association in 283 Caucasian, multiplex T1D families for which complete human leukocyte antigen (HLA) genotyping data are available. |
| 5259 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5260 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5261 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5262 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5263 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5264 | 17174749 | Initially, association with T1D was seen for LT-alpha A1069G (intron A, p=0.011, rs909253) and TNF G(-308)A (p<1x10(-5), rs1800629), but no association was observed for TNF G(-238)A (rs361525). |
| 5265 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5266 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5267 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5268 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5269 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5270 | 17174749 | Including HLA-B data in the analysis revealed that TNF (-238)A is present exclusively on DR3 haplotypes that also carry HLA-B18. |
| 5271 | 17170102 | The role of 12/15-lipoxygenase in the expression of interleukin-6 and tumor necrosis factor-alpha in macrophages. |
| 5272 | 17170102 | The role of 12/15-lipoxygenase in the expression of interleukin-6 and tumor necrosis factor-alpha in macrophages. |
| 5273 | 17170102 | The role of 12/15-lipoxygenase in the expression of interleukin-6 and tumor necrosis factor-alpha in macrophages. |
| 5274 | 17170102 | The role of 12/15-lipoxygenase in the expression of interleukin-6 and tumor necrosis factor-alpha in macrophages. |
| 5275 | 17170102 | To study the role of 12/15-LO in cytokine expression, experiments with direct additions of the12/15-LO products, 12(S)-hydroxyeicosa tetraenoic acid or 12(S)-hydroperoxyeicosa-5Z, 8Z, 10E, or 14Z-tetraenoic acid to macrophages were first carried out, and results showed that the 12/15-LO products stimulated mRNA and protein expression of IL-6 and TNF-alpha in a dose-dependent manner. |
| 5276 | 17170102 | To study the role of 12/15-LO in cytokine expression, experiments with direct additions of the12/15-LO products, 12(S)-hydroxyeicosa tetraenoic acid or 12(S)-hydroperoxyeicosa-5Z, 8Z, 10E, or 14Z-tetraenoic acid to macrophages were first carried out, and results showed that the 12/15-LO products stimulated mRNA and protein expression of IL-6 and TNF-alpha in a dose-dependent manner. |
| 5277 | 17170102 | To study the role of 12/15-LO in cytokine expression, experiments with direct additions of the12/15-LO products, 12(S)-hydroxyeicosa tetraenoic acid or 12(S)-hydroperoxyeicosa-5Z, 8Z, 10E, or 14Z-tetraenoic acid to macrophages were first carried out, and results showed that the 12/15-LO products stimulated mRNA and protein expression of IL-6 and TNF-alpha in a dose-dependent manner. |
| 5278 | 17170102 | To study the role of 12/15-LO in cytokine expression, experiments with direct additions of the12/15-LO products, 12(S)-hydroxyeicosa tetraenoic acid or 12(S)-hydroperoxyeicosa-5Z, 8Z, 10E, or 14Z-tetraenoic acid to macrophages were first carried out, and results showed that the 12/15-LO products stimulated mRNA and protein expression of IL-6 and TNF-alpha in a dose-dependent manner. |
| 5279 | 17170102 | The results showed a clear increase in IL-6 and TNF-alpha expression in Plox-86 cells and MPMs from 12/15-LO transgenic mice, compared with mock-transfected J774A.1 cells and MPMs from control C57BL6 mice. |
| 5280 | 17170102 | The results showed a clear increase in IL-6 and TNF-alpha expression in Plox-86 cells and MPMs from 12/15-LO transgenic mice, compared with mock-transfected J774A.1 cells and MPMs from control C57BL6 mice. |
| 5281 | 17170102 | The results showed a clear increase in IL-6 and TNF-alpha expression in Plox-86 cells and MPMs from 12/15-LO transgenic mice, compared with mock-transfected J774A.1 cells and MPMs from control C57BL6 mice. |
| 5282 | 17170102 | The results showed a clear increase in IL-6 and TNF-alpha expression in Plox-86 cells and MPMs from 12/15-LO transgenic mice, compared with mock-transfected J774A.1 cells and MPMs from control C57BL6 mice. |
| 5283 | 17170102 | IL-1beta, IL-12, and monocyte chemoattractant protein (MCP)-1 mRNA were also increased in Plox-86 cells. |
| 5284 | 17170102 | IL-1beta, IL-12, and monocyte chemoattractant protein (MCP)-1 mRNA were also increased in Plox-86 cells. |
| 5285 | 17170102 | IL-1beta, IL-12, and monocyte chemoattractant protein (MCP)-1 mRNA were also increased in Plox-86 cells. |
| 5286 | 17170102 | IL-1beta, IL-12, and monocyte chemoattractant protein (MCP)-1 mRNA were also increased in Plox-86 cells. |
| 5287 | 17170102 | We also demonstrated that signaling pathways including protein kinase C, p38 MAPK (p38), c-jun NH(2)-terminal kinase as well as nicotinamide adenine dinucleotide phosphate oxidase are important for 12-(S)-hydroxyeicosatetraenoic acid-induced increases in IL-6 and TNF-alpha gene expression. |
| 5288 | 17170102 | We also demonstrated that signaling pathways including protein kinase C, p38 MAPK (p38), c-jun NH(2)-terminal kinase as well as nicotinamide adenine dinucleotide phosphate oxidase are important for 12-(S)-hydroxyeicosatetraenoic acid-induced increases in IL-6 and TNF-alpha gene expression. |
| 5289 | 17170102 | We also demonstrated that signaling pathways including protein kinase C, p38 MAPK (p38), c-jun NH(2)-terminal kinase as well as nicotinamide adenine dinucleotide phosphate oxidase are important for 12-(S)-hydroxyeicosatetraenoic acid-induced increases in IL-6 and TNF-alpha gene expression. |
| 5290 | 17170102 | We also demonstrated that signaling pathways including protein kinase C, p38 MAPK (p38), c-jun NH(2)-terminal kinase as well as nicotinamide adenine dinucleotide phosphate oxidase are important for 12-(S)-hydroxyeicosatetraenoic acid-induced increases in IL-6 and TNF-alpha gene expression. |
| 5291 | 17166396 | We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. |
| 5292 | 17166396 | We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. |
| 5293 | 17166396 | TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. |
| 5294 | 17166396 | TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. |
| 5295 | 17162361 | HLA-DRB1, TNF and PTPN22) influence the susceptibility for acquiring different ADs. |
| 5296 | 17161237 | Fasting serum haptoglobin, insulin, and C-peptide were assayed, and select messenger RNA (mRNA) and protein markers of inflammation and glucose metabolism were measured in adipose and liver tissues. |
| 5297 | 17161237 | The CLA-fed fa/fa rats also had greater adipose glucose transporter-4 mRNA and less adipose tumor necrosis factor alpha mRNA and protein compared with control-fed fa/fa rats. |
| 5298 | 17161237 | In contrast, other markers of inflammation and glucose metabolism including adipose macrophage inflammatory factor, macrophage inflammatory protein-2, and liver pyruvate carboxylase and pyruvate dehydrogenase kinase 4 were not significantly changed. |
| 5299 | 17160670 | Using quantitative real-time PCR, we could show that the expression of intercellular adhesion molecule 1 (ICAM-1), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) significantly increased in peripheral blood leukocytes from "MetS" subjects (n=39) compared to "no MetS" subjects (n=35) 2 h after an oral glucose tolerance test (ICAM-1 +52%, TNF-alpha +107%, and IL-6 +38%) and also in vitro after 72 h cultivation in high-glucose medium (ICAM-1 +74%, TNF-alpha +71%, and IL-6 +44%). |
| 5300 | 17160670 | Using quantitative real-time PCR, we could show that the expression of intercellular adhesion molecule 1 (ICAM-1), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) significantly increased in peripheral blood leukocytes from "MetS" subjects (n=39) compared to "no MetS" subjects (n=35) 2 h after an oral glucose tolerance test (ICAM-1 +52%, TNF-alpha +107%, and IL-6 +38%) and also in vitro after 72 h cultivation in high-glucose medium (ICAM-1 +74%, TNF-alpha +71%, and IL-6 +44%). |
| 5301 | 17160670 | Using ELISA and Luminex technique, we further observed a trend towards increased immune mediator concentrations in the corresponding cell culture supernatants from MetS patients (ICAM-1 +21%, TNF-alpha +31%, and IL-6 +175%). |
| 5302 | 17160670 | Using ELISA and Luminex technique, we further observed a trend towards increased immune mediator concentrations in the corresponding cell culture supernatants from MetS patients (ICAM-1 +21%, TNF-alpha +31%, and IL-6 +175%). |
| 5303 | 17151300 | Four different diabetic groups allocated on the basis of the subjects' age (Group A: 15-25 years old; Group B: 26-40 years old; Group C: 40-60 years old; Group D: 60-80 years old) and consisting of 10 patients each, in parallel with 10 healthy controls matched for age, sex, and ethnic origin were screened for glucose, insulin, lipid profile (total cholesterol, triglycerides, LDL, and HDL), and inflammatory mediators (CRP, IL-6, and TNF-alpha). |
| 5304 | 17151295 | The main cytokines involved in the pathogenesis of T2D are interleukin-1beta (IL-1beta), with an action similar to the one present in type 1 diabetes, tumor necrosis factor-alpha (TNF-alpha), and IL-6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein-1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. |
| 5305 | 17148780 | The animals receiving VGX-1027 exhibited reduced production of the proinflammatory mediators tumor necrosis factor-alpha, IL-1beta, macrophage migration inhibitory factor, and inducible nitric-oxide synthase-mediated nitric oxide generation in both pancreatic islets and peripheral compartments. |
| 5306 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 5307 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 5308 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 5309 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 5310 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 5311 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 5312 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 5313 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 5314 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 5315 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 5316 | 17144883 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra (interleukin-1 receptor antagonist) and IL-10 (interleukin-10) and inhibits the production of the pro-inflammatory cytokine TNF-alpha (tumour necrosis factor-alpha). |
| 5317 | 17144883 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra (interleukin-1 receptor antagonist) and IL-10 (interleukin-10) and inhibits the production of the pro-inflammatory cytokine TNF-alpha (tumour necrosis factor-alpha). |
| 5318 | 17144883 | It is suggested that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 5319 | 17144883 | It is suggested that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 5320 | 17142138 | This study was designed to investigate the effect of spironolactone, a representative aldosterone blocker, on adipocytokines such as adiponectin, visfatin, plasminogen activator inhibitor (PAI)-1 and tumor necrosis factor alpha in patients with type 2 diabetic nephropathy: the study included 33 patients, 22 of whom were randomly assigned to the spironolactone (50 mg/d) group and 11 to the amlodipine (2.5 mg/d) group. |
| 5321 | 17142138 | Adiponectin and visfatin levels did not change in the spironolactone and amlodipine groups, but significant increases in these adipocytokines were found in a subgroup of patients in the spironolactone group with glycated hemoglobin A(1c) (HbA(1c)) 8.0% or greater (11.8 +/- 6.4 to 13.3 +/- 7.4 microg/mL, P = .0344; and 1.39 +/- 0.92 to 2.26 +/- 0.76 ng/mL, P =.0397, respectively). |
| 5322 | 17142138 | Moreover, neither spironolactone nor amlodipine therapy caused a change in high-sensitivity C-reactive protein or soluble CD40 ligand, but a significant decrease in the level of brain natriuretic peptide was found in the spironolactone group only. |
| 5323 | 17142138 | Furthermore, significant increases of HbA(1c), creatinine, potassium, and aldosterone levels and plasma renin activity, and a decrease in urinary albumin excretion were also observed only in the spironolactone group. |
| 5324 | 17142138 | In conclusion, our data suggest that in patients with type 2 diabetes mellitus complicated by diabetic nephropathy, spironolactone can decrease plasminogen activator inhibitor 1 and brain natriuretic peptide levels in addition to urinary albumin excretion, and systolic blood pressure, and that in patients with poor glycemic control, spironolactone can increase the levels of adiponectin and visfatin. |
| 5325 | 17141246 | Stimulation of the peroxisome proliferator-activated receptor gamma (PPAR gamma) and the expression of selected blood monocyte cytokine genes in diabetic macroangiopathy. |
| 5326 | 17141246 | Stimulation of the peroxisome proliferator-activated receptor gamma (PPAR gamma) and the expression of selected blood monocyte cytokine genes in diabetic macroangiopathy. |
| 5327 | 17141246 | Stimulation of the peroxisome proliferator-activated receptor gamma (PPAR gamma) and the expression of selected blood monocyte cytokine genes in diabetic macroangiopathy. |
| 5328 | 17141246 | Stimulation of the peroxisome proliferator-activated receptor gamma (PPAR gamma) and the expression of selected blood monocyte cytokine genes in diabetic macroangiopathy. |
| 5329 | 17141246 | The peroxisome proliferator-activated receptor gamma (PPAR gamma) can limit macroangiopathy through the control of cytokine transcription. |
| 5330 | 17141246 | The peroxisome proliferator-activated receptor gamma (PPAR gamma) can limit macroangiopathy through the control of cytokine transcription. |
| 5331 | 17141246 | The peroxisome proliferator-activated receptor gamma (PPAR gamma) can limit macroangiopathy through the control of cytokine transcription. |
| 5332 | 17141246 | The peroxisome proliferator-activated receptor gamma (PPAR gamma) can limit macroangiopathy through the control of cytokine transcription. |
| 5333 | 17141246 | The objectives of this study were to examine the influence of PPAR gamma and its agonist (rosiglitazone) on the TNFalpha, IL-6, IL-8 and IL-10 gene expression in monocytes of patients with diabetic macroangiopathy and to analyse obtained results in context of selected atherogenic factors ant direct indicators of endothelial lesion. |
| 5334 | 17141246 | The objectives of this study were to examine the influence of PPAR gamma and its agonist (rosiglitazone) on the TNFalpha, IL-6, IL-8 and IL-10 gene expression in monocytes of patients with diabetic macroangiopathy and to analyse obtained results in context of selected atherogenic factors ant direct indicators of endothelial lesion. |
| 5335 | 17141246 | The objectives of this study were to examine the influence of PPAR gamma and its agonist (rosiglitazone) on the TNFalpha, IL-6, IL-8 and IL-10 gene expression in monocytes of patients with diabetic macroangiopathy and to analyse obtained results in context of selected atherogenic factors ant direct indicators of endothelial lesion. |
| 5336 | 17141246 | The objectives of this study were to examine the influence of PPAR gamma and its agonist (rosiglitazone) on the TNFalpha, IL-6, IL-8 and IL-10 gene expression in monocytes of patients with diabetic macroangiopathy and to analyse obtained results in context of selected atherogenic factors ant direct indicators of endothelial lesion. |
| 5337 | 17141246 | TNFalpha, IL-6, IL-8, IL-10 and PPAR gamma gene expression was assessed in peripheral blood monocytes in 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy (real-time PCR [Applied Biosystems]). |
| 5338 | 17141246 | TNFalpha, IL-6, IL-8, IL-10 and PPAR gamma gene expression was assessed in peripheral blood monocytes in 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy (real-time PCR [Applied Biosystems]). |
| 5339 | 17141246 | TNFalpha, IL-6, IL-8, IL-10 and PPAR gamma gene expression was assessed in peripheral blood monocytes in 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy (real-time PCR [Applied Biosystems]). |
| 5340 | 17141246 | TNFalpha, IL-6, IL-8, IL-10 and PPAR gamma gene expression was assessed in peripheral blood monocytes in 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy (real-time PCR [Applied Biosystems]). |
| 5341 | 17141246 | Following rosiglitazone therapy, a statistically significant downward tendency of TNFalpha (p=0.026) and IL-8 (p=0.008) gene expression was noted. |
| 5342 | 17141246 | Following rosiglitazone therapy, a statistically significant downward tendency of TNFalpha (p=0.026) and IL-8 (p=0.008) gene expression was noted. |
| 5343 | 17141246 | Following rosiglitazone therapy, a statistically significant downward tendency of TNFalpha (p=0.026) and IL-8 (p=0.008) gene expression was noted. |
| 5344 | 17141246 | Following rosiglitazone therapy, a statistically significant downward tendency of TNFalpha (p=0.026) and IL-8 (p=0.008) gene expression was noted. |
| 5345 | 17141246 | Before and following rosiglitazone treatment, PPAR gamma, IL-6 and IL-10 gene expression was undetectable in studied monocytes in vivo. |
| 5346 | 17141246 | Before and following rosiglitazone treatment, PPAR gamma, IL-6 and IL-10 gene expression was undetectable in studied monocytes in vivo. |
| 5347 | 17141246 | Before and following rosiglitazone treatment, PPAR gamma, IL-6 and IL-10 gene expression was undetectable in studied monocytes in vivo. |
| 5348 | 17141246 | Before and following rosiglitazone treatment, PPAR gamma, IL-6 and IL-10 gene expression was undetectable in studied monocytes in vivo. |
| 5349 | 17141246 | In conclusion, TNFalpha and IL-8 play an important role in monocyte atherogenic activity. |
| 5350 | 17141246 | In conclusion, TNFalpha and IL-8 play an important role in monocyte atherogenic activity. |
| 5351 | 17141246 | In conclusion, TNFalpha and IL-8 play an important role in monocyte atherogenic activity. |
| 5352 | 17141246 | In conclusion, TNFalpha and IL-8 play an important role in monocyte atherogenic activity. |
| 5353 | 17141246 | Rosiglitazone reduces monocyte proinflammatory readiness by influencing the expression of selected atherogenic cytokines (PPAR gamma-independent pathway). |
| 5354 | 17141246 | Rosiglitazone reduces monocyte proinflammatory readiness by influencing the expression of selected atherogenic cytokines (PPAR gamma-independent pathway). |
| 5355 | 17141246 | Rosiglitazone reduces monocyte proinflammatory readiness by influencing the expression of selected atherogenic cytokines (PPAR gamma-independent pathway). |
| 5356 | 17141246 | Rosiglitazone reduces monocyte proinflammatory readiness by influencing the expression of selected atherogenic cytokines (PPAR gamma-independent pathway). |
| 5357 | 17135326 | We have previously reported that HCV core gene-transgenic (PA28gamma(+/+)CoreTg) mice develop marked insulin resistance and that the HCV core protein is degraded in the nucleus through a PA28gamma-dependent pathway. |
| 5358 | 17135326 | In this study, we examined whether PA28gamma is required for HCV core-induced insulin resistance in vivo. |
| 5359 | 17135326 | Although there was no significant difference in the glucose tolerance test results among the mice, the insulin sensitivity in PA28gamma(-/-)CoreTg mice was recovered to a normal level in the insulin tolerance test. |
| 5360 | 17135326 | Tyrosine phosphorylation of insulin receptor substrate 1 (IRS1), production of IRS2, and phosphorylation of Akt were suppressed in the livers of PA28gamma(+/+)CoreTg mice in response to insulin stimulation, whereas they were restored in the livers of PA28gamma(-/-)CoreTg mice. |
| 5361 | 17135326 | Furthermore, activation of the tumor necrosis factor alpha promoter in human liver cell lines or mice by the HCV core protein was suppressed by the knockdown or knockout of the PA28gamma gene. |
| 5362 | 17131467 | Hepatitis C virus (HCV) infection promotes insulin resistance, mainly by increased TNF production together with enhancement of suppressor of cytokine (SOC-3); both events block PI3K and Akt phosphorylation. |
| 5363 | 17131467 | Hepatitis C virus (HCV) infection promotes insulin resistance, mainly by increased TNF production together with enhancement of suppressor of cytokine (SOC-3); both events block PI3K and Akt phosphorylation. |
| 5364 | 17131467 | The mechanisms by which insulin resistance promotes fibrosis progression include: (1) steatosis, (2) hyperleptinemia, (3) increased TNF production, (4) impaired expression of PPARgamma receptors. |
| 5365 | 17131467 | The mechanisms by which insulin resistance promotes fibrosis progression include: (1) steatosis, (2) hyperleptinemia, (3) increased TNF production, (4) impaired expression of PPARgamma receptors. |
| 5366 | 17130569 | TNF microsatellite together with HLA polymorphisms is associated with type 1 diabetes in Brazilian patients, corroborating the participation of the MHC genes in disease susceptibility. |
| 5367 | 17130551 | In vitro TNF-alpha and IL-6 production by adherent peripheral blood mononuclear cells obtained from type 1 and type 2 diabetic patients evaluated according to the metabolic control. |
| 5368 | 17130551 | In vitro TNF-alpha and IL-6 production by adherent peripheral blood mononuclear cells obtained from type 1 and type 2 diabetic patients evaluated according to the metabolic control. |
| 5369 | 17130551 | In vitro TNF-alpha and IL-6 production by adherent peripheral blood mononuclear cells obtained from type 1 and type 2 diabetic patients evaluated according to the metabolic control. |
| 5370 | 17130551 | In vitro TNF-alpha and IL-6 production by adherent peripheral blood mononuclear cells obtained from type 1 and type 2 diabetic patients evaluated according to the metabolic control. |
| 5371 | 17130551 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels were evaluated in lipopolysaccharide (LPS)-stimulated cell cultured monocytes obtained from 24 type 1 and type 2 diabetic patients presenting inadequate (IN) or adequate (AD) metabolic control, and in 21 healthy individuals paired to patients for sex and age. |
| 5372 | 17130551 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels were evaluated in lipopolysaccharide (LPS)-stimulated cell cultured monocytes obtained from 24 type 1 and type 2 diabetic patients presenting inadequate (IN) or adequate (AD) metabolic control, and in 21 healthy individuals paired to patients for sex and age. |
| 5373 | 17130551 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels were evaluated in lipopolysaccharide (LPS)-stimulated cell cultured monocytes obtained from 24 type 1 and type 2 diabetic patients presenting inadequate (IN) or adequate (AD) metabolic control, and in 21 healthy individuals paired to patients for sex and age. |
| 5374 | 17130551 | Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels were evaluated in lipopolysaccharide (LPS)-stimulated cell cultured monocytes obtained from 24 type 1 and type 2 diabetic patients presenting inadequate (IN) or adequate (AD) metabolic control, and in 21 healthy individuals paired to patients for sex and age. |
| 5375 | 17130551 | The TNF-alpha levels in stimulated cultures of diabetic patients were similar to healthy individuals, and type 1 diabetic patients showed increased IL-6 supernatant levels. |
| 5376 | 17130551 | The TNF-alpha levels in stimulated cultures of diabetic patients were similar to healthy individuals, and type 1 diabetic patients showed increased IL-6 supernatant levels. |
| 5377 | 17130551 | The TNF-alpha levels in stimulated cultures of diabetic patients were similar to healthy individuals, and type 1 diabetic patients showed increased IL-6 supernatant levels. |
| 5378 | 17130551 | The TNF-alpha levels in stimulated cultures of diabetic patients were similar to healthy individuals, and type 1 diabetic patients showed increased IL-6 supernatant levels. |
| 5379 | 17130551 | The tendency toward increased TNF-alpha and IL-6 levels was observed with metabolic control of type 1 and type 2 diabetic patients, suggesting that the control of diabetes improves the capacity of activation and maintenance of the proinflammatory immune response. |
| 5380 | 17130551 | The tendency toward increased TNF-alpha and IL-6 levels was observed with metabolic control of type 1 and type 2 diabetic patients, suggesting that the control of diabetes improves the capacity of activation and maintenance of the proinflammatory immune response. |
| 5381 | 17130551 | The tendency toward increased TNF-alpha and IL-6 levels was observed with metabolic control of type 1 and type 2 diabetic patients, suggesting that the control of diabetes improves the capacity of activation and maintenance of the proinflammatory immune response. |
| 5382 | 17130551 | The tendency toward increased TNF-alpha and IL-6 levels was observed with metabolic control of type 1 and type 2 diabetic patients, suggesting that the control of diabetes improves the capacity of activation and maintenance of the proinflammatory immune response. |
| 5383 | 17130485 | Endogenous ApoE expression modulates adipocyte triglyceride content and turnover. |
| 5384 | 17130485 | Apolipoprotein E (apoE) is highly expressed in adipose tissue and adipocytes in which its expression is regulated by peroxisome proliferator-activated receptor (PPAR)-gamma agonists and tumor necrosis factor-alpha. |
| 5385 | 17130485 | There is, however, no information regarding a role for endogenous apoE in differentiated adipocyte function. |
| 5386 | 17130485 | In this report, we define a novel role for apoE in modulating adipocyte lipid metabolism. |
| 5387 | 17130485 | Markers of adipocyte differentiation were lower in freshly isolated and cultured apoE(-/-) adipocytes. |
| 5388 | 17130485 | Importantly, PPAR-gamma-mediated changes in lipid content and gene expression are markedly altered in cultured apoE(-/-) adipocytes. |
| 5389 | 17130485 | These results establish a novel role for endogenous apoE in adipocyte lipid metabolism and have implications for constructing an integrated model of adipocyte physiology in health and disease. |
| 5390 | 17130263 | Insulin resistance, inflammatory biomarkers, and adipokines in patients with chronic kidney disease: effects of angiotensin II blockade. |
| 5391 | 17130263 | In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-alpha, and IL-6. |
| 5392 | 17130263 | In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. |
| 5393 | 17130263 | Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 +/- 16 versus 92 +/- 14 mg/dl; P < 0.05), insulin (23.1 +/- 8.8 versus 19.9 +/- 9; P < 0.05), HOMA index (6.0 +/- 2.7 versus 4.7 +/- 2.8; P < 0.05), and glycated hemoglobin (5.33 +/- 0.58 versus 4.85 +/- 0.81%; P < 0.01). |
| 5394 | 17127716 | Lipoic acid (LA) is a sulfated antioxidant produced physiologically as a coenzyme of the pyruvate dehydrogenase complex; it is currently used for treatment of non-insulin-dependent diabetes to favor the cellular uptake of glucose. |
| 5395 | 17127716 | LA induced the production of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL) in KS-Imm and activin-A in KS-Imm and endothelial cells; these factors show anti-angiogenic activity in vivo contributing to explain the inhibitory effect of LA on neovascularization. |
| 5396 | 17125935 | There is even more evidence that implicates the presence of autoimmune mechanisms in the proliferative stage of this disease: elevated levels of tumor necrosis factor-alpha, interleukin-8 and soluble interleukin-2 receptor in the serum of diabetic patients, increased vitreous concentration of the interleukin-6 and interleukin-8 in patients with proliferative retinopathy. |
| 5397 | 17119268 | PPARalpha is most common in the liver, but also found in kidney, gut, skeletal muscle and adipose tissue, while PPARbeta/delta, is fairly ubiquitous; it may be found in body tissues and brain (for myelination process and lipid metabolism in the brain). |
| 5398 | 17119268 | PPARalpha is most common in the liver, but also found in kidney, gut, skeletal muscle and adipose tissue, while PPARbeta/delta, is fairly ubiquitous; it may be found in body tissues and brain (for myelination process and lipid metabolism in the brain). |
| 5399 | 17119268 | This metabolic syndrome represents a "Cluster" of metabolic disorders and cardiovascular risk factors which has been collected and summarized by the author and such a cluster includes: insulin resistance/hyperinsulinemia, central obesity, glucose intolerance/DM, atherogenic dyslipidemia (increase TG, decrease HDL-cholesterol, increase Apo-B, increase small dense LDL), hypertension, prothrombotic state (increase PAI-1, increase F-VII, increase fibrinogen, increase vWF, increase adhesion molecules), endothelial dysfunction, hyperuricemia, and increased hsC-RP and cytokines. |
| 5400 | 17119268 | This metabolic syndrome represents a "Cluster" of metabolic disorders and cardiovascular risk factors which has been collected and summarized by the author and such a cluster includes: insulin resistance/hyperinsulinemia, central obesity, glucose intolerance/DM, atherogenic dyslipidemia (increase TG, decrease HDL-cholesterol, increase Apo-B, increase small dense LDL), hypertension, prothrombotic state (increase PAI-1, increase F-VII, increase fibrinogen, increase vWF, increase adhesion molecules), endothelial dysfunction, hyperuricemia, and increased hsC-RP and cytokines. |
| 5401 | 17119268 | PPARgamma can be activated by TZDs and it appears to be fundamental to the pathophysiology of diabetes mellitus i.e increase GLUT-4, increase glucokinase, decrease PEPCK, increase GLUT-4, and decreases production by fat cell of several mediators that may cause insulin resistance, such as TNFalpha and resistin. |
| 5402 | 17119268 | PPARgamma can be activated by TZDs and it appears to be fundamental to the pathophysiology of diabetes mellitus i.e increase GLUT-4, increase glucokinase, decrease PEPCK, increase GLUT-4, and decreases production by fat cell of several mediators that may cause insulin resistance, such as TNFalpha and resistin. |
| 5403 | 17119268 | PPARgamma also mediates increased production of Adiponectin and the insulin signaling intermediate PI3K, and both actions lead to increase insulin sensitivity. |
| 5404 | 17119268 | PPARgamma also mediates increased production of Adiponectin and the insulin signaling intermediate PI3K, and both actions lead to increase insulin sensitivity. |
| 5405 | 17119268 | Current evidence suggests a close relationship between activation of PPARgamma and restoration of insulin sensitivity by reductions in TNFalpha and FFAs, and the enhancement of insulin stimulation of PI3-K Pathway and also increase adiponectin & decrease resistin. |
| 5406 | 17119268 | Current evidence suggests a close relationship between activation of PPARgamma and restoration of insulin sensitivity by reductions in TNFalpha and FFAs, and the enhancement of insulin stimulation of PI3-K Pathway and also increase adiponectin & decrease resistin. |
| 5407 | 17112855 | Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. |
| 5408 | 17112855 | Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. |
| 5409 | 17112855 | Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. |
| 5410 | 17112855 | Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. |
| 5411 | 17112855 | Pentoxifylline (PTX) is a nonselective phosphodiesterase inhibitor that inhibits the production of TNFalpha and IL6 and IL-10 cytokines. |
| 5412 | 17112855 | In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. |
| 5413 | 17112855 | In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. |
| 5414 | 17112855 | In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. |
| 5415 | 17112855 | In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. |
| 5416 | 17112855 | In renal rejection TNFalpha, IL-6, and IL-10 may have important roles. |
| 5417 | 17112855 | At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. |
| 5418 | 17112855 | At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. |
| 5419 | 17112855 | At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. |
| 5420 | 17112855 | At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. |
| 5421 | 17112855 | At the end of 3 months TNF-alpha decreased from 4.2 +/- 2.1 to 2.4 +/- 0.7 (P = .001) and 4.0 +/- 2.2 to 3.9 +/- 1.7 (P = .718), IL-10 also decreased from 3.90 +/- 1.9 to 2.38 +/- 0.6 (P = .001) and 4.02 +/- 1.6 to 3.82 +/- 1.5 (P = .225) in GI and GII, respectively. |
| 5422 | 17112855 | For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). |
| 5423 | 17112855 | For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). |
| 5424 | 17112855 | For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). |
| 5425 | 17112855 | For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). |
| 5426 | 17112855 | For IL-10 and TNF-alpha the alterations between baseline and the last visit of GI and GII were significant (P < .002 for all). |
| 5427 | 17112855 | In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. |
| 5428 | 17112855 | In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. |
| 5429 | 17112855 | In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. |
| 5430 | 17112855 | In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. |
| 5431 | 17112855 | In summary IL-10 and TNF-alpha levels decreased in stable recipients treated with PTx. |
| 5432 | 17112620 | Type 2 diabetic patients showed significantly higher expression levels of TNF-alpha, IL-6, IL-1, IL-8, COX-2, ICAM-1 and B7-1 compared to controls and type 1 diabetic patients. 1,25-Dihydroxyvitamin D(3) was able to down-regulate the expression of TNF-alpha, IL-6, IL-1, and IL-8, confirming its immunomodulatory properties. |
| 5433 | 17100770 | Evidence for immunological priming and increased frequency of CD4+ CD25+ cord blood T cells in children born to mothers with type 1 diabetes. |
| 5434 | 17100770 | Levels of interleukin (IL)-1beta (P = 0.022), tumour necrosis factor (TNF)-alpha (P = 0.002) and IL-8 (P = 0.0012), as well as the frequency of CD4(+) CD25(+) T cells (P < 0.01) were significantly increased, and the increased levels correlated positively with anti-GAD65 autoantibody (GADA) levels. |
| 5435 | 17100770 | Moreover, CD4(+) CD25(+) T cells of children born to T1D mothers exhibited a more pronounced memory phenotype with increased CCR4 expression and down-regulation of CD62L. |
| 5436 | 17100763 | Given the importance of cytokines in the progression of chronic and acute inflammatory processes, we aimed to ascertain whether the release of interleukin (IL)-8, IL-1beta, tumour necrosis factor (TNF)-alpha and IL-1ra of neutrophils and monocytes was modified in diabetes. |
| 5437 | 17100763 | Given the importance of cytokines in the progression of chronic and acute inflammatory processes, we aimed to ascertain whether the release of interleukin (IL)-8, IL-1beta, tumour necrosis factor (TNF)-alpha and IL-1ra of neutrophils and monocytes was modified in diabetes. |
| 5438 | 17100763 | Given the importance of cytokines in the progression of chronic and acute inflammatory processes, we aimed to ascertain whether the release of interleukin (IL)-8, IL-1beta, tumour necrosis factor (TNF)-alpha and IL-1ra of neutrophils and monocytes was modified in diabetes. |
| 5439 | 17100763 | In basal conditions, neutrophils of diabetics release 1.6, 3.2, 1.9 and 1.9-fold higher amounts of IL-8, IL-1beta, TNF-alpha and IL-1ra, respectively, than do healthy controls. |
| 5440 | 17100763 | In basal conditions, neutrophils of diabetics release 1.6, 3.2, 1.9 and 1.9-fold higher amounts of IL-8, IL-1beta, TNF-alpha and IL-1ra, respectively, than do healthy controls. |
| 5441 | 17100763 | In basal conditions, neutrophils of diabetics release 1.6, 3.2, 1.9 and 1.9-fold higher amounts of IL-8, IL-1beta, TNF-alpha and IL-1ra, respectively, than do healthy controls. |
| 5442 | 17100763 | IL-8, IL-1beta and TNF-alpha increased, respectively, by 4.0, 1.7 and 2.8-fold. |
| 5443 | 17100763 | IL-8, IL-1beta and TNF-alpha increased, respectively, by 4.0, 1.7 and 2.8-fold. |
| 5444 | 17100763 | IL-8, IL-1beta and TNF-alpha increased, respectively, by 4.0, 1.7 and 2.8-fold. |
| 5445 | 17097222 | Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. |
| 5446 | 17097222 | Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. |
| 5447 | 17097222 | Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. |
| 5448 | 17097222 | Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. |
| 5449 | 17097222 | Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. |
| 5450 | 17097222 | In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. |
| 5451 | 17097222 | In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. |
| 5452 | 17097222 | In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. |
| 5453 | 17097222 | In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. |
| 5454 | 17097222 | In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. |
| 5455 | 17097222 | Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. |
| 5456 | 17097222 | Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. |
| 5457 | 17097222 | Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. |
| 5458 | 17097222 | Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. |
| 5459 | 17097222 | Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. |
| 5460 | 17097222 | The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. |
| 5461 | 17097222 | The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. |
| 5462 | 17097222 | The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. |
| 5463 | 17097222 | The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. |
| 5464 | 17097222 | The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. |
| 5465 | 17097222 | Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. |
| 5466 | 17097222 | Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. |
| 5467 | 17097222 | Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. |
| 5468 | 17097222 | Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. |
| 5469 | 17097222 | Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. |
| 5470 | 17087190 | The purpose of the study was to investigate the effects of dietotherapy on oxidative stress (OS) condition, the fl-cell functional activity (BCFA), insulin resistance index (IRI), and the serum tumor necrosis factor alpha (alpha-TNF) level in patients with type 2 diabetes mellitus (DM 2). |
| 5471 | 17084639 | Adipokines including tumor necrosis factor alpha, interleukin-6, leptin and adiponectin influence insulin signaling in skeletal muscle. |
| 5472 | 17083157 | Tumor necrosis factor-alpha (TNF-alpha) system is potentially involved in the development of insulin resistance during pregnancy. |
| 5473 | 17083157 | Tumor necrosis factor-alpha (TNF-alpha) system is potentially involved in the development of insulin resistance during pregnancy. |
| 5474 | 17083157 | In conclusion, increased TNF-alpha concentrations in women with GDM class G1 indicates its contribution to the development of insulin resistance during pregnancy, but the lack of the differences in sTNFR concentrations between the groups studied suggests only moderate TNF-alpha system activation in relatively slim patients treated with diet. |
| 5475 | 17083157 | In conclusion, increased TNF-alpha concentrations in women with GDM class G1 indicates its contribution to the development of insulin resistance during pregnancy, but the lack of the differences in sTNFR concentrations between the groups studied suggests only moderate TNF-alpha system activation in relatively slim patients treated with diet. |
| 5476 | 17079333 | Phosphorylation of SIMPL modulates RelA-associated NF-kappaB-dependent transcription. |
| 5477 | 17079333 | Phosphorylation of SIMPL modulates RelA-associated NF-kappaB-dependent transcription. |
| 5478 | 17079333 | Phosphorylation of SIMPL modulates RelA-associated NF-kappaB-dependent transcription. |
| 5479 | 17079333 | Phosphorylation of SIMPL modulates RelA-associated NF-kappaB-dependent transcription. |
| 5480 | 17079333 | SIMPL (signaling molecule that associates with mouse Pelle-like kinase) is a component of a signaling pathway through which tumor necrosis factor-alpha (TNF-alpha) induces NF-kappaB-controlled gene transcription. |
| 5481 | 17079333 | SIMPL (signaling molecule that associates with mouse Pelle-like kinase) is a component of a signaling pathway through which tumor necrosis factor-alpha (TNF-alpha) induces NF-kappaB-controlled gene transcription. |
| 5482 | 17079333 | SIMPL (signaling molecule that associates with mouse Pelle-like kinase) is a component of a signaling pathway through which tumor necrosis factor-alpha (TNF-alpha) induces NF-kappaB-controlled gene transcription. |
| 5483 | 17079333 | SIMPL (signaling molecule that associates with mouse Pelle-like kinase) is a component of a signaling pathway through which tumor necrosis factor-alpha (TNF-alpha) induces NF-kappaB-controlled gene transcription. |
| 5484 | 17079333 | SIMPL interacts with the nuclear pool of the NF-kappaB subunit, p65, in a TNF-alpha-dependent manner to enhance p65-dependent gene transcription. |
| 5485 | 17079333 | SIMPL interacts with the nuclear pool of the NF-kappaB subunit, p65, in a TNF-alpha-dependent manner to enhance p65-dependent gene transcription. |
| 5486 | 17079333 | SIMPL interacts with the nuclear pool of the NF-kappaB subunit, p65, in a TNF-alpha-dependent manner to enhance p65-dependent gene transcription. |
| 5487 | 17079333 | SIMPL interacts with the nuclear pool of the NF-kappaB subunit, p65, in a TNF-alpha-dependent manner to enhance p65-dependent gene transcription. |
| 5488 | 17079333 | Under basal as well as TNF-alpha-stimulated conditions, SIMPL phosphopeptides were identified. |
| 5489 | 17079333 | Under basal as well as TNF-alpha-stimulated conditions, SIMPL phosphopeptides were identified. |
| 5490 | 17079333 | Under basal as well as TNF-alpha-stimulated conditions, SIMPL phosphopeptides were identified. |
| 5491 | 17079333 | Under basal as well as TNF-alpha-stimulated conditions, SIMPL phosphopeptides were identified. |
| 5492 | 17079333 | SIMPL mutants lacking sites of TNF-alpha-enhanced phosphorylation impaired nuclear localization and prevented TNF-alpha-induced p65 transactivation activity. |
| 5493 | 17079333 | SIMPL mutants lacking sites of TNF-alpha-enhanced phosphorylation impaired nuclear localization and prevented TNF-alpha-induced p65 transactivation activity. |
| 5494 | 17079333 | SIMPL mutants lacking sites of TNF-alpha-enhanced phosphorylation impaired nuclear localization and prevented TNF-alpha-induced p65 transactivation activity. |
| 5495 | 17079333 | SIMPL mutants lacking sites of TNF-alpha-enhanced phosphorylation impaired nuclear localization and prevented TNF-alpha-induced p65 transactivation activity. |
| 5496 | 17075045 | By neutralizing IL-18 activity with IL-18 binding protein (IL-18BP), we observed that islets produce bioactive IL-18. |
| 5497 | 17075045 | In related studies, IL-18R-deficient splenocytes and macrophages produced 2- to 3-fold greater amounts of IL-18, TNFalpha, macrophage inflammatory protein 1, macrophage inflammatory protein 2, and IFNgamma upon stimulation with Con A, Toll-like receptor 2 agonist, or anti-CD3 antibodies. |
| 5498 | 17075045 | Importantly, discrepancies between IL-18- and IL-18R-deficient cells suggest that IL-18Ralpha chain is used by an inflammation-suppressing signal. |
| 5499 | 17072583 | Liver X receptor agonists ameliorate TNFalpha-induced insulin resistance in murine brown adipocytes by downregulating protein tyrosine phosphatase-1B gene expression. |
| 5500 | 17068144 | Acylated and unacylated ghrelin promote proliferation and inhibit apoptosis of pancreatic beta-cells and human islets: involvement of 3',5'-cyclic adenosine monophosphate/protein kinase A, extracellular signal-regulated kinase 1/2, and phosphatidyl inositol 3-Kinase/Akt signaling. |
| 5501 | 17068144 | Acylated and unacylated ghrelin promote proliferation and inhibit apoptosis of pancreatic beta-cells and human islets: involvement of 3',5'-cyclic adenosine monophosphate/protein kinase A, extracellular signal-regulated kinase 1/2, and phosphatidyl inositol 3-Kinase/Akt signaling. |
| 5502 | 17068144 | Among its pleiotropic actions, ghrelin modulates insulin secretion and glucose metabolism. |
| 5503 | 17068144 | Among its pleiotropic actions, ghrelin modulates insulin secretion and glucose metabolism. |
| 5504 | 17068144 | Herein we investigated the role of ghrelin in pancreatic beta-cell proliferation and apoptosis induced by serum starvation or interferon (IFN)-gamma/TNF-alpha, whose synergism is a major cause for beta-cell destruction in type I diabetes. |
| 5505 | 17068144 | Herein we investigated the role of ghrelin in pancreatic beta-cell proliferation and apoptosis induced by serum starvation or interferon (IFN)-gamma/TNF-alpha, whose synergism is a major cause for beta-cell destruction in type I diabetes. |
| 5506 | 17068144 | HIT-T15 beta-cells expressed ghrelin but not ghrelin receptor (GRLN-R), which binds acylated ghrelin (AG) only. |
| 5507 | 17068144 | HIT-T15 beta-cells expressed ghrelin but not ghrelin receptor (GRLN-R), which binds acylated ghrelin (AG) only. |
| 5508 | 17068144 | Either AG or UAG stimulated cell proliferation through Galpha(s) protein and prevented serum starvation- and IFN-gamma/TNF-alpha-induced apoptosis. |
| 5509 | 17068144 | Either AG or UAG stimulated cell proliferation through Galpha(s) protein and prevented serum starvation- and IFN-gamma/TNF-alpha-induced apoptosis. |
| 5510 | 17068144 | Blockade of adenylyl cyclase/cAMP/protein kinase A signaling prevented the ghrelin cytoprotective effect. |
| 5511 | 17068144 | Blockade of adenylyl cyclase/cAMP/protein kinase A signaling prevented the ghrelin cytoprotective effect. |
| 5512 | 17068144 | AG and UAG also activated phosphatidyl inositol 3-kinase (PI3K)/Akt and ERK1/2, whereas PI3K and MAPK inhibitors counteracted the ghrelin antiapoptotic effect. |
| 5513 | 17068144 | AG and UAG also activated phosphatidyl inositol 3-kinase (PI3K)/Akt and ERK1/2, whereas PI3K and MAPK inhibitors counteracted the ghrelin antiapoptotic effect. |
| 5514 | 17068144 | These effects are independent of GRLN-R, are likely mediated by AG/UAG binding sites, and involve cAMP/PKA, ERK1/2, and PI3K/Akt. |
| 5515 | 17068144 | These effects are independent of GRLN-R, are likely mediated by AG/UAG binding sites, and involve cAMP/PKA, ERK1/2, and PI3K/Akt. |
| 5516 | 17065389 | Cell death was significantly increased after 4 weeks, as was caspase-8 activation, although circulating levels of TNF-alpha were increased as early as 1 week. |
| 5517 | 17048997 | In transgenic mice models the HCV core protein has been found to induce insulin resistance via TNF production. |
| 5518 | 17048997 | In transgenic mice models the HCV core protein has been found to induce insulin resistance via TNF production. |
| 5519 | 17048997 | In genotype-1 patients, the mechanisms by which insulin resistance promotes fibrosis progression include: a) steatosis; b) hyperleptinemia; c) increased TNF production; and d) impaired expression of PPARg receptors. |
| 5520 | 17048997 | In genotype-1 patients, the mechanisms by which insulin resistance promotes fibrosis progression include: a) steatosis; b) hyperleptinemia; c) increased TNF production; and d) impaired expression of PPARg receptors. |
| 5521 | 17047287 | Is the association between TNF-alpha-308 A allele and DMT1 independent of HLA-DRB1, DQB1 alleles? |
| 5522 | 17047287 | Is the association between TNF-alpha-308 A allele and DMT1 independent of HLA-DRB1, DQB1 alleles? |
| 5523 | 17047287 | Is the association between TNF-alpha-308 A allele and DMT1 independent of HLA-DRB1, DQB1 alleles? |
| 5524 | 17047287 | Is the association between TNF-alpha-308 A allele and DMT1 independent of HLA-DRB1, DQB1 alleles? |
| 5525 | 17047287 | Is the association between TNF-alpha-308 A allele and DMT1 independent of HLA-DRB1, DQB1 alleles? |
| 5526 | 17047287 | The aim of the study was to assess chosen factors of genetic susceptibility to DMT1: DRB1, DQB1, and TNF-alpha polymorphisms-308 (G/A) in children with DMT1 and their up-to-now healthy siblings. |
| 5527 | 17047287 | The aim of the study was to assess chosen factors of genetic susceptibility to DMT1: DRB1, DQB1, and TNF-alpha polymorphisms-308 (G/A) in children with DMT1 and their up-to-now healthy siblings. |
| 5528 | 17047287 | The aim of the study was to assess chosen factors of genetic susceptibility to DMT1: DRB1, DQB1, and TNF-alpha polymorphisms-308 (G/A) in children with DMT1 and their up-to-now healthy siblings. |
| 5529 | 17047287 | The aim of the study was to assess chosen factors of genetic susceptibility to DMT1: DRB1, DQB1, and TNF-alpha polymorphisms-308 (G/A) in children with DMT1 and their up-to-now healthy siblings. |
| 5530 | 17047287 | The aim of the study was to assess chosen factors of genetic susceptibility to DMT1: DRB1, DQB1, and TNF-alpha polymorphisms-308 (G/A) in children with DMT1 and their up-to-now healthy siblings. |
| 5531 | 17047287 | Then we tested whether the association between TNF-alpha genes and DMT1 is independent of HLA. 87 diabetic children, their 78 siblings, and 85 persons from healthy control group were followed up. |
| 5532 | 17047287 | Then we tested whether the association between TNF-alpha genes and DMT1 is independent of HLA. 87 diabetic children, their 78 siblings, and 85 persons from healthy control group were followed up. |
| 5533 | 17047287 | Then we tested whether the association between TNF-alpha genes and DMT1 is independent of HLA. 87 diabetic children, their 78 siblings, and 85 persons from healthy control group were followed up. |
| 5534 | 17047287 | Then we tested whether the association between TNF-alpha genes and DMT1 is independent of HLA. 87 diabetic children, their 78 siblings, and 85 persons from healthy control group were followed up. |
| 5535 | 17047287 | Then we tested whether the association between TNF-alpha genes and DMT1 is independent of HLA. 87 diabetic children, their 78 siblings, and 85 persons from healthy control group were followed up. |
| 5536 | 17047287 | The highest risk of DMT1 was connected with alleles: DRB1*0401 (OR = 3.39; CI: 1.55-7.41), DRB1*0301 (OR = 2.72; CI: 1.48-5.01), DQB1*0201 (OR = 4.04; CI: 2.17-7.52), DQB1*0302 (OR = 5.08; CI: 2.54-10.14), and TNF-alpha-308 A allele (OR = 2.59; CI: 1.23-5.44). |
| 5537 | 17047287 | The highest risk of DMT1 was connected with alleles: DRB1*0401 (OR = 3.39; CI: 1.55-7.41), DRB1*0301 (OR = 2.72; CI: 1.48-5.01), DQB1*0201 (OR = 4.04; CI: 2.17-7.52), DQB1*0302 (OR = 5.08; CI: 2.54-10.14), and TNF-alpha-308 A allele (OR = 2.59; CI: 1.23-5.44). |
| 5538 | 17047287 | The highest risk of DMT1 was connected with alleles: DRB1*0401 (OR = 3.39; CI: 1.55-7.41), DRB1*0301 (OR = 2.72; CI: 1.48-5.01), DQB1*0201 (OR = 4.04; CI: 2.17-7.52), DQB1*0302 (OR = 5.08; CI: 2.54-10.14), and TNF-alpha-308 A allele (OR = 2.59; CI: 1.23-5.44). |
| 5539 | 17047287 | The highest risk of DMT1 was connected with alleles: DRB1*0401 (OR = 3.39; CI: 1.55-7.41), DRB1*0301 (OR = 2.72; CI: 1.48-5.01), DQB1*0201 (OR = 4.04; CI: 2.17-7.52), DQB1*0302 (OR = 5.08; CI: 2.54-10.14), and TNF-alpha-308 A allele (OR = 2.59; CI: 1.23-5.44). |
| 5540 | 17047287 | The highest risk of DMT1 was connected with alleles: DRB1*0401 (OR = 3.39; CI: 1.55-7.41), DRB1*0301 (OR = 2.72; CI: 1.48-5.01), DQB1*0201 (OR = 4.04; CI: 2.17-7.52), DQB1*0302 (OR = 5.08; CI: 2.54-10.14), and TNF-alpha-308 A allele (OR = 2.59; CI: 1.23-5.44). |
| 5541 | 17047287 | The association between TNF-alpha-308 A allele and DMT1 is dependent of HLA-DRB1 and DQB1 alleles. |
| 5542 | 17047287 | The association between TNF-alpha-308 A allele and DMT1 is dependent of HLA-DRB1 and DQB1 alleles. |
| 5543 | 17047287 | The association between TNF-alpha-308 A allele and DMT1 is dependent of HLA-DRB1 and DQB1 alleles. |
| 5544 | 17047287 | The association between TNF-alpha-308 A allele and DMT1 is dependent of HLA-DRB1 and DQB1 alleles. |
| 5545 | 17047287 | The association between TNF-alpha-308 A allele and DMT1 is dependent of HLA-DRB1 and DQB1 alleles. |
| 5546 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5547 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5548 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5549 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5550 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5551 | 17046548 | Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line. |
| 5552 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5553 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5554 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5555 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5556 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5557 | 17046548 | Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. |
| 5558 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5559 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5560 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5561 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5562 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5563 | 17046548 | To address the mechanism underlying the up-regulation of hepatic PAI-1 in obesity, we tested the effects of tumor necrosis factor alpha (TNF-alpha), an important link between obesity and insulin resistance, on PAI-1 production in the nonmalignant human hepatocyte cell line, THLE-5b. |
| 5564 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5565 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5566 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5567 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5568 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5569 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 5570 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5571 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5572 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5573 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5574 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5575 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 5576 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5577 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5578 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5579 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5580 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5581 | 17046548 | The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor cerivastatin inhibited TNF-alpha-induced PAI-1 production by 59%, which was reversed by coincubation with mevalonic acid. |
| 5582 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5583 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5584 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5585 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5586 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5587 | 17046548 | In conclusion, obesity and TNF-alpha up-regulation of PAI-1 expression in human hepatocytes may contribute to the impairment of the fibrinolytic system, leading to the development of atherosclerosis and liver fibrosis in insulin-resistant individuals. |
| 5588 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5589 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5590 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5591 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5592 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5593 | 17046548 | A thiazolidinedione and a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor may thus be candidate drugs to inhibit obesity-associated hepatic PAI-1 production. |
| 5594 | 17045460 | SOCS-1 protects from virally-induced CD8 T cell mediated type 1 diabetes. |
| 5595 | 17045460 | CTL-mediated beta-cell killing can occur via perforin-mediated lysis, Fas-Fas-L interaction, and the secretion of TNF-alpha or IFN-gamma. |
| 5596 | 17045460 | Suppressor of cytokine signaling-1 (SOCS-1) represses several crucial cytokine signaling pathways simultaneously, among them IFN-gamma and IL-1-beta. |
| 5597 | 17045460 | We therefore evaluated the protective capacity of islet cell SOCS-1 expression in the CD8(+) mediated RIP-LCMV diabetes model. |
| 5598 | 17045460 | Not only absence of MHC-I and Fas upregulation, but also resistance to cytokine-induced killing of beta-cells and a complete lack of CXCL-10 (IP10) production in islets led to a lack of islet infiltration and impaired activation of autoaggressive CD4(+) and CD8(+) T-cells in these mice. |
| 5599 | 17036509 | Numerous angiogenic and mitogenic factors have been demonstrated to be present in the eye, including transforming growth factor-beta (TGF-beta), insulin-like growth factors, fibroblast growth factor, tumor necrosis factor and vascular endothelial growth factor. |
| 5600 | 17027526 | The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. |
| 5601 | 17027526 | The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. |
| 5602 | 17027526 | Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. |
| 5603 | 17027526 | Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. |
| 5604 | 17027526 | The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. |
| 5605 | 17027526 | The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. |
| 5606 | 17027526 | However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. |
| 5607 | 17027526 | However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. |
| 5608 | 17027526 | Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. |
| 5609 | 17027526 | Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. |
| 5610 | 17027526 | Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. |
| 5611 | 17027526 | Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. |
| 5612 | 17027526 | In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids. |
| 5613 | 17027526 | In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids. |
| 5614 | 17026986 | N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression. |
| 5615 | 17026986 | N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression. |
| 5616 | 17026986 | N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression. |
| 5617 | 17026986 | N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression. |
| 5618 | 17026986 | TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. |
| 5619 | 17026986 | TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. |
| 5620 | 17026986 | TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. |
| 5621 | 17026986 | TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. |
| 5622 | 17026986 | Treatment with NAC at 30 mmol/l restored eNOS expression and further increased NO production as compared to TNF-alpha alone, resulting in improved cell viability and reduced apoptosis. |
| 5623 | 17026986 | Treatment with NAC at 30 mmol/l restored eNOS expression and further increased NO production as compared to TNF-alpha alone, resulting in improved cell viability and reduced apoptosis. |
| 5624 | 17026986 | Treatment with NAC at 30 mmol/l restored eNOS expression and further increased NO production as compared to TNF-alpha alone, resulting in improved cell viability and reduced apoptosis. |
| 5625 | 17026986 | Treatment with NAC at 30 mmol/l restored eNOS expression and further increased NO production as compared to TNF-alpha alone, resulting in improved cell viability and reduced apoptosis. |
| 5626 | 17026986 | N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression. |
| 5627 | 17026986 | N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression. |
| 5628 | 17026986 | N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression. |
| 5629 | 17026986 | N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression. |
| 5630 | 17026849 | We enrolled 60 patients (32 diabetics; 28 non- diabetics) with acute ischemic stroke and 123 subjects without acute ischemic stroke, and measured levels of IL-1beta, TNF-alpha IL-6, IL-10, E-selectin, P-selectin, sICAM-1, sVCAM-1, VWF, 24-72 h and 7-10 days after stroke onset; TPA, PAI-1 plasma levels at 24-72h. |
| 5631 | 17026849 | We enrolled 60 patients (32 diabetics; 28 non- diabetics) with acute ischemic stroke and 123 subjects without acute ischemic stroke, and measured levels of IL-1beta, TNF-alpha IL-6, IL-10, E-selectin, P-selectin, sICAM-1, sVCAM-1, VWF, 24-72 h and 7-10 days after stroke onset; TPA, PAI-1 plasma levels at 24-72h. |
| 5632 | 17026849 | Lacunar strokes in comparison with those non-lacunar exhibited significantly lower levels of TNF-alpha and IL1-beta P-selectin and ICAM-1. |
| 5633 | 17026849 | Lacunar strokes in comparison with those non-lacunar exhibited significantly lower levels of TNF-alpha and IL1-beta P-selectin and ICAM-1. |
| 5634 | 17022850 | Effect of gliclazide modified release on adiponectin, interleukin-6, and tumor necrosis factor-alpha plasma levels in individuals with type 2 diabetes mellitus. |
| 5635 | 17022108 | Interleukin-1beta, Tumor Necrosis Factor-alpha, Interleukin- 6, Interleukin- 8, and Transforming Grow Factor beta were quantified by ELISA. |
| 5636 | 17018452 | Thus, in the present study we compared the GC sensitivity of the immune system, assessed by determining the dexamethasone inhibition of LPS-induced TNF-alpha production in peripheral leukocytes, with the feedback sensitivity of the HPA axis, assessed by a very low dose dexamethasone (0.25 mg) suppression test, in sixteen healthy volunteers. |
| 5637 | 17015694 | A 20-Mb region of chromosome 4 controls TNF-alpha-mediated CD8+ T cell aggression toward beta cells in type 1 diabetes. |
| 5638 | 17015694 | A 20-Mb region of chromosome 4 controls TNF-alpha-mediated CD8+ T cell aggression toward beta cells in type 1 diabetes. |
| 5639 | 17015694 | To identify some of these recessive alleles, we crossed TNF-alpha-NOD mice to diabetes-resistant congenic NOD mice having protective alleles at insulin-dependent diabetes (Idd) loci that control spontaneous T1D at either the preinsulitis (Idd3.Idd5) or postinsulitis (Idd9) phases. |
| 5640 | 17015694 | To identify some of these recessive alleles, we crossed TNF-alpha-NOD mice to diabetes-resistant congenic NOD mice having protective alleles at insulin-dependent diabetes (Idd) loci that control spontaneous T1D at either the preinsulitis (Idd3.Idd5) or postinsulitis (Idd9) phases. |
| 5641 | 17015694 | Lack of protection was not at the level of T cell priming, the efficacy of islet-infiltrating APCs to present islet peptides, nor the ability of high levels of CD4+ Foxp3+ T cells to accumulate in the islets. |
| 5642 | 17015694 | Lack of protection was not at the level of T cell priming, the efficacy of islet-infiltrating APCs to present islet peptides, nor the ability of high levels of CD4+ Foxp3+ T cells to accumulate in the islets. |
| 5643 | 17014868 | Significantly reduced levels of IL-6 and TNFalpha were observed in the culture supernatants of Raga treated 3T3L1 cells. |
| 5644 | 17014868 | Raga resulted in significant insulin dependent glucose uptake in 3T3L1 with a corresponding increase in GLUT4 expression. |
| 5645 | 17014868 | Further, Raga showed a significant cholesterol efflux with a corresponding increase in ABCA1 protein expression in THP-1 macrophages. |
| 5646 | 20527377 | The adipose tissue releases free fatty acids but also hormones and cytokines such as leptin, adiponectin, resistin, TNF-alpha and others. |
| 5647 | 17002473 | Dietary conjugated linoleic acid lowered tumor necrosis factor-alpha content and altered expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of Zucker rats. |
| 5648 | 17002473 | Dietary conjugated linoleic acid lowered tumor necrosis factor-alpha content and altered expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of Zucker rats. |
| 5649 | 17002473 | Dietary conjugated linoleic acid lowered tumor necrosis factor-alpha content and altered expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of Zucker rats. |
| 5650 | 17002473 | Additionally, expression of genes-related insulin sensitivity, such as adiponectin receptor 1, was significantly enhanced, and mRNA level of peroxisome proliferator activated receptor-alpha, known as a transcriptional factor related lipid metabolism and insulin signaling in skeletal muscle, was markedly increased in CLA-fed rats. |
| 5651 | 17002473 | Additionally, expression of genes-related insulin sensitivity, such as adiponectin receptor 1, was significantly enhanced, and mRNA level of peroxisome proliferator activated receptor-alpha, known as a transcriptional factor related lipid metabolism and insulin signaling in skeletal muscle, was markedly increased in CLA-fed rats. |
| 5652 | 17002473 | Additionally, expression of genes-related insulin sensitivity, such as adiponectin receptor 1, was significantly enhanced, and mRNA level of peroxisome proliferator activated receptor-alpha, known as a transcriptional factor related lipid metabolism and insulin signaling in skeletal muscle, was markedly increased in CLA-fed rats. |
| 5653 | 17002473 | We also showed that dietary CLA significantly decreased the level of tumor necrosis factor-alpha (TNF-alpha), associated with the development of insulin resistance, in the skeletal muscle of Zucker rats. |
| 5654 | 17002473 | We also showed that dietary CLA significantly decreased the level of tumor necrosis factor-alpha (TNF-alpha), associated with the development of insulin resistance, in the skeletal muscle of Zucker rats. |
| 5655 | 17002473 | We also showed that dietary CLA significantly decreased the level of tumor necrosis factor-alpha (TNF-alpha), associated with the development of insulin resistance, in the skeletal muscle of Zucker rats. |
| 5656 | 17002473 | We suppose that the attenuated TNF-alpha accumulation in skeletal muscle may contribute to the alteration of expression of several genes and the alleviation of insulin resistance in CLA-fed Zucker rats. |
| 5657 | 17002473 | We suppose that the attenuated TNF-alpha accumulation in skeletal muscle may contribute to the alteration of expression of several genes and the alleviation of insulin resistance in CLA-fed Zucker rats. |
| 5658 | 17002473 | We suppose that the attenuated TNF-alpha accumulation in skeletal muscle may contribute to the alteration of expression of several genes and the alleviation of insulin resistance in CLA-fed Zucker rats. |
| 5659 | 17000905 | Systemic tumor necrosis factor-related apoptosis-inducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. |
| 5660 | 16986170 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that is characterized by selective destruction of insulin secreting pancreatic islets beta-cells. |
| 5661 | 16986170 | The formation of cytokines (IL-1beta, IL-6, TNF-alpha, etc.) leads to extensive morphological damage of beta-cells, DNA fragmentation, decrease of glucose oxidation, impaired glucose-insulin secretion and decreased insulin action and proinsulin biosynthesis. |
| 5662 | 16979413 | Relationship between polymorphisms 804C/A and 252A/G of lymphotoxin-alpha gene and -308G/A of tumor necrosis factor alpha gene and diabetic retinopathy in Japanese patients with type 2 diabetes mellitus. |
| 5663 | 16979413 | Relationship between polymorphisms 804C/A and 252A/G of lymphotoxin-alpha gene and -308G/A of tumor necrosis factor alpha gene and diabetic retinopathy in Japanese patients with type 2 diabetes mellitus. |
| 5664 | 16979413 | Relationship between polymorphisms 804C/A and 252A/G of lymphotoxin-alpha gene and -308G/A of tumor necrosis factor alpha gene and diabetic retinopathy in Japanese patients with type 2 diabetes mellitus. |
| 5665 | 16979413 | Relationship between polymorphisms 804C/A and 252A/G of lymphotoxin-alpha gene and -308G/A of tumor necrosis factor alpha gene and diabetic retinopathy in Japanese patients with type 2 diabetes mellitus. |
| 5666 | 16979413 | To clarify whether polymorphisms of the lymphotoxin-alpha (LTA) gene and tumor necrosis factor alpha (TNF-alpha) gene were related to diabetic retinopathy (DR), we performed a case-control study in 251 Japanese patients with type 2 diabetes mellitus participating in a multicenter research protocol. |
| 5667 | 16979413 | To clarify whether polymorphisms of the lymphotoxin-alpha (LTA) gene and tumor necrosis factor alpha (TNF-alpha) gene were related to diabetic retinopathy (DR), we performed a case-control study in 251 Japanese patients with type 2 diabetes mellitus participating in a multicenter research protocol. |
| 5668 | 16979413 | To clarify whether polymorphisms of the lymphotoxin-alpha (LTA) gene and tumor necrosis factor alpha (TNF-alpha) gene were related to diabetic retinopathy (DR), we performed a case-control study in 251 Japanese patients with type 2 diabetes mellitus participating in a multicenter research protocol. |
| 5669 | 16979413 | To clarify whether polymorphisms of the lymphotoxin-alpha (LTA) gene and tumor necrosis factor alpha (TNF-alpha) gene were related to diabetic retinopathy (DR), we performed a case-control study in 251 Japanese patients with type 2 diabetes mellitus participating in a multicenter research protocol. |
| 5670 | 16979413 | Multivariate logistic regression analyses showed that significant associations with DR were glycosylated hemoglobin level and diabetes duration, but not polymorphisms of the LTA gene or TNF-alpha gene. |
| 5671 | 16979413 | Multivariate logistic regression analyses showed that significant associations with DR were glycosylated hemoglobin level and diabetes duration, but not polymorphisms of the LTA gene or TNF-alpha gene. |
| 5672 | 16979413 | Multivariate logistic regression analyses showed that significant associations with DR were glycosylated hemoglobin level and diabetes duration, but not polymorphisms of the LTA gene or TNF-alpha gene. |
| 5673 | 16979413 | Multivariate logistic regression analyses showed that significant associations with DR were glycosylated hemoglobin level and diabetes duration, but not polymorphisms of the LTA gene or TNF-alpha gene. |
| 5674 | 16979413 | In conclusion, the present study showed no association between polymorphisms 804C/A and 252A/G of the LTA gene and -302A/G of the TNF-alpha gene and DR in Japanese type 2 diabetic patients. |
| 5675 | 16979413 | In conclusion, the present study showed no association between polymorphisms 804C/A and 252A/G of the LTA gene and -302A/G of the TNF-alpha gene and DR in Japanese type 2 diabetic patients. |
| 5676 | 16979413 | In conclusion, the present study showed no association between polymorphisms 804C/A and 252A/G of the LTA gene and -302A/G of the TNF-alpha gene and DR in Japanese type 2 diabetic patients. |
| 5677 | 16979413 | In conclusion, the present study showed no association between polymorphisms 804C/A and 252A/G of the LTA gene and -302A/G of the TNF-alpha gene and DR in Japanese type 2 diabetic patients. |
| 5678 | 16979382 | In a previous study, we identified a biologically active form of tumor necrosis factor-alpha receptor 2 (sTNFR2) produced by differential splicing (DS-TNFR2) which antagonized TNF-alpha biological activity. |
| 5679 | 16979382 | In a previous study, we identified a biologically active form of tumor necrosis factor-alpha receptor 2 (sTNFR2) produced by differential splicing (DS-TNFR2) which antagonized TNF-alpha biological activity. |
| 5680 | 16979382 | Obesity, insulin resistance and type 2 diabetes are linked to increased TNF-alpha action. |
| 5681 | 16979382 | Obesity, insulin resistance and type 2 diabetes are linked to increased TNF-alpha action. |
| 5682 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5683 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5684 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5685 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5686 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5687 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5688 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5689 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5690 | 16960890 | Long-term effects of tumor necrosis factor-alpha treatment on insulin signaling pathway in HepG2 cells and HepG2 cells overexpressing constitutively active Akt/PKB. |
| 5691 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5692 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5693 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5694 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5695 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5696 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5697 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5698 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5699 | 16960890 | Tumor necrosis factor-alpha (TNF-alpha) mediated attenuation of insulin signaling pathway is an important cause in several disorders like obesity, obesity linked diabetes mellitus. |
| 5700 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5701 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5702 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5703 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5704 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5705 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5706 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5707 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5708 | 16960890 | In the present study, the effects of long-term TNF-alpha (1 ng/ml) exposure on the components of insulin signaling pathway in HepG2 and HepG2 cells overexpressing constitutively active Akt1/PKB-alpha (HepG2-CA-Akt/PKB) have been investigated. |
| 5709 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5710 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5711 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5712 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5713 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5714 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5715 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5716 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5717 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 5718 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5719 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5720 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5721 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5722 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5723 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5724 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5725 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5726 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 5727 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5728 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5729 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5730 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5731 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5732 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5733 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5734 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5735 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 5736 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5737 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5738 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5739 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5740 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5741 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5742 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5743 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5744 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 5745 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5746 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5747 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5748 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5749 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5750 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5751 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5752 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5753 | 16960890 | TNF-alpha pre-incubation also showed reduced insulin-stimulated Tyr phosphorylation of insulin receptor (IR-beta) in both the cell types, moreover hyperphosphorylation of IRS-1 at Ser 312 residue was observed in TNF-alpha pre-incubated cells. |
| 5754 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5755 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5756 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5757 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5758 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5759 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5760 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5761 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5762 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 5763 | 16954332 | Leptin and apelin mRNA levels in white and brown AT were higher in +/+ offspring from db/+ vs. +/+ dams; however, leptin, apelin, and tumor necrosis factor-alpha expression were boosted more robustly in db/+ offspring. |
| 5764 | 16941280 | Although Pg and E. coli LPS had no effect on HMG-CoA reductase gene expression, both tumor necrosis factor-alpha and interleukin-6 (IL-6), especially IL-6 at low concentration, markedly up-regulated HMG-CoA reductase gene expression. |
| 5765 | 16936207 | Expression of enzymes involved in ceramide generation (neutral sphingomyelinase [NSMase], acid sphingomyelinase [ASMase], and serine-palmitoyl-transferase [SPT]) and ceramide hydrolysis (ceramidase) are elevated in obese adipose tissues. |
| 5766 | 16936207 | Expression of enzymes involved in ceramide generation (neutral sphingomyelinase [NSMase], acid sphingomyelinase [ASMase], and serine-palmitoyl-transferase [SPT]) and ceramide hydrolysis (ceramidase) are elevated in obese adipose tissues. |
| 5767 | 16936207 | Our data also suggest that hyperinsulinemia and elevated tumor necrosis factor (TNF)-alpha associated with obesity may contribute to the observed increase in adipose NSMase, ASMase, and SPT mRNA in this murine model of obesity. |
| 5768 | 16936207 | Our data also suggest that hyperinsulinemia and elevated tumor necrosis factor (TNF)-alpha associated with obesity may contribute to the observed increase in adipose NSMase, ASMase, and SPT mRNA in this murine model of obesity. |
| 5769 | 16936207 | In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine. |
| 5770 | 16936207 | In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine. |
| 5771 | 16936197 | Regulation of A20 was nuclear factor-kappaB (NF-kappaB)-dependent, two NF-kappaB sites within the A20 promoter were found to be necessary and sufficient for A20 expression in beta-cells. |
| 5772 | 16936197 | Regulation of A20 was nuclear factor-kappaB (NF-kappaB)-dependent, two NF-kappaB sites within the A20 promoter were found to be necessary and sufficient for A20 expression in beta-cells. |
| 5773 | 16936197 | Activation of NF-kappaB by TNF receptor-associated factor (TRAF) 2, TRAF6, NF-kappaB-inducing kinase, or protein kinase D, which transduce signals downstream of Toll-like receptors, TNF receptors, and free radicals, respectively, were all potent activators of the A20 promoter. |
| 5774 | 16936197 | Activation of NF-kappaB by TNF receptor-associated factor (TRAF) 2, TRAF6, NF-kappaB-inducing kinase, or protein kinase D, which transduce signals downstream of Toll-like receptors, TNF receptors, and free radicals, respectively, were all potent activators of the A20 promoter. |
| 5775 | 16936197 | Finally, A20 expression was sufficient to protect beta-cells from TNF-induced apoptosis. |
| 5776 | 16936197 | Finally, A20 expression was sufficient to protect beta-cells from TNF-induced apoptosis. |
| 5777 | 16936197 | Further, A20 expression is NF-kappaB dependent, thus linking islet proinflammatory gene responses with protection from apoptosis. |
| 5778 | 16936197 | Further, A20 expression is NF-kappaB dependent, thus linking islet proinflammatory gene responses with protection from apoptosis. |
| 5779 | 16936191 | We recently discovered that CD40, a member of tumor necrosis factor (TNF) receptor family, is expressed in pancreatic beta-cells. |
| 5780 | 16936191 | Islet beta-cells responded to CD40L interaction by secreting interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and macrophage inflammatory protein (MIP)-1beta, the latter a chemokine first reported to be produced by islets. |
| 5781 | 16936191 | Induction of IL-8 and MIP-1beta was confirmed at the transcriptional level by quantitative RT-PCR. |
| 5782 | 16936191 | CD40-CD40L interaction activates extracellular signal-regulated kinase 1/2 and nuclear factor-kappaB pathways in insulinoma NIT-1 cells, and inhibitors of either pathway suppress cytokine/chemokine production in islets. |
| 5783 | 16936191 | Moreover, ligation of CD40 receptor upregulates intercellular adhesion molecule-1, associated with inflammation, at both transcriptional and translational levels. |
| 5784 | 16934758 | Regulation of death and survival in astrocytes by ADP activating P2Y1 and P2Y12 receptors. |
| 5785 | 16934758 | ADP is the endogenous agonist for both P2Y(1) and P2Y(12) receptors, which are important therapeutic targets. |
| 5786 | 16934758 | We demonstrated here that, unlike with the G(q)-coupled P2Y(1) receptor, activation of the G(i)-coupled P2Y(12) receptor does not induce apoptosis. |
| 5787 | 16934758 | Furthermore, activation of the P2Y(12) receptor by either ADP or 2MeSADP significantly attenuates the tumor necrosis factor alpha (TNFalpha)-induced apoptosis in 1321N1 human astrocytoma cells. |
| 5788 | 16934758 | This protective effect was blocked by the P2Y(12) receptor antagonist 2-methylthioAMP and by inhibitors of phospholipase C (U73122) and protein kinase C (chelerythrin), but not by the P2Y(1) receptor antagonist MRS2179. |
| 5789 | 16934758 | Toward a greater mechanistic understanding, we showed that hP2Y(12) receptor activation by 10nM 2MeSADP, activates Erk1/2, Akt, and JNK by phosphorylation. |
| 5790 | 16934758 | However, at a lower protective concentration of 100pM 2MeSADP, activation of the hP2Y(12) receptor involves only phosphorylated Erk1/2, but not Akt or JNK. |
| 5791 | 16934758 | These results may have important implications for understanding the signaling cascades that follow activation of P2Y(1) and P2Y(12) receptors and their opposing effects on cell death pathways. |
| 5792 | 16934497 | We have now observed that TNF superfamily 14 (TNFSF14) is upregulated in aged nonobese diabetic (NOD) pancreas with the appearance of TLO. |
| 5793 | 16934497 | Blockade of TNFSF14 signaling caused a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration factors within the islets and disrupts organization of tertiary structures, leading to prevention of diabetes. |
| 5794 | 16933788 | Serum levels of glucose, insulin, the pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), as well as insulin resistance index (IRI), decreased with CLA, whereas CLA and Cr in combination had significant effects on insulin and IL-6 concentrations and IRI. |
| 5795 | 16931452 | It has become evident that adipose tissue represents an active secretory organ capable of releasing a variety of cytokines such as TNFalpha, IL-6, adiponectin and other still unknown factors that might constitute the missing link between adipose tissue and insulin resistance. |
| 5796 | 16931452 | Positive regulators of insulin sensitivity include the adipocyte hormone adiponectin and inhibitors of inflammatory pathways such as JNK-, IKK- and ERK-inhibitors. |
| 5797 | 16930851 | Leptin controls adiponectin production via the hypothalamus. |
| 5798 | 16930851 | Adipocyte generated endocrine signals, including leptin and adiponectin, control systemic insulin sensitivity as part of a broader control mechanism in energy balance. |
| 5799 | 16930851 | Leptin and adiponectin are inversely regulated in vivo, but not in vitro, suggesting that the inverse relationship is mediated via indirect mechanisms. |
| 5800 | 16930851 | The cytokine TNF-alpha has been proposed as a putative candidate in the reciprocal regulation of adiponectin and leptin. |
| 5801 | 16930851 | However, several recent findings, including the observation that adiponectin production is paradoxically increased in mouse models with selective hypothalamic leptin resistance, indicate that part of the inverse relationship between leptin and adiponectin is mediated via a neural interface. |
| 5802 | 16930761 | The significance of tumor necrosis factor-alpha in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. |
| 5803 | 16930761 | The significance of tumor necrosis factor-alpha in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. |
| 5804 | 16930761 | The significance of tumor necrosis factor-alpha in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. |
| 5805 | 16930761 | The significance of tumor necrosis factor-alpha in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. |
| 5806 | 16930761 | The significance of tumor necrosis factor-alpha in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment. |
| 5807 | 16930761 | This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-alpha (TNF-alpha) and explore whether the decrease of serum TNF-alpha has correlation with the improvement of islet beta-Cell function and the decrease of insulin resistance. |
| 5808 | 16930761 | This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-alpha (TNF-alpha) and explore whether the decrease of serum TNF-alpha has correlation with the improvement of islet beta-Cell function and the decrease of insulin resistance. |
| 5809 | 16930761 | This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-alpha (TNF-alpha) and explore whether the decrease of serum TNF-alpha has correlation with the improvement of islet beta-Cell function and the decrease of insulin resistance. |
| 5810 | 16930761 | This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-alpha (TNF-alpha) and explore whether the decrease of serum TNF-alpha has correlation with the improvement of islet beta-Cell function and the decrease of insulin resistance. |
| 5811 | 16930761 | This study was performed to investigate whether transient intensive insulin therapy with an insulin pump (TIIT) can decrease serum tumor necrosis factor-alpha (TNF-alpha) and explore whether the decrease of serum TNF-alpha has correlation with the improvement of islet beta-Cell function and the decrease of insulin resistance. |
| 5812 | 16930761 | TNF-alpha, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. |
| 5813 | 16930761 | TNF-alpha, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. |
| 5814 | 16930761 | TNF-alpha, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. |
| 5815 | 16930761 | TNF-alpha, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. |
| 5816 | 16930761 | TNF-alpha, free fatty acids (FFAs), glucose, and insulin (INS) had been measured before and after TIIT, respectively. |
| 5817 | 16930761 | TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. |
| 5818 | 16930761 | TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. |
| 5819 | 16930761 | TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. |
| 5820 | 16930761 | TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. |
| 5821 | 16930761 | TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. |
| 5822 | 16930761 | It is inferred that the decrease of serum TNF-alpha might be involved in the improvement of beta-Cell function and the decrease of insulin resistance by TIIT. |
| 5823 | 16930761 | It is inferred that the decrease of serum TNF-alpha might be involved in the improvement of beta-Cell function and the decrease of insulin resistance by TIIT. |
| 5824 | 16930761 | It is inferred that the decrease of serum TNF-alpha might be involved in the improvement of beta-Cell function and the decrease of insulin resistance by TIIT. |
| 5825 | 16930761 | It is inferred that the decrease of serum TNF-alpha might be involved in the improvement of beta-Cell function and the decrease of insulin resistance by TIIT. |
| 5826 | 16930761 | It is inferred that the decrease of serum TNF-alpha might be involved in the improvement of beta-Cell function and the decrease of insulin resistance by TIIT. |
| 5827 | 16926846 | In situ hybridization using bfl-1 (microglia) and glial fibrillary acidic protein (GFAP) (astrocytes) revealed expression of both bfl-1 and GFAP in the ipsilateral hemisphere at 4 h in the db/+ mice, which was delayed and minimal in the db/db mice. |
| 5828 | 16926846 | In situ hybridization using bfl-1 (microglia) and glial fibrillary acidic protein (GFAP) (astrocytes) revealed expression of both bfl-1 and GFAP in the ipsilateral hemisphere at 4 h in the db/+ mice, which was delayed and minimal in the db/db mice. |
| 5829 | 16926846 | RNase protection assays showed a robust increase in expression of the proinflammatory cytokines tumor necrosis factor-alpha (TNFalpha), interleukin-1 IL-1alpha, and IL-1beta mRNA in the db/+ mice at 6 to 8 h of reperfusion peaking at 8 to 12 h; in db/db mice expression was markedly delayed and diminished. |
| 5830 | 16926846 | RNase protection assays showed a robust increase in expression of the proinflammatory cytokines tumor necrosis factor-alpha (TNFalpha), interleukin-1 IL-1alpha, and IL-1beta mRNA in the db/+ mice at 6 to 8 h of reperfusion peaking at 8 to 12 h; in db/db mice expression was markedly delayed and diminished. |
| 5831 | 16926846 | Real-time-polymerase chain reaction (RT-PCR) confirmed the reduced and delayed expression TNFalpha, IL-1alpha, IL-1beta, and the growth factors insulin-like growth factor-1 and ciliary neurotrophic factor in the db/db mice; enzyme-linked immunosorbent assays confirmed the reduced and delayed translation of IL-1beta protein. |
| 5832 | 16926846 | Real-time-polymerase chain reaction (RT-PCR) confirmed the reduced and delayed expression TNFalpha, IL-1alpha, IL-1beta, and the growth factors insulin-like growth factor-1 and ciliary neurotrophic factor in the db/db mice; enzyme-linked immunosorbent assays confirmed the reduced and delayed translation of IL-1beta protein. |
| 5833 | 16919536 | Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor kappaB (NF-kappaB) binding, the reduction of inhibitor kappaB alpha (IkappaBalpha) protein, and an increase in the activity of inhibitor kappaB kinase (IKK) and the expression of IKKalpha and IKKbeta, the enzymes that phosphorylate IkappaBalpha, in MNCs. |
| 5834 | 16919536 | Glucose ingestion (75 g in 300 mL water) in healthy human subjects resulted in an increase in intranuclear nuclear factor kappaB (NF-kappaB) binding, the reduction of inhibitor kappaB alpha (IkappaBalpha) protein, and an increase in the activity of inhibitor kappaB kinase (IKK) and the expression of IKKalpha and IKKbeta, the enzymes that phosphorylate IkappaBalpha, in MNCs. |
| 5835 | 16919536 | Glucose intake caused an increase in NF-kappaB binding to NF-kappaB2, NF-kappaB2a, and NF-kappaB3 sequences in the promoter site of tumor necrosis factor alpha (TNF-alpha) gene along with an increase in the expression of TNF-alpha messenger RNA in MNCs. |
| 5836 | 16919536 | Glucose intake caused an increase in NF-kappaB binding to NF-kappaB2, NF-kappaB2a, and NF-kappaB3 sequences in the promoter site of tumor necrosis factor alpha (TNF-alpha) gene along with an increase in the expression of TNF-alpha messenger RNA in MNCs. |
| 5837 | 16919536 | Membranous p47(phox) subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after glucose intake. |
| 5838 | 16919536 | Membranous p47(phox) subunit, an index of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression and activation, also increased after glucose intake. |
| 5839 | 16919536 | We conclude that glucose intake induces an immediate increase in intranuclear NF-kappaB binding, a fall in IkappaBalpha, an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha in MNCs in healthy subjects. |
| 5840 | 16919536 | We conclude that glucose intake induces an immediate increase in intranuclear NF-kappaB binding, a fall in IkappaBalpha, an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha in MNCs in healthy subjects. |
| 5841 | 16918372 | The signaling axis constituted by osteoprotegerin (OPG), receptor activator nuclear factor kB (RANK) and its ligand (RANKL), along with the monocyte colony stimulating factor (M-CSF) and the transcription factor core Binding protein (Cbfa-1), play a pivotal role in the control of VC. |
| 5842 | 16918372 | In contrast, fetuin-A, matrix G1a protein (MGP) and osteopontin (OPN) control the inhibition of VC. |
| 5843 | 16918372 | The inflammatory cytokines interleukin (IL-1) and tumor necrosis factor (TNF)-alpha enhance OPG and RANKL function in the vessel wall leading to VC. |
| 5844 | 16901933 | Tumor necrosis factor-alpha (TNF-alpha), a cytokine largely expressed in adipose tissue, stimulates chronic lipolysis, which may be associated with increased systemic FFA and insulin resistance in obesity and NIDDM. |
| 5845 | 16901933 | Tumor necrosis factor-alpha (TNF-alpha), a cytokine largely expressed in adipose tissue, stimulates chronic lipolysis, which may be associated with increased systemic FFA and insulin resistance in obesity and NIDDM. |
| 5846 | 16901933 | Tumor necrosis factor-alpha (TNF-alpha), a cytokine largely expressed in adipose tissue, stimulates chronic lipolysis, which may be associated with increased systemic FFA and insulin resistance in obesity and NIDDM. |
| 5847 | 16901933 | Treatment with metformin attenuated TNF-alpha-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 and reversing the downregulation of perilipin protein in TNF-alpha-stimulated adipocytes. |
| 5848 | 16901933 | Treatment with metformin attenuated TNF-alpha-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 and reversing the downregulation of perilipin protein in TNF-alpha-stimulated adipocytes. |
| 5849 | 16901933 | Treatment with metformin attenuated TNF-alpha-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 and reversing the downregulation of perilipin protein in TNF-alpha-stimulated adipocytes. |
| 5850 | 16901933 | A high concentration of glucose in the adipocyte culture promoted the basal rate of glycerol release and significantly enhanced the lipolytic action stimulated by either TNF-alpha or isoproterenol. |
| 5851 | 16901933 | A high concentration of glucose in the adipocyte culture promoted the basal rate of glycerol release and significantly enhanced the lipolytic action stimulated by either TNF-alpha or isoproterenol. |
| 5852 | 16901933 | A high concentration of glucose in the adipocyte culture promoted the basal rate of glycerol release and significantly enhanced the lipolytic action stimulated by either TNF-alpha or isoproterenol. |
| 5853 | 16889756 | Among these gene products are TNF and members of its superfamily, IL-1alpha, IL-1beta, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. |
| 5854 | 16886840 | Fasting endothelium-dependent flow-mediated dilatation (FMD) of the brachial artery, endothelium-independent nitroglycerin-mediated dilatation (NMD), plasma homocysteine, serum lipids, folate, and inflammatory markers (high-sensitivity C-reactive protein, soluble intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, interleukin-18, tumor necrosis factor-alpha) were assessed after each 2-week treatment period. |
| 5855 | 16883042 | Several studies of adipocyte function have revealed that adipose tissue is not merely an energy-storing organ but it secretes a variety of biologically active molecules, conceptualized as "adipocytokines", including tumor necrosis factor-alpha, estrogen, leptin and adiponectin and that abnormal secretion of these adipocytokines causes metabolic syndrome. |
| 5856 | 16880599 | TNFalpha induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 5857 | 16873816 | Case report of Klinefelter's syndrome with severe diabetes, dyslipidemia, and stroke: The effect of pioglitazone and other anti-inflammatory agents on interleukin-6 and -8, tumor necrosis factor-alpha, and C-reactive protein. |
| 5858 | 16870144 | The aim of this study was to evaluate whether imidazolines RX871024 and efaroxan protect beta-cells against death in the presence of a combination of the cytokines IL-1beta, IFNgamma, and TNFalpha. |
| 5859 | 16870144 | The aim of this study was to evaluate whether imidazolines RX871024 and efaroxan protect beta-cells against death in the presence of a combination of the cytokines IL-1beta, IFNgamma, and TNFalpha. |
| 5860 | 16870144 | Our data indicate that a combination of pro-inflammatory cytokines IL-1beta, IFNgamma, and TNFalpha, conditions modelling those that take place in type 1 diabetes, induces pancreatic beta-cell death that does not directly correlate with NO production and cannot be counteracted with imidazoline compounds. |
| 5861 | 16870144 | Our data indicate that a combination of pro-inflammatory cytokines IL-1beta, IFNgamma, and TNFalpha, conditions modelling those that take place in type 1 diabetes, induces pancreatic beta-cell death that does not directly correlate with NO production and cannot be counteracted with imidazoline compounds. |
| 5862 | 16870142 | Insulin suppressed angptl4 mRNA expression in time- and dose-dependent manners, and the inhibitory effect was attenuated by a RNA synthesis inhibitor actinomycin D and a phosphoinositide 3-kinase (PI3K) inhibitor LY294002. |
| 5863 | 16870142 | Adenoviral-mediated overexpression of forkhead transcription factor Foxo1 increased angptl4 mRNA expression, and insulin significantly suppressed its effect. |
| 5864 | 16870142 | In addition, insulin failed to decrease angptl4 mRNA expression in an insulin-resistant state induced by TNF-alpha in 3T3-L1 adipocytes. |
| 5865 | 16870142 | These results suggest that insulin downregulates angptl4 mRNA expression via PI3K/Foxo1 pathway in 3T3-L1 adipocytes, and that the reduction of angptl4 mRNA by insulin is attenuated in insulin resistance. |
| 5866 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 5867 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 5868 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 5869 | 16864906 | Serum IL-1beta, IL-2, and IL-6 in insulin-dependent diabetic children. |
| 5870 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 5871 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 5872 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 5873 | 16864906 | Insulin-dependent diabetes mellitus (IDDM) is a chronic disease characterized by T-cell-dependent autoimmune destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans, resulting in an absolute lack of insulin. |
| 5874 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 5875 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 5876 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 5877 | 16864906 | Insulin is one of the islet autoantigens responsible for the activation of T-lymphocyte functions, inflammatory cytokine production, and development of IDDM. |
| 5878 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 5879 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 5880 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 5881 | 16864906 | The aim of this study was to investigate serum concentrations of interleukin (IL)-1beta, IL-2, IL-6, and tumor necrosis factor (TNF)-alpha in children IDDM. |
| 5882 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 5883 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 5884 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 5885 | 16864906 | In all stages of diabetes higher levels of IL-1beta and TNF-alpha and lower levels of IL-2 and IL-6 were detected. |
| 5886 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 5887 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 5888 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 5889 | 16864906 | Our data about elevated serum IL-1beta, TNF-alpha and decreased IL-2, IL-6 levels in newly diagnosed IDDM patients in comparison with longer standing cases supports an activation of systemic inflammatory process during early phases of IDDM which may be indicative of an ongoing beta-cell destruction. |
| 5890 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 5891 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 5892 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 5893 | 16864906 | Persistence of significant difference between the cases with IDDM monitored for a long time and controls in terms of IL-1beta, IL-2, IL-6, and TNF-alpha supports continuous activation during the late stages of diabetes. |
| 5894 | 16864902 | This study compared the results of tumour necrosis factor alpha (TNF-alpha), interleukin-2 soluble receptor (sIL-2R), nitric oxide metabolites (NO(x)), C-reactive protein (CRP), and lipids (total cholesterol, high-density lipoprotein (HDL-cholesterol), low-density lipoprotein (LDL-cholesterol), and triglycerides) between control group (nondiabetic subjects) and overweight type 2 DM subjects. |
| 5895 | 16844399 | The worsening of sepsis and arthritis was associated with a significant increase in systemic and local production of IL-6, IL-1 beta, TNF-alpha, IL-10, macrophage inflammatory protein 1 alpha (MIP-1alpha), and MIP-2 and with a decrease in IFN-gamma production. |
| 5896 | 16835866 | The purpose of this study was to observe the islet changes of pancreas in insulin-dependent diabetes mellitus (IDDM) mice in comparison to normal mice after application of an extract from Siraitia grosvenori fruits containing mogrosides, in particular, mogroside V. |
| 5897 | 16835866 | In addition, alloxan induced a notable increase in the expression of CD8+ lymphocytes to form a dramatic decrease in CD4+/CD8+ ratio (while CD4+ was unchanged). |
| 5898 | 16835866 | Furthermore, at low dose, MG regulated the immune imbalance observed in alloxan-induced IDDM mice by up-regulating the CD4+ T-lymphocyte subsets and CD4/CD8 ratio, and altering the intracellular cytokine profiles. |
| 5899 | 16835866 | The expression of the pro-inflammatory Th1 cytokines: IFN-gamma, TNF-alpha in splenic lymphocytes was altered toward a beneficial Th2 pattern. |
| 5900 | 20351804 | Other accompanying abnormalities may include elevated serum levels of leptin, TNFalpha, plasminogen activator inhibitor-1 and testosterone. |
| 5901 | 16805436 | Several cytokines such as interleukin 6 (IL6) and tumour necrosis factor alpha (TNFalpha) in the dorsal horn are also increased after nerve lesion and have been implicated in contributing to nerve-injury pain. |
| 5902 | 16803995 | Results regarding genes involved in inflammation (IL-1 cluster, IL-6, IL-10, TNF-alpha, TGF-beta, TLR-4, PPARgamma), insulin/IGF-1 signaling pathway and lipid metabolism (apolipoproteins, CETP, PON1), and oxidative stress (p53, p66(shc)) will be described. |
| 5903 | 16801615 | Areca nut chewing is associated with metabolic syndrome: role of tumor necrosis factor-alpha, leptin, and white blood cell count in betel nut chewing-related metabolic derangements. |
| 5904 | 16784178 | Tumour necrosis factor (TNF)alpha is implicated in the relationship between obesity and insulin resistance/ type 2 diabetes. |
| 5905 | 16784178 | In an effort to understand this association better we (i) profiled gene expression patterns of TNF, TNFR1 and TNFR2 and (ii) investigated the effects of TNF on glucose uptake in isolated adipocytes and adipose tissue explants from omental and subcutaneous depots from lean, overweight and obese individuals. |
| 5906 | 16784178 | TNF expression correlated with expression of TNFR2, but not TNFR1, and TNF and TNFR2 expression increased in obesity. |
| 5907 | 16781673 | Activation of Toll-like receptor 4 is associated with insulin resistance in adipocytes. |
| 5908 | 16781673 | Here, we observed that mRNA level of TLR4 was induced during adipocyte differentiation and remarkably enhanced in fat tissues of obese db/db mice. |
| 5909 | 16781673 | In addition, activation of TLR4 with either LPS or free fatty acids stimulated NFkappaB signaling and expression of inflammatory cytokine genes, such as TNFalpha and IL-6 in 3T3-L1 adipocytes. |
| 5910 | 16781673 | Furthermore, we discovered that TLR4 activation in 3T3-L1 adipocytes provoked insulin resistance. |
| 5911 | 16781673 | Taken together, these results suggest that activation of TLR4 in adipocyte might be implicated in the onset of insulin resistance in obesity and type 2 diabetes. |
| 5912 | 16781084 | It contains a rich blood and nerve supply as well as proinflammatory molecules such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), leptin, and resistin, the adipocytokines, and acute phase proteins (APP) which are activated from adipocytes and/or macrophages by sympathetic signaling. |
| 5913 | 16781084 | It contains a rich blood and nerve supply as well as proinflammatory molecules such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), leptin, and resistin, the adipocytokines, and acute phase proteins (APP) which are activated from adipocytes and/or macrophages by sympathetic signaling. |
| 5914 | 16781084 | Sympathetic signaling induces TNF which stimulates the production of IL-6 and leptin from adipocytes; these molecules promote lipolysis and ffa fluxes from adipocytes. |
| 5915 | 16781084 | Sympathetic signaling induces TNF which stimulates the production of IL-6 and leptin from adipocytes; these molecules promote lipolysis and ffa fluxes from adipocytes. |
| 5916 | 16781084 | Leptin stimulates corticotrophin releasing hormone in the brain which stimulates the SNS and HPA axes, i.e. the stress response. |
| 5917 | 16781084 | Leptin stimulates corticotrophin releasing hormone in the brain which stimulates the SNS and HPA axes, i.e. the stress response. |
| 5918 | 16777978 | C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. |
| 5919 | 16777978 | C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. |
| 5920 | 16777978 | C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. |
| 5921 | 16777978 | C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. |
| 5922 | 16777978 | C-jun N-terminal kinase mediates tumor necrosis factor-alpha suppression of differentiation in myoblasts. |
| 5923 | 16777978 | The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes. |
| 5924 | 16777978 | The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes. |
| 5925 | 16777978 | The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes. |
| 5926 | 16777978 | The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes. |
| 5927 | 16777978 | The stress kinase c-jun N-terminal kinase (JNK) was recently shown to be involved in the pathophysiology of major inflammatory conditions, including Alzheimer's disease, stroke, obesity, and type II diabetes. |
| 5928 | 16777978 | Here we used a novel, JNK interacting protein (JIP)-derived JNK peptide inhibitor to establish that JNK suppresses the biological activity of IGF-I in skeletal muscle progenitor cells. |
| 5929 | 16777978 | Here we used a novel, JNK interacting protein (JIP)-derived JNK peptide inhibitor to establish that JNK suppresses the biological activity of IGF-I in skeletal muscle progenitor cells. |
| 5930 | 16777978 | Here we used a novel, JNK interacting protein (JIP)-derived JNK peptide inhibitor to establish that JNK suppresses the biological activity of IGF-I in skeletal muscle progenitor cells. |
| 5931 | 16777978 | Here we used a novel, JNK interacting protein (JIP)-derived JNK peptide inhibitor to establish that JNK suppresses the biological activity of IGF-I in skeletal muscle progenitor cells. |
| 5932 | 16777978 | Here we used a novel, JNK interacting protein (JIP)-derived JNK peptide inhibitor to establish that JNK suppresses the biological activity of IGF-I in skeletal muscle progenitor cells. |
| 5933 | 16777978 | In these myoblasts, TNFalpha and its downstream receptor substrates, neutral-sphingomyelinase (N-SMase) and N-acetyl-d-sphingosine (C2-ceramide), induce JNK kinase activity in a time-dependent manner. |
| 5934 | 16777978 | In these myoblasts, TNFalpha and its downstream receptor substrates, neutral-sphingomyelinase (N-SMase) and N-acetyl-d-sphingosine (C2-ceramide), induce JNK kinase activity in a time-dependent manner. |
| 5935 | 16777978 | In these myoblasts, TNFalpha and its downstream receptor substrates, neutral-sphingomyelinase (N-SMase) and N-acetyl-d-sphingosine (C2-ceramide), induce JNK kinase activity in a time-dependent manner. |
| 5936 | 16777978 | In these myoblasts, TNFalpha and its downstream receptor substrates, neutral-sphingomyelinase (N-SMase) and N-acetyl-d-sphingosine (C2-ceramide), induce JNK kinase activity in a time-dependent manner. |
| 5937 | 16777978 | In these myoblasts, TNFalpha and its downstream receptor substrates, neutral-sphingomyelinase (N-SMase) and N-acetyl-d-sphingosine (C2-ceramide), induce JNK kinase activity in a time-dependent manner. |
| 5938 | 16777978 | Consistent with these results, TNFalpha induces JNK binding to insulin receptor substrate 1 (IRS-1) but is unable to inhibit IGF-I-induced IRS-1 tyrosine phosphorylation in myoblasts that are treated with the JNK peptide inhibitor. |
| 5939 | 16777978 | Consistent with these results, TNFalpha induces JNK binding to insulin receptor substrate 1 (IRS-1) but is unable to inhibit IGF-I-induced IRS-1 tyrosine phosphorylation in myoblasts that are treated with the JNK peptide inhibitor. |
| 5940 | 16777978 | Consistent with these results, TNFalpha induces JNK binding to insulin receptor substrate 1 (IRS-1) but is unable to inhibit IGF-I-induced IRS-1 tyrosine phosphorylation in myoblasts that are treated with the JNK peptide inhibitor. |
| 5941 | 16777978 | Consistent with these results, TNFalpha induces JNK binding to insulin receptor substrate 1 (IRS-1) but is unable to inhibit IGF-I-induced IRS-1 tyrosine phosphorylation in myoblasts that are treated with the JNK peptide inhibitor. |
| 5942 | 16777978 | Consistent with these results, TNFalpha induces JNK binding to insulin receptor substrate 1 (IRS-1) but is unable to inhibit IGF-I-induced IRS-1 tyrosine phosphorylation in myoblasts that are treated with the JNK peptide inhibitor. |
| 5943 | 16777978 | More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC). |
| 5944 | 16777978 | More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC). |
| 5945 | 16777978 | More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC). |
| 5946 | 16777978 | More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC). |
| 5947 | 16777978 | More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC). |
| 5948 | 16777978 | The JNK peptide inhibitor, but not the control peptide, completely reverses this inhibition of both myogenin and MHC. |
| 5949 | 16777978 | The JNK peptide inhibitor, but not the control peptide, completely reverses this inhibition of both myogenin and MHC. |
| 5950 | 16777978 | The JNK peptide inhibitor, but not the control peptide, completely reverses this inhibition of both myogenin and MHC. |
| 5951 | 16777978 | The JNK peptide inhibitor, but not the control peptide, completely reverses this inhibition of both myogenin and MHC. |
| 5952 | 16777978 | The JNK peptide inhibitor, but not the control peptide, completely reverses this inhibition of both myogenin and MHC. |
| 5953 | 16777978 | In the absence of IGF-I, TNFalpha, C2-ceramide, N-SMase and the JNK inhibitor are inactive, as shown by their inability to affect IRS tyrosine phosphorylation and protein expression of myogenin and MHC. |
| 5954 | 16777978 | In the absence of IGF-I, TNFalpha, C2-ceramide, N-SMase and the JNK inhibitor are inactive, as shown by their inability to affect IRS tyrosine phosphorylation and protein expression of myogenin and MHC. |
| 5955 | 16777978 | In the absence of IGF-I, TNFalpha, C2-ceramide, N-SMase and the JNK inhibitor are inactive, as shown by their inability to affect IRS tyrosine phosphorylation and protein expression of myogenin and MHC. |
| 5956 | 16777978 | In the absence of IGF-I, TNFalpha, C2-ceramide, N-SMase and the JNK inhibitor are inactive, as shown by their inability to affect IRS tyrosine phosphorylation and protein expression of myogenin and MHC. |
| 5957 | 16777978 | In the absence of IGF-I, TNFalpha, C2-ceramide, N-SMase and the JNK inhibitor are inactive, as shown by their inability to affect IRS tyrosine phosphorylation and protein expression of myogenin and MHC. |
| 5958 | 16777978 | These results establish that the resistance of muscle progenitor cells to IGF-I, which is caused by inflammatory stimuli, is mediated by the JNK stress kinase pathway. |
| 5959 | 16777978 | These results establish that the resistance of muscle progenitor cells to IGF-I, which is caused by inflammatory stimuli, is mediated by the JNK stress kinase pathway. |
| 5960 | 16777978 | These results establish that the resistance of muscle progenitor cells to IGF-I, which is caused by inflammatory stimuli, is mediated by the JNK stress kinase pathway. |
| 5961 | 16777978 | These results establish that the resistance of muscle progenitor cells to IGF-I, which is caused by inflammatory stimuli, is mediated by the JNK stress kinase pathway. |
| 5962 | 16777978 | These results establish that the resistance of muscle progenitor cells to IGF-I, which is caused by inflammatory stimuli, is mediated by the JNK stress kinase pathway. |
| 5963 | 16777430 | The spontaneous production of IFN-gamma, TNF-alpha and IL-10 by mononuclear cells in children with both asthma and diabetes was elevated compared to the other study groups (p=0.02, p=0.001 and p=0.04, respectively). |
| 5964 | 16767296 | Thus, increased adipose tissue mass is associated with alteration in adipokine production as over expression of tumor necrosis factor alpha, interleukin 6, plasminogen activator inhibitor 1, and under expression of adiponectin in adipocite tissue. |
| 5965 | 16767296 | Thus, increased adipose tissue mass is associated with alteration in adipokine production as over expression of tumor necrosis factor alpha, interleukin 6, plasminogen activator inhibitor 1, and under expression of adiponectin in adipocite tissue. |
| 5966 | 16767296 | Thus, increased adipose tissue mass is associated with alteration in adipokine production as over expression of tumor necrosis factor alpha, interleukin 6, plasminogen activator inhibitor 1, and under expression of adiponectin in adipocite tissue. |
| 5967 | 16767296 | Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-alpha, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. |
| 5968 | 16767296 | Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-alpha, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. |
| 5969 | 16767296 | Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-alpha, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. |
| 5970 | 16767296 | This review will focus on the evidence for regulation of endothelial function by insulin and the adypokines such as adyponectin, leptin, resistin, IL-6 and TNF-alpha. |
| 5971 | 16767296 | This review will focus on the evidence for regulation of endothelial function by insulin and the adypokines such as adyponectin, leptin, resistin, IL-6 and TNF-alpha. |
| 5972 | 16767296 | This review will focus on the evidence for regulation of endothelial function by insulin and the adypokines such as adyponectin, leptin, resistin, IL-6 and TNF-alpha. |
| 5973 | 16767291 | IR may reflect a more aggressive form of autoimmune disease mediated by immuno-inflammatory factors that also mediate beta cell destruction (TNF-alpha and IL-6). |
| 5974 | 16762982 | TNF-alpha induces endothelial dysfunction in diabetic adults, an effect reversible by the PPAR-gamma agonist pioglitazone. |
| 5975 | 16741160 | Real-time PCR and Western blotting revealed that mRNA and protein of TNF-alpha were higher in ZOF rats than that in lean rats, whereas eNOS protein levels were reduced in the ZOF versus lean rats. |
| 5976 | 16739872 | This increased IDR may be a consequence of the synergy between interferon-gamma and tumor necrosis factor alpha which is a significant factor in diabetes. |
| 5977 | 16734992 | The effect of periodontal therapy on TNF-alpha, IL-6 and metabolic control in type 2 diabetics. |
| 5978 | 16732051 | Divergent relationships among soluble tumor necrosis factor-alpha receptors 1 and 2, insulin resistance, and endothelial function. |
| 5979 | 16731844 | Tumor necrosis factor-alpha (TNF-alpha) is a major factor behind inflammation and insulin resistance in adipose tissue. |
| 5980 | 16731825 | We confirmed that t10,c12-CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes hyperinsulinemia. |
| 5981 | 16731825 | In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such as tumor necrosis factor-alpha and interleukin-6 gene expression in WAT without affecting their serum levels. |
| 5982 | 16731790 | In the present study we prospectively analyzed the serial effects of androgen-replacement therapy on both the distribution of peripheral blood lymphocytes, monocytes and dendritic cells as well as on the production of interleukin (IL)-1beta, IL-6 and tumor necrosis factor alpha (TNFalpha) inflammatory cytokines by circulating monocytes and CD33 myeloid, CD16 and plasmacytoid dendritic cell subsets, the most potent antigen-presenting cells (APCs) in type-2 diabetic men with partial androgen deficiency. |
| 5983 | 16731790 | In the present study we prospectively analyzed the serial effects of androgen-replacement therapy on both the distribution of peripheral blood lymphocytes, monocytes and dendritic cells as well as on the production of interleukin (IL)-1beta, IL-6 and tumor necrosis factor alpha (TNFalpha) inflammatory cytokines by circulating monocytes and CD33 myeloid, CD16 and plasmacytoid dendritic cell subsets, the most potent antigen-presenting cells (APCs) in type-2 diabetic men with partial androgen deficiency. |
| 5984 | 16731790 | Our results show for the first time that testosterone-replacement therapy is associated with a reduction or complete abrogation of spontaneous ex vivo production of IL-1beta, IL-6 and TNFalpha by APCs. |
| 5985 | 16731790 | Our results show for the first time that testosterone-replacement therapy is associated with a reduction or complete abrogation of spontaneous ex vivo production of IL-1beta, IL-6 and TNFalpha by APCs. |
| 5986 | 16728431 | Expression of TLR3 and TLR5 was significantly higher in newly diabetic non-obese diabetic (NOD) mice when compared with pre-diabetic and control strains of mice. |
| 5987 | 16728431 | Expression of TLR3 and TLR5 was significantly higher in newly diabetic non-obese diabetic (NOD) mice when compared with pre-diabetic and control strains of mice. |
| 5988 | 16728431 | Dysregulation of TLR4 expression in the diabetic state correlated with increased nuclear factor kappa B (NF-kappaB) activation in response to the TLR4 ligand LPS and higher expression of IL-12p40, tumor necrosis factor alpha (TNFalpha), IL-6 and inducible nitric oxide synthase but lowered expression of IL-10. |
| 5989 | 16728431 | Dysregulation of TLR4 expression in the diabetic state correlated with increased nuclear factor kappa B (NF-kappaB) activation in response to the TLR4 ligand LPS and higher expression of IL-12p40, tumor necrosis factor alpha (TNFalpha), IL-6 and inducible nitric oxide synthase but lowered expression of IL-10. |
| 5990 | 16728431 | Exposure of bone marrow precursor cells from NOD mice to a hyperglycemic environment during differentiation into macrophages resulted in elevated levels of TLR2 and TLR4 and the cytokine TNFalpha. |
| 5991 | 16728431 | Exposure of bone marrow precursor cells from NOD mice to a hyperglycemic environment during differentiation into macrophages resulted in elevated levels of TLR2 and TLR4 and the cytokine TNFalpha. |
| 5992 | 16720206 | Modulation of cytokine release through humanized monoclonal antibodies was moderate and selective: anti-CD25 led to increased release of IL-2 and reduced production of TNFalpha, whereas anti-CD3 decreased release of interferon-y and IL-5 and increased secretion of IL-10. |
| 5993 | 16718633 | Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. |
| 5994 | 16718633 | Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. |
| 5995 | 16718633 | Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation. |
| 5996 | 16718633 | Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation. |
| 5997 | 16715619 | Genetics, oxidative stress: superoxide anion (O2*-) and hydrogen peroxide (H2O2), endothelial nitric oxide (eNO), lipid peroxides, anti-oxidants, endothelin, angiotensin converting enzyme (ACE) activity, angiotensinII, transforming growth factor-beta (TGF-beta), insulin, homocysteine, asymmetrical dimethyl arginine, proinflammatory cytokines: interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), C-reactive protein (hs-CRP), and long-chain polyunsaturated fatty acids (LCPUFAs), and activity of NAD(P)H oxidase have a role in human essential hypertension. |
| 5998 | 16713232 | Caloric restriction inhibits up-regulation of inflammatory cytokines and TNF-alpha, and activates IL-10 and haptoglobin in the plasma of streptozotocin-induced diabetic rats. |
| 5999 | 16713232 | Caloric restriction inhibits up-regulation of inflammatory cytokines and TNF-alpha, and activates IL-10 and haptoglobin in the plasma of streptozotocin-induced diabetic rats. |
| 6000 | 16713232 | The inflammatory cytokines [interleukin (IL)-1beta, IL-4 and IL-6] and tumor necrosis factor alpha up-regulated in diabetes were found to be significantly depressed by CR, whereas the antiinflammatory mediators, haptoglobin and IL-10 levels, were increased. |
| 6001 | 16713232 | The inflammatory cytokines [interleukin (IL)-1beta, IL-4 and IL-6] and tumor necrosis factor alpha up-regulated in diabetes were found to be significantly depressed by CR, whereas the antiinflammatory mediators, haptoglobin and IL-10 levels, were increased. |
| 6002 | 16713007 | The concentrations of circulating inflammatory markers C-reactive protein (CRP) and tumour necrosis factor-alpha (TNF-alpha) and serum fructosamine were determined. |
| 6003 | 16713007 | The concentrations of circulating inflammatory markers C-reactive protein (CRP) and tumour necrosis factor-alpha (TNF-alpha) and serum fructosamine were determined. |
| 6004 | 16713007 | The results showed that DBT had no direct effect in lowering serum fructosamine level, but can decrease the concentrations of CRP and TNF-alpha, produce a higher survival rate and less body weight loss, and decrease water intake in diabetic atherosclerosis in GK rats. |
| 6005 | 16713007 | The results showed that DBT had no direct effect in lowering serum fructosamine level, but can decrease the concentrations of CRP and TNF-alpha, produce a higher survival rate and less body weight loss, and decrease water intake in diabetic atherosclerosis in GK rats. |
| 6006 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 6007 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 6008 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 6009 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 6010 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 6011 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 6012 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 6013 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 6014 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 6015 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 6016 | 16709900 | TNF-alpha upregulated pro-MMP9 in AMFs isolated from wild-type (OPN(+/+)) mice, but pro-MMP9 induction was abrogated in AMFs from OPN(-/-) mice. |
| 6017 | 16709900 | TNF-alpha upregulated pro-MMP9 in AMFs isolated from wild-type (OPN(+/+)) mice, but pro-MMP9 induction was abrogated in AMFs from OPN(-/-) mice. |
| 6018 | 16709900 | TNF-alpha upregulated pro-MMP9 in AMFs isolated from wild-type (OPN(+/+)) mice, but pro-MMP9 induction was abrogated in AMFs from OPN(-/-) mice. |
| 6019 | 16709900 | TNF-alpha upregulated pro-MMP9 in AMFs isolated from wild-type (OPN(+/+)) mice, but pro-MMP9 induction was abrogated in AMFs from OPN(-/-) mice. |
| 6020 | 16709900 | TNF-alpha upregulated pro-MMP9 in AMFs isolated from wild-type (OPN(+/+)) mice, but pro-MMP9 induction was abrogated in AMFs from OPN(-/-) mice. |
| 6021 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 6022 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 6023 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 6024 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 6025 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 6026 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 6027 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 6028 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 6029 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 6030 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 6031 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 6032 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 6033 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 6034 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 6035 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 6036 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 6037 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 6038 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 6039 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 6040 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 6041 | 16709900 | OPN structure/function studies mapped these activities to the SVVYGLR heptapeptide motif in the thrombin-liberated human OPN N-terminal domain (SLAYGLR in mouse OPN). |
| 6042 | 16709900 | OPN structure/function studies mapped these activities to the SVVYGLR heptapeptide motif in the thrombin-liberated human OPN N-terminal domain (SLAYGLR in mouse OPN). |
| 6043 | 16709900 | OPN structure/function studies mapped these activities to the SVVYGLR heptapeptide motif in the thrombin-liberated human OPN N-terminal domain (SLAYGLR in mouse OPN). |
| 6044 | 16709900 | OPN structure/function studies mapped these activities to the SVVYGLR heptapeptide motif in the thrombin-liberated human OPN N-terminal domain (SLAYGLR in mouse OPN). |
| 6045 | 16709900 | OPN structure/function studies mapped these activities to the SVVYGLR heptapeptide motif in the thrombin-liberated human OPN N-terminal domain (SLAYGLR in mouse OPN). |
| 6046 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 6047 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 6048 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 6049 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 6050 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 6051 | 16709900 | Injection of OPN-deficient OPN(+/-) mice with SVVYGLR peptide upregulated pro-MMP9 activity, 8-IsoP levels, and Nox2 protein levels in aorta and increased panmural superoxide production (dihydroethidium staining). |
| 6052 | 16709900 | Injection of OPN-deficient OPN(+/-) mice with SVVYGLR peptide upregulated pro-MMP9 activity, 8-IsoP levels, and Nox2 protein levels in aorta and increased panmural superoxide production (dihydroethidium staining). |
| 6053 | 16709900 | Injection of OPN-deficient OPN(+/-) mice with SVVYGLR peptide upregulated pro-MMP9 activity, 8-IsoP levels, and Nox2 protein levels in aorta and increased panmural superoxide production (dihydroethidium staining). |
| 6054 | 16709900 | Injection of OPN-deficient OPN(+/-) mice with SVVYGLR peptide upregulated pro-MMP9 activity, 8-IsoP levels, and Nox2 protein levels in aorta and increased panmural superoxide production (dihydroethidium staining). |
| 6055 | 16709900 | Injection of OPN-deficient OPN(+/-) mice with SVVYGLR peptide upregulated pro-MMP9 activity, 8-IsoP levels, and Nox2 protein levels in aorta and increased panmural superoxide production (dihydroethidium staining). |
| 6056 | 16709900 | At equivalent hyperglycemia and dyslipidemia, 8-IsoP levels and aortic pro-MMP9 were reduced with complete OPN deficiency in a model of diet-induced diabetes, achieved by comparing OPN(-/-)/LDLR(-/-) versus OPN(+/-)/LDLR(-/-) siblings. |
| 6057 | 16709900 | At equivalent hyperglycemia and dyslipidemia, 8-IsoP levels and aortic pro-MMP9 were reduced with complete OPN deficiency in a model of diet-induced diabetes, achieved by comparing OPN(-/-)/LDLR(-/-) versus OPN(+/-)/LDLR(-/-) siblings. |
| 6058 | 16709900 | At equivalent hyperglycemia and dyslipidemia, 8-IsoP levels and aortic pro-MMP9 were reduced with complete OPN deficiency in a model of diet-induced diabetes, achieved by comparing OPN(-/-)/LDLR(-/-) versus OPN(+/-)/LDLR(-/-) siblings. |
| 6059 | 16709900 | At equivalent hyperglycemia and dyslipidemia, 8-IsoP levels and aortic pro-MMP9 were reduced with complete OPN deficiency in a model of diet-induced diabetes, achieved by comparing OPN(-/-)/LDLR(-/-) versus OPN(+/-)/LDLR(-/-) siblings. |
| 6060 | 16709900 | At equivalent hyperglycemia and dyslipidemia, 8-IsoP levels and aortic pro-MMP9 were reduced with complete OPN deficiency in a model of diet-induced diabetes, achieved by comparing OPN(-/-)/LDLR(-/-) versus OPN(+/-)/LDLR(-/-) siblings. |
| 6061 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 6062 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 6063 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 6064 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 6065 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 6066 | 16698671 | CBD treatment also resulted in the significant reduction of plasma levels of the pro-inflammatory cytokines, IFN-gamma and TNF-alpha. |
| 6067 | 16698671 | Th1-associated cytokine production of in vitro activated T-cells and peritoneal macrophages was also significantly reduced in CBD-treated mice, whereas production of the Th2-associated cytokines, IL-4 and IL-10, was increased when compared to untreated control mice. |
| 6068 | 16689001 | [Effects of Jiangtang Bushen Recipe on serum C-reactive protein, tumor necrosis factor-alpha and interleukin-6 in patients with type 2 diabetes mellitus]. |
| 6069 | 16687123 | NRTIs are able to induce mitochondrial dysfonction and to modify adipocyte phenotype and adipose tissue pattern of secretion of cytokines (TNFalpha, IL-6) and other adipokines (adiponectin, leptin) probably through the production of reactive oxygen species. |
| 6070 | 16687123 | Some PIs also act on adipocyte, alter its differentiation and insulin sensitivity and also the pattern of secretion of adipokines by adipose tissue. |
| 6071 | 16677285 | Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease. |
| 6072 | 16677059 | Recent studies show that serum levels of inflammatory mediators, such as tumor necrosis factor-alpha and interleukin-6, are increased in the insulin-resistant conditions of obesity and PCOS. |
| 6073 | 16677059 | The optimal modality for long-term treatment should have positive effects on androgen synthesis, sex hormone-binding globulin production, the lipid profile, insulin sensitivity, inflammatory mediators, and clinical symptoms including acne, hirsutism, and irregular menstrual cycles. |
| 6074 | 16674947 | Among adipocytokines, tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and may contribute to the development of vascular diseases. |
| 6075 | 16674947 | Among adipocytokines, tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and may contribute to the development of vascular diseases. |
| 6076 | 16674947 | On the contrary to these adipocytokines, adiponectin, an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. |
| 6077 | 16674947 | On the contrary to these adipocytokines, adiponectin, an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. |
| 6078 | 16674947 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin binding epidermal growth factor-like growth and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. |
| 6079 | 16674947 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin binding epidermal growth factor-like growth and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. |
| 6080 | 16645020 | An alternative spliced variant of circulating soluble tumor necrosis factor-alpha receptor-2 is paradoxically associated with insulin action. |
| 6081 | 16644698 | The IL-1 cytokine trap used herein comprised extracellular domains of the IL-1 receptor accessory protein and the human IL-1 receptor 1 arranged inline and fused to the Fc portion of human IgG1. |
| 6082 | 16644698 | IL-1beta alone induced a strong inhibition of insulin secretion and glucose oxidation rate and a marked increase in medium nitrite accumulation as an indicator of nitric oxide generation. |
| 6083 | 16644698 | Moreover, the IL-1 trap (100:1) blocked the increased islet cell death seen in islets treated with a combination of IL-1beta + tumor necrosis factor-alpha + interferon-gamma as well as functional suppression induced by the cytokine combination. |
| 6084 | 16644677 | One of the mechanisms involved in the progression of diabetic nephropathy, the most common cause of end-stage renal failure, is angiogenic phenomenon associated with the increase of angiogenic factors such as vascular endothelial growth factor (VEGF)-A and angiopoietin (Ang)-2, an antagonist of Ang-1. |
| 6085 | 16644677 | Increases in kidney weight, glomerular volume, creatinine clearance, urinary albumin excretion, total mesangial fraction, glomerular type IV collagen, glomerular endothelial area (CD31(+)), and monocyte/macrophage accumulation (F4/80(+)) observed in control db/db mice were significantly suppressed by daily intraperitoneal injection of NM-3 (100 mg/kg, for 8 weeks). |
| 6086 | 16644677 | Increases in renal expression of VEGF-A, Ang-2, fibrogenic factor transforming growth factor (TGF)-beta1, and chemokine monocyte chemoattractant protein-1 but not tumor necrosis factor-alpha were also inhibited by NM-3 in db/db mice. |
| 6087 | 16644677 | NM-3 significantly suppressed the increase of VEGF induced by high glucose in cultured podocytes and also suppressed the increase of VEGF and TGF-beta induced by high glucose in cultured mesangial cells. |
| 6088 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6089 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6090 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6091 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6092 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6093 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6094 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6095 | 16644673 | Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling. |
| 6096 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6097 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6098 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6099 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6100 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6101 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6102 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6103 | 16644673 | Tumor necrosis factor (TNF)-alpha inhibits insulin action; however, the precise mechanisms are unknown. |
| 6104 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6105 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6106 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6107 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6108 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6109 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6110 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6111 | 16644673 | It was reported that TNF-alpha could increase mitochondrial reactive oxygen species (ROS) production, and apoptosis signal-regulating kinase 1 (ASK1) was reported to be required for TNF-alpha-induced apoptosis. |
| 6112 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6113 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6114 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6115 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6116 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6117 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6118 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6119 | 16644673 | Here, we examined roles of mitochondrial ROS and ASK1 in TNF-alpha-induced impaired insulin signaling in cultured human hepatoma (Huh7) cells. |
| 6120 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6121 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6122 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6123 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6124 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6125 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6126 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6127 | 16644673 | Using reduced MitoTracker Red probe, we confirmed that TNF-alpha increased mitochondrial ROS production, which was suppressed by overexpression of either uncoupling protein-1 (UCP)-1 or manganese superoxide dismutase (MnSOD). |
| 6128 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6129 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6130 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6131 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6132 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6133 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6134 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6135 | 16644673 | TNF-alpha significantly activated ASK1, increased serine phosphorylation of insulin receptor substrate (IRS)-1, and decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, and all of these effects were inhibited by overexpression of either UCP-1 or MnSOD. |
| 6136 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6137 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6138 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6139 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6140 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6141 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6142 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6143 | 16644673 | Similar to TNF-alpha, overexpression of wild-type ASK1 increased serine phosphorylation of IRS-1 and decreased insulin-stimulated tyrosine phosphorylation of IRS-1, whereas overexpression of dominant-negative ASK1 ameliorated these TNF-alpha-induced events. |
| 6144 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6145 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6146 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6147 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6148 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6149 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6150 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6151 | 16644673 | In addition, TNF-alpha activated c-jun NH(2)-terminal kinases (JNKs), and this observation was partially inhibited by overexpression of UCP-1, MnSOD, or dominant-negative ASK1. |
| 6152 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6153 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6154 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6155 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6156 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6157 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6158 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6159 | 16644673 | These results suggest that TNF-alpha increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these TNF-alpha-induced phenomena contribute, at least in part, to impaired insulin signaling. |
| 6160 | 16641887 | Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. |
| 6161 | 16641887 | Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. |
| 6162 | 16641887 | This suggests that in metabolic syndrome X, obesity, hypertension, diabetes mellitus, and cancer (where insulin resistance is common due to enhanced TNF-alpha production) pyruvate plays a role. |
| 6163 | 16641887 | This suggests that in metabolic syndrome X, obesity, hypertension, diabetes mellitus, and cancer (where insulin resistance is common due to enhanced TNF-alpha production) pyruvate plays a role. |
| 6164 | 16634986 | Adiponectin antagonizes many effects of tumour necrosis factor-alpha(TNF-alpha) and this, in turn, suppresses adiponectin production. |
| 6165 | 16634986 | Adiponectin antagonizes many effects of tumour necrosis factor-alpha(TNF-alpha) and this, in turn, suppresses adiponectin production. |
| 6166 | 16634986 | Adiponectin antagonizes many effects of tumour necrosis factor-alpha(TNF-alpha) and this, in turn, suppresses adiponectin production. |
| 6167 | 16634986 | Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). |
| 6168 | 16634986 | Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). |
| 6169 | 16634986 | Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). |
| 6170 | 16634986 | Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. |
| 6171 | 16634986 | Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. |
| 6172 | 16634986 | Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. |
| 6173 | 16634986 | Two adiponectin receptors, termed AdipoR1 and AdipoR2, have been identified and these are ubiquitously expressed. |
| 6174 | 16634986 | Two adiponectin receptors, termed AdipoR1 and AdipoR2, have been identified and these are ubiquitously expressed. |
| 6175 | 16634986 | Two adiponectin receptors, termed AdipoR1 and AdipoR2, have been identified and these are ubiquitously expressed. |
| 6176 | 16634986 | AdipoR1 is most highly expressed in skeletal muscle and has a prominent action to activate AMPK, and hence promote lipid oxidation. |
| 6177 | 16634986 | AdipoR1 is most highly expressed in skeletal muscle and has a prominent action to activate AMPK, and hence promote lipid oxidation. |
| 6178 | 16634986 | AdipoR1 is most highly expressed in skeletal muscle and has a prominent action to activate AMPK, and hence promote lipid oxidation. |
| 6179 | 16634986 | AdipoR2 is most highly expressed in liver, where it enhances insulin sensitivity and reduces steatosis via activation of AMPK and increased peroxisome-proliferator-activated receptor alpha ligand activity. |
| 6180 | 16634986 | AdipoR2 is most highly expressed in liver, where it enhances insulin sensitivity and reduces steatosis via activation of AMPK and increased peroxisome-proliferator-activated receptor alpha ligand activity. |
| 6181 | 16634986 | AdipoR2 is most highly expressed in liver, where it enhances insulin sensitivity and reduces steatosis via activation of AMPK and increased peroxisome-proliferator-activated receptor alpha ligand activity. |
| 6182 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6183 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6184 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6185 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6186 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6187 | 16613757 | In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. |
| 6188 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6189 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6190 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6191 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6192 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6193 | 16613757 | Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. |
| 6194 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6195 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6196 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6197 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6198 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6199 | 16613757 | Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. |
| 6200 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6201 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6202 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6203 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6204 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6205 | 16613757 | Leptin could modulate TNF-alpha production and macrophage activation. |
| 6206 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6207 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6208 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6209 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6210 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6211 | 16613757 | TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. |
| 6212 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6213 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6214 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6215 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6216 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6217 | 16613757 | Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. |
| 6218 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6219 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6220 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6221 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6222 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6223 | 16613757 | In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. |
| 6224 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6225 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6226 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6227 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6228 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6229 | 16613757 | Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. |
| 6230 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6231 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6232 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6233 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6234 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6235 | 16613757 | In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. |
| 6236 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6237 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6238 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6239 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6240 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6241 | 16613757 | In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. |
| 6242 | 16600299 | We evaluated the plasma levels of IL-6, TNF-alpha, IL-1beta, and IL-10 in four groups of older individuals: 60 patients with LOAD, 80 patients with VD, 40 subjects with cerebrovascular disease but without dementia (CDND), and 42 controls (C). |
| 6243 | 16600299 | We evaluated the plasma levels of IL-6, TNF-alpha, IL-1beta, and IL-10 in four groups of older individuals: 60 patients with LOAD, 80 patients with VD, 40 subjects with cerebrovascular disease but without dementia (CDND), and 42 controls (C). |
| 6244 | 16600299 | We evaluated the plasma levels of IL-6, TNF-alpha, IL-1beta, and IL-10 in four groups of older individuals: 60 patients with LOAD, 80 patients with VD, 40 subjects with cerebrovascular disease but without dementia (CDND), and 42 controls (C). |
| 6245 | 16600299 | By logistic regression analysis, we demonstrated that high levels (defined as above the median) of IL-1beta and TNF-alpha, but not of IL-6, were associated with increased likelihood of having VD and LOAD compared to C, while high IL-6 levels were associated with a increased probability of having VD, compared with LOAD. |
| 6246 | 16600299 | By logistic regression analysis, we demonstrated that high levels (defined as above the median) of IL-1beta and TNF-alpha, but not of IL-6, were associated with increased likelihood of having VD and LOAD compared to C, while high IL-6 levels were associated with a increased probability of having VD, compared with LOAD. |
| 6247 | 16600299 | By logistic regression analysis, we demonstrated that high levels (defined as above the median) of IL-1beta and TNF-alpha, but not of IL-6, were associated with increased likelihood of having VD and LOAD compared to C, while high IL-6 levels were associated with a increased probability of having VD, compared with LOAD. |
| 6248 | 16600299 | Our study support the notion of a low-grade systemic inflammation in older patients with LOAD or VD, characterized by an increase in plasma IL-1beta and TNF-alpha levels. |
| 6249 | 16600299 | Our study support the notion of a low-grade systemic inflammation in older patients with LOAD or VD, characterized by an increase in plasma IL-1beta and TNF-alpha levels. |
| 6250 | 16600299 | Our study support the notion of a low-grade systemic inflammation in older patients with LOAD or VD, characterized by an increase in plasma IL-1beta and TNF-alpha levels. |
| 6251 | 16598903 | The two main transduction pathways are the phosphatidylinositol 3 kinase pathway activating protein kinase B which is involved in priority in metabolic effects, and the MAP kinase pathway involved in nuclear effects, proliferation and differentiation. |
| 6252 | 16598903 | This phosphorylation is activated in response to different signals involved in insulin resistance, hyperinsulinism, TNFalpha or increased free fatty acids from adipose tissue, which are transformed inside the cell in acyl-CoA. |
| 6253 | 16598899 | Here, we review new advances in our understanding of mechanisms leading to insulin resistance and type 2 diabetes from the perspective of the role and interactions of recently identified adipocyte-specific chemical messengers, the adipocytokines, such as adiponectin, tumor necrosis factor-alpha, interleukin 6, and resistin. |
| 6254 | 16585568 | Control of autoimmune myocarditis and multiorgan inflammation by glucocorticoid-induced TNF receptor family-related protein(high), Foxp3-expressing CD25+ and CD25- regulatory T cells. |
| 6255 | 16585568 | The transcription factor Foxp3 is currently the most specific marker for natural CD4+ Treg, but it would be useful if other Treg markers, particularly cell surface molecules, could be elucidated. |
| 6256 | 16585568 | We demonstrate in this study that the vast majority of Foxp3-expressing CD4+ T cells (whether CD25+ or CD25-) show constitutive high-level expression of glucocorticoid-induced TNFR family-related gene/protein (GITR). |
| 6257 | 16585568 | Transfer of T cell or thymocyte suspensions depleted of GITR(high) cells produces in BALB/c nude mice a wider spectrum and more severe forms of autoimmune diseases than does transfer of similar cell suspensions depleted of CD25+ CD4+ T cells only. |
| 6258 | 16574667 | Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL. |
| 6259 | 16574667 | Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL. |
| 6260 | 16574667 | Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL. |
| 6261 | 16574667 | Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL. |
| 6262 | 16574667 | Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL. |
| 6263 | 16574667 | It was also prevented by pre-incubation with anti-tumor necrosis factor-alpha (anti-TNFalpha) antibody or by blocking IFNgamma responsiveness through expressing a dominant negative IFNgamma receptor. |
| 6264 | 16574667 | It was also prevented by pre-incubation with anti-tumor necrosis factor-alpha (anti-TNFalpha) antibody or by blocking IFNgamma responsiveness through expressing a dominant negative IFNgamma receptor. |
| 6265 | 16574667 | It was also prevented by pre-incubation with anti-tumor necrosis factor-alpha (anti-TNFalpha) antibody or by blocking IFNgamma responsiveness through expressing a dominant negative IFNgamma receptor. |
| 6266 | 16574667 | It was also prevented by pre-incubation with anti-tumor necrosis factor-alpha (anti-TNFalpha) antibody or by blocking IFNgamma responsiveness through expressing a dominant negative IFNgamma receptor. |
| 6267 | 16574667 | It was also prevented by pre-incubation with anti-tumor necrosis factor-alpha (anti-TNFalpha) antibody or by blocking IFNgamma responsiveness through expressing a dominant negative IFNgamma receptor. |
| 6268 | 16574667 | Perforin-deficient CTL produced IFNgamma and TNFalpha that was shown to directly induce islet Fas expression during the assays. |
| 6269 | 16574667 | Perforin-deficient CTL produced IFNgamma and TNFalpha that was shown to directly induce islet Fas expression during the assays. |
| 6270 | 16574667 | Perforin-deficient CTL produced IFNgamma and TNFalpha that was shown to directly induce islet Fas expression during the assays. |
| 6271 | 16574667 | Perforin-deficient CTL produced IFNgamma and TNFalpha that was shown to directly induce islet Fas expression during the assays. |
| 6272 | 16574667 | Perforin-deficient CTL produced IFNgamma and TNFalpha that was shown to directly induce islet Fas expression during the assays. |
| 6273 | 16574667 | This suggests that Fas-deficiency, SOCS-1 overexpression and blockade of IFNgamma and TNFalpha all protect beta cells from residual cytotoxicity of perforin-deficient CTL by blocking Fas upregulation. |
| 6274 | 16574667 | This suggests that Fas-deficiency, SOCS-1 overexpression and blockade of IFNgamma and TNFalpha all protect beta cells from residual cytotoxicity of perforin-deficient CTL by blocking Fas upregulation. |
| 6275 | 16574667 | This suggests that Fas-deficiency, SOCS-1 overexpression and blockade of IFNgamma and TNFalpha all protect beta cells from residual cytotoxicity of perforin-deficient CTL by blocking Fas upregulation. |
| 6276 | 16574667 | This suggests that Fas-deficiency, SOCS-1 overexpression and blockade of IFNgamma and TNFalpha all protect beta cells from residual cytotoxicity of perforin-deficient CTL by blocking Fas upregulation. |
| 6277 | 16574667 | This suggests that Fas-deficiency, SOCS-1 overexpression and blockade of IFNgamma and TNFalpha all protect beta cells from residual cytotoxicity of perforin-deficient CTL by blocking Fas upregulation. |
| 6278 | 16574667 | However, in the absence of perforin, the Fas/FasL pathway provides an alternative mechanism dependent on islet cell Fas upregulation by cytokines IFNgamma and TNFalpha. |
| 6279 | 16574667 | However, in the absence of perforin, the Fas/FasL pathway provides an alternative mechanism dependent on islet cell Fas upregulation by cytokines IFNgamma and TNFalpha. |
| 6280 | 16574667 | However, in the absence of perforin, the Fas/FasL pathway provides an alternative mechanism dependent on islet cell Fas upregulation by cytokines IFNgamma and TNFalpha. |
| 6281 | 16574667 | However, in the absence of perforin, the Fas/FasL pathway provides an alternative mechanism dependent on islet cell Fas upregulation by cytokines IFNgamma and TNFalpha. |
| 6282 | 16574667 | However, in the absence of perforin, the Fas/FasL pathway provides an alternative mechanism dependent on islet cell Fas upregulation by cytokines IFNgamma and TNFalpha. |
| 6283 | 16567828 | Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB1*02-DQA1*05 and TNF -308A. |
| 6284 | 16567539 | We measured insulin sensitivity (euglycemic clamp), forearm blood flow responses to graded local acetylcholine (Ach) and sodium nitroprusside (SNP) infusions, plasma concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, von Willebrand factor (vWF), plasminogen activator inhibitor (PAI)-1, tissue plasminogen activator (tPA), and high-sensitivity C-reactive protein (hs-CRP) in 81 diabetic patients. |
| 6285 | 16567539 | We measured insulin sensitivity (euglycemic clamp), forearm blood flow responses to graded local acetylcholine (Ach) and sodium nitroprusside (SNP) infusions, plasma concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, von Willebrand factor (vWF), plasminogen activator inhibitor (PAI)-1, tissue plasminogen activator (tPA), and high-sensitivity C-reactive protein (hs-CRP) in 81 diabetic patients. |
| 6286 | 16567539 | In multivariate analysis, inflammatory markers (IL-6, hs-CRP, and TNF-alpha) were independently associated with insulin resistance and fasting glycemia, fibrinolytic markers PAI-1 and tPA with insulin resistance and central fat distribution, and vascular indexes (vWF, Ach, and SNP vasodilation) with insulin resistance and obesity or cytokines (TNF-alpha or IL-6). |
| 6287 | 16567539 | In multivariate analysis, inflammatory markers (IL-6, hs-CRP, and TNF-alpha) were independently associated with insulin resistance and fasting glycemia, fibrinolytic markers PAI-1 and tPA with insulin resistance and central fat distribution, and vascular indexes (vWF, Ach, and SNP vasodilation) with insulin resistance and obesity or cytokines (TNF-alpha or IL-6). |
| 6288 | 16556731 | Cytokines, such as IL-1beta and TNF-alpha, contribute to pancreatic beta-cell death in type 1 diabetes mellitus. |
| 6289 | 16556731 | Cytokines, such as IL-1beta and TNF-alpha, contribute to pancreatic beta-cell death in type 1 diabetes mellitus. |
| 6290 | 16556731 | Cytokines, such as IL-1beta and TNF-alpha, contribute to pancreatic beta-cell death in type 1 diabetes mellitus. |
| 6291 | 16556731 | To clarify the reasons behind the proapoptotic effects of NF-kappaB in pancreatic beta-cells, we compared the pattern of cytokine-induced NF-kappaB activation between rat insulin-producing cells (INS-1E cells) and fibroblasts (208F cells). |
| 6292 | 16556731 | To clarify the reasons behind the proapoptotic effects of NF-kappaB in pancreatic beta-cells, we compared the pattern of cytokine-induced NF-kappaB activation between rat insulin-producing cells (INS-1E cells) and fibroblasts (208F cells). |
| 6293 | 16556731 | To clarify the reasons behind the proapoptotic effects of NF-kappaB in pancreatic beta-cells, we compared the pattern of cytokine-induced NF-kappaB activation between rat insulin-producing cells (INS-1E cells) and fibroblasts (208F cells). |
| 6294 | 16556731 | NF-kappaB activation was induced in INS-1E cells and in 208F cells after exposure to cytokines, but apoptosis was induced only in INS-1E cells, with a more pronounced proapoptotic effect of IL-1beta than of TNF-alpha. |
| 6295 | 16556731 | NF-kappaB activation was induced in INS-1E cells and in 208F cells after exposure to cytokines, but apoptosis was induced only in INS-1E cells, with a more pronounced proapoptotic effect of IL-1beta than of TNF-alpha. |
| 6296 | 16556731 | NF-kappaB activation was induced in INS-1E cells and in 208F cells after exposure to cytokines, but apoptosis was induced only in INS-1E cells, with a more pronounced proapoptotic effect of IL-1beta than of TNF-alpha. |
| 6297 | 16556731 | NF-kappaB activation in IL-1beta-exposed INS-1E cells was earlier and more marked as compared with TNF-alpha-exposed INS-1E cells or IL-1beta-exposed 208F cells. |
| 6298 | 16556731 | NF-kappaB activation in IL-1beta-exposed INS-1E cells was earlier and more marked as compared with TNF-alpha-exposed INS-1E cells or IL-1beta-exposed 208F cells. |
| 6299 | 16556731 | NF-kappaB activation in IL-1beta-exposed INS-1E cells was earlier and more marked as compared with TNF-alpha-exposed INS-1E cells or IL-1beta-exposed 208F cells. |
| 6300 | 16556731 | Both cytokines induced a prolonged (up to 48 h) and stable NF-kappaB activation in INS-1E cells, whereas IL-1beta induced an oscillatory NF-kappaB activation in 208F cells. p65/p65 and p65/p50 were the predominant NF-kappaB dimers in IL-1beta-exposed INS-1E cells and 208F cells, respectively. |
| 6301 | 16556731 | Both cytokines induced a prolonged (up to 48 h) and stable NF-kappaB activation in INS-1E cells, whereas IL-1beta induced an oscillatory NF-kappaB activation in 208F cells. p65/p65 and p65/p50 were the predominant NF-kappaB dimers in IL-1beta-exposed INS-1E cells and 208F cells, respectively. |
| 6302 | 16556731 | Both cytokines induced a prolonged (up to 48 h) and stable NF-kappaB activation in INS-1E cells, whereas IL-1beta induced an oscillatory NF-kappaB activation in 208F cells. p65/p65 and p65/p50 were the predominant NF-kappaB dimers in IL-1beta-exposed INS-1E cells and 208F cells, respectively. |
| 6303 | 16556731 | IL-1beta induced a differential usage of cis-elements in the inducible nitric oxide synthase promoter region in the two cell-lines and an increase in ERK1/2 activity in INS-1E cells but not in 208F cells. |
| 6304 | 16556731 | IL-1beta induced a differential usage of cis-elements in the inducible nitric oxide synthase promoter region in the two cell-lines and an increase in ERK1/2 activity in INS-1E cells but not in 208F cells. |
| 6305 | 16556731 | IL-1beta induced a differential usage of cis-elements in the inducible nitric oxide synthase promoter region in the two cell-lines and an increase in ERK1/2 activity in INS-1E cells but not in 208F cells. |
| 6306 | 16556731 | Cytokine-induced expression of IkappaB isoforms and other NF-kappaB target genes (Fas, MCP-1, and inducible nitric oxide synthase) was severalfold higher in INS-1E cells than in 208F cells. |
| 6307 | 16556731 | Cytokine-induced expression of IkappaB isoforms and other NF-kappaB target genes (Fas, MCP-1, and inducible nitric oxide synthase) was severalfold higher in INS-1E cells than in 208F cells. |
| 6308 | 16556731 | Cytokine-induced expression of IkappaB isoforms and other NF-kappaB target genes (Fas, MCP-1, and inducible nitric oxide synthase) was severalfold higher in INS-1E cells than in 208F cells. |
| 6309 | 16556731 | These results suggest that cytokine-induced NF-kappaB activation in insulin-producing cells is more rapid, marked, and sustained than in fibroblasts, which correlates with a more pronounced activation of downstream genes and a proapoptotic outcome. |
| 6310 | 16556731 | These results suggest that cytokine-induced NF-kappaB activation in insulin-producing cells is more rapid, marked, and sustained than in fibroblasts, which correlates with a more pronounced activation of downstream genes and a proapoptotic outcome. |
| 6311 | 16556731 | These results suggest that cytokine-induced NF-kappaB activation in insulin-producing cells is more rapid, marked, and sustained than in fibroblasts, which correlates with a more pronounced activation of downstream genes and a proapoptotic outcome. |
| 6312 | 16554868 | The findings suggest the involvement of cytokines (TNF-alpha) in preeclampsia and may have a role in gestational diabetes mellitus and insulin resistance. |
| 6313 | 16554480 | Human astrocytes are resistant to Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis. |
| 6314 | 16554480 | Human astrocytes are resistant to Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis. |
| 6315 | 16554480 | Here, we report that calcium/calmodulin-dependent protein kinase II (CaMKII) is constitutively activated in human astrocytes and protects the cells from apoptotic stimulation by Fas agonist. |
| 6316 | 16554480 | Here, we report that calcium/calmodulin-dependent protein kinase II (CaMKII) is constitutively activated in human astrocytes and protects the cells from apoptotic stimulation by Fas agonist. |
| 6317 | 16554480 | Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death-inducing signaling complex (DISC); however, caspase-8 cleavage is inhibited in the DISC. |
| 6318 | 16554480 | Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death-inducing signaling complex (DISC); however, caspase-8 cleavage is inhibited in the DISC. |
| 6319 | 16554480 | Inhibition of CaMKII kinase activity inhibits the expression of phosphoprotein enriched astrocytes-15 kDa/phosphoprotein enriched in diabetes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP), thus releasing their inhibition of caspase-8 cleavage. |
| 6320 | 16554480 | Inhibition of CaMKII kinase activity inhibits the expression of phosphoprotein enriched astrocytes-15 kDa/phosphoprotein enriched in diabetes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP), thus releasing their inhibition of caspase-8 cleavage. |
| 6321 | 16554480 | Inhibition of PEA-15/PED or c-FLIP by small interfering RNA sensitizes human astrocytes to Fas-induced apoptosis. |
| 6322 | 16554480 | Inhibition of PEA-15/PED or c-FLIP by small interfering RNA sensitizes human astrocytes to Fas-induced apoptosis. |
| 6323 | 16554480 | In contrast, inhibition of CaMKII, PEA-15, or c-FLIP does not affect the sensitivity of human astrocytes to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). |
| 6324 | 16554480 | In contrast, inhibition of CaMKII, PEA-15, or c-FLIP does not affect the sensitivity of human astrocytes to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). |
| 6325 | 16554480 | TRAIL death receptors (DR4, DR5) are weakly expressed at mRNA, protein, and cell surface levels and thus fail to mediate the assembly of the DISC in human astrocytes. |
| 6326 | 16554480 | TRAIL death receptors (DR4, DR5) are weakly expressed at mRNA, protein, and cell surface levels and thus fail to mediate the assembly of the DISC in human astrocytes. |
| 6327 | 16554480 | Overexpression of DR5 restores TRAIL signaling pathways and sensitizes the human astrocytes to TRAIL-induced apoptosis if CaMKII kinase activity or expression of PEA-15 and c-FLIP is inhibited; the results suggest that CaMKII-mediated pathways prevent TRAIL-induced apoptosis in human astrocytes under conditions in which TRAIL death receptors are upregulated. |
| 6328 | 16554480 | Overexpression of DR5 restores TRAIL signaling pathways and sensitizes the human astrocytes to TRAIL-induced apoptosis if CaMKII kinase activity or expression of PEA-15 and c-FLIP is inhibited; the results suggest that CaMKII-mediated pathways prevent TRAIL-induced apoptosis in human astrocytes under conditions in which TRAIL death receptors are upregulated. |
| 6329 | 16554480 | This study has therefore identified the molecular mechanisms that protect normal human astrocytes from apoptosis induced by Fas ligand and TRAIL. |
| 6330 | 16554480 | This study has therefore identified the molecular mechanisms that protect normal human astrocytes from apoptosis induced by Fas ligand and TRAIL. |
| 6331 | 16552358 | The following analyses were performed 6 h there after: (a) total and differential cell counts in bronchoalveolar lavage (BAL) fluid, (b) quantification of tumor necrosis factor alpha, interleukin (IL) 1beta, IL-10, and cytokine-induced neutrophil chemoattractant 1 in the BAL (enzyme-linked immunosorbent assay), (c)immunohistochemistry for intercellular adhesion molecule 1 and E-selectin on lung vessels, and (d) quantification of metalloproteinases (MMP) 2 and 9 in the BAL (zymography). |
| 6332 | 16552358 | The following analyses were performed 6 h there after: (a) total and differential cell counts in bronchoalveolar lavage (BAL) fluid, (b) quantification of tumor necrosis factor alpha, interleukin (IL) 1beta, IL-10, and cytokine-induced neutrophil chemoattractant 1 in the BAL (enzyme-linked immunosorbent assay), (c)immunohistochemistry for intercellular adhesion molecule 1 and E-selectin on lung vessels, and (d) quantification of metalloproteinases (MMP) 2 and 9 in the BAL (zymography). |
| 6333 | 16552358 | Relative to controls, diabetic rats exhibited a reduction in the number of neutrophils (80%) and reduced concentrations of tumor necrosis factor alpha (56%), IL-1beta (66%), and IL-10 (35%) after LPS instillation. |
| 6334 | 16552358 | Relative to controls, diabetic rats exhibited a reduction in the number of neutrophils (80%) and reduced concentrations of tumor necrosis factor alpha (56%), IL-1beta (66%), and IL-10 (35%) after LPS instillation. |
| 6335 | 16552358 | Despite no significant differences between diabetic and control groups, there was a remarkable increase in intercellular adhesion molecule 1 and E-selectin expression on lung vessels after insulin treatment. |
| 6336 | 16552358 | Despite no significant differences between diabetic and control groups, there was a remarkable increase in intercellular adhesion molecule 1 and E-selectin expression on lung vessels after insulin treatment. |
| 6337 | 16552358 | Levels of MMP-2 and MMP-9 did not change after treatment with insulin. |
| 6338 | 16552358 | Levels of MMP-2 and MMP-9 did not change after treatment with insulin. |
| 6339 | 16552358 | Data presented suggest that insulin modulates the production/release of cytokines and the expression of adhesion molecules controlling, therefore, neutrophil migration during the course of LPS-induced acute lung inflammation. |
| 6340 | 16552358 | Data presented suggest that insulin modulates the production/release of cytokines and the expression of adhesion molecules controlling, therefore, neutrophil migration during the course of LPS-induced acute lung inflammation. |
| 6341 | 16546478 | Angiotensin II infusion decreases plasma adiponectin level via its type 1 receptor in rats: an implication for hypertension-related insulin resistance. |
| 6342 | 16546478 | We explored the mechanisms underlying the close association between hypertension and insulin resistance by measuring the changes in the plasma levels of adiponectin, a novel insulin sensitizer secreted by adipose tissue, in rats infused with angiotensin II (AII). |
| 6343 | 16546478 | Angiotensin II decreased plasma adiponectin levels from 3.7 to 2.9 microg/mL (P < .01) without affecting the expression of adiponectin messenger RNA in adipose tissue. |
| 6344 | 16546478 | Angiotensin II infusion did not affect plasma leptin and tumor necrosis factor alpha levels. |
| 6345 | 16546478 | Angiotensin II induced no further decrease of adiponectin, whereas olmesartan increased adiponectin remarkably both with and without AII infusion. |
| 6346 | 16546478 | These results suggest that AII suppresses adiponectin production via AII type 1 receptor, resulting in impaired insulin sensitivity. |
| 6347 | 16543409 | Suppressor of cytokine Signaling-3 inhibits interleukin-1 signaling by targeting the TRAF-6/TAK1 complex. |
| 6348 | 16543409 | IL-1 plays a major role in inflammation and autoimmunity through activation of nuclear factor kappa B (NFkappaB) and MAPKs. |
| 6349 | 16543409 | Although a great deal is known about the mechanism of activation of NFkappaB and MAPKs by IL-1, much less is known about the down-regulation of this pathway. |
| 6350 | 16543409 | Suppressor of cytokine signaling (SOCS)-3 was shown to inhibit IL-1-induced transcription and activation of NFkappaB and the MAPKs JNK and p38, but the mechanism is unknown. |
| 6351 | 16543409 | We show here that SOCS-3 inhibits NFkappaB-dependent transcription induced by overexpression of the upstream IL-1 signaling molecules MyD88, IL-1R-activated kinase 1, TNF receptor-associated factor (TRAF)6, and TGFbeta-activated kinase (TAK)1, but not when the MAP3K MAPK/ERK kinase kinase-1 is used instead of TAK1, indicating that the target for SOCS-3 is the TRAF6/TAK1 signaling complex. |
| 6352 | 16543409 | By coimmunoprecipitation, it was shown that SOCS-3 inhibited the association between TRAF6 and TAK1 and that SOCS-3 coimmunoprecipitated with TAK1 and TRAF6. |
| 6353 | 16543409 | Furthermore, SOCS-3 inhibited the IL-1-induced catalytic activity of TAK1. |
| 6354 | 16543409 | Because ubiquitination of TRAF6 is required for activation of TAK1, we analyzed the role of SOCS-3 on TRAF6 ubiquitination and found that SOCS-3 inhibited ubiquitin modification of TRAF6. |
| 6355 | 16543409 | These results indicate that SOCS-3 inhibits IL-1 signal transduction by inhibiting ubiquitination of TRAF6, thus preventing association and activation of TAK1. |
| 6356 | 16530289 | Plasma glucose, insulin (fasting and 2h after 75gm oral glucose) lipids and serum levels of C-reactive protein (CRP), tumour necrosis factor (TNF)-alpha and fibrinogen were measured after an overnight fast of 10-12h. |
| 6357 | 16510765 | The aim was to investigate whether C-peptide or insulin could modulate TNF-alpha-mediated cell death in opossum kidney proximal tubular cells and to examine the mechanism(s) of any effects observed. |
| 6358 | 16510765 | The aim was to investigate whether C-peptide or insulin could modulate TNF-alpha-mediated cell death in opossum kidney proximal tubular cells and to examine the mechanism(s) of any effects observed. |
| 6359 | 16510765 | The aim was to investigate whether C-peptide or insulin could modulate TNF-alpha-mediated cell death in opossum kidney proximal tubular cells and to examine the mechanism(s) of any effects observed. |
| 6360 | 16510765 | The aim was to investigate whether C-peptide or insulin could modulate TNF-alpha-mediated cell death in opossum kidney proximal tubular cells and to examine the mechanism(s) of any effects observed. |
| 6361 | 16510765 | The aim was to investigate whether C-peptide or insulin could modulate TNF-alpha-mediated cell death in opossum kidney proximal tubular cells and to examine the mechanism(s) of any effects observed. |
| 6362 | 16510765 | C-peptide and insulin protect against TNF-alpha-induced proximal tubular cell toxicity and apoptosis. |
| 6363 | 16510765 | C-peptide and insulin protect against TNF-alpha-induced proximal tubular cell toxicity and apoptosis. |
| 6364 | 16510765 | C-peptide and insulin protect against TNF-alpha-induced proximal tubular cell toxicity and apoptosis. |
| 6365 | 16510765 | C-peptide and insulin protect against TNF-alpha-induced proximal tubular cell toxicity and apoptosis. |
| 6366 | 16510765 | C-peptide and insulin protect against TNF-alpha-induced proximal tubular cell toxicity and apoptosis. |
| 6367 | 16510765 | By ELISA assay, 300 ng/ml TNF-alpha increased apoptosis by 145.8 +/- 4.9% compared with controls, whereas 5 nM C-peptide and 100 nM insulin reduced apoptosis to 81.6 +/- 4.8 and 77.4 +/- 3.1% of control, respectively. |
| 6368 | 16510765 | By ELISA assay, 300 ng/ml TNF-alpha increased apoptosis by 145.8 +/- 4.9% compared with controls, whereas 5 nM C-peptide and 100 nM insulin reduced apoptosis to 81.6 +/- 4.8 and 77.4 +/- 3.1% of control, respectively. |
| 6369 | 16510765 | By ELISA assay, 300 ng/ml TNF-alpha increased apoptosis by 145.8 +/- 4.9% compared with controls, whereas 5 nM C-peptide and 100 nM insulin reduced apoptosis to 81.6 +/- 4.8 and 77.4 +/- 3.1% of control, respectively. |
| 6370 | 16510765 | By ELISA assay, 300 ng/ml TNF-alpha increased apoptosis by 145.8 +/- 4.9% compared with controls, whereas 5 nM C-peptide and 100 nM insulin reduced apoptosis to 81.6 +/- 4.8 and 77.4 +/- 3.1% of control, respectively. |
| 6371 | 16510765 | By ELISA assay, 300 ng/ml TNF-alpha increased apoptosis by 145.8 +/- 4.9% compared with controls, whereas 5 nM C-peptide and 100 nM insulin reduced apoptosis to 81.6 +/- 4.8 and 77.4 +/- 3.1% of control, respectively. |
| 6372 | 16510765 | The protective effects of C-peptide and insulin were associated with activation of NF-kappaB. |
| 6373 | 16510765 | The protective effects of C-peptide and insulin were associated with activation of NF-kappaB. |
| 6374 | 16510765 | The protective effects of C-peptide and insulin were associated with activation of NF-kappaB. |
| 6375 | 16510765 | The protective effects of C-peptide and insulin were associated with activation of NF-kappaB. |
| 6376 | 16510765 | The protective effects of C-peptide and insulin were associated with activation of NF-kappaB. |
| 6377 | 16510765 | Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen-activated protein kinase mediated C-peptide and insulin activation of NF-kappaB. |
| 6378 | 16510765 | Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen-activated protein kinase mediated C-peptide and insulin activation of NF-kappaB. |
| 6379 | 16510765 | Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen-activated protein kinase mediated C-peptide and insulin activation of NF-kappaB. |
| 6380 | 16510765 | Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen-activated protein kinase mediated C-peptide and insulin activation of NF-kappaB. |
| 6381 | 16510765 | Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen-activated protein kinase mediated C-peptide and insulin activation of NF-kappaB. |
| 6382 | 16510765 | The cytoprotective effects of both C-peptide and insulin were related to increased expression of TNF receptor-associated factor 2, the product of an NF-kappaB-dependent survival gene. |
| 6383 | 16510765 | The cytoprotective effects of both C-peptide and insulin were related to increased expression of TNF receptor-associated factor 2, the product of an NF-kappaB-dependent survival gene. |
| 6384 | 16510765 | The cytoprotective effects of both C-peptide and insulin were related to increased expression of TNF receptor-associated factor 2, the product of an NF-kappaB-dependent survival gene. |
| 6385 | 16510765 | The cytoprotective effects of both C-peptide and insulin were related to increased expression of TNF receptor-associated factor 2, the product of an NF-kappaB-dependent survival gene. |
| 6386 | 16510765 | The cytoprotective effects of both C-peptide and insulin were related to increased expression of TNF receptor-associated factor 2, the product of an NF-kappaB-dependent survival gene. |
| 6387 | 16510765 | These data suggest that C-peptide and/or insulin activation of NF-kappaB-regulated survival genes protects against TNF-alpha-induced renal tubular injury in diabetes. |
| 6388 | 16510765 | These data suggest that C-peptide and/or insulin activation of NF-kappaB-regulated survival genes protects against TNF-alpha-induced renal tubular injury in diabetes. |
| 6389 | 16510765 | These data suggest that C-peptide and/or insulin activation of NF-kappaB-regulated survival genes protects against TNF-alpha-induced renal tubular injury in diabetes. |
| 6390 | 16510765 | These data suggest that C-peptide and/or insulin activation of NF-kappaB-regulated survival genes protects against TNF-alpha-induced renal tubular injury in diabetes. |
| 6391 | 16510765 | These data suggest that C-peptide and/or insulin activation of NF-kappaB-regulated survival genes protects against TNF-alpha-induced renal tubular injury in diabetes. |
| 6392 | 16507892 | Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. |
| 6393 | 16507892 | Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. |
| 6394 | 16507892 | Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. |
| 6395 | 16507892 | Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. |
| 6396 | 16507892 | Here, we investigated insulin-mediated signaling in nonwounded skin and in cutaneous tissue regeneration of healthy C57BL/6 and diabetes-impaired leptin-deficient obese/obese (ob/ob) mice. |
| 6397 | 16507892 | Here, we investigated insulin-mediated signaling in nonwounded skin and in cutaneous tissue regeneration of healthy C57BL/6 and diabetes-impaired leptin-deficient obese/obese (ob/ob) mice. |
| 6398 | 16507892 | Here, we investigated insulin-mediated signaling in nonwounded skin and in cutaneous tissue regeneration of healthy C57BL/6 and diabetes-impaired leptin-deficient obese/obese (ob/ob) mice. |
| 6399 | 16507892 | Here, we investigated insulin-mediated signaling in nonwounded skin and in cutaneous tissue regeneration of healthy C57BL/6 and diabetes-impaired leptin-deficient obese/obese (ob/ob) mice. |
| 6400 | 16507892 | Remarkably, active signaling from the InsR, as assessed by phosphorylation of downstream targets such as protein tyrosine phosphatase-1B, glycogen synthase (GS), and GS kinase, was nearly absent in nonwounded and acutely healing skin from ob/ob mice. |
| 6401 | 16507892 | Remarkably, active signaling from the InsR, as assessed by phosphorylation of downstream targets such as protein tyrosine phosphatase-1B, glycogen synthase (GS), and GS kinase, was nearly absent in nonwounded and acutely healing skin from ob/ob mice. |
| 6402 | 16507892 | Remarkably, active signaling from the InsR, as assessed by phosphorylation of downstream targets such as protein tyrosine phosphatase-1B, glycogen synthase (GS), and GS kinase, was nearly absent in nonwounded and acutely healing skin from ob/ob mice. |
| 6403 | 16507892 | Remarkably, active signaling from the InsR, as assessed by phosphorylation of downstream targets such as protein tyrosine phosphatase-1B, glycogen synthase (GS), and GS kinase, was nearly absent in nonwounded and acutely healing skin from ob/ob mice. |
| 6404 | 16507892 | Systemic leptin administration to ob/ob mice reverted the diabetic phenotype and improved tissue regeneration as well as the impaired expression of InsR, insulin receptor substrate-1 and insulin receptor substrate-2, and downstream signaling (phosphorylation of GS kinase and GS) in late wounds and nonwounded skin of ob/ob mice. |
| 6405 | 16507892 | Systemic leptin administration to ob/ob mice reverted the diabetic phenotype and improved tissue regeneration as well as the impaired expression of InsR, insulin receptor substrate-1 and insulin receptor substrate-2, and downstream signaling (phosphorylation of GS kinase and GS) in late wounds and nonwounded skin of ob/ob mice. |
| 6406 | 16507892 | Systemic leptin administration to ob/ob mice reverted the diabetic phenotype and improved tissue regeneration as well as the impaired expression of InsR, insulin receptor substrate-1 and insulin receptor substrate-2, and downstream signaling (phosphorylation of GS kinase and GS) in late wounds and nonwounded skin of ob/ob mice. |
| 6407 | 16507892 | Systemic leptin administration to ob/ob mice reverted the diabetic phenotype and improved tissue regeneration as well as the impaired expression of InsR, insulin receptor substrate-1 and insulin receptor substrate-2, and downstream signaling (phosphorylation of GS kinase and GS) in late wounds and nonwounded skin of ob/ob mice. |
| 6408 | 16507892 | Importantly, tumor necrosis factor (TNF)-alpha was a mediator of insulin resistance in keratinocytes in vitro and in ob/ob wound tissue in vivo. |
| 6409 | 16507892 | Importantly, tumor necrosis factor (TNF)-alpha was a mediator of insulin resistance in keratinocytes in vitro and in ob/ob wound tissue in vivo. |
| 6410 | 16507892 | Importantly, tumor necrosis factor (TNF)-alpha was a mediator of insulin resistance in keratinocytes in vitro and in ob/ob wound tissue in vivo. |
| 6411 | 16507892 | Importantly, tumor necrosis factor (TNF)-alpha was a mediator of insulin resistance in keratinocytes in vitro and in ob/ob wound tissue in vivo. |
| 6412 | 16507892 | Systemic administration of a monoclonal anti-TNF-alpha antibody (V1q) in wounded ob/ob mice attenuated wound inflammation, improved re-epithelialization, and restored InsR expression and signaling in wound tissue of ob/ob mice. |
| 6413 | 16507892 | Systemic administration of a monoclonal anti-TNF-alpha antibody (V1q) in wounded ob/ob mice attenuated wound inflammation, improved re-epithelialization, and restored InsR expression and signaling in wound tissue of ob/ob mice. |
| 6414 | 16507892 | Systemic administration of a monoclonal anti-TNF-alpha antibody (V1q) in wounded ob/ob mice attenuated wound inflammation, improved re-epithelialization, and restored InsR expression and signaling in wound tissue of ob/ob mice. |
| 6415 | 16507892 | Systemic administration of a monoclonal anti-TNF-alpha antibody (V1q) in wounded ob/ob mice attenuated wound inflammation, improved re-epithelialization, and restored InsR expression and signaling in wound tissue of ob/ob mice. |
| 6416 | 16507892 | These data suggest that InsR signaling in diabetes-impaired wounds is sensitive to inflammatory conditions and that anti-inflammatory approaches, such as anti-TNF-alpha strategies, improve diabetic wound healing. |
| 6417 | 16507892 | These data suggest that InsR signaling in diabetes-impaired wounds is sensitive to inflammatory conditions and that anti-inflammatory approaches, such as anti-TNF-alpha strategies, improve diabetic wound healing. |
| 6418 | 16507892 | These data suggest that InsR signaling in diabetes-impaired wounds is sensitive to inflammatory conditions and that anti-inflammatory approaches, such as anti-TNF-alpha strategies, improve diabetic wound healing. |
| 6419 | 16507892 | These data suggest that InsR signaling in diabetes-impaired wounds is sensitive to inflammatory conditions and that anti-inflammatory approaches, such as anti-TNF-alpha strategies, improve diabetic wound healing. |
| 6420 | 16507891 | At 21 hours, TNF-alpha inhibition significantly reduced fibroblast apoptosis and caspase-3 activity in both diabetic and normoglycemic mice (P < 0.05). |
| 6421 | 16505240 | In subjects with type 2 diabetes, training increased IkappaB alpha and IkappaB beta protein to levels comparable with that of control subjects, and these increments were accompanied by a 40% decrease in tumor necrosis factor alpha muscle content and a 37% increase in insulin-stimulated glucose disposal. |
| 6422 | 16505233 | Overexpression of suppressor of cytokine signaling 3 in adipose tissue causes local but not systemic insulin resistance. |
| 6423 | 16505233 | In adipocytes, suppressor of cytokine signaling (SOCS)3 deficiency increases insulin-stimulated insulin receptor substrate (IRS)-1 and -2 phosphorylation, IRS-associated phosphatidylinositol 3 kinase activity, and insulin-stimulated glucose uptake. |
| 6424 | 16505233 | Moreover, SOCS3 is required for tumor necrosis factor-alpha full inhibition of insulin-stimulated IRS-1 and -2 phosphorylation, phosphatidylinositol 3 kinase activity, and glucose uptake. |
| 6425 | 16505233 | Whether SOCS3 also inhibits adipocyte insulin signaling in vivo and whether this action further affects systemic insulin sensitivity is not clear. |
| 6426 | 16505233 | Overexpression of SOCS3 in adipocytes decreases IRS1 protein levels and subsequent insulin-stimulated IRS-1 and -2 phosphorylation, decreases p85 binding to IRS-1, and leads to decreased insulin-stimulated glucose uptake in adipocytes. |
| 6427 | 16505233 | This impaired insulin signaling in adipose tissue of aP2-SOCS3 mice causes decreased lipogenesis and blocks insulin's antilipolytic action. |
| 6428 | 16505233 | However, because of decreased energy partitioning in adipose tissue, aP2-SOCS3 mice are resistant to diet-induced obesity and are protected against systemic insulin resistance caused by a high-fat diet. |
| 6429 | 16505233 | Therefore, overexpression of SOCS3 in adipocytes causes local adipocyte insulin resistance, but it is not sufficient to cause systemic insulin resistance. |
| 6430 | 16505224 | We evaluated ubiquitin-proteasome activity in carotid plaques of asymptomatic diabetic and nondiabetic patients, as well as the effect of rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma activator, in diabetic plaques. |
| 6431 | 16505224 | We evaluated ubiquitin-proteasome activity in carotid plaques of asymptomatic diabetic and nondiabetic patients, as well as the effect of rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma activator, in diabetic plaques. |
| 6432 | 16505224 | We evaluated ubiquitin-proteasome activity in carotid plaques of asymptomatic diabetic and nondiabetic patients, as well as the effect of rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma activator, in diabetic plaques. |
| 6433 | 16505224 | Plaques were analyzed for macrophages (CD68), T-cells (CD3), inflammatory cells (HLA-DR), ubiquitin, proteasome 20S activity, nuclear factor (NF)-kappaB, inhibitor of kappaB (IkappaB)-beta, tumor necrosis factor (TNF)-alpha, nitrotyrosine, matrix metalloproteinase (MMP)-9, and collagen content (immunohistochemistry and enzyme-linked immunosorbent assay). |
| 6434 | 16505224 | Plaques were analyzed for macrophages (CD68), T-cells (CD3), inflammatory cells (HLA-DR), ubiquitin, proteasome 20S activity, nuclear factor (NF)-kappaB, inhibitor of kappaB (IkappaB)-beta, tumor necrosis factor (TNF)-alpha, nitrotyrosine, matrix metalloproteinase (MMP)-9, and collagen content (immunohistochemistry and enzyme-linked immunosorbent assay). |
| 6435 | 16505224 | Plaques were analyzed for macrophages (CD68), T-cells (CD3), inflammatory cells (HLA-DR), ubiquitin, proteasome 20S activity, nuclear factor (NF)-kappaB, inhibitor of kappaB (IkappaB)-beta, tumor necrosis factor (TNF)-alpha, nitrotyrosine, matrix metalloproteinase (MMP)-9, and collagen content (immunohistochemistry and enzyme-linked immunosorbent assay). |
| 6436 | 16505224 | Compared with nondiabetic plaques, diabetic plaques had more macrophages, T-cells, and HLA-DR+ cells (P < 0.001); more ubiquitin, proteasome 20S activity (TNF-alpha), and NF-kappaB (P < 0.001); and more markers of oxidative stress (nitrotyrosine and O2(-) production) and MMP-9 (P < 0.01), along with a lesser collagen content and IkappaB-beta levels (P < 0.001). |
| 6437 | 16505224 | Compared with nondiabetic plaques, diabetic plaques had more macrophages, T-cells, and HLA-DR+ cells (P < 0.001); more ubiquitin, proteasome 20S activity (TNF-alpha), and NF-kappaB (P < 0.001); and more markers of oxidative stress (nitrotyrosine and O2(-) production) and MMP-9 (P < 0.01), along with a lesser collagen content and IkappaB-beta levels (P < 0.001). |
| 6438 | 16505224 | Compared with nondiabetic plaques, diabetic plaques had more macrophages, T-cells, and HLA-DR+ cells (P < 0.001); more ubiquitin, proteasome 20S activity (TNF-alpha), and NF-kappaB (P < 0.001); and more markers of oxidative stress (nitrotyrosine and O2(-) production) and MMP-9 (P < 0.01), along with a lesser collagen content and IkappaB-beta levels (P < 0.001). |
| 6439 | 16505224 | Compared with placebo-treated plaques, rosiglitazone-treated diabetic plaques presented less inflammatory cells (P < 0.01); less ubiquitin, proteasome 20S, TNF-alpha, and NF-kappaB (P < 0.01); less nitrotyrosine and superoxide anion production (P < 0.01); and greater collagen content (P < 0.01), indicating a more stable plaque phenotype. |
| 6440 | 16505224 | Compared with placebo-treated plaques, rosiglitazone-treated diabetic plaques presented less inflammatory cells (P < 0.01); less ubiquitin, proteasome 20S, TNF-alpha, and NF-kappaB (P < 0.01); less nitrotyrosine and superoxide anion production (P < 0.01); and greater collagen content (P < 0.01), indicating a more stable plaque phenotype. |
| 6441 | 16505224 | Compared with placebo-treated plaques, rosiglitazone-treated diabetic plaques presented less inflammatory cells (P < 0.01); less ubiquitin, proteasome 20S, TNF-alpha, and NF-kappaB (P < 0.01); less nitrotyrosine and superoxide anion production (P < 0.01); and greater collagen content (P < 0.01), indicating a more stable plaque phenotype. |
| 6442 | 16505224 | Ubiquitin-proteasome over-activity is associated with enhanced inflammatory reaction and NF-kappaB expression in diabetic plaques. |
| 6443 | 16505224 | Ubiquitin-proteasome over-activity is associated with enhanced inflammatory reaction and NF-kappaB expression in diabetic plaques. |
| 6444 | 16505224 | Ubiquitin-proteasome over-activity is associated with enhanced inflammatory reaction and NF-kappaB expression in diabetic plaques. |
| 6445 | 16505224 | The inhibition of ubiquitin-proteasome activity in atherosclerotic lesions of diabetic patients by rosiglitazone is associated with morphological and compositional characteristics of a potential stable plaque phenotype, possibly by downregulating NF-kappaB-mediated inflammatory pathways. |
| 6446 | 16505224 | The inhibition of ubiquitin-proteasome activity in atherosclerotic lesions of diabetic patients by rosiglitazone is associated with morphological and compositional characteristics of a potential stable plaque phenotype, possibly by downregulating NF-kappaB-mediated inflammatory pathways. |
| 6447 | 16505224 | The inhibition of ubiquitin-proteasome activity in atherosclerotic lesions of diabetic patients by rosiglitazone is associated with morphological and compositional characteristics of a potential stable plaque phenotype, possibly by downregulating NF-kappaB-mediated inflammatory pathways. |
| 6448 | 16504840 | Emerging evidence in animals and humans has shown that HCV infection induces hepatic steatosis and increases tumor necrosis factor-alpha level, both resulting in the development of insulin resistance and subsequent type 2 diabetes. |
| 6449 | 16504463 | Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of beta-blockers, BMI, and psychosocial factors in older adults. |
| 6450 | 16504463 | Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of beta-blockers, BMI, and psychosocial factors in older adults. |
| 6451 | 16504463 | Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of beta-blockers, BMI, and psychosocial factors in older adults. |
| 6452 | 16504463 | The inflammatory mediators [C-reactive protein (CRP), IL-6, tumor necrosis factor (TNF)-alpha, and IL-18] and the psychosocial factors (depression, perceived stress, optimism, sense of coherence, and social support) were measured pre- and post-intervention. |
| 6453 | 16504463 | The inflammatory mediators [C-reactive protein (CRP), IL-6, tumor necrosis factor (TNF)-alpha, and IL-18] and the psychosocial factors (depression, perceived stress, optimism, sense of coherence, and social support) were measured pre- and post-intervention. |
| 6454 | 16504463 | The inflammatory mediators [C-reactive protein (CRP), IL-6, tumor necrosis factor (TNF)-alpha, and IL-18] and the psychosocial factors (depression, perceived stress, optimism, sense of coherence, and social support) were measured pre- and post-intervention. |
| 6455 | 16504463 | The CARDIO treatment resulted in significant reductions in serum CRP, IL-6, and IL-18 compared to the FLEX treatment (significant treatment x time interaction, p<.05), whereas TNFalpha declined in both groups (main effect of time, p=.001). |
| 6456 | 16504463 | The CARDIO treatment resulted in significant reductions in serum CRP, IL-6, and IL-18 compared to the FLEX treatment (significant treatment x time interaction, p<.05), whereas TNFalpha declined in both groups (main effect of time, p=.001). |
| 6457 | 16504463 | The CARDIO treatment resulted in significant reductions in serum CRP, IL-6, and IL-18 compared to the FLEX treatment (significant treatment x time interaction, p<.05), whereas TNFalpha declined in both groups (main effect of time, p=.001). |
| 6458 | 16504463 | However, several psychosocial factors (depression, optimism, and sense of coherence) improved in both groups suggesting that the reduction of CRP, IL-6, and IL-18 in the CARDIO group was not mediated by improvements in psychosocial scores. |
| 6459 | 16504463 | However, several psychosocial factors (depression, optimism, and sense of coherence) improved in both groups suggesting that the reduction of CRP, IL-6, and IL-18 in the CARDIO group was not mediated by improvements in psychosocial scores. |
| 6460 | 16504463 | However, several psychosocial factors (depression, optimism, and sense of coherence) improved in both groups suggesting that the reduction of CRP, IL-6, and IL-18 in the CARDIO group was not mediated by improvements in psychosocial scores. |
| 6461 | 16504463 | With respect to the potential role of beta-adrenergic receptors, both CARDIO subjects treated with beta-adrenergic antagonists and those who were not treated with those medications demonstrated similar reductions in serum CRP, IL-6, IL-18, and TNFalpha. |
| 6462 | 16504463 | With respect to the potential role of beta-adrenergic receptors, both CARDIO subjects treated with beta-adrenergic antagonists and those who were not treated with those medications demonstrated similar reductions in serum CRP, IL-6, IL-18, and TNFalpha. |
| 6463 | 16504463 | With respect to the potential role of beta-adrenergic receptors, both CARDIO subjects treated with beta-adrenergic antagonists and those who were not treated with those medications demonstrated similar reductions in serum CRP, IL-6, IL-18, and TNFalpha. |
| 6464 | 16503147 | In the present work we have evaluated the expression of many pro-inflammatory TNF system cytokines (TNF-alpha, TWEAK and their respective receptors, TNFR1, TNFR2 and Fn14) in human adipose tissue of 84 subjects some with different degree of obesity and type 2 diabetes, and its relation with inflammation by also measuring the expression of macrophage marker CD68. |
| 6465 | 16503147 | In the present work we have evaluated the expression of many pro-inflammatory TNF system cytokines (TNF-alpha, TWEAK and their respective receptors, TNFR1, TNFR2 and Fn14) in human adipose tissue of 84 subjects some with different degree of obesity and type 2 diabetes, and its relation with inflammation by also measuring the expression of macrophage marker CD68. |
| 6466 | 16503147 | We detected expression of TWEAK and Fn14 in isolated mature adipocytes and in the stromovascular fraction. |
| 6467 | 16503147 | We detected expression of TWEAK and Fn14 in isolated mature adipocytes and in the stromovascular fraction. |
| 6468 | 16503147 | The data obtained here also showed that TNF-alpha and TNFR2 mRNAs were significantly more expressed in subcutaneous adipose tissue of subjects with morbid obesity compared to obese and non-obese subjects. |
| 6469 | 16503147 | The data obtained here also showed that TNF-alpha and TNFR2 mRNAs were significantly more expressed in subcutaneous adipose tissue of subjects with morbid obesity compared to obese and non-obese subjects. |
| 6470 | 16497732 | Coactivator-associated arginine methyltransferase-1 (CARM1) is known to enhance transcriptional activation by nuclear receptors through interactions with the coactivators p160 and cAMP response element binding protein-binding protein (CBP) and methylation of histone H3 at arginine 17 (H3-R17). |
| 6471 | 16497732 | Here, we show that CARM1 can act as a coactivator for the transcription factor nuclear factor-kappaB (NF-kappaB) and enhance NF-kappaB activity in a CBP (p300)-dependent manner. |
| 6472 | 16497732 | Chromatin immunoprecipitation demonstrated CARM1 recruitment in vivo to the promoters of NF-kappaB p65-regulated genes along with CBP and steroid receptor coactivator-1. |
| 6473 | 16497732 | Immunoprecipitation with anti-p65 antibody revealed that CARM1 physically interacts with NF-kappaB p65. |
| 6474 | 16497732 | Furthermore, we demonstrated the physiological significance by observing that similar events occurred when THP-1 monocytic cells were stimulated with TNF-alpha or with S100b, a ligand for the receptor of advanced glycation end products, both of which are associated with diabetic complications and also known inducers of NF-kappaB and inflammatory genes in monocytes. |
| 6475 | 16497732 | These results demonstrate that CARM1 participates in NF-kappaB-mediated transcription through H3-R17 methylation and support a nonnuclear receptor-associated function for CARM1. |
| 6476 | 16493877 | [Possible connection between ghrelin, resistin and TNF-alpha levels and the metabolic syndrome caused by atypical antipsychotics]. |
| 6477 | 16493877 | [Possible connection between ghrelin, resistin and TNF-alpha levels and the metabolic syndrome caused by atypical antipsychotics]. |
| 6478 | 16493877 | [Possible connection between ghrelin, resistin and TNF-alpha levels and the metabolic syndrome caused by atypical antipsychotics]. |
| 6479 | 16493877 | [Possible connection between ghrelin, resistin and TNF-alpha levels and the metabolic syndrome caused by atypical antipsychotics]. |
| 6480 | 16493877 | [Possible connection between ghrelin, resistin and TNF-alpha levels and the metabolic syndrome caused by atypical antipsychotics]. |
| 6481 | 16493877 | Role of ghrelin (RIA), resistin and TNF-alpha (ELISA) in weight gain and insulin resistance (fasting plasma insulin, HOMA, ELISA) was studied in Hungarian psychiatryic patients (n=60) treated with SGA (clozapine, olanzapine, risperidone, quetiapine, 15 each). |
| 6482 | 16493877 | Role of ghrelin (RIA), resistin and TNF-alpha (ELISA) in weight gain and insulin resistance (fasting plasma insulin, HOMA, ELISA) was studied in Hungarian psychiatryic patients (n=60) treated with SGA (clozapine, olanzapine, risperidone, quetiapine, 15 each). |
| 6483 | 16493877 | Role of ghrelin (RIA), resistin and TNF-alpha (ELISA) in weight gain and insulin resistance (fasting plasma insulin, HOMA, ELISA) was studied in Hungarian psychiatryic patients (n=60) treated with SGA (clozapine, olanzapine, risperidone, quetiapine, 15 each). |
| 6484 | 16493877 | Role of ghrelin (RIA), resistin and TNF-alpha (ELISA) in weight gain and insulin resistance (fasting plasma insulin, HOMA, ELISA) was studied in Hungarian psychiatryic patients (n=60) treated with SGA (clozapine, olanzapine, risperidone, quetiapine, 15 each). |
| 6485 | 16493877 | Role of ghrelin (RIA), resistin and TNF-alpha (ELISA) in weight gain and insulin resistance (fasting plasma insulin, HOMA, ELISA) was studied in Hungarian psychiatryic patients (n=60) treated with SGA (clozapine, olanzapine, risperidone, quetiapine, 15 each). |
| 6486 | 16493877 | Ghrelin (1.3 +/- 0.6 ng/ml), resistin (9.8 +/- 3.7 ng/ml), TNF-alpha (5.8 +/- 1.7 pg/ml), insulin (10.4 +/- 7.6 U/ml, HOMA A: 2.5 +/- 1.8, HOMA B: 133 +/- 62.5) were significantly higher in patients than in healthy matched controls. |
| 6487 | 16493877 | Ghrelin (1.3 +/- 0.6 ng/ml), resistin (9.8 +/- 3.7 ng/ml), TNF-alpha (5.8 +/- 1.7 pg/ml), insulin (10.4 +/- 7.6 U/ml, HOMA A: 2.5 +/- 1.8, HOMA B: 133 +/- 62.5) were significantly higher in patients than in healthy matched controls. |
| 6488 | 16493877 | Ghrelin (1.3 +/- 0.6 ng/ml), resistin (9.8 +/- 3.7 ng/ml), TNF-alpha (5.8 +/- 1.7 pg/ml), insulin (10.4 +/- 7.6 U/ml, HOMA A: 2.5 +/- 1.8, HOMA B: 133 +/- 62.5) were significantly higher in patients than in healthy matched controls. |
| 6489 | 16493877 | Ghrelin (1.3 +/- 0.6 ng/ml), resistin (9.8 +/- 3.7 ng/ml), TNF-alpha (5.8 +/- 1.7 pg/ml), insulin (10.4 +/- 7.6 U/ml, HOMA A: 2.5 +/- 1.8, HOMA B: 133 +/- 62.5) were significantly higher in patients than in healthy matched controls. |
| 6490 | 16493877 | Ghrelin (1.3 +/- 0.6 ng/ml), resistin (9.8 +/- 3.7 ng/ml), TNF-alpha (5.8 +/- 1.7 pg/ml), insulin (10.4 +/- 7.6 U/ml, HOMA A: 2.5 +/- 1.8, HOMA B: 133 +/- 62.5) were significantly higher in patients than in healthy matched controls. |
| 6491 | 16493877 | Resistin and TNF-alpha positively correlated with each other, insulin, HOMA, and negatively with ghrelin. |
| 6492 | 16493877 | Resistin and TNF-alpha positively correlated with each other, insulin, HOMA, and negatively with ghrelin. |
| 6493 | 16493877 | Resistin and TNF-alpha positively correlated with each other, insulin, HOMA, and negatively with ghrelin. |
| 6494 | 16493877 | Resistin and TNF-alpha positively correlated with each other, insulin, HOMA, and negatively with ghrelin. |
| 6495 | 16493877 | Resistin and TNF-alpha positively correlated with each other, insulin, HOMA, and negatively with ghrelin. |
| 6496 | 16493877 | Ghrelin contributes to weight gain, resistin and TNF-alpha to insulin resistance. |
| 6497 | 16493877 | Ghrelin contributes to weight gain, resistin and TNF-alpha to insulin resistance. |
| 6498 | 16493877 | Ghrelin contributes to weight gain, resistin and TNF-alpha to insulin resistance. |
| 6499 | 16493877 | Ghrelin contributes to weight gain, resistin and TNF-alpha to insulin resistance. |
| 6500 | 16493877 | Ghrelin contributes to weight gain, resistin and TNF-alpha to insulin resistance. |
| 6501 | 16493495 | Changes in adhesion molecule expression, i.e. vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin were determined by cell-bound Elisa on human endothelial cells after incubation with CML-modified albumin and MGO-modified albumin. |
| 6502 | 16493495 | We demonstrated that CML-albumin or MGO-albumin did not induce activation of endothelial cells as measured by the expression of adhesion molecules, while, under the same conditions, TNF-alpha did. |
| 6503 | 16492207 | Pioglitazone increases circulating adiponectin levels and subsequently reduces TNF-alpha levels in Type 2 diabetic patients: a randomized study. |
| 6504 | 16478779 | Elevated resistin levels in cirrhosis are associated with the proinflammatory state and altered hepatic glucose metabolism but not with insulin resistance. |
| 6505 | 16478779 | The adipokine resistin has been implicated in obesity and insulin resistance. |
| 6506 | 16478779 | Circulating resistin was significantly correlated with plasma TNF-alpha levels (r = 0.62, P < 0.001). |
| 6507 | 16478779 | No correlation was observed between resistin and hepatic hemodynamics, body fat mass, systemic energy metabolism, and the degree of insulin resistance. |
| 6508 | 16478779 | After liver transplantation, plasma resistin levels remained unchanged, whereas insulin resistance was significantly improved (P < 0.01). |
| 6509 | 16478779 | These data provide novel insights into the role of resistin in the pathophysiological background of a catabolic disease in humans and also indicate that resistin inhibition may not represent a suitable therapeutic strategy for the treatment of insulin resistance and diabetes in patients with liver cirrhosis. |
| 6510 | 16477544 | Chromium chloride inhibits TNFalpha and IL-6 secretion in isolated human blood mononuclear cells exposed to high glucose. |
| 6511 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6512 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6513 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6514 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6515 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6516 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6517 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6518 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6519 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 6520 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6521 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6522 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6523 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6524 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6525 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6526 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6527 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6528 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 6529 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6530 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6531 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6532 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6533 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6534 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6535 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6536 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6537 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 6538 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6539 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6540 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6541 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6542 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6543 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6544 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6545 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6546 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 6547 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6548 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6549 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6550 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6551 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6552 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6553 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6554 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6555 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 6556 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6557 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6558 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6559 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6560 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6561 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6562 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6563 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6564 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 6565 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6566 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6567 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6568 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6569 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6570 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6571 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6572 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6573 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 6574 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6575 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6576 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6577 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6578 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6579 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6580 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6581 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6582 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 6583 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6584 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6585 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6586 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6587 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6588 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6589 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6590 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6591 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 6592 | 16474306 | The state of lipid transport function of the blood, blood contents of stable nitrogen metabolites, and proinflammatory cytokines (TNF-a and IL-1b) during therapy with simvastatin were studied in 29 patients receiving combination antihypertensive therapy with angiotensin converting enzyme inhibitors (ACEI) and verapamil. |
| 6593 | 16472051 | The evolutive advantages of increased inflammatory responses, hypersecretion of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, and IL-18], or decreased anti-inflammatory molecules (adiponectin, certain TNF-alpha isoforms, soluble CD14, etc.), would lead in westernized countries to chronic inflammation conditions, such as obesity and type 2 diabetes, resulting in cardiovascular disease. |
| 6594 | 16466346 | Endothelium-dependent [FMD (flow-mediated dilation)] and -independent [NTG (nitroglycerine)] vasodilatation (determined by ultrasound), S(I) (insulin sensitivity index; determined by isoglycaemic-hyperinsulinaemic clamp) and serum levels of CRP (C-reactive protein), TNF-alpha (tumour necrosis factor-alpha), IL-6 (interleukin 6), resistin and adiponectin (determined by ELISA) were measured. |
| 6595 | 16466346 | Endothelium-dependent [FMD (flow-mediated dilation)] and -independent [NTG (nitroglycerine)] vasodilatation (determined by ultrasound), S(I) (insulin sensitivity index; determined by isoglycaemic-hyperinsulinaemic clamp) and serum levels of CRP (C-reactive protein), TNF-alpha (tumour necrosis factor-alpha), IL-6 (interleukin 6), resistin and adiponectin (determined by ELISA) were measured. |
| 6596 | 16466346 | Endothelium-dependent [FMD (flow-mediated dilation)] and -independent [NTG (nitroglycerine)] vasodilatation (determined by ultrasound), S(I) (insulin sensitivity index; determined by isoglycaemic-hyperinsulinaemic clamp) and serum levels of CRP (C-reactive protein), TNF-alpha (tumour necrosis factor-alpha), IL-6 (interleukin 6), resistin and adiponectin (determined by ELISA) were measured. |
| 6597 | 16466346 | Associations between FMD/NTG and S(I), and CRP, TNF-alpha, IL-6, adiponectin, resistin, lipids, blood pressure, BMI (body mass index) and brachial artery diameter were then assessed. |
| 6598 | 16466346 | Associations between FMD/NTG and S(I), and CRP, TNF-alpha, IL-6, adiponectin, resistin, lipids, blood pressure, BMI (body mass index) and brachial artery diameter were then assessed. |
| 6599 | 16466346 | Associations between FMD/NTG and S(I), and CRP, TNF-alpha, IL-6, adiponectin, resistin, lipids, blood pressure, BMI (body mass index) and brachial artery diameter were then assessed. |
| 6600 | 16466346 | TNF-alpha (6.9 compared with 1.8 pg/ml; P<0.01) and IL-6 (2.3 compared with 1.2 pg/ml; P<0.01) levels were higher in patients with T2DM, whereas differences in CRP and resistin levels did not attain statistical significance between the two groups. |
| 6601 | 16466346 | TNF-alpha (6.9 compared with 1.8 pg/ml; P<0.01) and IL-6 (2.3 compared with 1.2 pg/ml; P<0.01) levels were higher in patients with T2DM, whereas differences in CRP and resistin levels did not attain statistical significance between the two groups. |
| 6602 | 16466346 | TNF-alpha (6.9 compared with 1.8 pg/ml; P<0.01) and IL-6 (2.3 compared with 1.2 pg/ml; P<0.01) levels were higher in patients with T2DM, whereas differences in CRP and resistin levels did not attain statistical significance between the two groups. |
| 6603 | 16464856 | Obesity with enlarged fat cells is associated with high local concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) in the adipose tissue. |
| 6604 | 16464856 | Obesity with enlarged fat cells is associated with high local concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) in the adipose tissue. |
| 6605 | 16464856 | Obesity with enlarged fat cells is associated with high local concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) in the adipose tissue. |
| 6606 | 16464856 | Obesity with enlarged fat cells is associated with high local concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) in the adipose tissue. |
| 6607 | 16464856 | Obesity with enlarged fat cells is associated with high local concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) in the adipose tissue. |
| 6608 | 16464856 | Both IL-6 and TNFalpha impaired the normal differentiation pattern and lipid accumulation. |
| 6609 | 16464856 | Both IL-6 and TNFalpha impaired the normal differentiation pattern and lipid accumulation. |
| 6610 | 16464856 | Both IL-6 and TNFalpha impaired the normal differentiation pattern and lipid accumulation. |
| 6611 | 16464856 | Both IL-6 and TNFalpha impaired the normal differentiation pattern and lipid accumulation. |
| 6612 | 16464856 | Both IL-6 and TNFalpha impaired the normal differentiation pattern and lipid accumulation. |
| 6613 | 16464856 | However, IL-6 allowed a normal early induction of differentiation with inhibition of Wnt10b and Pref-1, whereas expression of CCAAT/enhancer-binding protein alpha, in contrast to peroxisome proliferator-activated receptor gamma, was markedly reduced. |
| 6614 | 16464856 | However, IL-6 allowed a normal early induction of differentiation with inhibition of Wnt10b and Pref-1, whereas expression of CCAAT/enhancer-binding protein alpha, in contrast to peroxisome proliferator-activated receptor gamma, was markedly reduced. |
| 6615 | 16464856 | However, IL-6 allowed a normal early induction of differentiation with inhibition of Wnt10b and Pref-1, whereas expression of CCAAT/enhancer-binding protein alpha, in contrast to peroxisome proliferator-activated receptor gamma, was markedly reduced. |
| 6616 | 16464856 | However, IL-6 allowed a normal early induction of differentiation with inhibition of Wnt10b and Pref-1, whereas expression of CCAAT/enhancer-binding protein alpha, in contrast to peroxisome proliferator-activated receptor gamma, was markedly reduced. |
| 6617 | 16464856 | However, IL-6 allowed a normal early induction of differentiation with inhibition of Wnt10b and Pref-1, whereas expression of CCAAT/enhancer-binding protein alpha, in contrast to peroxisome proliferator-activated receptor gamma, was markedly reduced. |
| 6618 | 16464856 | Remarkably, both IL-6 and TNFalpha maintained and augmented the canonical Wnt signaling associated with low axin and high low density lipoprotein receptor-related protein (LRD), Dishevelled, and beta-catenin levels. |
| 6619 | 16464856 | Remarkably, both IL-6 and TNFalpha maintained and augmented the canonical Wnt signaling associated with low axin and high low density lipoprotein receptor-related protein (LRD), Dishevelled, and beta-catenin levels. |
| 6620 | 16464856 | Remarkably, both IL-6 and TNFalpha maintained and augmented the canonical Wnt signaling associated with low axin and high low density lipoprotein receptor-related protein (LRD), Dishevelled, and beta-catenin levels. |
| 6621 | 16464856 | Remarkably, both IL-6 and TNFalpha maintained and augmented the canonical Wnt signaling associated with low axin and high low density lipoprotein receptor-related protein (LRD), Dishevelled, and beta-catenin levels. |
| 6622 | 16464856 | Remarkably, both IL-6 and TNFalpha maintained and augmented the canonical Wnt signaling associated with low axin and high low density lipoprotein receptor-related protein (LRD), Dishevelled, and beta-catenin levels. |
| 6623 | 16464856 | TNFalpha, but not IL-6, activated Wnt10b expression, whereas IL-6 increased the apparent phosphorylation of Dishevelled. |
| 6624 | 16464856 | TNFalpha, but not IL-6, activated Wnt10b expression, whereas IL-6 increased the apparent phosphorylation of Dishevelled. |
| 6625 | 16464856 | TNFalpha, but not IL-6, activated Wnt10b expression, whereas IL-6 increased the apparent phosphorylation of Dishevelled. |
| 6626 | 16464856 | TNFalpha, but not IL-6, activated Wnt10b expression, whereas IL-6 increased the apparent phosphorylation of Dishevelled. |
| 6627 | 16464856 | TNFalpha, but not IL-6, activated Wnt10b expression, whereas IL-6 increased the apparent phosphorylation of Dishevelled. |
| 6628 | 16464856 | Thus, both IL-6 and TNFalpha prevent the normal development of preadipocytes to fully differentiated adipose cells and, instead, promote an inflammatory phenotype of the adipocytes. |
| 6629 | 16464856 | Thus, both IL-6 and TNFalpha prevent the normal development of preadipocytes to fully differentiated adipose cells and, instead, promote an inflammatory phenotype of the adipocytes. |
| 6630 | 16464856 | Thus, both IL-6 and TNFalpha prevent the normal development of preadipocytes to fully differentiated adipose cells and, instead, promote an inflammatory phenotype of the adipocytes. |
| 6631 | 16464856 | Thus, both IL-6 and TNFalpha prevent the normal development of preadipocytes to fully differentiated adipose cells and, instead, promote an inflammatory phenotype of the adipocytes. |
| 6632 | 16464856 | Thus, both IL-6 and TNFalpha prevent the normal development of preadipocytes to fully differentiated adipose cells and, instead, promote an inflammatory phenotype of the adipocytes. |
| 6633 | 16464741 | Interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha play a central role in the autoimmune destruction of pancreatic beta-cells, whereas IL-6 inhibits TNF-alpha secretion, and may have some protecting effects. |
| 6634 | 16464741 | Interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha play a central role in the autoimmune destruction of pancreatic beta-cells, whereas IL-6 inhibits TNF-alpha secretion, and may have some protecting effects. |
| 6635 | 16464741 | Interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha play a central role in the autoimmune destruction of pancreatic beta-cells, whereas IL-6 inhibits TNF-alpha secretion, and may have some protecting effects. |
| 6636 | 16464741 | Interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha play a central role in the autoimmune destruction of pancreatic beta-cells, whereas IL-6 inhibits TNF-alpha secretion, and may have some protecting effects. |
| 6637 | 16464741 | Interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha play a central role in the autoimmune destruction of pancreatic beta-cells, whereas IL-6 inhibits TNF-alpha secretion, and may have some protecting effects. |
| 6638 | 16464741 | In our study, we aimed to investigate the association between these three cytokines' single nucleotide polymorphisms (IL-6 gene G(-174)C, TNF-alpha gene G(-308)A and IL-1beta gene C(3954)T polymorphisms) and age-at-onset of type 1 diabetes mellitus (T1DM) in 165 diabetic children (median age: 17 years). |
| 6639 | 16464741 | In our study, we aimed to investigate the association between these three cytokines' single nucleotide polymorphisms (IL-6 gene G(-174)C, TNF-alpha gene G(-308)A and IL-1beta gene C(3954)T polymorphisms) and age-at-onset of type 1 diabetes mellitus (T1DM) in 165 diabetic children (median age: 17 years). |
| 6640 | 16464741 | In our study, we aimed to investigate the association between these three cytokines' single nucleotide polymorphisms (IL-6 gene G(-174)C, TNF-alpha gene G(-308)A and IL-1beta gene C(3954)T polymorphisms) and age-at-onset of type 1 diabetes mellitus (T1DM) in 165 diabetic children (median age: 17 years). |
| 6641 | 16464741 | In our study, we aimed to investigate the association between these three cytokines' single nucleotide polymorphisms (IL-6 gene G(-174)C, TNF-alpha gene G(-308)A and IL-1beta gene C(3954)T polymorphisms) and age-at-onset of type 1 diabetes mellitus (T1DM) in 165 diabetic children (median age: 17 years). |
| 6642 | 16464741 | In our study, we aimed to investigate the association between these three cytokines' single nucleotide polymorphisms (IL-6 gene G(-174)C, TNF-alpha gene G(-308)A and IL-1beta gene C(3954)T polymorphisms) and age-at-onset of type 1 diabetes mellitus (T1DM) in 165 diabetic children (median age: 17 years). |
| 6643 | 16464741 | Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients. |
| 6644 | 16464741 | Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients. |
| 6645 | 16464741 | Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients. |
| 6646 | 16464741 | Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients. |
| 6647 | 16464741 | Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients. |
| 6648 | 16464741 | However, we found this association to be present only in patients who carried the TNF-alpha (-308)A or IL-1beta (3954)T allele, i.e. in patients with high TNF-alpha and high IL-1beta producer genotypes. |
| 6649 | 16464741 | However, we found this association to be present only in patients who carried the TNF-alpha (-308)A or IL-1beta (3954)T allele, i.e. in patients with high TNF-alpha and high IL-1beta producer genotypes. |
| 6650 | 16464741 | However, we found this association to be present only in patients who carried the TNF-alpha (-308)A or IL-1beta (3954)T allele, i.e. in patients with high TNF-alpha and high IL-1beta producer genotypes. |
| 6651 | 16464741 | However, we found this association to be present only in patients who carried the TNF-alpha (-308)A or IL-1beta (3954)T allele, i.e. in patients with high TNF-alpha and high IL-1beta producer genotypes. |
| 6652 | 16464741 | However, we found this association to be present only in patients who carried the TNF-alpha (-308)A or IL-1beta (3954)T allele, i.e. in patients with high TNF-alpha and high IL-1beta producer genotypes. |
| 6653 | 16464741 | We suppose that in the case of high TNF-alpha and IL-1beta producer genotypes, elevated proinflammatory cytokine levels result in a higher production of IL-6 in (-174)G allele carrier patients. |
| 6654 | 16464741 | We suppose that in the case of high TNF-alpha and IL-1beta producer genotypes, elevated proinflammatory cytokine levels result in a higher production of IL-6 in (-174)G allele carrier patients. |
| 6655 | 16464741 | We suppose that in the case of high TNF-alpha and IL-1beta producer genotypes, elevated proinflammatory cytokine levels result in a higher production of IL-6 in (-174)G allele carrier patients. |
| 6656 | 16464741 | We suppose that in the case of high TNF-alpha and IL-1beta producer genotypes, elevated proinflammatory cytokine levels result in a higher production of IL-6 in (-174)G allele carrier patients. |
| 6657 | 16464741 | We suppose that in the case of high TNF-alpha and IL-1beta producer genotypes, elevated proinflammatory cytokine levels result in a higher production of IL-6 in (-174)G allele carrier patients. |
| 6658 | 16461467 | An RNA interference-based screen identifies MAP4K4/NIK as a negative regulator of PPARgamma, adipogenesis, and insulin-responsive hexose transport. |
| 6659 | 16461467 | An RNA interference-based screen identifies MAP4K4/NIK as a negative regulator of PPARgamma, adipogenesis, and insulin-responsive hexose transport. |
| 6660 | 16461467 | The insulin-regulated glucose transporter GLUT4 is a key modulator of whole body glucose homeostasis, and its selective loss in adipose tissue or skeletal muscle causes insulin resistance and diabetes. |
| 6661 | 16461467 | The insulin-regulated glucose transporter GLUT4 is a key modulator of whole body glucose homeostasis, and its selective loss in adipose tissue or skeletal muscle causes insulin resistance and diabetes. |
| 6662 | 16461467 | Here we report an RNA interference-based screen of protein kinases expressed in adipocytes and identify four negative regulators of insulin-responsive glucose transport: the protein kinases PCTAIRE-1 (PCTK1), PFTAIRE-1 (PFTK1), IkappaB kinase alpha, and MAP4K4/NIK. |
| 6663 | 16461467 | Here we report an RNA interference-based screen of protein kinases expressed in adipocytes and identify four negative regulators of insulin-responsive glucose transport: the protein kinases PCTAIRE-1 (PCTK1), PFTAIRE-1 (PFTK1), IkappaB kinase alpha, and MAP4K4/NIK. |
| 6664 | 16461467 | We characterized one of these hits, MAP4K4/NIK, and found that it is unique among mitogen-activated protein (MAP) kinases expressed in cultured adipocytes in attenuating hexose transport. |
| 6665 | 16461467 | We characterized one of these hits, MAP4K4/NIK, and found that it is unique among mitogen-activated protein (MAP) kinases expressed in cultured adipocytes in attenuating hexose transport. |
| 6666 | 16461467 | Remarkably, MAP4K4/NIK suppresses expression of the adipogenic transcription factors C/EBPalpha, C/EBPbeta, and PPARgamma and of GLUT4 itself in these cells. |
| 6667 | 16461467 | Remarkably, MAP4K4/NIK suppresses expression of the adipogenic transcription factors C/EBPalpha, C/EBPbeta, and PPARgamma and of GLUT4 itself in these cells. |
| 6668 | 16461467 | RNA interference-mediated depletion of MAP4K4/NIK early in differentiation enhances adipogenesis and triglyceride deposition, and even in fully differentiated adipocytes its loss up-regulates GLUT4. |
| 6669 | 16461467 | RNA interference-mediated depletion of MAP4K4/NIK early in differentiation enhances adipogenesis and triglyceride deposition, and even in fully differentiated adipocytes its loss up-regulates GLUT4. |
| 6670 | 16461467 | Conversely, conditions that inhibit adipogenesis such as TNF-alpha treatment or depletion of PPARgamma markedly up-regulate MAP4K4/NIK expression in cultured adipocytes. |
| 6671 | 16461467 | Conversely, conditions that inhibit adipogenesis such as TNF-alpha treatment or depletion of PPARgamma markedly up-regulate MAP4K4/NIK expression in cultured adipocytes. |
| 6672 | 16461467 | Furthermore, TNF-alpha signaling to down-regulate GLUT4 is impaired in the absence of MAP4K4/NIK, indicating that MAP4K4 expression is required for optimal TNF-alpha action. |
| 6673 | 16461467 | Furthermore, TNF-alpha signaling to down-regulate GLUT4 is impaired in the absence of MAP4K4/NIK, indicating that MAP4K4 expression is required for optimal TNF-alpha action. |
| 6674 | 16461467 | These results reveal a MAP4K4/NIK-dependent signaling pathway that potently inhibits PPARgamma-responsive gene expression, adipogenesis, and insulin-stimulated glucose transport. |
| 6675 | 16461467 | These results reveal a MAP4K4/NIK-dependent signaling pathway that potently inhibits PPARgamma-responsive gene expression, adipogenesis, and insulin-stimulated glucose transport. |
| 6676 | 16455783 | IL-1beta, IL-6, IL12, IL-18, TNFalpha, and interferon-gamma are produced primarily in macrophages and have been associated with accelerated atherosclerosis and altered vascular wall function. |
| 6677 | 16455783 | HG increased the activity of protein kinase C, p38 MAPK (p38), c-Jun terminal kinase, and inhibitory-kappaB kinase in MPM. |
| 6678 | 16452547 | Plasma adiponectin concentration and tumor necrosis factor-alpha system activity in lean non-diabetic offspring of type 2 diabetic subjects. |
| 6679 | 16450750 | Advanced glycation end products stimulate tumor necrosis factor-alpha and interleukin-1 beta secretion by peritoneal macrophages in patients on continuous ambulatory peritoneal dialysis. |
| 6680 | 16445986 | The sphingolipid ceramide is a putative intermediate linking both excess nutrients (i.e. saturated fatty acids) and inflammatory cytokines (e.g. tumor necrosis factor-alpha, TNFalpha) to the induction of insulin resistance. |
| 6681 | 16437243 | We analyzed, in a cross-sectional pilot study, HIV-antigen-stimulated IL-10 and tumor necrosis factor alpha (TNFalpha) production, and intracellular concentration (ICC), as well as B7-H1 expression, a marker preferentially presented by IL-10-producing cells, in 20 ARV-treated individuals in whom diabetes did (n=10; diabetes mellitus, DM) or did not (n=10; controls) develop. |
| 6682 | 16437243 | We analyzed, in a cross-sectional pilot study, HIV-antigen-stimulated IL-10 and tumor necrosis factor alpha (TNFalpha) production, and intracellular concentration (ICC), as well as B7-H1 expression, a marker preferentially presented by IL-10-producing cells, in 20 ARV-treated individuals in whom diabetes did (n=10; diabetes mellitus, DM) or did not (n=10; controls) develop. |
| 6683 | 16437243 | Results showed that: (1) IL-10 production was lower; (2) IL-10 ICC was reduced; (3) B7-H1-expressing CD19(+) cells were diminished; and (4) TNFalpha production and ICC by CD4(+) T cells was augmented in DM patients. |
| 6684 | 16437243 | Results showed that: (1) IL-10 production was lower; (2) IL-10 ICC was reduced; (3) B7-H1-expressing CD19(+) cells were diminished; and (4) TNFalpha production and ICC by CD4(+) T cells was augmented in DM patients. |
| 6685 | 16437024 | Augmented fat intake is associated with an increased mass of adipose tissue which releases free fatty acids (FFA) but also hormones and cytokines such as leptin, adiponectin, resistin, tumor necrosis factor-a and interleukin-6. |
| 6686 | 16435302 | The dual role of Fas-ligand as an injury effector and defense strategy in diabetes and islet transplantation. |
| 6687 | 16435302 | The information on the molecular mechanisms of the emergence of beta cell injury is controversial and points to possibly important roles for the perforin-granzyme, Fas-Fas-ligand (FasL) and tumor-necrosis-factor-mediated apoptotic pathways. |
| 6688 | 16434028 | Kaempferol but not quercetin dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced production of the osteoclastogenic cytokines interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1/CCL2) in osteoblasts. |
| 6689 | 16434028 | Kaempferol but not quercetin dose-dependently inhibited tumor necrosis factor alpha (TNFalpha)-induced production of the osteoclastogenic cytokines interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1/CCL2) in osteoblasts. |
| 6690 | 16434028 | The effect on IL-6 was posttranscriptional, whereas kaempferol reduced MCP-1 mRNA levels. |
| 6691 | 16434028 | The effect on IL-6 was posttranscriptional, whereas kaempferol reduced MCP-1 mRNA levels. |
| 6692 | 16434028 | In addition, in mouse primary calvarial osteoblasts, kaempferol but not quercetin blocked TNFalpha-induced translocation of the nuclear factor kappaB (NF-kappaB) subunit p65 from the cytoplasm to the nucleus. |
| 6693 | 16434028 | In addition, in mouse primary calvarial osteoblasts, kaempferol but not quercetin blocked TNFalpha-induced translocation of the nuclear factor kappaB (NF-kappaB) subunit p65 from the cytoplasm to the nucleus. |
| 6694 | 16434028 | In RAW264.7 cells, a monocyte/macrophage precursor for osteoclasts, both kaempferol and quercetin dose-dependently inhibited the receptor activator of NF-kappaB ligand (RANKL)-induced immediate-early oncogene c-fos expression at 6 h. |
| 6695 | 16434028 | In RAW264.7 cells, a monocyte/macrophage precursor for osteoclasts, both kaempferol and quercetin dose-dependently inhibited the receptor activator of NF-kappaB ligand (RANKL)-induced immediate-early oncogene c-fos expression at 6 h. |
| 6696 | 16434028 | After 3-5 days, both flavonols robustly inhibited RANKL-induced expression of the osteoclastic differentiation markers, RANK and calcitonin receptor. |
| 6697 | 16434028 | After 3-5 days, both flavonols robustly inhibited RANKL-induced expression of the osteoclastic differentiation markers, RANK and calcitonin receptor. |
| 6698 | 16433757 | Pro-inflammatory cytokines, IL-1beta and IL-6, were significantly increased 3 h after IPIT, while TNF-alpha was elevated for up to 5 days post-IPIT. |
| 6699 | 16431926 | Pioglitazone ameliorates insulin resistance and diabetes by both adiponectin-dependent and -independent pathways. |
| 6700 | 16431926 | Thiazolidinediones have been shown to up-regulate adiponectin expression in white adipose tissue and plasma adiponectin levels, and these up-regulations have been proposed to be a major mechanism of the thiazolidinedione-induced amelioration of insulin resistance linked to obesity. |
| 6701 | 16431926 | After 14 days of 10 mg/kg pioglitazone, the insulin resistance and diabetes of ob/ob mice were significantly improved in association with significant up-regulation of serum adiponectin levels. |
| 6702 | 16431926 | Amelioration of insulin resistance in ob/ob mice was attributed to decreased glucose production and increased AMP-activated protein kinase in the liver but not to increased glucose uptake in skeletal muscle. |
| 6703 | 16431926 | Moreover, the expressions of TNFalpha and resistin in adipose tissues of ob/ob and adipo-/-ob/ob mice were unchanged after 10 mg/kg pioglitazone but were decreased after 30 mg/kg pioglitazone. |
| 6704 | 16431926 | Thus, pioglitazone-induced amelioration of insulin resistance and diabetes may occur adiponectin dependently in the liver and adiponectin independently in skeletal muscle. |
| 6705 | 16425035 | The Idd9.3 interval contains the candidate molecule cluster of differentiation (CD)137, which is a member of the tumor necrosis factor (TNF) receptor superfamily, functions as an inducible costimulator of T cells, and controls T-B interactions. |
| 6706 | 16425035 | The NOD and B10 CD137 alleles have sequence polymorphisms and different functional effects on T cells; the NOD CD137 allele mediates weaker T cell proliferative responses and decreased interleukin (IL)-2 production after CD137-mediated costimulation. |
| 6707 | 16424352 | Atherosclerosis is a long-term chronic inflammatory disease associated with increased concentrations of inflammatory hepatic markers, such as CRP and fibrinogen, and of peripheral origin, such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6. |
| 6708 | 16424352 | Atherosclerosis is a long-term chronic inflammatory disease associated with increased concentrations of inflammatory hepatic markers, such as CRP and fibrinogen, and of peripheral origin, such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6. |
| 6709 | 16424352 | PPAR-alpha agonists impact on different steps of atherogenesis: (1) early markers of atherosclerosis, such as vascular wall reactivity, are improved, (2) however, reduced expression of adhesion molecules on the surface of endothelial cells, accompanied by decreased levels of inflammatory cytokines, such as TNF-alpha, IL-1, and IL-6, leads to a decreased leukocyte recruitment into the arterial wall; (3) in later stages of the atherosclerotic process, PPAR-alpha agonists may promote plaque stabilization and reduce cardiovascular events, via effects on metalloproteinases, such as MMP9. |
| 6710 | 16424352 | PPAR-alpha agonists impact on different steps of atherogenesis: (1) early markers of atherosclerosis, such as vascular wall reactivity, are improved, (2) however, reduced expression of adhesion molecules on the surface of endothelial cells, accompanied by decreased levels of inflammatory cytokines, such as TNF-alpha, IL-1, and IL-6, leads to a decreased leukocyte recruitment into the arterial wall; (3) in later stages of the atherosclerotic process, PPAR-alpha agonists may promote plaque stabilization and reduce cardiovascular events, via effects on metalloproteinases, such as MMP9. |
| 6711 | 16403817 | Tumor necrosis factor alpha and glucocorticoid synergistically increase leptin production in human adipose tissue: role for p38 mitogen-activated protein kinase. |
| 6712 | 16400026 | These pathologies have been associated with oxidative stress and proinflammatory cytokines, which may operate by activating their downstream target p38 MAP kinase. |
| 6713 | 16400026 | These pathologies have been associated with oxidative stress and proinflammatory cytokines, which may operate by activating their downstream target p38 MAP kinase. |
| 6714 | 16400026 | These effects were associated with increased levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1 and activation of p38 MAP kinase, as assessed by enzyme-linked immunosorbent assay, immunohistochemistry, and/or Western blot. |
| 6715 | 16400026 | These effects were associated with increased levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1 and activation of p38 MAP kinase, as assessed by enzyme-linked immunosorbent assay, immunohistochemistry, and/or Western blot. |
| 6716 | 16400026 | CBD treatment significantly reduced oxidative stress; decreased the levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1; and prevented retinal cell death and vascular hyperpermeability in the diabetic retina. |
| 6717 | 16400026 | CBD treatment significantly reduced oxidative stress; decreased the levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1; and prevented retinal cell death and vascular hyperpermeability in the diabetic retina. |
| 6718 | 16400026 | Consistent with these effects, CBD treatment also significantly inhibited p38 MAP kinase in the diabetic retina. |
| 6719 | 16400026 | Consistent with these effects, CBD treatment also significantly inhibited p38 MAP kinase in the diabetic retina. |
| 6720 | 16400026 | These results demonstrate that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase. |
| 6721 | 16400026 | These results demonstrate that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase. |
| 6722 | 16395259 | Elevated resistin levels in chronic kidney disease are associated with decreased glomerular filtration rate and inflammation, but not with insulin resistance. |
| 6723 | 16395259 | In the present study, we explore the role of decreased renal function and a genetic polymorphism on the recently discovered protein resistin, apparently able to inhibit hepatic insulin action in mice. |
| 6724 | 16395259 | Plasma analysis of blood lipids, insulin, glucose, inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-alpha, vascular cellular adhesion molecule, intercellular adhesion molecule) and resistin (kit from LINCO Research, St Charles, MS) was performed using commercially available assays or routine methods. |
| 6725 | 16395259 | However, in a multiple regression model, resistin, as well as all the measured markers of inflammation, was only associated with insulin resistance if GFR was not taken into account. |
| 6726 | 16395259 | As the significant relationship between plasma resistin levels and insulin resistance was lost following the correction for GFR, resistin is not a likely mediator of insulin resistance in patients with CKD. |
| 6727 | 16394652 | Death receptors belong to the TNF (tumor necrosis factor)/NGF (nerve growth factor) receptor superfamily. |
| 6728 | 16391616 | Among adipocytokines, tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and contribute to the development of vascular diseases. |
| 6729 | 16391616 | Among adipocytokines, tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and contribute to the development of vascular diseases. |
| 6730 | 16391616 | In contrast to these adipocytokines, adiponectin, which is an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. |
| 6731 | 16391616 | In contrast to these adipocytokines, adiponectin, which is an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. |
| 6732 | 16391616 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor, and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. |
| 6733 | 16391616 | Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor, and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. |
| 6734 | 16389718 | According to current concepts, appetite and feeding are regulated by a complex of neurotransmitters, neuromodulators, cytokines and hormones interacting with the hypothalamus, including the leptin and the tumor necrosis factor system. |
| 6735 | 16387690 | On activation, NF-kappaB regulates the expression of almost 400 different genes, which include enzymes (e.g., COX-2, 5-LOX, and iNOS), cytokines (such as TNF, IL-1, IL-6, IL-8, and chemokines), adhesion molecules, cell cycle regulatory molecules, viral proteins, and angiogenic factors. |
| 6736 | 16387690 | Several agents are known to suppress NF-kappaB activation, including Th2 cytokines (IL-4, IL-13, and IL-10), interferons, endocrine hormones (LH, HCG, MSH, and GH), phytochemicals, corticosteroids, and immunosuppressive agents. |
| 6737 | 16387689 | Modern science has revealed that curcumin mediates its effects by modulation of several important molecular targets, including transcription factors (e.g., NF-kappaB, AP-1, Egr-1, beta-catenin, and PPAR-gamma), enzymes (e.g., COX2, 5-LOX, iNOS, and hemeoxygenase-1), cell cycle proteins (e.g., cyclin D1 and p21), cytokines (e.g., TNF, IL-1, IL-6, and chemokines), receptors (e.g., EGFR and HER2), and cell surface adhesion molecules. |
| 6738 | 16378747 | Leptin, free fatty acids, adiponectin, tumor necrosis factor-alpha and interleukin-6 are all produced and secreted by adipocytes, and may directly influence aspects of beta-cell function, including insulin synthesis and secretion, insulin cell survival and apoptosis. |
| 6739 | 16373399 | A novel partial agonist of peroxisome proliferator-activated receptor-gamma (PPARgamma) recruits PPARgamma-coactivator-1alpha, prevents triglyceride accumulation, and potentiates insulin signaling in vitro. |
| 6740 | 16373399 | Partial agonists of peroxisome proliferator-activated receptor-gamma (PPARgamma), also termed selective PPARgamma modulators, are expected to uncouple insulin sensitization from triglyceride (TG) storage in patients with type 2 diabetes mellitus. |
| 6741 | 16373399 | The compound displayed partial agonism in biochemical and cell-based transactivation assays and caused preferential recruitment of PPARgamma-coactivator-1alpha (PGC1alpha) to the receptor, a feature shared with other selective PPARgamma modulators. |
| 6742 | 16373399 | It potentiated glucose uptake and inhibited the negative cross-talk of TNFalpha on protein kinase B (AKT) phosphorylation in mature adipocytes and HepG2 human hepatoma cells. |
| 6743 | 16373399 | We thus propose that selective recruitment of PGC1alpha to favorable PPARgamma-target genes provides a possible molecular mechanism whereby partial PPARgamma agonists dissociate TG accumulation from insulin signaling. |
| 6744 | 16373396 | In an experiment using adenovirus vectors encoding TFAP2B, the expression of TNF-alpha gene was shown to be elevated in the TFAP2B overexpressing cells compared with those in control cells. |
| 6745 | 16373396 | In an experiment using adenovirus vectors encoding TFAP2B, the expression of TNF-alpha gene was shown to be elevated in the TFAP2B overexpressing cells compared with those in control cells. |
| 6746 | 16373396 | Furthermore, we demonstrated that the expression of TFAP2B was increased in the adipose tissues of subjects with the disease-susceptibility allele, and the plasma levels of TNF-alpha and high sensitivity C-reactive peptide were significantly elevated in the patients with the disease-susceptibility allele. |
| 6747 | 16373396 | Furthermore, we demonstrated that the expression of TFAP2B was increased in the adipose tissues of subjects with the disease-susceptibility allele, and the plasma levels of TNF-alpha and high sensitivity C-reactive peptide were significantly elevated in the patients with the disease-susceptibility allele. |
| 6748 | 16371802 | In addition, there appears to be a complex relationship between TNFalpha and tumor growth factor beta (TGF-beta), a cytokine which promotes collagen synthesis and deposition. |
| 6749 | 16370555 | C-reactive protein and tumor necrosis factor-alpha in gestational hyperglycemia. |
| 6750 | 16368716 | Pigment epithelium-derived factor (PEDF) is an endogenous antiinflammatory factor. |
| 6751 | 16368716 | Pigment epithelium-derived factor (PEDF) is an endogenous antiinflammatory factor. |
| 6752 | 16368716 | Pigment epithelium-derived factor (PEDF) is an endogenous antiinflammatory factor. |
| 6753 | 16368716 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor. |
| 6754 | 16368716 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor. |
| 6755 | 16368716 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor. |
| 6756 | 16368716 | Intravitreal injection of PEDF significantly reduced vascular hyper-permeability in rat models of diabetes and oxygen-induced retinopathy, correlating with the decreased levels of retinal inflammatory factors, including VEGF, VEGF receptor-2, MCP-1, TNF-alpha, and ICAM-1. |
| 6757 | 16368716 | Intravitreal injection of PEDF significantly reduced vascular hyper-permeability in rat models of diabetes and oxygen-induced retinopathy, correlating with the decreased levels of retinal inflammatory factors, including VEGF, VEGF receptor-2, MCP-1, TNF-alpha, and ICAM-1. |
| 6758 | 16368716 | Intravitreal injection of PEDF significantly reduced vascular hyper-permeability in rat models of diabetes and oxygen-induced retinopathy, correlating with the decreased levels of retinal inflammatory factors, including VEGF, VEGF receptor-2, MCP-1, TNF-alpha, and ICAM-1. |
| 6759 | 16368716 | In cultured retinal capillary endothelial cells, PEDF significantly decreased TNF-alpha and ICAM-1 expression under hypoxia. |
| 6760 | 16368716 | In cultured retinal capillary endothelial cells, PEDF significantly decreased TNF-alpha and ICAM-1 expression under hypoxia. |
| 6761 | 16368716 | In cultured retinal capillary endothelial cells, PEDF significantly decreased TNF-alpha and ICAM-1 expression under hypoxia. |
| 6762 | 16368716 | Moreover, down-regulation of PEDF expression by siRNA resulted in significantly increases of VEGF and TNF-alpha secretion in retinal Müller cells. |
| 6763 | 16368716 | Moreover, down-regulation of PEDF expression by siRNA resulted in significantly increases of VEGF and TNF-alpha secretion in retinal Müller cells. |
| 6764 | 16368716 | Moreover, down-regulation of PEDF expression by siRNA resulted in significantly increases of VEGF and TNF-alpha secretion in retinal Müller cells. |
| 6765 | 16367949 | Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb). |
| 6766 | 16367949 | Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb). |
| 6767 | 16367949 | Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb). |
| 6768 | 16367949 | The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens. |
| 6769 | 16367949 | The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens. |
| 6770 | 16367949 | The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens. |
| 6771 | 16367949 | During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens. |
| 6772 | 16367949 | During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens. |
| 6773 | 16367949 | During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens. |
| 6774 | 16367949 | The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs. |
| 6775 | 16367949 | The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs. |
| 6776 | 16367949 | The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs. |
| 6777 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 6778 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 6779 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 6780 | 16367949 | In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB. |
| 6781 | 16367949 | In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB. |
| 6782 | 16367949 | In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB. |
| 6783 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 6784 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 6785 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 6786 | 16366418 | Tumor necrosis factor-alpha and interleukin (IL)-6 concentrations tended to be higher in AS patients than in controls. |
| 6787 | 16358360 | IL-23, a proximal regulator of IL-17, may be a major driving force in the induction of autoimmune inflammation. |
| 6788 | 16358360 | Ten daily injections of 400 ng IL-23, starting on the first day of MLD-STZ administration led to significant and sustained hyperglycemia along with weight loss compared with controls (no IL-23), and a significant increase in the number of infiltrating cells, a lower insulin content, enhanced apoptosis, expression of IFN-gamma and IL-17 (not seen in the controls) and a significant increase in the expression of TNF-alpha and IL-18 in the pancreatic islets. |
| 6789 | 16358360 | We provide the first evidence in an animal model that IL-23 is involved in the development of type-1 diabetes, by inducing IL-17 and possibly IFN-gamma production in the target tissue. |
| 6790 | 16352667 | Plasma adiponectin (P < 0.001) increased, and C-reactive protein (P < 0.05), IL-6 (P < 0.01), IL-8 (P < 0.05), and monocyte chemoattractant protein-1 (P < 0.01) decreased. |
| 6791 | 16352667 | AT inflammation was reduced, determined from an increased mRNA expression of adiponectin (P < 0.001) and a decreased expression of macrophage-specific markers (CD14, CD68), IL-6, IL-8, and tumor necrosis factor-alpha (P < 0.01). |
| 6792 | 16352667 | The intervention had no effect on adiponectin receptor 1 and 2 mRNA in AT or SM. |
| 6793 | 16336586 | Tumor necrosis factor-alpha gene expression in diabetic nephropathy: relationship with urinary albumin excretion and effect of angiotensin-converting enzyme inhibition. |
| 6794 | 16332931 | The increase in UAE in the diabetes group was associated with a significant reduction in the expression of slit diaphragm-associated molecules compared with control (nephrin; P < 0.05 and podocin; P < 0.005) that was reversed by ATL146e treatment. |
| 6795 | 16332931 | Diabetes led to an increase in urinary excretion of monocyte chemoattractant protein-1 (705% of control), TNF-alpha (1,586% of control), IFN-gamma (298% of control), kidney fibronectin mRNA (457% of control), and glomerular infiltration of macrophages (764% of control), effects significantly reduced by ATL146e treatment. |
| 6796 | 16331857 | In most cells, TNF mediates its effects through activation of caspases, NF-kappaB, AP-1, c-jun N-terminal kinase, p38 MAPK, and p44/p42 MAPK. |
| 6797 | 16328103 | Inhibition of tumor necrosis factor-alpha-induced intercellular adhesion molecule-1 expression in diabetic rats: role of insulin. |
| 6798 | 16324931 | Outcome measures were blood pressure, total cholesterol, high-density lipoprotein cholesterol, C-reactive protein, interleukin 6, tumor necrosis factor alpha (TNF-alpha), homocysteine, insulin resistance (IR), percentage of body fat, waist-to-hip ratio, physical activity levels, and cardiovascular fitness. |
| 6799 | 19079903 | It is suggested that the relationship between vitamin D and low-intensity chronic inflammation and insulin resistance in T2DM can be mediated in part by the immune-modulating properties of the active form of vitamin D (1-alpha,25-dihydroxyvitamin D3; 1,25(OH)2D3), which is able to down regulate the production of pro-inflammatory cytokines - particularly TNF-alpha, and IL-6. |
| 6800 | 16311222 | Tumour necrosis factor (TNF)-alphaalpha, plasminogen activator inhibitor-1 (PAI-1) and heparin-binding epidermal-growth-factor-like growth factor (HBEGF) are among these adipocytokines, and they contribute to the development of vascular diseases. |
| 6801 | 16311222 | In contrast, adiponectin, an adipose-tissue-specific collagen-like protein, has recently been reported as an important anti-atherogenic and anti-diabetic protein. |
| 6802 | 16311222 | Visceral fat accumulation leads to dysfunction of adipocytes (including hypersecretion of TNF-alphaalpha, PAI-1 and HBEGF, and hyposecretion of adiponectin), which results in the development of a variety of metabolic and circulatory diseases. |
| 6803 | 16307975 | Markers of 8-hydroxydeoxy-guanosine (8-OHdG), endothelin-1 (ET-1), and [nitrate+nitrite], an indicator of nitric oxide (NO) production, in addition to C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in peripheral blood were also determined. |
| 6804 | 16307975 | Markers of 8-hydroxydeoxy-guanosine (8-OHdG), endothelin-1 (ET-1), and [nitrate+nitrite], an indicator of nitric oxide (NO) production, in addition to C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in peripheral blood were also determined. |
| 6805 | 16307975 | Our results showed that diabetic rats were associated with increased 8-OHdG, IL-6, and ET-1 decreased [nitrate+nitrite]. |
| 6806 | 16307975 | Our results showed that diabetic rats were associated with increased 8-OHdG, IL-6, and ET-1 decreased [nitrate+nitrite]. |
| 6807 | 16307975 | In nondiabetic rats PM exposure was also associated with increased 8-OHdG, IL-6, TNF-alpha, and CRP but decreased [nitrate+nitrite]. |
| 6808 | 16307975 | In nondiabetic rats PM exposure was also associated with increased 8-OHdG, IL-6, TNF-alpha, and CRP but decreased [nitrate+nitrite]. |
| 6809 | 16306362 | FFA-induced hepatic insulin resistance was associated with increased hepatic diacylglycerol content (+210%), increased activities of two serine/threonine kinases (protein kinase C-delta and inhibitor of kappaB [IkappaB] kinase-beta), increased activation of the proinflammatory nuclear factor-kappaB (NF-kappaB) pathway (IkappaB kinase-beta, +640%; IkappaB-alpha, -54%; and NF-kappaB, +73%), and increased expression of inflammatory cytokines (tumor necrosis factor-alpha, +1,700% and interleukin-1beta, +440%) and plasma levels of monocyte chemoattractant protein-1 (+220%). |
| 6810 | 16306347 | In the insulitis lesion in type 1 diabetes, invading immune cells produce cytokines, such as IL-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. |
| 6811 | 16306347 | In the insulitis lesion in type 1 diabetes, invading immune cells produce cytokines, such as IL-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. |
| 6812 | 16306347 | IL-1beta and/or TNF-alpha plus IFN-gamma induce beta-cell apoptosis via the activation of beta-cell gene networks under the control of the transcription factors NF-kappaB and STAT-1. |
| 6813 | 16306347 | IL-1beta and/or TNF-alpha plus IFN-gamma induce beta-cell apoptosis via the activation of beta-cell gene networks under the control of the transcription factors NF-kappaB and STAT-1. |
| 6814 | 16306347 | High glucose, however, does not induce or activate IL-1beta, NF-kappaB, or inducible nitric oxide synthase in rat or human beta-cells in vitro or in vivo in Psammomys obesus. |
| 6815 | 16306347 | High glucose, however, does not induce or activate IL-1beta, NF-kappaB, or inducible nitric oxide synthase in rat or human beta-cells in vitro or in vivo in Psammomys obesus. |
| 6816 | 16306347 | Thus, cytokines and nutrients trigger beta-cell death by fundamentally different mechanisms, namely an NF-kappaB-dependent mechanism that culminates in caspase-3 activation for cytokines and an NF-kappaB-independent mechanism for nutrients. |
| 6817 | 16306347 | Thus, cytokines and nutrients trigger beta-cell death by fundamentally different mechanisms, namely an NF-kappaB-dependent mechanism that culminates in caspase-3 activation for cytokines and an NF-kappaB-independent mechanism for nutrients. |
| 6818 | 16306344 | Importantly, the inflammatory component in obesity and diabetes is now firmly established with the discovery of causal links between inflammatory mediators, such as tumor necrosis factor (TNF)-alpha and insulin receptor signaling and the elucidation of the underlying molecular mechanisms, such as c-Jun NH2-terminal kinase (JNK)- and inhibitor of nuclear factor-kappaB kinase-mediated transcriptional and posttranslational modifications that inhibit insulin action. |
| 6819 | 16306344 | More recently, obesity-induced endoplasmic reticulum stress has been demonstrated to underlie the initiation of obesity-induced JNK activation, inflammatory responses, and generation of peripheral insulin resistance. |
| 6820 | 16306335 | No significant differences between genotypes (24 I/I subjects versus 10 I/III or III/III subjects) were observed for gamma-interferon, tumor necrosis factor-alpha, or interleukin (IL)-4. |
| 6821 | 16306335 | By contrast, the I/III + III/III group showed a significant threefold higher IL-10 release in memory T-cells for whole proinsulin and the immunodominant region. |
| 6822 | 16306335 | Given that IL-10 is a marker of regulatory function, our data are consistent with the hypothesis that higher insulin levels in the thymus promote the formation of regulatory T-cells, a proposed explanation for the protective effect of the class III alleles. |
| 6823 | 16306329 | Mediators of inflammation such as tumor necrosis factor-alpha, interleukin (IL)-1beta, the IL-6 family of cytokines, IL-18, and certain chemokines have been proposed to be involved in the events causing both forms of diabetes. |
| 6824 | 16301684 | Effector function of diabetogenic CD4 Th1 T cell clones: a central role for TNF-alpha. |
| 6825 | 16301684 | Effector function of diabetogenic CD4 Th1 T cell clones: a central role for TNF-alpha. |
| 6826 | 16301684 | We have investigated cytokine production both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD mouse. |
| 6827 | 16301684 | We have investigated cytokine production both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD mouse. |
| 6828 | 16301684 | Ex vivo intracellular cytokine staining demonstrated that two important inflammatory cytokines, IFN-gamma and TNF-alpha, were being made by these T cells recovered from the pancreas 6 days following adoptive transfer. |
| 6829 | 16301684 | Ex vivo intracellular cytokine staining demonstrated that two important inflammatory cytokines, IFN-gamma and TNF-alpha, were being made by these T cells recovered from the pancreas 6 days following adoptive transfer. |
| 6830 | 16301684 | Similar analyses in other models demonstrated that disease induced by CD4 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells are required. |
| 6831 | 16301684 | Similar analyses in other models demonstrated that disease induced by CD4 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells are required. |
| 6832 | 16298496 | The specific pathogenic pathways of MetSyn development include: (1) increased tissue and plasma levels of proinflammatory cytokines Interleukin-1(IL-1), Interleukin-6 (IL-6 ) and tumor necrosis factor - alpha (TNF-alpha) caused by inflammatory and/or emotional distress; (2) increased plasma levels of neurotrophin - nerve growth factor (NGF) caused by the high IL-1, IL-6 and TNFalpha levels; (3) high plasma levels of NGF which enhance activation of: the autonomous nerve system--vegetodystonia (disbalance of neurotransmitters); Neuropeptide Y (NPY)--enhanced feeding, obesity and increased leptin plasma levels; hypothalamo-pituitary-adrenal axis--increased corticotropin-releasing hormone (CRH) and cortisol (hormonal disbalance); immune cells--increased number and degranulation of mastocytes (MC)--immunological disbalance; (4) as a result of 1-3 insulin resistance is exhibited leading to diabetes mellitus. |
| 6833 | 16294222 | Timp3 deficiency in insulin receptor-haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF-alpha. |
| 6834 | 16294222 | Timp3 deficiency in insulin receptor-haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF-alpha. |
| 6835 | 16294222 | Timp3 deficiency in insulin receptor-haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF-alpha. |
| 6836 | 16294222 | In insulin receptor heterozygous (Insr+/-) mice, we identified the deficiency of tissue inhibitor of metalloproteinase 3 (Timp3, an inhibitor of both TNF-alpha-converting enzyme [TACE] and MMPs) as a common bond between glucose intolerance and vascular inflammation. |
| 6837 | 16294222 | In insulin receptor heterozygous (Insr+/-) mice, we identified the deficiency of tissue inhibitor of metalloproteinase 3 (Timp3, an inhibitor of both TNF-alpha-converting enzyme [TACE] and MMPs) as a common bond between glucose intolerance and vascular inflammation. |
| 6838 | 16294222 | In insulin receptor heterozygous (Insr+/-) mice, we identified the deficiency of tissue inhibitor of metalloproteinase 3 (Timp3, an inhibitor of both TNF-alpha-converting enzyme [TACE] and MMPs) as a common bond between glucose intolerance and vascular inflammation. |
| 6839 | 16294222 | Among Insr+/- mice, those that develop diabetes have reduced Timp3 and increased TACE activity. |
| 6840 | 16294222 | Among Insr+/- mice, those that develop diabetes have reduced Timp3 and increased TACE activity. |
| 6841 | 16294222 | Among Insr+/- mice, those that develop diabetes have reduced Timp3 and increased TACE activity. |
| 6842 | 16294222 | Unchecked TACE activity causes an increase in levels of soluble TNF-alpha, which subsequently promotes diabetes and vascular inflammation. |
| 6843 | 16294222 | Unchecked TACE activity causes an increase in levels of soluble TNF-alpha, which subsequently promotes diabetes and vascular inflammation. |
| 6844 | 16294222 | Unchecked TACE activity causes an increase in levels of soluble TNF-alpha, which subsequently promotes diabetes and vascular inflammation. |
| 6845 | 16294222 | A therapeutic role for Timp3/TACE modulation is supported by the observation that pharmacological inhibition of TACE led to marked reduction of hyperglycemia and vascular inflammation in Insr+/- diabetic mice, as well as by the observation of increased insulin sensitivity in Tace+/- mice compared with WT mice. |
| 6846 | 16294222 | A therapeutic role for Timp3/TACE modulation is supported by the observation that pharmacological inhibition of TACE led to marked reduction of hyperglycemia and vascular inflammation in Insr+/- diabetic mice, as well as by the observation of increased insulin sensitivity in Tace+/- mice compared with WT mice. |
| 6847 | 16294222 | A therapeutic role for Timp3/TACE modulation is supported by the observation that pharmacological inhibition of TACE led to marked reduction of hyperglycemia and vascular inflammation in Insr+/- diabetic mice, as well as by the observation of increased insulin sensitivity in Tace+/- mice compared with WT mice. |
| 6848 | 16294222 | Our results suggest that an interplay between reduced insulin action and unchecked TACE activity promotes diabetes and vascular inflammation. |
| 6849 | 16294222 | Our results suggest that an interplay between reduced insulin action and unchecked TACE activity promotes diabetes and vascular inflammation. |
| 6850 | 16294222 | Our results suggest that an interplay between reduced insulin action and unchecked TACE activity promotes diabetes and vascular inflammation. |
| 6851 | 16288846 | Assessment of lipopolysaccharide (LPS)-stimulated secretion of IL-1beta, IL-6, and TNF-alpha was accomplished by ELISA of supernatant. |
| 6852 | 16288846 | Assessment of lipopolysaccharide (LPS)-stimulated secretion of IL-1beta, IL-6, and TNF-alpha was accomplished by ELISA of supernatant. |
| 6853 | 16288846 | Assessment of lipopolysaccharide (LPS)-stimulated secretion of IL-1beta, IL-6, and TNF-alpha was accomplished by ELISA of supernatant. |
| 6854 | 16288846 | Regression models controlling for age, body mass index, and race/ethnicity revealed that higher HOMA-IR values were associated with larger stress-induced increases in IL-1beta and TNF-alpha (p<.05). |
| 6855 | 16288846 | Regression models controlling for age, body mass index, and race/ethnicity revealed that higher HOMA-IR values were associated with larger stress-induced increases in IL-1beta and TNF-alpha (p<.05). |
| 6856 | 16288846 | Regression models controlling for age, body mass index, and race/ethnicity revealed that higher HOMA-IR values were associated with larger stress-induced increases in IL-1beta and TNF-alpha (p<.05). |
| 6857 | 16288846 | Furthermore, arousal of negative affect during the ARI was differentially associated with stress-induced changes in stimulated secretion of TNF-alpha and IL-6 as a function of HOMA-IR (p<.05). |
| 6858 | 16288846 | Furthermore, arousal of negative affect during the ARI was differentially associated with stress-induced changes in stimulated secretion of TNF-alpha and IL-6 as a function of HOMA-IR (p<.05). |
| 6859 | 16288846 | Furthermore, arousal of negative affect during the ARI was differentially associated with stress-induced changes in stimulated secretion of TNF-alpha and IL-6 as a function of HOMA-IR (p<.05). |
| 6860 | 16284605 | Determination of vitreous interleukin-1 (IL-1) and tumour necrosis factor (TNF) levels in proliferative diabetic retinopathy. |
| 6861 | 16284605 | Determination of vitreous interleukin-1 (IL-1) and tumour necrosis factor (TNF) levels in proliferative diabetic retinopathy. |
| 6862 | 16284605 | Determination of vitreous interleukin-1 (IL-1) and tumour necrosis factor (TNF) levels in proliferative diabetic retinopathy. |
| 6863 | 16284605 | Determination of vitreous interleukin-1 (IL-1) and tumour necrosis factor (TNF) levels in proliferative diabetic retinopathy. |
| 6864 | 16284605 | We measured interleukin-1 beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) in the vitreous humour and serum of patients with proliferative diabetic retinopathy (PDR), in order to determine the role of these cytokines in the pathogenesis of the disease. |
| 6865 | 16284605 | We measured interleukin-1 beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) in the vitreous humour and serum of patients with proliferative diabetic retinopathy (PDR), in order to determine the role of these cytokines in the pathogenesis of the disease. |
| 6866 | 16284605 | We measured interleukin-1 beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) in the vitreous humour and serum of patients with proliferative diabetic retinopathy (PDR), in order to determine the role of these cytokines in the pathogenesis of the disease. |
| 6867 | 16284605 | We measured interleukin-1 beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) in the vitreous humour and serum of patients with proliferative diabetic retinopathy (PDR), in order to determine the role of these cytokines in the pathogenesis of the disease. |
| 6868 | 16284605 | Vitreous IL-1beta and TNF-alpha concentrations in patients with PDR exceeded those of controls (P<0.05), as did serum IL-1beta and TNF-alpha. |
| 6869 | 16284605 | Vitreous IL-1beta and TNF-alpha concentrations in patients with PDR exceeded those of controls (P<0.05), as did serum IL-1beta and TNF-alpha. |
| 6870 | 16284605 | Vitreous IL-1beta and TNF-alpha concentrations in patients with PDR exceeded those of controls (P<0.05), as did serum IL-1beta and TNF-alpha. |
| 6871 | 16284605 | Vitreous IL-1beta and TNF-alpha concentrations in patients with PDR exceeded those of controls (P<0.05), as did serum IL-1beta and TNF-alpha. |
| 6872 | 16284605 | We suggest that increased vitreous IL-1beta and TNF-alpha levels may play a significant role in the pathogenesis of PDR, which features abnormal cell proliferation and neovascularisation. |
| 6873 | 16284605 | We suggest that increased vitreous IL-1beta and TNF-alpha levels may play a significant role in the pathogenesis of PDR, which features abnormal cell proliferation and neovascularisation. |
| 6874 | 16284605 | We suggest that increased vitreous IL-1beta and TNF-alpha levels may play a significant role in the pathogenesis of PDR, which features abnormal cell proliferation and neovascularisation. |
| 6875 | 16284605 | We suggest that increased vitreous IL-1beta and TNF-alpha levels may play a significant role in the pathogenesis of PDR, which features abnormal cell proliferation and neovascularisation. |
| 6876 | 16281079 | In this study we develop an experimental design to sensitize pancreatic islet cells by high glucose to streptozotocin (STZ) and proinflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma]-induced apoptosis. |
| 6877 | 16278052 | Inflammatory cytokines including IL-1beta, TNF-alpha and IFN-gamma are implicated in the pancreatic islet beta-cell death and functional loss during autoimmune diabetes and also seem to be involved in early loss of islet mass in islet transplantation. |
| 6878 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6879 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6880 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6881 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6882 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6883 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6884 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 6885 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6886 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6887 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6888 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6889 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6890 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6891 | 16277639 | Primary islets are not susceptible to cell death induced by TNF-alpha alone; however, they are killed by TNF-alpha and IFN-gamma in a nitric oxide-dependent manner. |
| 6892 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6893 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6894 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6895 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6896 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6897 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6898 | 16277639 | We examined signal transduction in NIT-1 cells in response to cytokines to determine the mechanism for TNF-alpha-induced apoptosis. |
| 6899 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6900 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6901 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6902 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6903 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6904 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6905 | 16277639 | We found that NIT-1 cells are defective in the activation of nuclear factor-kappaB (NFkappaB) as a result of functionally deficient RelA activity, because overexpression of RelA protected NIT-1 cells from apoptosis. |
| 6906 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6907 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6908 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6909 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6910 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6911 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6912 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 6913 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6914 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6915 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6916 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6917 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6918 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6919 | 16277639 | Together, these defects prevent expression of anti-apoptotic genes in NIT-1 cells and make them susceptible to TNF-alpha. |
| 6920 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6921 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6922 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6923 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6924 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6925 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6926 | 16277639 | To determine whether similar defects in primary beta cells would induce the same effect, we examined TNF-alpha-induced apoptosis in islets isolated from mice deficient in NFkappaB p50. |
| 6927 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6928 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6929 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6930 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6931 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6932 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6933 | 16277639 | These islets were as susceptible as wild-type islets to TNF-alpha and IFN-gamma-induced cell death. |
| 6934 | 16269465 | X-box binding protein-1 mRNA splicing and glucose-regulated protein 78 expression). |
| 6935 | 16269465 | These changes preceded and/or occurred independently of obesity and differences in leptin, TNFalpha, insulin action, and mitochondrial function. |
| 6936 | 16266866 | Compared with the neighborhood children, NUG victims showed significant (p < 0.05 or < 0.001) increases in serum levels of interleukin (IL)-8 (+ 233%), IL-18 (+ 30%), IL-6 (+ 190%), IL-1beta (+ 341%), IL-10 (+ 186%), with a small decrease in interferon (IFN)-gamma (-19%) and nonsignificant increases in soluble tumor necrosis factor (TNF) receptors (sTNFR-p55, p75). |
| 6937 | 16263129 | Supernatant samples were analysed by ELISA for TNFalpha, IFNgamma and IL-10 production. |
| 6938 | 16263129 | Supernatant samples were analysed by ELISA for TNFalpha, IFNgamma and IL-10 production. |
| 6939 | 16263129 | Plastic adhesion decreased the macrophage numbers by approximately 30% and CD4(+)CD25(+) cells by about 60%. |
| 6940 | 16263129 | Plastic adhesion decreased the macrophage numbers by approximately 30% and CD4(+)CD25(+) cells by about 60%. |
| 6941 | 16263129 | This was accompanied by increased medium levels of TNFalpha, IFNgamma and IL-10, which suggest that either CD4(+)CD25(+) cells, macrophages, or both, down-regulate production of both Th1 and certain Th2 cytokines. |
| 6942 | 16263129 | This was accompanied by increased medium levels of TNFalpha, IFNgamma and IL-10, which suggest that either CD4(+)CD25(+) cells, macrophages, or both, down-regulate production of both Th1 and certain Th2 cytokines. |
| 6943 | 16261264 | Interleukin-17 stimulates inducible nitric oxide synthase-dependent toxicity in mouse beta cells. |
| 6944 | 16261264 | The influence of the proinflammatory cytokine interleukin (IL)-17 on inducible nitric oxide (NO) synthase (iNOS)-mediated NO release was investigated in the mouse insulinoma cell line MIN6 and mouse pancreatic islets. |
| 6945 | 16261264 | IL-17 markedly augmented iNOS mRNA/protein expression and subsequent NO production induced in MIN6 cells or pancreatic islets by different combinations of interferon-gamma, tumor necrosis factor-alpha, and IL-1beta. |
| 6946 | 16261264 | The induction of iNOS by IL-17 was preceded by phosphorylation of p38 mitogen-activated protein kinase (MAPK), and inhibition of p38 MAPK activation completely abolished IL-17-stimulated NO release. |
| 6947 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6948 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6949 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6950 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6951 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6952 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 6953 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6954 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6955 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6956 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6957 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6958 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 6959 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6960 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6961 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6962 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6963 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6964 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 6965 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6966 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6967 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6968 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6969 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6970 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 6971 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6972 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6973 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6974 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6975 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6976 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 6977 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6978 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6979 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6980 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6981 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6982 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 6983 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6984 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6985 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6986 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6987 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6988 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 6989 | 16259488 | Discrepancies in the regulation of plasma adiponectin and TNF-alpha levels and adipose tissue gene expression in obese African Americans with glucose intolerance: a pilot study using rosiglitazone. |
| 6990 | 16254197 | Interaction of the -308G/A promoter polymorphism of the tumor necrosis factor-alpha gene with single-nucleotide polymorphism 45 of the adiponectin gene: effect on serum adiponectin concentrations in a Spanish population. |
| 6991 | 16254033 | Donor treatment with bilirubin up-regulated mRNA expression of protective genes such as HO-1 and bcl-2 and suppressed proinflammatory and proapoptotic genes including monocyte chemoattractant protein-1 and caspase-3 and -8 in the islet grafts before transplantation. |
| 6992 | 16254033 | Furthermore, treatment of only the donor suppressed the expression of proinflammatory cytokines including TNF-alpha, inducible nitric oxide synthase, monocyte chemoattractant protein-1, and other proapoptotic and proinflammatory genes normally seen in the islets after transplantation. |
| 6993 | 16248970 | We discovered that IFNgamma/TNFalpha synergism, rather than the Fas ligand as currently believed, is responsible for the apoptosis of pancreatic islet cells both in vitro and in vivo. |
| 6994 | 16247001 | Moreover, neonatal treatment with TNF-alpha resulted in skewed development of a CD8alpha(+)CD11b(-)CD11c(+) DC subset such that TNF-alpha decreases the CD8alpha(+)CD11c(+) DC subset, increases the CD11c(+)CD11b(+) subset, and causes an increase in the expression of CD40 and CD54 on mature DCs capable of inducing immunity. |
| 6995 | 16247001 | Moreover, neonatal treatment with TNF-alpha resulted in skewed development of a CD8alpha(+)CD11b(-)CD11c(+) DC subset such that TNF-alpha decreases the CD8alpha(+)CD11c(+) DC subset, increases the CD11c(+)CD11b(+) subset, and causes an increase in the expression of CD40 and CD54 on mature DCs capable of inducing immunity. |
| 6996 | 16247001 | Moreover, neonatal treatment with TNF-alpha resulted in skewed development of a CD8alpha(+)CD11b(-)CD11c(+) DC subset such that TNF-alpha decreases the CD8alpha(+)CD11c(+) DC subset, increases the CD11c(+)CD11b(+) subset, and causes an increase in the expression of CD40 and CD54 on mature DCs capable of inducing immunity. |
| 6997 | 16247001 | Anti-TNF-alpha-treated mice had an increase in the CD8alpha(+)CD11c(+) DCs. |
| 6998 | 16247001 | Anti-TNF-alpha-treated mice had an increase in the CD8alpha(+)CD11c(+) DCs. |
| 6999 | 16247001 | Anti-TNF-alpha-treated mice had an increase in the CD8alpha(+)CD11c(+) DCs. |
| 7000 | 16247001 | Notably, adoptively transferred naïve CD4(+) T cells from BDC2.5 T cell receptor transgenic mice proliferated in the pancreatic lymph nodes in TNF-alpha-treated NOD mice but not in anti-TNF-alpha-treated mice. |
| 7001 | 16247001 | Notably, adoptively transferred naïve CD4(+) T cells from BDC2.5 T cell receptor transgenic mice proliferated in the pancreatic lymph nodes in TNF-alpha-treated NOD mice but not in anti-TNF-alpha-treated mice. |
| 7002 | 16247001 | Notably, adoptively transferred naïve CD4(+) T cells from BDC2.5 T cell receptor transgenic mice proliferated in the pancreatic lymph nodes in TNF-alpha-treated NOD mice but not in anti-TNF-alpha-treated mice. |
| 7003 | 16246903 | The KpL1-infected mice showed a tendency to increase the blood interleukin 1beta (IL-1beta) level in both nondiabetic and diabetic groups, whereas the tumor necrosis factor-alpha (TNF-alpha) level was significantly decreased in the KpL1-infected diabetic mice (P = 0.002). |
| 7004 | 16246903 | The KpL1-infected mice showed a tendency to increase the blood interleukin 1beta (IL-1beta) level in both nondiabetic and diabetic groups, whereas the tumor necrosis factor-alpha (TNF-alpha) level was significantly decreased in the KpL1-infected diabetic mice (P = 0.002). |
| 7005 | 16246903 | The infection with KP from liver abscess significantly decreased the blood TNF-alpha level in diabetes mellitus (DM) mice and the blood IL-1beta level tended to increase in both infected nondiabetic and diabetic groups. |
| 7006 | 16246903 | The infection with KP from liver abscess significantly decreased the blood TNF-alpha level in diabetes mellitus (DM) mice and the blood IL-1beta level tended to increase in both infected nondiabetic and diabetic groups. |
| 7007 | 16242770 | For example, the accumulation of leptin and TNF-alpha is associated with an increased production for markers of inflammation, fibrotic response, vascular remodeling and proteins facilitating lipid storage within the placenta. |
| 7008 | 16242708 | A subpopulation of CD8+ T cells that constitutes approximately 3-7% of the total CD8+ T cell population underwent apoptosis on exposure to low concentrations of TNF-alpha. |
| 7009 | 16235772 | Hemoglobin, high sensitive C-reactive protein (hsCRP), creatinine, blood lipids, white blood cells (WBC); CD11b/CD18; vascular cell adhesion molecule (sVCAM-1), intercellular adhesion molecule (sICAM-1), sE-selectin, sP-selectin; IL-6, IL-8, tumour necrosis factor (TNF)alpha, sTNFalpha-R1 and sTNFalpha-R2 were analysed. |
| 7010 | 16231364 | Circulating levels of four adipokines (adiponectin, TNF-alpha, leptin, and resistin) and the postprandial lipid and adiponectin responses to an oral fat load were assessed in 25 non-obese, non-diabetic patients with biopsy-proven nonalcoholic steatohepatitis (NASH) and correlated with metabolic indices and liver histology. |
| 7011 | 16227461 | Intermittent hypoxemia and sleep fragmentation in sleep apnea can trigger a cascade of pathophysiological events, including autonomic activation, alterations in neuroendocrine function, and release of potent proinflammatory mediators such as tumor necrosis factor-alpha and interleukin-6. |
| 7012 | 16226915 | Role of suppressors of cytokine signaling SOCS-1 and SOCS-3 in hepatic steatosis and the metabolic syndrome. |
| 7013 | 16226915 | In this study, we show that expression of suppressor of cytokine signaling SOCS-1 and SOCS-3 is increased in livers of obese insulin-resistant animals, and that adenoviral-mediated overexpression of SOCS-1 or SOCS-3 in liver causes insulin resistance through down-regulation of tyrosine phosphorylation of insulin receptor substrate (IRS) proteins. |
| 7014 | 16226915 | Moreover, the increased SOCS-1 and SOCS-3 also cause a prominent up-regulation of the key regulator of fatty acid synthesis in liver, sterol regulatory element binding protein (SREBP)-1. |
| 7015 | 16226915 | Conversely, inhibition of SOCS-1 and SOCS-3 in livers of obese diabetic db/db mice by antisense treatment modestly improves insulin sensitivity, but completely normalizes the increased expression of SREBP-1. |
| 7016 | 16226915 | Promoter activity analysis reveals that expression of SOCS-1 or SOCS-3 with SOCS-3 being more potent enhances SREBP-1c expression, while it is inhibited by expression of STAT3. |
| 7017 | 16226915 | This STAT3-mediated inhibition of SREBP-1c expression is antagonized by co-expression of SOCS proteins. |
| 7018 | 16226915 | Moreover, db/db mice display decreased STAT3 phosphorylation in liver that is normalized by antisense treatment of SOCS proteins. |
| 7019 | 16226915 | These data suggest that obese subjects in the persistent inflammatory states, such as elevated circulating tumor necrosis factor-alpha, may have down-regulated STAT3-mediated signaling by increased SOCS proteins, leading to up-regulation of SREBP-1c expression and increased fatty acid synthesis in liver. |
| 7020 | 16226915 | Thus, SOCS proteins play an important role in pathogenesis of the metabolic syndrome by concordantly modulating cytokine signaling and insulin signaling. |
| 7021 | 16225463 | White adipose tissue is secreting several hormones, particularly leptin and adiponectin, and a variety of other protein signals: the adipocytokines. |
| 7022 | 16225463 | A growing list of adipocytokines involved in inflammation (IL-1beta, IL-6, IL-8, IL-10, TNF-alpha, TGF-beta,) and the acute-phase response (serum amyloid A, PAI-1) have been found to be increased in the metabolic syndrome. |
| 7023 | 16218490 | Furthermore, TZD treatment results in decreased plasma levels of inflammation and cardiovascular risk markers such as CRP, MMP9, PAI-1 and sCD40 in both obese and type 2 diabetic patients. |
| 7024 | 16218490 | Finally, TZDs induce synoviocyte apoptosis and reduce secretion of TNFalpha, IL-6 and IL-8 in synoviocyte from rheumatoid arthritis patients. |
| 7025 | 16217983 | Recent studies have shown that women who have PCOS have higher circulating levels of inflammatory mediators such as C-reactive protein, tumor necrosis factor, tissue plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1). |
| 7026 | 16217126 | It is a direct scavenger of free radicals and has indirect antioxidant effects due to its stimulation of the expression and activity of antioxidative enzymes such as glutathione peroxidase, superoxide dismutase and catalase, and NO synthase, in mammalian cells. |
| 7027 | 16217126 | It was recently reported that melatonin enhanced insulin-receptor kinase and IRS-1 phosphorylation, suggesting the potential existence of signaling pathway cross-talk between melatonin and insulin. |
| 7028 | 16217126 | Because TNF-alpha has been shown to impair insulin action by suppressing insulin receptor-tyrosine kinase activity and its IRS-1 tyrosine phosphorylation in peripheral tissues such as skeletal muscle cells, it was speculated that melatonin might counteract TNF-alpha-associated insulin resistance in type 2 diabetes. |
| 7029 | 16217019 | Here we report that peripherally administered insulin-like growth factor 1 (IGF-1) attenuates LPS-dependent depression of social exploration (sickness) in nondiabetic (db/+) but not in diabetic (db/db) mice. |
| 7030 | 16217019 | We show that the insulin/IGF-1 mimetic vanadyl sulfate (VS) is effective at augmenting recovery from sickness in both db/+ and db/db mice. |
| 7031 | 16217019 | Examination of the mechanism of VS action in db/+ mice showed that VS paradoxically augmented peritoneal macrophage responsivity to LPS, increasing both peritoneal and ex vivo macrophage production of IL-1beta and IL-6 but not TNF-alpha. |
| 7032 | 16217019 | VS also inhibited LPS-dependent up-regulation of IL-1beta and IL-6 mRNA in the brain, while increasing by 50% the cerebral expression of transcripts of the specific antagonist of IL-1 receptors IL-1RA and IL-1R2. |
| 7033 | 16214938 | STAT5 activation by human GH protects insulin-producing cells against interleukin-1beta, interferon-gamma and tumour necrosis factor-alpha-induced apoptosis independent of nitric oxide production. |
| 7034 | 16214938 | STAT5 activation by human GH protects insulin-producing cells against interleukin-1beta, interferon-gamma and tumour necrosis factor-alpha-induced apoptosis independent of nitric oxide production. |
| 7035 | 16214938 | STAT5 activation by human GH protects insulin-producing cells against interleukin-1beta, interferon-gamma and tumour necrosis factor-alpha-induced apoptosis independent of nitric oxide production. |
| 7036 | 16214938 | STAT5 activation by human GH protects insulin-producing cells against interleukin-1beta, interferon-gamma and tumour necrosis factor-alpha-induced apoptosis independent of nitric oxide production. |
| 7037 | 16214938 | The proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) are toxic to pancreatic beta-cells and are implicated in the pathogenesis of type 1 diabetes. |
| 7038 | 16214938 | The proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) are toxic to pancreatic beta-cells and are implicated in the pathogenesis of type 1 diabetes. |
| 7039 | 16214938 | The proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) are toxic to pancreatic beta-cells and are implicated in the pathogenesis of type 1 diabetes. |
| 7040 | 16214938 | The proinflammatory cytokines interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) are toxic to pancreatic beta-cells and are implicated in the pathogenesis of type 1 diabetes. |
| 7041 | 16214938 | We have previously found that GH and prolactin (PRL) stimulate both proliferation and insulin production in pancreatic beta-cells and rat insulin-producing INS-1 cells. |
| 7042 | 16214938 | We have previously found that GH and prolactin (PRL) stimulate both proliferation and insulin production in pancreatic beta-cells and rat insulin-producing INS-1 cells. |
| 7043 | 16214938 | We have previously found that GH and prolactin (PRL) stimulate both proliferation and insulin production in pancreatic beta-cells and rat insulin-producing INS-1 cells. |
| 7044 | 16214938 | We have previously found that GH and prolactin (PRL) stimulate both proliferation and insulin production in pancreatic beta-cells and rat insulin-producing INS-1 cells. |
| 7045 | 16214938 | Here we report that human (h) GH can prevent the apoptotic effects of IL-1beta, IFN-gamma and TNF-alpha in INS-1 and INS-1E cells. |
| 7046 | 16214938 | Here we report that human (h) GH can prevent the apoptotic effects of IL-1beta, IFN-gamma and TNF-alpha in INS-1 and INS-1E cells. |
| 7047 | 16214938 | Here we report that human (h) GH can prevent the apoptotic effects of IL-1beta, IFN-gamma and TNF-alpha in INS-1 and INS-1E cells. |
| 7048 | 16214938 | Here we report that human (h) GH can prevent the apoptotic effects of IL-1beta, IFN-gamma and TNF-alpha in INS-1 and INS-1E cells. |
| 7049 | 16214938 | In order to identify possible targets for the STAT5-mediated protection of INS-1E cells, we studied the effect of hGH on activation of the transcription factors STAT1 and nuclear factor-kappaB (NF-kappaB) by IFN-gamma and IL-1beta+TNF-alpha respectively. |
| 7050 | 16214938 | In order to identify possible targets for the STAT5-mediated protection of INS-1E cells, we studied the effect of hGH on activation of the transcription factors STAT1 and nuclear factor-kappaB (NF-kappaB) by IFN-gamma and IL-1beta+TNF-alpha respectively. |
| 7051 | 16214938 | In order to identify possible targets for the STAT5-mediated protection of INS-1E cells, we studied the effect of hGH on activation of the transcription factors STAT1 and nuclear factor-kappaB (NF-kappaB) by IFN-gamma and IL-1beta+TNF-alpha respectively. |
| 7052 | 16214938 | In order to identify possible targets for the STAT5-mediated protection of INS-1E cells, we studied the effect of hGH on activation of the transcription factors STAT1 and nuclear factor-kappaB (NF-kappaB) by IFN-gamma and IL-1beta+TNF-alpha respectively. |
| 7053 | 16214938 | Gel retardation experiments showed that hGH affects neither IFN-gamma+TNF-alpha-induced STAT1 DNA binding nor IL-1beta and IFN-gamma+TNF-alpha-induced NFkappaB DNA binding. |
| 7054 | 16214938 | Gel retardation experiments showed that hGH affects neither IFN-gamma+TNF-alpha-induced STAT1 DNA binding nor IL-1beta and IFN-gamma+TNF-alpha-induced NFkappaB DNA binding. |
| 7055 | 16214938 | Gel retardation experiments showed that hGH affects neither IFN-gamma+TNF-alpha-induced STAT1 DNA binding nor IL-1beta and IFN-gamma+TNF-alpha-induced NFkappaB DNA binding. |
| 7056 | 16214938 | Gel retardation experiments showed that hGH affects neither IFN-gamma+TNF-alpha-induced STAT1 DNA binding nor IL-1beta and IFN-gamma+TNF-alpha-induced NFkappaB DNA binding. |
| 7057 | 16214938 | The lack of influence of hGH on cytokine-mediated activation of STAT1 and NFkappaB is in accordance with the finding that hGH had only a minor effect on cytokine-induced inducible nitric oxide synthase (iNOS) gene expression and in fact augmented the IL-1beta-stimulated nitric oxide production. |
| 7058 | 16214938 | The lack of influence of hGH on cytokine-mediated activation of STAT1 and NFkappaB is in accordance with the finding that hGH had only a minor effect on cytokine-induced inducible nitric oxide synthase (iNOS) gene expression and in fact augmented the IL-1beta-stimulated nitric oxide production. |
| 7059 | 16214938 | The lack of influence of hGH on cytokine-mediated activation of STAT1 and NFkappaB is in accordance with the finding that hGH had only a minor effect on cytokine-induced inducible nitric oxide synthase (iNOS) gene expression and in fact augmented the IL-1beta-stimulated nitric oxide production. |
| 7060 | 16214938 | The lack of influence of hGH on cytokine-mediated activation of STAT1 and NFkappaB is in accordance with the finding that hGH had only a minor effect on cytokine-induced inducible nitric oxide synthase (iNOS) gene expression and in fact augmented the IL-1beta-stimulated nitric oxide production. |
| 7061 | 16214938 | As the anti-apoptotic Bcl-xL gene has been shown to harbour a STAT5-binding element we measured the expression of Bcl-xL as well as the pro-apoptotic Bax. |
| 7062 | 16214938 | As the anti-apoptotic Bcl-xL gene has been shown to harbour a STAT5-binding element we measured the expression of Bcl-xL as well as the pro-apoptotic Bax. |
| 7063 | 16214938 | As the anti-apoptotic Bcl-xL gene has been shown to harbour a STAT5-binding element we measured the expression of Bcl-xL as well as the pro-apoptotic Bax. |
| 7064 | 16214938 | As the anti-apoptotic Bcl-xL gene has been shown to harbour a STAT5-binding element we measured the expression of Bcl-xL as well as the pro-apoptotic Bax. |
| 7065 | 16214938 | We found that hGH increased the Bcl-xL/Bax ratio both in the absence and in the presence of cytotoxic cytokines. |
| 7066 | 16214938 | We found that hGH increased the Bcl-xL/Bax ratio both in the absence and in the presence of cytotoxic cytokines. |
| 7067 | 16214938 | We found that hGH increased the Bcl-xL/Bax ratio both in the absence and in the presence of cytotoxic cytokines. |
| 7068 | 16214938 | We found that hGH increased the Bcl-xL/Bax ratio both in the absence and in the presence of cytotoxic cytokines. |
| 7069 | 16214938 | In conclusion, these results suggested that GH and PRL protect beta-cells against cytotoxic cytokines via STAT5-dependent mechanisms distal to iNOS activation possibly at the level of Bcl-xL. |
| 7070 | 16214938 | In conclusion, these results suggested that GH and PRL protect beta-cells against cytotoxic cytokines via STAT5-dependent mechanisms distal to iNOS activation possibly at the level of Bcl-xL. |
| 7071 | 16214938 | In conclusion, these results suggested that GH and PRL protect beta-cells against cytotoxic cytokines via STAT5-dependent mechanisms distal to iNOS activation possibly at the level of Bcl-xL. |
| 7072 | 16214938 | In conclusion, these results suggested that GH and PRL protect beta-cells against cytotoxic cytokines via STAT5-dependent mechanisms distal to iNOS activation possibly at the level of Bcl-xL. |
| 7073 | 16203173 | Other studies have shown defects in insulin signaling possibly secondary to activation of Protein Kinase C resulting from the accumulation of active fatty acyl CoA's. |
| 7074 | 16203173 | In vivo it has been shown that rats over-expressing the gluconeogenic enzyme Phosphoenol Pyruvate Carboxykinase (PEPCK) develop insulin resistance in fat and muscle tissues and some features of the metabolic syndrome including mild obesity and dyslipidemia. |
| 7075 | 16203173 | Obesity resulting from excess nutrient intake can also cause insulin resistance by an increase in the production of agents that impair insulin action such as TNFalpha and resistin and a decrease in the production of an insulin sensitizing compound adiponectin. |
| 7076 | 16201273 | Gene expression of adiponectin and adiponectin receptor 1 in type 2 diabetic rats and the relationship with the parameters of glucose and lipid metabolism. |
| 7077 | 16201273 | In order to confirm whether the mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were correlated with the serum parameters of glucose and lipid metabolism and to clarify the regulation of adiponectin receptor gene expression in diabetic states, serum adiponectin, mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were examined in type 2 diabetic rats. |
| 7078 | 16201273 | No siglificant changes were observed in the expression of adiponectin receptor 1 in the skeletal muscle of type 2 diabetic rats. |
| 7079 | 16201273 | The mRNA levels of adiponectin in adipose tissue were reversely correlated with serum insulin (r=-0.66, P<0.05), triglyceride (r= -0.58, P<0.05), cholesterol (r=-0.49, P<0.05), interleukin-6 (r=-0.49, P<0. 05) and tumor necrosis factor (r= -0.43, P<0.05). |
| 7080 | 16192669 | The OMp showed reduced TNF-alpha, IL-12, and NO production as well as defective phagocytosis activity compared to nondiabetic controls; however, there was no significant difference with IL-6 production. |
| 7081 | 16192669 | On the other hand, the levels of IFN-gamma or IL-4 of splenocytes in diabetic mice were significantly higher compared to the control mice. |
| 7082 | 16192669 | The ratio of IFN-gamma to IL-4 was also higher at the early stage of diabetes and then declined several weeks later after the occurrence of diabetes, suggesting a pathogenetic TH1 phenotype from the beginning gradually to a tendency of TH2 during the development of diabetes. |
| 7083 | 16189279 | Therefore, we studied the expression of additional genes (Bmp-1, Bmp-4, Vegf, Bglap, Il-1b, Infg, Tnfa, Calca, Sp1, Yy1) in bone of nondiabetic BB rats compared with newly diagnosed and well- and poorly compensated diabetic rats as well as two nondiabetes-prone congenic BB.SHR rats, BB rat-related (WOKW) and -unrelated rat strains (F344). |
| 7084 | 16186410 | The cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) gene is implicated as an important regulator of body weight in mice and humans and is therefore a candidate gene for human obesity. |
| 7085 | 16186410 | The cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) gene is implicated as an important regulator of body weight in mice and humans and is therefore a candidate gene for human obesity. |
| 7086 | 16186410 | CIDEA-deficient mice display higher metabolic rate, and the gene cross-talks with tumor necrosis factor-alpha (TNF-alpha) in fat cells. |
| 7087 | 16186410 | CIDEA-deficient mice display higher metabolic rate, and the gene cross-talks with tumor necrosis factor-alpha (TNF-alpha) in fat cells. |
| 7088 | 16186410 | We hypothesize that CIDEA alleles regulate human obesity through impact on basal metabolic rate and adipocyte TNF-alpha signaling. |
| 7089 | 16186410 | We hypothesize that CIDEA alleles regulate human obesity through impact on basal metabolic rate and adipocyte TNF-alpha signaling. |
| 7090 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7091 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7092 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7093 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7094 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7095 | 16186396 | Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. |
| 7096 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7097 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7098 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7099 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7100 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7101 | 16186396 | Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. |
| 7102 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7103 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7104 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7105 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7106 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7107 | 16186396 | Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. |
| 7108 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7109 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7110 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7111 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7112 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7113 | 16186396 | TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. |
| 7114 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7115 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7116 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7117 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7118 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7119 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 7120 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7121 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7122 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7123 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7124 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7125 | 16186396 | These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. |
| 7126 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7127 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7128 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7129 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7130 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7131 | 16186396 | Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. |
| 7132 | 16180338 | The release of soluble VAP-1/SSAO by 3T3-L1 adipocytes is stimulated by isoproterenol and low concentrations of TNFalpha. |
| 7133 | 16180338 | The release of soluble VAP-1/SSAO by 3T3-L1 adipocytes is stimulated by isoproterenol and low concentrations of TNFalpha. |
| 7134 | 16180338 | The release of soluble VAP-1/SSAO by 3T3-L1 adipocytes is stimulated by isoproterenol and low concentrations of TNFalpha. |
| 7135 | 16180338 | Plasma level of the protein VAP-1/SSAO (Vascular Adhesion Protein-1/Semicarbazide-Sensitive Amine Oxidase) is increased in diabetes and/or obesity and may be related to vascular complications associated to these pathologies. |
| 7136 | 16180338 | Plasma level of the protein VAP-1/SSAO (Vascular Adhesion Protein-1/Semicarbazide-Sensitive Amine Oxidase) is increased in diabetes and/or obesity and may be related to vascular complications associated to these pathologies. |
| 7137 | 16180338 | Plasma level of the protein VAP-1/SSAO (Vascular Adhesion Protein-1/Semicarbazide-Sensitive Amine Oxidase) is increased in diabetes and/or obesity and may be related to vascular complications associated to these pathologies. |
| 7138 | 16180338 | Here we focused on the previously observed effect produced by TNFalpha in the release of VAP-1/SSAO and studied the effect of a beta-adrenergic compound, isoproterenol. |
| 7139 | 16180338 | Here we focused on the previously observed effect produced by TNFalpha in the release of VAP-1/SSAO and studied the effect of a beta-adrenergic compound, isoproterenol. |
| 7140 | 16180338 | Here we focused on the previously observed effect produced by TNFalpha in the release of VAP-1/SSAO and studied the effect of a beta-adrenergic compound, isoproterenol. |
| 7141 | 16180338 | While TNFalpha produced a decrease on VAP-1/SSAO membrane form content, isoproterenol did not modify it. |
| 7142 | 16180338 | While TNFalpha produced a decrease on VAP-1/SSAO membrane form content, isoproterenol did not modify it. |
| 7143 | 16180338 | While TNFalpha produced a decrease on VAP-1/SSAO membrane form content, isoproterenol did not modify it. |
| 7144 | 16177203 | A diet supplemented with husks of Plantago ovata reduces the development of endothelial dysfunction, hypertension, and obesity by affecting adiponectin and TNF-alpha in obese Zucker rats. |
| 7145 | 16177203 | A diet supplemented with husks of Plantago ovata reduces the development of endothelial dysfunction, hypertension, and obesity by affecting adiponectin and TNF-alpha in obese Zucker rats. |
| 7146 | 16177203 | A diet supplemented with husks of Plantago ovata reduces the development of endothelial dysfunction, hypertension, and obesity by affecting adiponectin and TNF-alpha in obese Zucker rats. |
| 7147 | 16177203 | A diet supplemented with husks of Plantago ovata reduces the development of endothelial dysfunction, hypertension, and obesity by affecting adiponectin and TNF-alpha in obese Zucker rats. |
| 7148 | 16177203 | At the end of the treatment, plasma concentrations of triglycerides, total cholesterol, FFAs, glucose, insulin, adiponectin, and tumor necrosis factor alpha (TNF-alpha) were determined, and studies on vascular function were performed using aortic rings. |
| 7149 | 16177203 | At the end of the treatment, plasma concentrations of triglycerides, total cholesterol, FFAs, glucose, insulin, adiponectin, and tumor necrosis factor alpha (TNF-alpha) were determined, and studies on vascular function were performed using aortic rings. |
| 7150 | 16177203 | At the end of the treatment, plasma concentrations of triglycerides, total cholesterol, FFAs, glucose, insulin, adiponectin, and tumor necrosis factor alpha (TNF-alpha) were determined, and studies on vascular function were performed using aortic rings. |
| 7151 | 16177203 | At the end of the treatment, plasma concentrations of triglycerides, total cholesterol, FFAs, glucose, insulin, adiponectin, and tumor necrosis factor alpha (TNF-alpha) were determined, and studies on vascular function were performed using aortic rings. |
| 7152 | 16177203 | The greater SBP, higher plasma concentrations of triglycerides, total cholesterol, FFA, glucose, insulin, and TNF-alpha, and the hypoadinectinemia that occurred in obese Zucker rats that consumed the control diet were significantly improved in those fed the fiber-supplemented diet. |
| 7153 | 16177203 | The greater SBP, higher plasma concentrations of triglycerides, total cholesterol, FFA, glucose, insulin, and TNF-alpha, and the hypoadinectinemia that occurred in obese Zucker rats that consumed the control diet were significantly improved in those fed the fiber-supplemented diet. |
| 7154 | 16177203 | The greater SBP, higher plasma concentrations of triglycerides, total cholesterol, FFA, glucose, insulin, and TNF-alpha, and the hypoadinectinemia that occurred in obese Zucker rats that consumed the control diet were significantly improved in those fed the fiber-supplemented diet. |
| 7155 | 16177203 | The greater SBP, higher plasma concentrations of triglycerides, total cholesterol, FFA, glucose, insulin, and TNF-alpha, and the hypoadinectinemia that occurred in obese Zucker rats that consumed the control diet were significantly improved in those fed the fiber-supplemented diet. |
| 7156 | 16177203 | We conclude that intake of a P. ovata husk-supplemented diet prevents endothelial dysfunction, hypertension, and obesity development, and ameliorates dyslipidemia and abnormal plasma concentrations of adiponectin and TNF-alpha in obese Zucker rats. |
| 7157 | 16177203 | We conclude that intake of a P. ovata husk-supplemented diet prevents endothelial dysfunction, hypertension, and obesity development, and ameliorates dyslipidemia and abnormal plasma concentrations of adiponectin and TNF-alpha in obese Zucker rats. |
| 7158 | 16177203 | We conclude that intake of a P. ovata husk-supplemented diet prevents endothelial dysfunction, hypertension, and obesity development, and ameliorates dyslipidemia and abnormal plasma concentrations of adiponectin and TNF-alpha in obese Zucker rats. |
| 7159 | 16177203 | We conclude that intake of a P. ovata husk-supplemented diet prevents endothelial dysfunction, hypertension, and obesity development, and ameliorates dyslipidemia and abnormal plasma concentrations of adiponectin and TNF-alpha in obese Zucker rats. |
| 7160 | 16175602 | Obese WAT showed increased TNFalpha and leptin expression and reciprocally reduced adiponectin expression. |
| 7161 | 16175602 | Obese WAT showed increased TNFalpha and leptin expression and reciprocally reduced adiponectin expression. |
| 7162 | 16175602 | The expression of lipogenic transcription factors (SREBP-1c, PPARgamma, LXRalpha) was increased, whereas that of a lipolytic nuclear factor PPARalpha was reduced in SH. |
| 7163 | 16175602 | The expression of lipogenic transcription factors (SREBP-1c, PPARgamma, LXRalpha) was increased, whereas that of a lipolytic nuclear factor PPARalpha was reduced in SH. |
| 7164 | 16175602 | SH was associated with reduced cytochrome P450 (Cyp)2e1 but increased Cyp4a. |
| 7165 | 16175602 | SH was associated with reduced cytochrome P450 (Cyp)2e1 but increased Cyp4a. |
| 7166 | 16175602 | In conclusion, forced overfeeding with a high-fat diet in mice induces obesity, insulin resistance, and SH in the absence of TNF signaling or Cyp2e1 induction. |
| 7167 | 16175602 | In conclusion, forced overfeeding with a high-fat diet in mice induces obesity, insulin resistance, and SH in the absence of TNF signaling or Cyp2e1 induction. |
| 7168 | 16174285 | Among them, -511 C/T in interleukin-1beta (IL-1beta), tandem repeat in IL-1 receptor antagonist (IL-1Ra), -308 G/A in tumour necrosis factor-alpha (TNF-alpha) were significantly associated with an increased risk of kidney failure. |
| 7169 | 16171951 | At that time, does pravastatin treatment increase serum levels of adiponectin, a key adipokine with insulin-sensitizing property? |
| 7170 | 16171951 | How about the effects of pravastatin treatment on adipokines that could elicit insulin resistance such as tumor necrosis factor-alpha? |
| 7171 | 16170833 | Do adiponectin, TNFalpha, leptin and CRP relate to insulin resistance in pregnancy? |
| 7172 | 16170395 | High adiponectin and TNF-alpha levels in moderate drinkers suffering from liver steatosis: comparison with non drinkers suffering from similar hepatopathy. |
| 7173 | 16170395 | High adiponectin and TNF-alpha levels in moderate drinkers suffering from liver steatosis: comparison with non drinkers suffering from similar hepatopathy. |
| 7174 | 16170395 | High adiponectin and TNF-alpha levels in moderate drinkers suffering from liver steatosis: comparison with non drinkers suffering from similar hepatopathy. |
| 7175 | 16170395 | High adiponectin and TNF-alpha levels in moderate drinkers suffering from liver steatosis: comparison with non drinkers suffering from similar hepatopathy. |
| 7176 | 16170395 | High adiponectin and TNF-alpha levels in moderate drinkers suffering from liver steatosis: comparison with non drinkers suffering from similar hepatopathy. |
| 7177 | 16170395 | An important endogenous mediator of insulin sensitivity is adiponectin (AN), an adipokine that displays numerous antiatherogenic, antidiabetogenic and antiinflammatory effects. |
| 7178 | 16170395 | An important endogenous mediator of insulin sensitivity is adiponectin (AN), an adipokine that displays numerous antiatherogenic, antidiabetogenic and antiinflammatory effects. |
| 7179 | 16170395 | An important endogenous mediator of insulin sensitivity is adiponectin (AN), an adipokine that displays numerous antiatherogenic, antidiabetogenic and antiinflammatory effects. |
| 7180 | 16170395 | An important endogenous mediator of insulin sensitivity is adiponectin (AN), an adipokine that displays numerous antiatherogenic, antidiabetogenic and antiinflammatory effects. |
| 7181 | 16170395 | An important endogenous mediator of insulin sensitivity is adiponectin (AN), an adipokine that displays numerous antiatherogenic, antidiabetogenic and antiinflammatory effects. |
| 7182 | 16170395 | Recently, acute increase in alcohol consumption has been shown to be associated with increase in plasma adiponectin and, concomitantly, insulin sensitivity. |
| 7183 | 16170395 | Recently, acute increase in alcohol consumption has been shown to be associated with increase in plasma adiponectin and, concomitantly, insulin sensitivity. |
| 7184 | 16170395 | Recently, acute increase in alcohol consumption has been shown to be associated with increase in plasma adiponectin and, concomitantly, insulin sensitivity. |
| 7185 | 16170395 | Recently, acute increase in alcohol consumption has been shown to be associated with increase in plasma adiponectin and, concomitantly, insulin sensitivity. |
| 7186 | 16170395 | Recently, acute increase in alcohol consumption has been shown to be associated with increase in plasma adiponectin and, concomitantly, insulin sensitivity. |
| 7187 | 16170395 | All individuals were examined for serum concentrations of AN, glucose, triglycerides, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate transferase (GMT) activity; carbohydrate-deficient transferrin (CDT%) a marker of chronic alcohol consumption, insulin and TNF-alpha. |
| 7188 | 16170395 | All individuals were examined for serum concentrations of AN, glucose, triglycerides, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate transferase (GMT) activity; carbohydrate-deficient transferrin (CDT%) a marker of chronic alcohol consumption, insulin and TNF-alpha. |
| 7189 | 16170395 | All individuals were examined for serum concentrations of AN, glucose, triglycerides, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate transferase (GMT) activity; carbohydrate-deficient transferrin (CDT%) a marker of chronic alcohol consumption, insulin and TNF-alpha. |
| 7190 | 16170395 | All individuals were examined for serum concentrations of AN, glucose, triglycerides, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate transferase (GMT) activity; carbohydrate-deficient transferrin (CDT%) a marker of chronic alcohol consumption, insulin and TNF-alpha. |
| 7191 | 16170395 | All individuals were examined for serum concentrations of AN, glucose, triglycerides, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and glutamate transferase (GMT) activity; carbohydrate-deficient transferrin (CDT%) a marker of chronic alcohol consumption, insulin and TNF-alpha. |
| 7192 | 16170395 | Plasma AN concentrations in the whole group were positively correlated with TNF-alpha concentrations (r = 0.6; p = 0.0001), CDT (r = 0.26; p = 0.0084), AST/ALT index (r = 0.3, p = 0.009), AST (r = 0.29; p = 0.011) and GMT (r = 0.29; p = 0.011) and negatively with BMI (r = -0.48; p = 0.0002) and glycemia (r = -0.22; p = 0.049). |
| 7193 | 16170395 | Plasma AN concentrations in the whole group were positively correlated with TNF-alpha concentrations (r = 0.6; p = 0.0001), CDT (r = 0.26; p = 0.0084), AST/ALT index (r = 0.3, p = 0.009), AST (r = 0.29; p = 0.011) and GMT (r = 0.29; p = 0.011) and negatively with BMI (r = -0.48; p = 0.0002) and glycemia (r = -0.22; p = 0.049). |
| 7194 | 16170395 | Plasma AN concentrations in the whole group were positively correlated with TNF-alpha concentrations (r = 0.6; p = 0.0001), CDT (r = 0.26; p = 0.0084), AST/ALT index (r = 0.3, p = 0.009), AST (r = 0.29; p = 0.011) and GMT (r = 0.29; p = 0.011) and negatively with BMI (r = -0.48; p = 0.0002) and glycemia (r = -0.22; p = 0.049). |
| 7195 | 16170395 | Plasma AN concentrations in the whole group were positively correlated with TNF-alpha concentrations (r = 0.6; p = 0.0001), CDT (r = 0.26; p = 0.0084), AST/ALT index (r = 0.3, p = 0.009), AST (r = 0.29; p = 0.011) and GMT (r = 0.29; p = 0.011) and negatively with BMI (r = -0.48; p = 0.0002) and glycemia (r = -0.22; p = 0.049). |
| 7196 | 16170395 | Plasma AN concentrations in the whole group were positively correlated with TNF-alpha concentrations (r = 0.6; p = 0.0001), CDT (r = 0.26; p = 0.0084), AST/ALT index (r = 0.3, p = 0.009), AST (r = 0.29; p = 0.011) and GMT (r = 0.29; p = 0.011) and negatively with BMI (r = -0.48; p = 0.0002) and glycemia (r = -0.22; p = 0.049). |
| 7197 | 16170395 | The positive associations of AN with TNF-alpha (0.8; p = 0.001), CDT (0.55; p = 0.017), AST/ALT index (0.55; p = 0.019) and the negative correlation with glycemia (-0.35; p = 0.0158) were independent of BMI. |
| 7198 | 16170395 | The positive associations of AN with TNF-alpha (0.8; p = 0.001), CDT (0.55; p = 0.017), AST/ALT index (0.55; p = 0.019) and the negative correlation with glycemia (-0.35; p = 0.0158) were independent of BMI. |
| 7199 | 16170395 | The positive associations of AN with TNF-alpha (0.8; p = 0.001), CDT (0.55; p = 0.017), AST/ALT index (0.55; p = 0.019) and the negative correlation with glycemia (-0.35; p = 0.0158) were independent of BMI. |
| 7200 | 16170395 | The positive associations of AN with TNF-alpha (0.8; p = 0.001), CDT (0.55; p = 0.017), AST/ALT index (0.55; p = 0.019) and the negative correlation with glycemia (-0.35; p = 0.0158) were independent of BMI. |
| 7201 | 16170395 | The positive associations of AN with TNF-alpha (0.8; p = 0.001), CDT (0.55; p = 0.017), AST/ALT index (0.55; p = 0.019) and the negative correlation with glycemia (-0.35; p = 0.0158) were independent of BMI. |
| 7202 | 16170395 | Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found. |
| 7203 | 16170395 | Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found. |
| 7204 | 16170395 | Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found. |
| 7205 | 16170395 | Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found. |
| 7206 | 16170395 | Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found. |
| 7207 | 16169595 | Several cytokines such as interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the dorsal horn are increased after nerve lesion and have been implicated in contributing to nerve-injury pain, presumably by altering synaptic transmission in the CNS, including the spinal cord. |
| 7208 | 16169595 | Nerve injury also leads to persistent activation of p38 mitogen-activated protein kinase (MAPK) in microglia. |
| 7209 | 16159895 | Markers of oxidative stress (plasma and urine albumin carbonyl and total protein carbonyls and malondialdehyde), inflammation [white blood cell (WBC) count, C-reactive protein (CRP), plasma IL-6, TNF-alpha], and plaque stability [matrix metalloproteinase 9 (MMP-9)] were measured in frozen samples obtained from patients with overt diabetic nephropathy participating in a randomized, open-label, blinded end-point, 16-wk trial with glipizide (n = 22) or pioglitazone (n = 22). |
| 7210 | 16159895 | Pioglitazone therapy in men with advanced diabetic nephropathy reduced WBC count by 1,125/mul (P < 0.001), CRP by 41% (P = 0.042), IL-6 by 38% (P = 0.009), and MMP-9 by 29% (P = 0.016). |
| 7211 | 16157299 | Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats. |
| 7212 | 16157299 | Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats. |
| 7213 | 16157299 | Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats. |
| 7214 | 16157299 | Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats. |
| 7215 | 16157299 | Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats. |
| 7216 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 7217 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 7218 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 7219 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 7220 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 7221 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 7222 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 7223 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 7224 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 7225 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 7226 | 16157299 | The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). |
| 7227 | 16157299 | The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). |
| 7228 | 16157299 | The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). |
| 7229 | 16157299 | The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). |
| 7230 | 16157299 | The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). |
| 7231 | 16157299 | These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha. |
| 7232 | 16157299 | These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha. |
| 7233 | 16157299 | These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha. |
| 7234 | 16157299 | These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha. |
| 7235 | 16157299 | These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha. |
| 7236 | 16154537 | IFN-gamma sensitizes MIN6N8 insulinoma cells to TNF-alpha-induced apoptosis by inhibiting NF-kappaB-mediated XIAP upregulation. |
| 7237 | 16154537 | IFN-gamma sensitizes MIN6N8 insulinoma cells to TNF-alpha-induced apoptosis by inhibiting NF-kappaB-mediated XIAP upregulation. |
| 7238 | 16154537 | IFN-gamma sensitizes MIN6N8 insulinoma cells to TNF-alpha-induced apoptosis by inhibiting NF-kappaB-mediated XIAP upregulation. |
| 7239 | 16154537 | Here, we found that: (i) XIAP level was inversely correlated with tumor necrosis factor (TNF)-alpha-induced apoptosis in MIN6N8 insulinoma cells; (ii) adenoviral XIAP overexpression abrogated the TNF-alpha-induced apoptosis through inhibition of caspase activity; (iii) downregulation of XIAP by antisense oligonucleotide or Smac peptide sensitized MIN6N8 cells to TNF-alpha-induced apoptosis; (iv) XIAP expression was induced by TNF-alpha through a nuclear factor-kappaB (NF-kappaB)-dependent pathway, and interferon (IFN)-gamma prevented such an induction in a manner independent of NF-kappaB, which presents a potential mechanism underlying cytotoxic IFN-gamma/TNF-alpha synergism. |
| 7240 | 16154537 | Here, we found that: (i) XIAP level was inversely correlated with tumor necrosis factor (TNF)-alpha-induced apoptosis in MIN6N8 insulinoma cells; (ii) adenoviral XIAP overexpression abrogated the TNF-alpha-induced apoptosis through inhibition of caspase activity; (iii) downregulation of XIAP by antisense oligonucleotide or Smac peptide sensitized MIN6N8 cells to TNF-alpha-induced apoptosis; (iv) XIAP expression was induced by TNF-alpha through a nuclear factor-kappaB (NF-kappaB)-dependent pathway, and interferon (IFN)-gamma prevented such an induction in a manner independent of NF-kappaB, which presents a potential mechanism underlying cytotoxic IFN-gamma/TNF-alpha synergism. |
| 7241 | 16154537 | Here, we found that: (i) XIAP level was inversely correlated with tumor necrosis factor (TNF)-alpha-induced apoptosis in MIN6N8 insulinoma cells; (ii) adenoviral XIAP overexpression abrogated the TNF-alpha-induced apoptosis through inhibition of caspase activity; (iii) downregulation of XIAP by antisense oligonucleotide or Smac peptide sensitized MIN6N8 cells to TNF-alpha-induced apoptosis; (iv) XIAP expression was induced by TNF-alpha through a nuclear factor-kappaB (NF-kappaB)-dependent pathway, and interferon (IFN)-gamma prevented such an induction in a manner independent of NF-kappaB, which presents a potential mechanism underlying cytotoxic IFN-gamma/TNF-alpha synergism. |
| 7242 | 16154537 | Taken together, our results suggest that XIAP is an important modulator of TNF-alpha-induced apoptosis of MIN6N8 cells, and XIAP regulation in pancreatic beta-cells might play an important role in pancreatic beta-cell apoptosis and in the pathogenesis of type 1 diabetes. |
| 7243 | 16154537 | Taken together, our results suggest that XIAP is an important modulator of TNF-alpha-induced apoptosis of MIN6N8 cells, and XIAP regulation in pancreatic beta-cells might play an important role in pancreatic beta-cell apoptosis and in the pathogenesis of type 1 diabetes. |
| 7244 | 16154537 | Taken together, our results suggest that XIAP is an important modulator of TNF-alpha-induced apoptosis of MIN6N8 cells, and XIAP regulation in pancreatic beta-cells might play an important role in pancreatic beta-cell apoptosis and in the pathogenesis of type 1 diabetes. |
| 7245 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7246 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7247 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7248 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7249 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7250 | 16154427 | Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7251 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7252 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7253 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7254 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7255 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7256 | 16154427 | The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. |
| 7257 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7258 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7259 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7260 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7261 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7262 | 16154427 | In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. |
| 7263 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7264 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7265 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7266 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7267 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7268 | 16154427 | Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. |
| 7269 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7270 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7271 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7272 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7273 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7274 | 16154427 | In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. |
| 7275 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7276 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7277 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7278 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7279 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7280 | 16154427 | There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. |
| 7281 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7282 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7283 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7284 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7285 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7286 | 16154427 | From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients. |
| 7287 | 16145910 | [Effect of rosiglitazone on level of serum TNF-alpha and its relation with insulin resistance in type 2 diabetes mellitus]. |
| 7288 | 16143422 | TNFalpha genotype affects TNFalpha release, insulin sensitivity and the severity of liver disease in HCV chronic hepatitis. |
| 7289 | 16135665 | Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies. |
| 7290 | 16135665 | Release and regulation of leptin, resistin and adiponectin from human placenta, fetal membranes, and maternal adipose tissue and skeletal muscle from normal and gestational diabetes mellitus-complicated pregnancies. |
| 7291 | 16135665 | The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. |
| 7292 | 16135665 | The aim of this study was to determine the release and regulation of leptin, resistin and adiponectin from human placenta and fetal membranes, and maternal subcutaneous adipose tissue and skeletal muscle obtained from normal and gestational diabetes mellitus (GDM)-complicated pregnancies at the time of Cesarean section. |
| 7293 | 16135665 | Tissue explants were incubated in the absence (basal control) or presence of 10 mug/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-8, 1 microM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0.1, 1 and 10 microM insulin and 0.1 1 and 10 microM dexamethasone, progesterone and estrogen. |
| 7294 | 16135665 | Tissue explants were incubated in the absence (basal control) or presence of 10 mug/ml lipopolysaccharide (LPS), 10, 20 or 40 ng/ml tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-8, 1 microM phorbol myristate acetate, 10, 20 and 40 mM glucose, 0.1, 1 and 10 microM insulin and 0.1 1 and 10 microM dexamethasone, progesterone and estrogen. |
| 7295 | 16135665 | After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. |
| 7296 | 16135665 | After an 18-h incubation, the medium was collected and the release of leptin, resistin and adiponectin was quantified by ELISA. |
| 7297 | 16135665 | Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. |
| 7298 | 16135665 | Human gestational tissues and maternal tissues released immunoreactive leptin, resistin and adiponectin; however, there was no difference in the release of either resistin or adiponectin between normal pregnant women and women with gestational diabetes. |
| 7299 | 16135665 | In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. |
| 7300 | 16135665 | In adipose tissue and skeletal muscle the release of leptin was significantly greater in insulin-controlled GDM compared with diet-controlled GDM, and leptin release from adipose tissue was significantly correlated with maternal body mass index. |
| 7301 | 16135665 | In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-alpha on leptin, resistin or adiponectin release. |
| 7302 | 16135665 | In all tissues tested, there was no effect of incubation with LPS, IL-6, IL-8 or TNF-alpha on leptin, resistin or adiponectin release. |
| 7303 | 16135665 | Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. |
| 7304 | 16135665 | Insulin increased placental resistin release, whereas the hormones dexamethasone, progesterone and estrogen significantly decreased placental resistin release. |
| 7305 | 16132956 | Large-scale studies of the association between variation at the TNF/LTA locus and susceptibility to type 2 diabetes. |
| 7306 | 16130407 | To elucidate the etiopathological role of IP-10 in type 2 DM, we measured the concentrations of IP-10 together with IFN-gamma, TNF-alpha, IL-18, IL-6 and MCP-1 in plasma samples from 103 type 2 DM patients with various degrees of nephropathy. |
| 7307 | 16130407 | To elucidate the etiopathological role of IP-10 in type 2 DM, we measured the concentrations of IP-10 together with IFN-gamma, TNF-alpha, IL-18, IL-6 and MCP-1 in plasma samples from 103 type 2 DM patients with various degrees of nephropathy. |
| 7308 | 16130407 | To elucidate the etiopathological role of IP-10 in type 2 DM, we measured the concentrations of IP-10 together with IFN-gamma, TNF-alpha, IL-18, IL-6 and MCP-1 in plasma samples from 103 type 2 DM patients with various degrees of nephropathy. |
| 7309 | 16130407 | IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1. |
| 7310 | 16130407 | IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1. |
| 7311 | 16130407 | IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1. |
| 7312 | 16130407 | IP-10 levels became higher with the progression of nephropathy : IP-10 levels were 148.9+/-14.5, 174.2+/-17.2 and 231.9+/-31.3 pg/m/ in patients with an urinary albumin creatinine ratio of <30, 30 to 300 and >300 microg/mg Cr, respectively. |
| 7313 | 16130407 | IP-10 levels became higher with the progression of nephropathy : IP-10 levels were 148.9+/-14.5, 174.2+/-17.2 and 231.9+/-31.3 pg/m/ in patients with an urinary albumin creatinine ratio of <30, 30 to 300 and >300 microg/mg Cr, respectively. |
| 7314 | 16130407 | IP-10 levels became higher with the progression of nephropathy : IP-10 levels were 148.9+/-14.5, 174.2+/-17.2 and 231.9+/-31.3 pg/m/ in patients with an urinary albumin creatinine ratio of <30, 30 to 300 and >300 microg/mg Cr, respectively. |
| 7315 | 16130407 | Similarly, IL-18, IL-6, MCP-1 and TNF-alpha levels in patients with overt albuminuria were significantly higher as compared with those without albuminuria (IL-18, 367.3 45.6 vs 203.5+/-17.6 pg/ml; IL-6, 1.61+/-0.26 vs 0.87+/-0.13 pg/ml; TNF-alpha, 1.83+/-0.48 vs 0.61+/-0.07 pg/ml; p<0.05, respectively) in consistent with previous reports. |
| 7316 | 16130407 | Similarly, IL-18, IL-6, MCP-1 and TNF-alpha levels in patients with overt albuminuria were significantly higher as compared with those without albuminuria (IL-18, 367.3 45.6 vs 203.5+/-17.6 pg/ml; IL-6, 1.61+/-0.26 vs 0.87+/-0.13 pg/ml; TNF-alpha, 1.83+/-0.48 vs 0.61+/-0.07 pg/ml; p<0.05, respectively) in consistent with previous reports. |
| 7317 | 16130407 | Similarly, IL-18, IL-6, MCP-1 and TNF-alpha levels in patients with overt albuminuria were significantly higher as compared with those without albuminuria (IL-18, 367.3 45.6 vs 203.5+/-17.6 pg/ml; IL-6, 1.61+/-0.26 vs 0.87+/-0.13 pg/ml; TNF-alpha, 1.83+/-0.48 vs 0.61+/-0.07 pg/ml; p<0.05, respectively) in consistent with previous reports. |
| 7318 | 16129698 | Six weeks after STZ injection, impairment of left ventricular (LV) function parameters measured by a Millar-tip catheter (peak LV systolic pressure; dP/dtmax; dP/dtmin) was accompanied by a significant increment of ICAM-1 and VCAM-1 (CAMs) expression, as well as of beta2-leukocyte-integrins+ (CD18+, CD11a+, CD11b+) and cytokine (TNF-alpha and IL-1beta)-expressing infiltrates in male Sprague-Dawley (SD-STZ) rats compared with normoglycemic littermates. |
| 7319 | 20476989 | Many immune cytokines are subject to circadian variation, for example, interleukin-1, -6, -10 and -12, macrophage migration inhibitory factor, tumor necrosis factor-alpha and interferon-gamma. |
| 7320 | 16123358 | Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6. |
| 7321 | 16123358 | Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6. |
| 7322 | 16123358 | Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6. |
| 7323 | 16123358 | Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6. |
| 7324 | 16123358 | Based on the presence of mitochondrial dysfunction in insulin-resistant conditions, we have examined whether Mfn2 expression is dysregulated in skeletal muscle from obese or nonobese type 2 diabetic subjects, whether muscle Mfn2 expression is regulated by body weight loss, and the potential regulatory role of tumor necrosis factor (TNF)alpha or interleukin-6. |
| 7325 | 16123358 | Based on the presence of mitochondrial dysfunction in insulin-resistant conditions, we have examined whether Mfn2 expression is dysregulated in skeletal muscle from obese or nonobese type 2 diabetic subjects, whether muscle Mfn2 expression is regulated by body weight loss, and the potential regulatory role of tumor necrosis factor (TNF)alpha or interleukin-6. |
| 7326 | 16123358 | Based on the presence of mitochondrial dysfunction in insulin-resistant conditions, we have examined whether Mfn2 expression is dysregulated in skeletal muscle from obese or nonobese type 2 diabetic subjects, whether muscle Mfn2 expression is regulated by body weight loss, and the potential regulatory role of tumor necrosis factor (TNF)alpha or interleukin-6. |
| 7327 | 16123358 | Based on the presence of mitochondrial dysfunction in insulin-resistant conditions, we have examined whether Mfn2 expression is dysregulated in skeletal muscle from obese or nonobese type 2 diabetic subjects, whether muscle Mfn2 expression is regulated by body weight loss, and the potential regulatory role of tumor necrosis factor (TNF)alpha or interleukin-6. |
| 7328 | 16123358 | A positive correlation between the Mfn2 expression and the insulin sensitivity was also detected in nondiabetic and type 2 diabetic subjects. |
| 7329 | 16123358 | A positive correlation between the Mfn2 expression and the insulin sensitivity was also detected in nondiabetic and type 2 diabetic subjects. |
| 7330 | 16123358 | A positive correlation between the Mfn2 expression and the insulin sensitivity was also detected in nondiabetic and type 2 diabetic subjects. |
| 7331 | 16123358 | A positive correlation between the Mfn2 expression and the insulin sensitivity was also detected in nondiabetic and type 2 diabetic subjects. |
| 7332 | 16123358 | Mean expression of muscle Mfn2 mRNA increased threefold after reduction in body weight, and a positive correlation between muscle Mfn2 expression and insulin sensitivity was again detected. |
| 7333 | 16123358 | Mean expression of muscle Mfn2 mRNA increased threefold after reduction in body weight, and a positive correlation between muscle Mfn2 expression and insulin sensitivity was again detected. |
| 7334 | 16123358 | Mean expression of muscle Mfn2 mRNA increased threefold after reduction in body weight, and a positive correlation between muscle Mfn2 expression and insulin sensitivity was again detected. |
| 7335 | 16123358 | Mean expression of muscle Mfn2 mRNA increased threefold after reduction in body weight, and a positive correlation between muscle Mfn2 expression and insulin sensitivity was again detected. |
| 7336 | 16123358 | In vitro experiments revealed an inhibitory effect of TNFalpha or interleukin-6 on Mfn2 expression in cultured cells. |
| 7337 | 16123358 | In vitro experiments revealed an inhibitory effect of TNFalpha or interleukin-6 on Mfn2 expression in cultured cells. |
| 7338 | 16123358 | In vitro experiments revealed an inhibitory effect of TNFalpha or interleukin-6 on Mfn2 expression in cultured cells. |
| 7339 | 16123358 | In vitro experiments revealed an inhibitory effect of TNFalpha or interleukin-6 on Mfn2 expression in cultured cells. |
| 7340 | 16123358 | We conclude that body weight loss upregulates the expression of Mfn2 mRNA in skeletal muscle of obese humans, type 2 diabetes downregulates the expression of Mfn2 mRNA in skeletal muscle, Mfn2 expression in skeletal muscle is directly proportional to insulin sensitivity and is inversely proportional to the BMI, TNFalpha and interleukin-6 downregulate Mfn2 expression and may participate in the dysregulation of Mfn2 expression in obesity or type 2 diabetes, and the in vivo modulation of Mfn2 mRNA levels is an additional level of regulation for the control of muscle metabolism and could provide a molecular mechanism for alterations in mitochondrial function in obesity or type 2 diabetes. |
| 7341 | 16123358 | We conclude that body weight loss upregulates the expression of Mfn2 mRNA in skeletal muscle of obese humans, type 2 diabetes downregulates the expression of Mfn2 mRNA in skeletal muscle, Mfn2 expression in skeletal muscle is directly proportional to insulin sensitivity and is inversely proportional to the BMI, TNFalpha and interleukin-6 downregulate Mfn2 expression and may participate in the dysregulation of Mfn2 expression in obesity or type 2 diabetes, and the in vivo modulation of Mfn2 mRNA levels is an additional level of regulation for the control of muscle metabolism and could provide a molecular mechanism for alterations in mitochondrial function in obesity or type 2 diabetes. |
| 7342 | 16123358 | We conclude that body weight loss upregulates the expression of Mfn2 mRNA in skeletal muscle of obese humans, type 2 diabetes downregulates the expression of Mfn2 mRNA in skeletal muscle, Mfn2 expression in skeletal muscle is directly proportional to insulin sensitivity and is inversely proportional to the BMI, TNFalpha and interleukin-6 downregulate Mfn2 expression and may participate in the dysregulation of Mfn2 expression in obesity or type 2 diabetes, and the in vivo modulation of Mfn2 mRNA levels is an additional level of regulation for the control of muscle metabolism and could provide a molecular mechanism for alterations in mitochondrial function in obesity or type 2 diabetes. |
| 7343 | 16123358 | We conclude that body weight loss upregulates the expression of Mfn2 mRNA in skeletal muscle of obese humans, type 2 diabetes downregulates the expression of Mfn2 mRNA in skeletal muscle, Mfn2 expression in skeletal muscle is directly proportional to insulin sensitivity and is inversely proportional to the BMI, TNFalpha and interleukin-6 downregulate Mfn2 expression and may participate in the dysregulation of Mfn2 expression in obesity or type 2 diabetes, and the in vivo modulation of Mfn2 mRNA levels is an additional level of regulation for the control of muscle metabolism and could provide a molecular mechanism for alterations in mitochondrial function in obesity or type 2 diabetes. |
| 7344 | 16121292 | Among these were a number of presentations investigating novel anti-inflammatory targets, including the search for a selective COX-2 inhibitor and the potential of cytokines/cytokine receptor targets (eg TNFalpha) as treatments for rheumatoid arthritis (RA) and other chronic inflammatory conditions. |
| 7345 | 16116345 | Plasma lipid and high-sensitivity C-reactive protein (hsCRP) levels, and the release of tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta from monocytes were assessed at baseline and 30 and 90 days following randomization of IIa dyslipidemic patients into fluvastatin or simvastatin groups and randomization of type IIb dyslipidemic patients to the micronized form of either ciprofibrate or fenofibrate. |
| 7346 | 16114068 | Tumor necrosis factor-alpha-induced changes in insulin-producing beta-cells. |
| 7347 | 16114068 | Tumor necrosis factor-alpha-induced changes in insulin-producing beta-cells. |
| 7348 | 16114068 | Tumor necrosis factor-alpha-induced changes in insulin-producing beta-cells. |
| 7349 | 16114068 | Tumor necrosis factor-alpha-induced changes in insulin-producing beta-cells. |
| 7350 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 7351 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 7352 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 7353 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 7354 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 7355 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 7356 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 7357 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 7358 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 7359 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 7360 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 7361 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 7362 | 16112958 | The adipose tissue has been recognized as an important source of metabolically active secretory products (adipocytokines), free fatty acids, leptin, TNF-alpha, Iinterleucin-6, plasminogen activator inhibitor-1, adiponectin and resistin. |
| 7363 | 16112617 | Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans. |
| 7364 | 16112617 | Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans. |
| 7365 | 16112617 | Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans. |
| 7366 | 16112617 | Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. |
| 7367 | 16112617 | Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. |
| 7368 | 16112617 | Elevated plasma IL-18 is present in several conditions sharing insulin-resistance as common trait, but the association with insulin-resistance per se is not established. |
| 7369 | 16112617 | Plasma/serum IL-6, IL-18, TNF-alpha, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). |
| 7370 | 16112617 | Plasma/serum IL-6, IL-18, TNF-alpha, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). |
| 7371 | 16112617 | Plasma/serum IL-6, IL-18, TNF-alpha, soluble TNF receptor II (sTNFR2), and C-reactive protein (CRP) were measured in 97 patients with type 2 diabetes (DM) and 84 non-diabetic controls (CON). |
| 7372 | 16112617 | Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF-alpha was lower (P = 0.017). |
| 7373 | 16112617 | Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF-alpha was lower (P = 0.017). |
| 7374 | 16112617 | Compared to CON, DM demonstrated higher plasma levels of IL-18 (P = 0.001), IL-6 (P < 0.001), sTNFR2 (P = 0.005), and CRP (P < 0.001), while TNF-alpha was lower (P = 0.017). |
| 7375 | 16112617 | In contrast, neither IL-6, TNF-alpha, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. |
| 7376 | 16112617 | In contrast, neither IL-6, TNF-alpha, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. |
| 7377 | 16112617 | In contrast, neither IL-6, TNF-alpha, sTNFR2, nor CRP was associated with HOMA-IR in CON when adjusting for confounders. |
| 7378 | 16100093 | Specifically, it is suggested that the disorder arises because of abnormal expression of the nuclear transcription factor, NFkappaB, in diabetic neuropathy and that this is further enhanced at the onset of the acute arthropathy as a result of the release of proinflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-1. |
| 7379 | 16093309 | Compared to untreated or albumin-control-treated graft recipients, which rejected islets at day 10, AAT-treated mice displayed diminished cellular infiltrates and intact intragraft insulin production throughout treatment. |
| 7380 | 16093309 | In vitro, several islet responses to IL-1beta/IFNgamma stimulation were examined. |
| 7381 | 16093309 | In the presence of AAT, islets displayed enhanced viability and inducible insulin secretion. |
| 7382 | 16093309 | TNFalpha release from IL-1beta/IFNgamma-stimulated islet cells was reduced by 99%, accompanied by an 8-fold increase in the accumulation of membrane TNFalpha on CD45-positive islet cells. |
| 7383 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7384 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7385 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7386 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7387 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7388 | 16081485 | Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. |
| 7389 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7390 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7391 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7392 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7393 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7394 | 16081485 | We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. |
| 7395 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7396 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7397 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7398 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7399 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7400 | 16081485 | Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. |
| 7401 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7402 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7403 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7404 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7405 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7406 | 16081485 | IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. |
| 7407 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7408 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7409 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7410 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7411 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7412 | 16081485 | IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. |
| 7413 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7414 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7415 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7416 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7417 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7418 | 16081485 | Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. |
| 7419 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7420 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7421 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7422 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7423 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7424 | 16081485 | Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. |
| 7425 | 16080843 | [The role of tumor necrosis factor alpha and leptin in obesity and insulin resistance]. |
| 7426 | 16054232 | Prolactin regulation of the expression of TNF-alpha, IFN-gamma and IL-10 by splenocytes in murine multiple low dose streptozotocin diabetes. |
| 7427 | 16054232 | Prolactin regulation of the expression of TNF-alpha, IFN-gamma and IL-10 by splenocytes in murine multiple low dose streptozotocin diabetes. |
| 7428 | 16054232 | Prolactin regulation of the expression of TNF-alpha, IFN-gamma and IL-10 by splenocytes in murine multiple low dose streptozotocin diabetes. |
| 7429 | 16054232 | Spleen cell preparations depleted in erythrocytes and macrophages were stained for cytoplasmic TNF-alpha, IFN-gamma and IL-10 and analyzed with flow cytometry. |
| 7430 | 16054232 | Spleen cell preparations depleted in erythrocytes and macrophages were stained for cytoplasmic TNF-alpha, IFN-gamma and IL-10 and analyzed with flow cytometry. |
| 7431 | 16054232 | Spleen cell preparations depleted in erythrocytes and macrophages were stained for cytoplasmic TNF-alpha, IFN-gamma and IL-10 and analyzed with flow cytometry. |
| 7432 | 16054232 | Freshly isolated spleen cell preparations from PRL and STZ+PRL treated animals seemed to have an increased frequency of IL-10 positive cells compared to controls. |
| 7433 | 16054232 | Freshly isolated spleen cell preparations from PRL and STZ+PRL treated animals seemed to have an increased frequency of IL-10 positive cells compared to controls. |
| 7434 | 16054232 | Freshly isolated spleen cell preparations from PRL and STZ+PRL treated animals seemed to have an increased frequency of IL-10 positive cells compared to controls. |
| 7435 | 16054232 | In cultured spleen cells isolated from STZ treated mice, IFN-gamma and IL-10 mRNA expression was up-regulated. |
| 7436 | 16054232 | In cultured spleen cells isolated from STZ treated mice, IFN-gamma and IL-10 mRNA expression was up-regulated. |
| 7437 | 16054232 | In cultured spleen cells isolated from STZ treated mice, IFN-gamma and IL-10 mRNA expression was up-regulated. |
| 7438 | 16054232 | PRL treatment down-regulated the mRNA expression of these cytokines and also TNF-alpha in the splenocytes obtained from animals treated with STZ. |
| 7439 | 16054232 | PRL treatment down-regulated the mRNA expression of these cytokines and also TNF-alpha in the splenocytes obtained from animals treated with STZ. |
| 7440 | 16054232 | PRL treatment down-regulated the mRNA expression of these cytokines and also TNF-alpha in the splenocytes obtained from animals treated with STZ. |
| 7441 | 16046295 | Expression of CD68 and macrophage chemoattractant protein-1 genes in human adipose and muscle tissues: association with cytokine expression, insulin resistance, and reduction by pioglitazone. |
| 7442 | 16046295 | Expression of CD68 and macrophage chemoattractant protein-1 genes in human adipose and muscle tissues: association with cytokine expression, insulin resistance, and reduction by pioglitazone. |
| 7443 | 16046295 | To examine the role of adipose-resident macrophages in insulin resistance, we examined the gene expression of CD68, a macrophage marker, along with macrophage chemoattractant protein-1 (MCP-1) in human subcutaneous adipose tissue using real-time RT-PCR. |
| 7444 | 16046295 | To examine the role of adipose-resident macrophages in insulin resistance, we examined the gene expression of CD68, a macrophage marker, along with macrophage chemoattractant protein-1 (MCP-1) in human subcutaneous adipose tissue using real-time RT-PCR. |
| 7445 | 16046295 | Both CD68 and MCP-1 mRNAs were expressed in human adipose tissue, primarily in the stromal vascular fraction. |
| 7446 | 16046295 | Both CD68 and MCP-1 mRNAs were expressed in human adipose tissue, primarily in the stromal vascular fraction. |
| 7447 | 16046295 | When measured in the adipose tissue from subjects with normal glucose tolerance, covering a wide range of BMI (21-51 kg/m2) and insulin sensitivity (S(I)) (0.6-8.0 x 10(-4)min(-1).microU(-1).ml(-1)), CD68 mRNA abundance, which correlated with the number of CD68-positive cells by immunohistochemistry, tended to increase with BMI but was not statistically significant. |
| 7448 | 16046295 | When measured in the adipose tissue from subjects with normal glucose tolerance, covering a wide range of BMI (21-51 kg/m2) and insulin sensitivity (S(I)) (0.6-8.0 x 10(-4)min(-1).microU(-1).ml(-1)), CD68 mRNA abundance, which correlated with the number of CD68-positive cells by immunohistochemistry, tended to increase with BMI but was not statistically significant. |
| 7449 | 16046295 | In addition, there was a strong positive relationship among adipose tissue CD68 mRNA, tumor necrosis factor-alpha (TNF-alpha) secretion in vitro (r=0.79, P<0.005), and plasma interleukin-6 (r=0.67, P < 0.005). |
| 7450 | 16046295 | In addition, there was a strong positive relationship among adipose tissue CD68 mRNA, tumor necrosis factor-alpha (TNF-alpha) secretion in vitro (r=0.79, P<0.005), and plasma interleukin-6 (r=0.67, P < 0.005). |
| 7451 | 16046295 | Pioglitazone increased S(I) by 60% and in the same subjects reduced both CD68 and MCP-1 mRNAs by >50%. |
| 7452 | 16046295 | Pioglitazone increased S(I) by 60% and in the same subjects reduced both CD68 and MCP-1 mRNAs by >50%. |
| 7453 | 16046295 | Furthermore, pioglitazone resulted in a reduction in the number of CD68-positive cells in adipose tissue and reduced plasma TNF-alpha. |
| 7454 | 16046295 | Furthermore, pioglitazone resulted in a reduction in the number of CD68-positive cells in adipose tissue and reduced plasma TNF-alpha. |
| 7455 | 16046295 | Thus, treatment with pioglitazone reduces expression of CD68 and MCP-1 in adipose tissue, apparently by reducing macrophage numbers, resulting in reduced inflammatory cytokine production and improvement in S(I). |
| 7456 | 16046295 | Thus, treatment with pioglitazone reduces expression of CD68 and MCP-1 in adipose tissue, apparently by reducing macrophage numbers, resulting in reduced inflammatory cytokine production and improvement in S(I). |
| 7457 | 16046222 | The cysteine protease inhibitor cystatin-C may be involved in this phenomenon. |
| 7458 | 16046222 | Cystatin-C was positively correlated with body mass index (BMI), low-density lipoprotein (LDL)-cholesterol, triglycerides and several inflammatory markers such as fibrinogen (r = 0.18), C-reactive protein (CRP) (r = 0.24), interleukin-6 (= 0.20), tumor necrosis factor-alpha (TNFalpha) (r = 0.27) and two TNFalpha receptors: TNFR1A (r = 0.43) and TNFR1B (r = 0.41); and negatively with high-density lipoprotein (HDL)-cholesterol (r = -0.25). |
| 7459 | 16046222 | Cystatin-C is not a more predictive risk marker of CHD than CRP or interleukin-6, but could be useful in detecting moderate chronic renal disease. |
| 7460 | 16043194 | Physical exercise increases the expression of TNFalpha and GLUT 1 in muscle tissue of diabetes prone Psammomys obesus. |
| 7461 | 16039994 | Human resistin stimulates the pro-inflammatory cytokines TNF-alpha and IL-12 in macrophages by NF-kappaB-dependent pathway. |
| 7462 | 16039994 | Human resistin stimulates the pro-inflammatory cytokines TNF-alpha and IL-12 in macrophages by NF-kappaB-dependent pathway. |
| 7463 | 16039994 | Human resistin stimulates the pro-inflammatory cytokines TNF-alpha and IL-12 in macrophages by NF-kappaB-dependent pathway. |
| 7464 | 16039994 | Resistin, a recently discovered 92 amino acid protein involved in the development of insulin resistance, has been associated with obesity and type 2 diabetes. |
| 7465 | 16039994 | Resistin, a recently discovered 92 amino acid protein involved in the development of insulin resistance, has been associated with obesity and type 2 diabetes. |
| 7466 | 16039994 | Resistin, a recently discovered 92 amino acid protein involved in the development of insulin resistance, has been associated with obesity and type 2 diabetes. |
| 7467 | 16039994 | Addition of recombinant human resistin protein (hResistin) to macrophages (both murine and human) resulted in enhanced secretion of pro-inflammatory cytokines, TNF-alpha and IL-12, similar to that obtained using 5 microg/ml lipopolysaccharide. |
| 7468 | 16039994 | Addition of recombinant human resistin protein (hResistin) to macrophages (both murine and human) resulted in enhanced secretion of pro-inflammatory cytokines, TNF-alpha and IL-12, similar to that obtained using 5 microg/ml lipopolysaccharide. |
| 7469 | 16039994 | Addition of recombinant human resistin protein (hResistin) to macrophages (both murine and human) resulted in enhanced secretion of pro-inflammatory cytokines, TNF-alpha and IL-12, similar to that obtained using 5 microg/ml lipopolysaccharide. |
| 7470 | 16039994 | Induction of TNF-alpha in U937 cells by hResistin was markedly reduced in the presence of either dominant negative IkappaBalpha plasmid or PDTC, a pharmacological inhibitor of NF-kappaB. |
| 7471 | 16039994 | Induction of TNF-alpha in U937 cells by hResistin was markedly reduced in the presence of either dominant negative IkappaBalpha plasmid or PDTC, a pharmacological inhibitor of NF-kappaB. |
| 7472 | 16039994 | Induction of TNF-alpha in U937 cells by hResistin was markedly reduced in the presence of either dominant negative IkappaBalpha plasmid or PDTC, a pharmacological inhibitor of NF-kappaB. |
| 7473 | 16035296 | These include tumor necrosis factors (TNF)-alpha, leptin, resistin, adiponectin or visfatin. |
| 7474 | 16035296 | These include tumor necrosis factors (TNF)-alpha, leptin, resistin, adiponectin or visfatin. |
| 7475 | 16035296 | These include tumor necrosis factors (TNF)-alpha, leptin, resistin, adiponectin or visfatin. |
| 7476 | 16035296 | Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of leptin, resistin or TNF-alpha in obesity, its level is negatively correlated with body mass index, and is decreased in presence of insulin resistance and in type 2 diabetes. |
| 7477 | 16035296 | Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of leptin, resistin or TNF-alpha in obesity, its level is negatively correlated with body mass index, and is decreased in presence of insulin resistance and in type 2 diabetes. |
| 7478 | 16035296 | Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of leptin, resistin or TNF-alpha in obesity, its level is negatively correlated with body mass index, and is decreased in presence of insulin resistance and in type 2 diabetes. |
| 7479 | 16035296 | For instance, thiazolidinediones treatment in patients with type 2 diabetes resulted in an increased in plasma adiponectin levels and a decrease in circulating TNF-alpha concentrations. |
| 7480 | 16035296 | For instance, thiazolidinediones treatment in patients with type 2 diabetes resulted in an increased in plasma adiponectin levels and a decrease in circulating TNF-alpha concentrations. |
| 7481 | 16035296 | For instance, thiazolidinediones treatment in patients with type 2 diabetes resulted in an increased in plasma adiponectin levels and a decrease in circulating TNF-alpha concentrations. |
| 7482 | 16034719 | Tumor necrosis factor alpha system and plasma adiponectin concentration in women with gestational diabetes. |
| 7483 | 16034719 | Tumor necrosis factor alpha system and plasma adiponectin concentration in women with gestational diabetes. |
| 7484 | 16034719 | Tumor necrosis factor alpha system and plasma adiponectin concentration in women with gestational diabetes. |
| 7485 | 16034719 | Plasma concentrations of adiponectin, tumor necrosis factor-alpha (TNF-alpha) and its soluble receptors sTNFR-1 and sTNFR-2 were measured in 80 patients with gestational diabetes (GDM) (mean age 29.0 +/- 4.9 years) and 30 pregnant women with normal glucose tolerance (NGT) (mean age 28.2 +/- 6.0 years). |
| 7486 | 16034719 | Plasma concentrations of adiponectin, tumor necrosis factor-alpha (TNF-alpha) and its soluble receptors sTNFR-1 and sTNFR-2 were measured in 80 patients with gestational diabetes (GDM) (mean age 29.0 +/- 4.9 years) and 30 pregnant women with normal glucose tolerance (NGT) (mean age 28.2 +/- 6.0 years). |
| 7487 | 16034719 | Plasma concentrations of adiponectin, tumor necrosis factor-alpha (TNF-alpha) and its soluble receptors sTNFR-1 and sTNFR-2 were measured in 80 patients with gestational diabetes (GDM) (mean age 29.0 +/- 4.9 years) and 30 pregnant women with normal glucose tolerance (NGT) (mean age 28.2 +/- 6.0 years). |
| 7488 | 16034719 | We found that GDM patients had significantly lower concentrations of adiponectin (11.28 +/- 5.91 vs. 16.31 +/- 6.04 microg/ml, p = 0.00009) and elevated levels of TNF-alpha (1.71 +/- 0.92 vs. 1.27 +/- 0.42 pg/ml, p = 0.0175) in comparison to NGT women. |
| 7489 | 16034719 | We found that GDM patients had significantly lower concentrations of adiponectin (11.28 +/- 5.91 vs. 16.31 +/- 6.04 microg/ml, p = 0.00009) and elevated levels of TNF-alpha (1.71 +/- 0.92 vs. 1.27 +/- 0.42 pg/ml, p = 0.0175) in comparison to NGT women. |
| 7490 | 16034719 | We found that GDM patients had significantly lower concentrations of adiponectin (11.28 +/- 5.91 vs. 16.31 +/- 6.04 microg/ml, p = 0.00009) and elevated levels of TNF-alpha (1.71 +/- 0.92 vs. 1.27 +/- 0.42 pg/ml, p = 0.0175) in comparison to NGT women. |
| 7491 | 16034719 | In conclusion, our results suggest that decreased adiponectin concentration in GDM may not simply reflect maternal adiposity and insulin resistant state, but may contribute to the impaired glucose metabolism during pregnancy, with potential implications for screening and prevention of the disease. |
| 7492 | 16034719 | In conclusion, our results suggest that decreased adiponectin concentration in GDM may not simply reflect maternal adiposity and insulin resistant state, but may contribute to the impaired glucose metabolism during pregnancy, with potential implications for screening and prevention of the disease. |
| 7493 | 16034719 | In conclusion, our results suggest that decreased adiponectin concentration in GDM may not simply reflect maternal adiposity and insulin resistant state, but may contribute to the impaired glucose metabolism during pregnancy, with potential implications for screening and prevention of the disease. |
| 7494 | 16032528 | Immunological analyses of the KORA Survey S4 (1999/2001) allowed us to show that levels of circulating acute-phase proteins like CRP and of IL-6 are highly correlated and associated not only with overt type 2 diabetes, but already with impaired glucose tolerance (IGT) pointing out a role of these mediators in the pathogenesis of type 2 diabetes. |
| 7495 | 16032528 | On the contrary, TNFalpha was neither coregulated with CRP nor associated with diabetes status. |
| 7496 | 16030142 | Vaspin was barely detectable in rats at 6 wk and was highly expressed in adipocytes of visceral WATs at 30 wk, the age when obesity, body weight, and insulin levels peak in OLETF rats. |
| 7497 | 16030142 | Administration of vaspin to obese CRL:CD-1 (ICR) (ICR) mice fed with high-fat high-sucrose chow improved glucose tolerance and insulin sensitivity reflected by normalized serum glucose levels. |
| 7498 | 16030142 | It also led to the reversal of altered expression of genes relevant to insulin resistance, e.g., leptin, resistin, TNFalpha, glucose transporter-4, and adiponectin. |
| 7499 | 16030142 | These findings indicate that vaspin exerts an insulin-sensitizing effect targeted toward WATs in states of obesity. |
| 7500 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7501 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7502 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7503 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7504 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7505 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7506 | 16025396 | PGE1 inhibits the expression of PAI-1 mRNA induced by TNF-alpha in human mesangial cells. |
| 7507 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7508 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7509 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7510 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7511 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7512 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7513 | 16025396 | We examined the effect of PGE1 on the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA induced by tumor necrosis factor-alpha (TNF-alpha) in human mesangial cells, because PAI-1 is one of major factors for the progression of glomerulosclerosis. |
| 7514 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7515 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7516 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7517 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7518 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7519 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7520 | 16025396 | The expression of PAI-1 mRNA was increased after stimulation with TNF-alpha, and it was diminished by pre-incubation with PGE1. |
| 7521 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7522 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7523 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7524 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7525 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7526 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7527 | 16025396 | Next, we examined the effect of PGE1 on the phosphorylation of mitogen activated protein kinase (MAPK) family and Akt. |
| 7528 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7529 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7530 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7531 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7532 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7533 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7534 | 16025396 | TNF-alpha activated the phosphorylation of p44/42 MAPK, p38 MAPK, SAPK/JNK and Akt in mesangial cells. |
| 7535 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7536 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7537 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7538 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7539 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7540 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7541 | 16025396 | PGE1 inhibited the TNF-alpha induced phosphorylation of SAPK/JNK and Akt, but not p44/42 MAPK and p38 MAPK. |
| 7542 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7543 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7544 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7545 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7546 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7547 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7548 | 16025396 | The TNF-alpha induced expression of PAI-1 mRNA was not affected by PD98059, an inhibitor of MEK, SB203580, an inhibitor of p38 MAPK, nor LY294002, an inhibitor of PI3 K. |
| 7549 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7550 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7551 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7552 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7553 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7554 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7555 | 16025396 | However, DMAP, an inhibitor of SAPK/JNK, inhibited the expression of PAI-1 mRNA, suggesting that the TNF-alpha induced expression of PAI-1 mRNA is regulated by the SAPK/JNK dependent pathway in human mesangial cells. |
| 7556 | 16023759 | The matrix metalloproteinase system (MMP and the TIMP inhibitors), and the ADAM metalloproteinases, have roles in maintaining vascular plaque stability and the shedding of cell surface molecules, such as TNF-alpha and adhesion molecules; aspirin suppresses MMP expression and ADAM activity from some cell lines in vitro. |
| 7557 | 16023759 | In a randomised prospective controlled study, we examined peripheral venous monocyte MMP-9, TIMP-1 and ADAM mRNA levels, and protein expression, in subjects with type 2 diabetes (n=10) and controls (n=14) before and after oral aspirin therapy (150mg daily for 14 days) or no active intervention. |
| 7558 | 16023759 | Baseline monocyte TIMP-1 mRNA levels were significantly lower in the diabetes group (p=0.0014), although monocyte MMP-9 mRNA, and MMP-9 and TIMP-1 protein expression after culture did not differ significantly between groups. |
| 7559 | 16023759 | Plasma MMP-9 (p=0.027) and TIMP-1 (p=0.016) concentrations were significantly greater, and the ratio of plasma TIMP-1:MMP-9 concentrations significantly lower, in the diabetes group (p=0.023). |
| 7560 | 16023759 | Type 2 diabetes is characterised by reduced monocyte TIMP-1 mRNA levels, and a lower plasma MMP-9 to TIMP-1 protein ratio compared to controls, a pattern that would promote coronary plaque instability if reproduced within vascular plaque. |
| 7561 | 16010587 | Th1 cells, characterized by secretion of IFN-gamma and TNF-alpha, are primarily responsible for activating and regulating the development and persistence of CTL. |
| 7562 | 16006032 | Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells. |
| 7563 | 16006032 | Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells. |
| 7564 | 16006032 | Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells. |
| 7565 | 16006032 | PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy. |
| 7566 | 16006032 | PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy. |
| 7567 | 16006032 | PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy. |
| 7568 | 16006032 | Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls. |
| 7569 | 16006032 | Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls. |
| 7570 | 16006032 | Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls. |
| 7571 | 16006032 | IL-1beta or TNFalpha alone had no effect. |
| 7572 | 16006032 | IL-1beta or TNFalpha alone had no effect. |
| 7573 | 16006032 | IL-1beta or TNFalpha alone had no effect. |
| 7574 | 16006032 | Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone. |
| 7575 | 16006032 | Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone. |
| 7576 | 16006032 | Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone. |
| 7577 | 16006032 | Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death. |
| 7578 | 16006032 | Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death. |
| 7579 | 16006032 | Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death. |
| 7580 | 16002729 | We analyzed the mechanism whereby isolated islets from ALR mice resisted proinflammatory stress mediated by combined cytokines (IL-1beta, TNF-alpha, and IFN-gamma) in vitro. |
| 7581 | 16002729 | In contrast to islets from other mouse strains, ALR islets expressed constitutively higher glutathione reductase, glutathione peroxidase, and higher ratios of reduced to oxidized glutathione. |
| 7582 | 16002729 | Western blot analysis showed that combined cytokines up-regulated the NF-kappaB inducible NO synthase in NOD-Rag and C3H/HeJ islets but not in ALR islets. |
| 7583 | 16002729 | This inability of cytokine-treated ALR islets to up-regulate inducible NO synthase and produce NO correlated both with reduced kinetics of IkappaB degradation and with markedly suppressed NF-kappaB p65 nuclear translocation. |
| 7584 | 16002729 | Hence, ALR/Lt islets resist cytokine-induced diabetogenic stress through enhanced dissipation and/or suppressed formation of reactive oxygen and nitrogen species, impaired IkappaB degradation, and blunted NF-kappaB activation. |
| 7585 | 15998581 | In the current report we reduce the size of the Idd9.3 interval to 1.2Mb containing 15 genes, including one encoding the immune signaling molecule, 4-1BB, which shows amino acid variation between diabetes sensitive and resistant strains. 4-1BB, a member of the TNF receptor superfamily expressed by a variety of immune cells, mediates growth and survival signals for T cells. |
| 7586 | 15998581 | Functional analyses demonstrate that purified T cells from NOD congenic mice with the C57BL/10 (B10) allele at Idd9.3 produce more IL-2 and proliferate more vigorously in response to anti-CD3 plus immobilized 4-1BB ligand than T cells from NOD mice with the NOD allele at Idd9.3. |
| 7587 | 15997235 | Additionally, Amadori adducts significantly increased the production of NF-kappaB-related proinflammatory molecules, including cytokines, such as TNF-alpha, IL-1beta or IL-6, and enzymes, such as cyclooxygenase-2 and inducible nitric oxide (NO) synthase, this latter leading to the release of NO by HPMCs. |
| 7588 | 15992611 | 1267 HSP70-2 polymorphism as a risk factor for carotid plaque rupture and cerebral ischaemia in old type 2 diabetes-atherosclerotic patients. |
| 7589 | 15992611 | 1267 HSP70-2 polymorphism as a risk factor for carotid plaque rupture and cerebral ischaemia in old type 2 diabetes-atherosclerotic patients. |
| 7590 | 15992611 | 1267 HSP70-2 polymorphism as a risk factor for carotid plaque rupture and cerebral ischaemia in old type 2 diabetes-atherosclerotic patients. |
| 7591 | 15992611 | 1267 HSP70-2 polymorphism as a risk factor for carotid plaque rupture and cerebral ischaemia in old type 2 diabetes-atherosclerotic patients. |
| 7592 | 15992611 | IFN-gamma inhibits collagen synthesis thereby affecting plaque stability. |
| 7593 | 15992611 | IFN-gamma inhibits collagen synthesis thereby affecting plaque stability. |
| 7594 | 15992611 | IFN-gamma inhibits collagen synthesis thereby affecting plaque stability. |
| 7595 | 15992611 | IFN-gamma inhibits collagen synthesis thereby affecting plaque stability. |
| 7596 | 15992611 | High IL-6, TNF-alpha, and dyslipidemia are risk factors for thrombosis. |
| 7597 | 15992611 | High IL-6, TNF-alpha, and dyslipidemia are risk factors for thrombosis. |
| 7598 | 15992611 | High IL-6, TNF-alpha, and dyslipidemia are risk factors for thrombosis. |
| 7599 | 15992611 | High IL-6, TNF-alpha, and dyslipidemia are risk factors for thrombosis. |
| 7600 | 15992611 | Abnormal increments of HSP70 in atherosclerotic plaques might lead to plaque instability and rupture caused by chronic inflammation, which up-regulates the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha) in human monocytes. |
| 7601 | 15992611 | Abnormal increments of HSP70 in atherosclerotic plaques might lead to plaque instability and rupture caused by chronic inflammation, which up-regulates the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha) in human monocytes. |
| 7602 | 15992611 | Abnormal increments of HSP70 in atherosclerotic plaques might lead to plaque instability and rupture caused by chronic inflammation, which up-regulates the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha) in human monocytes. |
| 7603 | 15992611 | Abnormal increments of HSP70 in atherosclerotic plaques might lead to plaque instability and rupture caused by chronic inflammation, which up-regulates the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha) in human monocytes. |
| 7604 | 15992611 | Studies of a polymorphic PstI site lying in the coding region at position 1267 of the HSP70-2 gene have shown that the BB genotype is associated with NIDDM. |
| 7605 | 15992611 | Studies of a polymorphic PstI site lying in the coding region at position 1267 of the HSP70-2 gene have shown that the BB genotype is associated with NIDDM. |
| 7606 | 15992611 | Studies of a polymorphic PstI site lying in the coding region at position 1267 of the HSP70-2 gene have shown that the BB genotype is associated with NIDDM. |
| 7607 | 15992611 | Studies of a polymorphic PstI site lying in the coding region at position 1267 of the HSP70-2 gene have shown that the BB genotype is associated with NIDDM. |
| 7608 | 15992611 | We screened 60 old NIDDM patients with carotid stenosis and 107 old healthy controls for 1267 HSP70-2 polymorphism in order to establish if an association with plaque frailty exists. |
| 7609 | 15992611 | We screened 60 old NIDDM patients with carotid stenosis and 107 old healthy controls for 1267 HSP70-2 polymorphism in order to establish if an association with plaque frailty exists. |
| 7610 | 15992611 | We screened 60 old NIDDM patients with carotid stenosis and 107 old healthy controls for 1267 HSP70-2 polymorphism in order to establish if an association with plaque frailty exists. |
| 7611 | 15992611 | We screened 60 old NIDDM patients with carotid stenosis and 107 old healthy controls for 1267 HSP70-2 polymorphism in order to establish if an association with plaque frailty exists. |
| 7612 | 15992611 | HSP70-2, IL-6, IFN-gamma, TNF-alpha gene expressions within the plaques and serum levels of triglyceride, total cholesterol and LDL cholesterol were tested from patients stratified according to their B+ (AB and BB) and B- (AA) genotypes. |
| 7613 | 15992611 | HSP70-2, IL-6, IFN-gamma, TNF-alpha gene expressions within the plaques and serum levels of triglyceride, total cholesterol and LDL cholesterol were tested from patients stratified according to their B+ (AB and BB) and B- (AA) genotypes. |
| 7614 | 15992611 | HSP70-2, IL-6, IFN-gamma, TNF-alpha gene expressions within the plaques and serum levels of triglyceride, total cholesterol and LDL cholesterol were tested from patients stratified according to their B+ (AB and BB) and B- (AA) genotypes. |
| 7615 | 15992611 | HSP70-2, IL-6, IFN-gamma, TNF-alpha gene expressions within the plaques and serum levels of triglyceride, total cholesterol and LDL cholesterol were tested from patients stratified according to their B+ (AB and BB) and B- (AA) genotypes. |
| 7616 | 15992611 | B+ patients showed increased HSP70-2, IL-6, IFN-gamma, TNF-alpha and dyslipidemia as compared to B- carriers. |
| 7617 | 15992611 | B+ patients showed increased HSP70-2, IL-6, IFN-gamma, TNF-alpha and dyslipidemia as compared to B- carriers. |
| 7618 | 15992611 | B+ patients showed increased HSP70-2, IL-6, IFN-gamma, TNF-alpha and dyslipidemia as compared to B- carriers. |
| 7619 | 15992611 | B+ patients showed increased HSP70-2, IL-6, IFN-gamma, TNF-alpha and dyslipidemia as compared to B- carriers. |
| 7620 | 15992611 | A higher frequency of cerebral ischaemia (ictus or transient ischaemic attack (TIA)) was present in B+ than in B- genotype (53% versus 20%; odds ratio 4.57, p < 0.05) Hence, 1267 HSP70-2 polymorphism may be of use in identifying B+ NIDDM patients at risk for carotid plaque rupture and cerebral ischaemia. |
| 7621 | 15992611 | A higher frequency of cerebral ischaemia (ictus or transient ischaemic attack (TIA)) was present in B+ than in B- genotype (53% versus 20%; odds ratio 4.57, p < 0.05) Hence, 1267 HSP70-2 polymorphism may be of use in identifying B+ NIDDM patients at risk for carotid plaque rupture and cerebral ischaemia. |
| 7622 | 15992611 | A higher frequency of cerebral ischaemia (ictus or transient ischaemic attack (TIA)) was present in B+ than in B- genotype (53% versus 20%; odds ratio 4.57, p < 0.05) Hence, 1267 HSP70-2 polymorphism may be of use in identifying B+ NIDDM patients at risk for carotid plaque rupture and cerebral ischaemia. |
| 7623 | 15992611 | A higher frequency of cerebral ischaemia (ictus or transient ischaemic attack (TIA)) was present in B+ than in B- genotype (53% versus 20%; odds ratio 4.57, p < 0.05) Hence, 1267 HSP70-2 polymorphism may be of use in identifying B+ NIDDM patients at risk for carotid plaque rupture and cerebral ischaemia. |
| 7624 | 15991565 | Both associations between the inflammatory mediators as CRP, fibrinogen, alpha1-glycoproteins, leptin, TNFalpha, PAI-1 and the metabolic syndrome variables, chiefly obesity, seem to suggest that both atherosclerosis and insulin resistance are the results of chronic activation of the nonspecific (innate) immune system. |
| 7625 | 15991254 | Surrogate markers for this low-grade chronic inflammation include CRP, IL-6 and TNF-alpha. |
| 7626 | 15988694 | Plasma resistin levels were not altered by the 3 interventions from pre- to posttreatment (D: pre = 6.9 +/- 0.6, post = 6.2 +/- 0.4 ng/mL; D + E: pre = 5.6 +/- 0.6, post = 5.7 +/- 0.4 ng/mL; E: pre = 6.2 +/- 0.6, post = 5.9 +/- 0.6 ng/mL, P > .05), and no differences in adiponectin and tumor necrosis factor alpha (TNF- alpha ) levels were found. |
| 7627 | 15983205 | With progressive islet infiltration, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were expressed in immune cells but not in beta-cells. |
| 7628 | 15983205 | With progressive islet infiltration, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were expressed in immune cells but not in beta-cells. |
| 7629 | 15983205 | The observed coincidence of IL-1beta and TNF-alpha expression in the immune cells and the induction of iNOS and procaspase 3 mRNA expression in the beta-cells depicts a sequence of pathological changes leading to apoptotic beta-cell death in the IDDM rat. |
| 7630 | 15983205 | The observed coincidence of IL-1beta and TNF-alpha expression in the immune cells and the induction of iNOS and procaspase 3 mRNA expression in the beta-cells depicts a sequence of pathological changes leading to apoptotic beta-cell death in the IDDM rat. |
| 7631 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 7632 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 7633 | 15975818 | Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). |
| 7634 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 7635 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 7636 | 15975818 | Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. |
| 7637 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 7638 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 7639 | 15975818 | Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. |
| 7640 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 7641 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 7642 | 15975818 | Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. |
| 7643 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 7644 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 7645 | 15975818 | Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease. |
| 7646 | 15971149 | This study was mainly aimed at investigating the effect of potential inhibitors of distinct protein kinases and protein phosphatase-1 upon insulin- and GLP-1-stimulated 2-deoxy-D-glucose net uptake by normal rat skeletal muscle. |
| 7647 | 15971149 | The basal uptake of the D-glucose analog was decreased by wortmannin--a phosphatidylinositol-3-kinase inhibitor--, PD98059--a mitogen-activated protein kinases inhibitor--, and TNFalpha--a protein phosphatase-1 inhibitor--, but not by either rapamycin--a p70s6 kinase inhibitor--, or H-7--, a protein kinase C inhibitor--. |
| 7648 | 15971149 | The enhancing action of both insulin and GLP-1 upon 2-deoxy-D-glucose transport was abolished by PD98059 and H-7, but largely unaffected by TNFalpha. |
| 7649 | 15955385 | Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. |
| 7650 | 15952917 | Among those, adiponectin, visfatin and omentin appear as insulin-sensitising adipocytokines, whereas TNF-alpha, IL-6 and resistin induce insulin resistance. |
| 7651 | 15952088 | Association of humoral immunity to human Hsp60 with the IL-6 gene polymorphism C-174G in patients with type 2 diabetes and controls. |
| 7652 | 15952088 | There was no significant association to age and sex, or to key clinical or metabolic parameters (BMI, WHR, HbA1c, total cholesterol, LDL cholesterol, HDL cholesterol, systolic and diastolic blood pressure, albumin, uric acid) or immunological parameters (CRP, IL-6, sIL-6R, TNFalpha, sTNFalpha R60, sTNFalpha R80). |
| 7653 | 15936183 | The effect of PPARgamma ligands on the adipose tissue in insulin resistance. |
| 7654 | 15936183 | Elevated levels of various cytokines, such as TNF-alpha and IL-6, are typically found in the adipose tissue in these conditions. |
| 7655 | 15936183 | Peroxisome proliferator-activated receptor (PPAR)gamma is essential for adipocyte proliferation and differentiation. |
| 7656 | 15936183 | In recent years, PPARgamma and its ligands, the thiazolidinediones (TZD), have achieved great attention due to their insulin sensitizing and anti-inflammatory properties. |
| 7657 | 15936183 | Treatment with TZDs result in improved insulin signaling and adipocyte differentiation, increased adipose tissue influx of free fatty acids and inhibition of cytokine expression and action. |
| 7658 | 15935983 | Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis. |
| 7659 | 15935983 | Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis. |
| 7660 | 15935983 | Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis. |
| 7661 | 15935983 | Insulin-like growth factors (IGFs) and their high affinity binding proteins (IGFBPs) exert major actions on mesangial cell survival, but their underlying mechanisms remain unclear. |
| 7662 | 15935983 | Insulin-like growth factors (IGFs) and their high affinity binding proteins (IGFBPs) exert major actions on mesangial cell survival, but their underlying mechanisms remain unclear. |
| 7663 | 15935983 | Insulin-like growth factors (IGFs) and their high affinity binding proteins (IGFBPs) exert major actions on mesangial cell survival, but their underlying mechanisms remain unclear. |
| 7664 | 15935983 | Anti-sense IGFBP-3 oligo at 10 microg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-alpha, serum-free conditions, or high (25 mM) glucose. |
| 7665 | 15935983 | Anti-sense IGFBP-3 oligo at 10 microg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-alpha, serum-free conditions, or high (25 mM) glucose. |
| 7666 | 15935983 | Anti-sense IGFBP-3 oligo at 10 microg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-alpha, serum-free conditions, or high (25 mM) glucose. |
| 7667 | 15935983 | Increased IGFBP-3 release associated with high ambient glucose or TNF-alpha was inhibited by pre-treatment with anti-sense oligo. |
| 7668 | 15935983 | Increased IGFBP-3 release associated with high ambient glucose or TNF-alpha was inhibited by pre-treatment with anti-sense oligo. |
| 7669 | 15935983 | Increased IGFBP-3 release associated with high ambient glucose or TNF-alpha was inhibited by pre-treatment with anti-sense oligo. |
| 7670 | 15935983 | Under serum-free conditions, recombinant human IGFBP-3 blocked Akt phosphorylation at threonine 308 (pThr308), whereas anti-sense oligo treatment was associated with enhanced pThr308 activity. |
| 7671 | 15935983 | Under serum-free conditions, recombinant human IGFBP-3 blocked Akt phosphorylation at threonine 308 (pThr308), whereas anti-sense oligo treatment was associated with enhanced pThr308 activity. |
| 7672 | 15935983 | Under serum-free conditions, recombinant human IGFBP-3 blocked Akt phosphorylation at threonine 308 (pThr308), whereas anti-sense oligo treatment was associated with enhanced pThr308 activity. |
| 7673 | 15935983 | In summary, these data support a novel mechanism for TNF-alpha-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action. |
| 7674 | 15935983 | In summary, these data support a novel mechanism for TNF-alpha-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action. |
| 7675 | 15935983 | In summary, these data support a novel mechanism for TNF-alpha-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action. |
| 7676 | 15925276 | Gene therapy and gene transfer, including site- and organ-specific targeted gene transfer, have become powerful tools for studying the potential role of HO-1/HO-2 in the treatment of various cardiovascular diseases as well as diabetes. |
| 7677 | 15925276 | HO-1 induction by pharmacological agents or gene transfer of human HO-1 into endothelial cells (ECs) in vitro increases cell-cycle progression and attenuates Ang II, TNF-, and heme-mediated DNA damage; administration in vivo acts to correct blood pressure elevation following Ang II exposure. |
| 7678 | 15920055 | A prospective study of soluble tumor necrosis factor-alpha receptor II (sTNF-RII) and risk of coronary heart disease among women with type 2 diabetes. |
| 7679 | 15919808 | This was accompanied by approximately 65% decrease in fed and approximately 30% decrease in fasted glucose levels, a 60% decrease in plasma insulin concentration, and approximately 20 and 35% decrease in plasma resistin and tumor necrosis factor-alpha levels, respectively. |
| 7680 | 15919808 | GCCR ASO treatment completely inhibited the increase in dexamethasone-induced PEPCK expression in the liver without causing any change in the dexamethasone-induced lymphopenia. |
| 7681 | 15919806 | Furthermore, primary cultures of cardiomyocytes from wild-type and MT-TG mice were exposed to lipopolysaccharide/tumor necrosis factor-alpha for generating intracellular peroxynitrite. |
| 7682 | 15919794 | A human-specific role of cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) in adipocyte lipolysis and obesity. |
| 7683 | 15919794 | A human-specific role of cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) in adipocyte lipolysis and obesity. |
| 7684 | 15919794 | A human-specific role of cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) in adipocyte lipolysis and obesity. |
| 7685 | 15919794 | A human-specific role of cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) in adipocyte lipolysis and obesity. |
| 7686 | 15919794 | Elevated circulating fatty acid concentration is a hallmark of insulin resistance and is at least in part attributed to the action of adipose tissue-derived tumor necrosis factor-alpha (TNF-alpha) on lipolysis. |
| 7687 | 15919794 | Elevated circulating fatty acid concentration is a hallmark of insulin resistance and is at least in part attributed to the action of adipose tissue-derived tumor necrosis factor-alpha (TNF-alpha) on lipolysis. |
| 7688 | 15919794 | Elevated circulating fatty acid concentration is a hallmark of insulin resistance and is at least in part attributed to the action of adipose tissue-derived tumor necrosis factor-alpha (TNF-alpha) on lipolysis. |
| 7689 | 15919794 | Elevated circulating fatty acid concentration is a hallmark of insulin resistance and is at least in part attributed to the action of adipose tissue-derived tumor necrosis factor-alpha (TNF-alpha) on lipolysis. |
| 7690 | 15919794 | Cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) belongs to a family of proapoptotic proteins that has five known members in humans and mice. |
| 7691 | 15919794 | Cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) belongs to a family of proapoptotic proteins that has five known members in humans and mice. |
| 7692 | 15919794 | Cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) belongs to a family of proapoptotic proteins that has five known members in humans and mice. |
| 7693 | 15919794 | Cell death-inducing DFFA (DNA fragmentation factor-alpha)-like effector A (CIDEA) belongs to a family of proapoptotic proteins that has five known members in humans and mice. |
| 7694 | 15919794 | Human adipocyte depletion of CIDEA by RNA interference stimulated lipolysis and increased TNF-alpha secretion by a posttranscriptional effect. |
| 7695 | 15919794 | Human adipocyte depletion of CIDEA by RNA interference stimulated lipolysis and increased TNF-alpha secretion by a posttranscriptional effect. |
| 7696 | 15919794 | Human adipocyte depletion of CIDEA by RNA interference stimulated lipolysis and increased TNF-alpha secretion by a posttranscriptional effect. |
| 7697 | 15919794 | Human adipocyte depletion of CIDEA by RNA interference stimulated lipolysis and increased TNF-alpha secretion by a posttranscriptional effect. |
| 7698 | 15919794 | Conversely, TNF-alpha treatment decreased adipocyte CIDEA expression via the mitogen-activated protein kinase c-Jun NH(2)-terminal kinase. |
| 7699 | 15919794 | Conversely, TNF-alpha treatment decreased adipocyte CIDEA expression via the mitogen-activated protein kinase c-Jun NH(2)-terminal kinase. |
| 7700 | 15919794 | Conversely, TNF-alpha treatment decreased adipocyte CIDEA expression via the mitogen-activated protein kinase c-Jun NH(2)-terminal kinase. |
| 7701 | 15919794 | Conversely, TNF-alpha treatment decreased adipocyte CIDEA expression via the mitogen-activated protein kinase c-Jun NH(2)-terminal kinase. |
| 7702 | 15919794 | We propose an important and human-specific role for CIDEA in lipolysis regulation and metabolic complications of obesity, which is at least in part mediated by cross-talk between CIDEA and TNF-alpha. |
| 7703 | 15919794 | We propose an important and human-specific role for CIDEA in lipolysis regulation and metabolic complications of obesity, which is at least in part mediated by cross-talk between CIDEA and TNF-alpha. |
| 7704 | 15919794 | We propose an important and human-specific role for CIDEA in lipolysis regulation and metabolic complications of obesity, which is at least in part mediated by cross-talk between CIDEA and TNF-alpha. |
| 7705 | 15919794 | We propose an important and human-specific role for CIDEA in lipolysis regulation and metabolic complications of obesity, which is at least in part mediated by cross-talk between CIDEA and TNF-alpha. |
| 7706 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 7707 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 7708 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 7709 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 7710 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 7711 | 15917841 | TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. |
| 7712 | 15917841 | TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. |
| 7713 | 15917841 | TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. |
| 7714 | 15917841 | TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. |
| 7715 | 15917841 | TNFalpha increased the mRNA levels of TNFalpha itself as well as IL-6, IL-8, IL-1beta and PAI-1, but not leptin. |
| 7716 | 15917841 | The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. |
| 7717 | 15917841 | The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. |
| 7718 | 15917841 | The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. |
| 7719 | 15917841 | The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. |
| 7720 | 15917841 | The medium concentrations of IL-1 RA, IL-6 and IL-8 were markedly increased by TNFalpha while no measurable release of TNFalpha, resistin or IL-1beta to the medium was found. |
| 7721 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 7722 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 7723 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 7724 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 7725 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 7726 | 15917841 | However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role. |
| 7727 | 15917841 | However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role. |
| 7728 | 15917841 | However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role. |
| 7729 | 15917841 | However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role. |
| 7730 | 15917841 | However, since neither TNFalpha, resistin or IL-1beta was found in the culture medium, such a regulatory effect by TNFalpha on adipose tissue in vivo is likely to be mediated through a paracrine mechanism where invaded inflammatory cells may play a critical role. |
| 7731 | 15917336 | Baseline characteristics were similar between groups, and correlation analysis showed a significant association between urinary albumin excretion (UAE) and urinary TNF-alpha (R = 0.53, P < 0.001). |
| 7732 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7733 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7734 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7735 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7736 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7737 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7738 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7739 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7740 | 15908180 | Synergistic activation of JNK/SAPK induced by TNF-alpha and IFN-gamma: apoptosis of pancreatic beta-cells via the p53 and ROS pathway. |
| 7741 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7742 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7743 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7744 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7745 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7746 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7747 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7748 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7749 | 15908180 | IFN-gamma and TNF-alpha are major proinflammatory cytokines implicated in islet beta-cell destruction, which results in type-1 diabetes; however, the underlying mechanism is not clear. |
| 7750 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7751 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7752 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7753 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7754 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7755 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7756 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7757 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7758 | 15908180 | Using pancreatic beta-cell line MIN6N8 cells, co-treatment with TNF-alpha and IFN-gamma, but neither cytokine alone, synergistically induced apoptosis, correlated with the activation of the JNK/SAPK, which resulted in the production of reactive oxidative species (ROS) and loss of mitochondrial transmembrane potential (delta psi m). |
| 7759 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7760 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7761 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7762 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7763 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7764 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7765 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7766 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7767 | 15908180 | Additionally, cells transfected with wild-type JNK1 became more susceptible to apoptosis induced by TNF-alpha/IFN-gamma through ROS production and loss of delta psi m, while cascading apoptotic events were prevented in dominant-negative JNK1-transfected or JNK inhibitor SP600125-treated cells. |
| 7768 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7769 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7770 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7771 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7772 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7773 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7774 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7775 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7776 | 15908180 | As the antioxidant, N-acetyl-cysteine, failed to completely suppress apoptosis induced by TNF-alpha/IFN-gamma, an additional pathway was considered to be involved. |
| 7777 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7778 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7779 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7780 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7781 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7782 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7783 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7784 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7785 | 15908180 | The level of p53 was significantly increased through synergistic activation of JNK by TNF-alpha/IFN-gamma. |
| 7786 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7787 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7788 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7789 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7790 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7791 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7792 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7793 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7794 | 15908180 | Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53. |
| 7795 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7796 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7797 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7798 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7799 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7800 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7801 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7802 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7803 | 15908180 | This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125. |
| 7804 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7805 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7806 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7807 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7808 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7809 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7810 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7811 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7812 | 15908180 | Collectively, these data demonstrate that TNF-alpha/IFN-gamma synergistically activates JNK/SAPK, playing an important role in promoting apoptosis of pancreatic beta-cell via activation of p53 pathway together with ROS. |
| 7813 | 15904993 | Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. |
| 7814 | 15904993 | Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. |
| 7815 | 15904993 | Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. |
| 7816 | 15904993 | LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. |
| 7817 | 15904993 | LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. |
| 7818 | 15904993 | LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. |
| 7819 | 15904993 | Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO. |
| 7820 | 15904993 | Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO. |
| 7821 | 15904993 | Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO. |
| 7822 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7823 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7824 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7825 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7826 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7827 | 15902099 | Proteome of H-411E (liver) cells exposed to insulin and tumor necrosis factor-alpha: analysis of proteins involved in insulin resistance. |
| 7828 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7829 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7830 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7831 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7832 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7833 | 15902099 | Insulin resistance may be modeled in H-411E liver cells in tissue culture with the use of the cytokine tumor necrosis factor-alpha (TNF-alpha) and insulin. |
| 7834 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7835 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7836 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7837 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7838 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7839 | 15902099 | After incubation of liver cells in tissue culture with INS alone, TNF-alpha alone, and TNF-alpha plus insulin, as well as a control sample, liver-cell extracts were separated on 2D polyacrylamide-gel electrophoresis on the basis of isoelectric point and molecular weight. |
| 7840 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7841 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7842 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7843 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7844 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7845 | 15902099 | We analyzed the gel images with the use of PD Quest software (Bio-Rad Laboratories, Hercules, Calif) to identify differentially expressed protein spots (ie, up or down with insulin vs down or up with TNF-alpha plus insulin). |
| 7846 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7847 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7848 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7849 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7850 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7851 | 15902099 | The first series of experiments identified 6 differentially expressed proteins: eukaryotic translation initiation factor-3, subunit 2, regulator of G-protein signaling-5, superoxide dismutase, protein disulfide isomerase A6, proteasome subunit-alpha type 3, and regucalcin. |
| 7852 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7853 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7854 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7855 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7856 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7857 | 15902099 | A second series of experiments identified 7 additional proteins with significantly altered differential expression: cell-division protein kinase-4, kinogen heavy chain, carbonic anhydrase-7, E 3 ubiquitin protein ligase, URE-B1; Rab GDP dissociation inhibitor-beta, Rab GDP dissociation inhibitor-beta2, and MAWDBP. |
| 7858 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7859 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7860 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7861 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7862 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7863 | 15902099 | It can be seen that differentially expressed proteins, affected by treatment with insulin or with TNF-alpha plus insulin, include regulators of translation, protein degradation, cellular Ca ++ , G-proteins, and free-radical production. |
| 7864 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7865 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7866 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7867 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7868 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7869 | 15902099 | Although one cannot detail the mechanism or mechanisms of TNF-alpha induced IR from this data alone, it is easy to relate all of these proteins to a role in insulin signal transduction and, hence, insulin resistance. |
| 7870 | 15899101 | Elevated serum tumor necrosis factor alpha and ferritin may contribute to the insulin resistance found in HCV positive Egyptian patients. |
| 7871 | 15899050 | First, we compared biomarkers of endothelial dysfunction (vascular cell adhesion molecule [VCAM]-1, intercellular adhesion molecule [ICAM]-1 and endothelial leucocyte adhesion molecule [ELAM]-1) in 74 RA patients and 80 healthy control individuals before and after controlling for traditional and nontraditional cardiovascular risk factors, including high-sensitivity C-reactive protein (hs-CRP), IL-1, IL-6 and tumor necrosis factor-alpha. |
| 7872 | 15899050 | First, we compared biomarkers of endothelial dysfunction (vascular cell adhesion molecule [VCAM]-1, intercellular adhesion molecule [ICAM]-1 and endothelial leucocyte adhesion molecule [ELAM]-1) in 74 RA patients and 80 healthy control individuals before and after controlling for traditional and nontraditional cardiovascular risk factors, including high-sensitivity C-reactive protein (hs-CRP), IL-1, IL-6 and tumor necrosis factor-alpha. |
| 7873 | 15899050 | The three biomarkers of endothelial dysfunction, as well as hs-CRP, IL-1, IL-6 and tumor necrosis factor-alpha, were higher in patients than in control individuals (P < 0.0001). |
| 7874 | 15899050 | The three biomarkers of endothelial dysfunction, as well as hs-CRP, IL-1, IL-6 and tumor necrosis factor-alpha, were higher in patients than in control individuals (P < 0.0001). |
| 7875 | 15899050 | In the 74 RA patients, IL-6 predicted levels of all three biomarkers (P <or= 0.03), and rheumatoid factor titres and low glomerular filtration rate (GFR) both predicted levels of VCAM-1 and ICAM-1, independent of traditional cardiovascular risk factors (P <or= 0.02). |
| 7876 | 15899050 | In the 74 RA patients, IL-6 predicted levels of all three biomarkers (P <or= 0.03), and rheumatoid factor titres and low glomerular filtration rate (GFR) both predicted levels of VCAM-1 and ICAM-1, independent of traditional cardiovascular risk factors (P <or= 0.02). |
| 7877 | 15895517 | Conjugated linoleic acid deteriorates insulin resistance in obese/diabetic mice in association with decreased production of adiponectin and leptin. |
| 7878 | 15895517 | The plasma and WAT mRNA levels of leptin were higher in KK and KKAy mice than C57BI. mice, whereas those of adiponectin were higher in C5 7BL mice. |
| 7879 | 15895517 | CLA-feeding decreased the levels of leptin, adiponectin and resistin, especially in KK and KKAy mice. |
| 7880 | 15895517 | The present results thus indicate that CLA feeding promotes insulin resistance in obese/diabetic mice by at least inverse regulation of leptin and adiponectin, and TNFalpha, adipocytokines known to either ameliorate or deteriorate insulin sensitivity, respectively. |
| 7881 | 15893251 | In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 7882 | 15893251 | In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 7883 | 15893251 | In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 7884 | 15893251 | Also, we reported a positive correlation between IL-6 or TNFalpha plasma levels and the body-mass-index (BMI). |
| 7885 | 15893251 | Also, we reported a positive correlation between IL-6 or TNFalpha plasma levels and the body-mass-index (BMI). |
| 7886 | 15893251 | Also, we reported a positive correlation between IL-6 or TNFalpha plasma levels and the body-mass-index (BMI). |
| 7887 | 15893251 | In subsequent studies, we showed that IL-6, TNFalpha, and insulin levels were elevated in sleep apnea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnea. |
| 7888 | 15893251 | In subsequent studies, we showed that IL-6, TNFalpha, and insulin levels were elevated in sleep apnea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnea. |
| 7889 | 15893251 | In subsequent studies, we showed that IL-6, TNFalpha, and insulin levels were elevated in sleep apnea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnea. |
| 7890 | 15893134 | Among them, TNF-alpha has been most widely studied; it not only suppresses the insulin signaling, but also elicits vascular inflammation. |
| 7891 | 15893134 | Among them, TNF-alpha has been most widely studied; it not only suppresses the insulin signaling, but also elicits vascular inflammation. |
| 7892 | 15893134 | Among them, TNF-alpha has been most widely studied; it not only suppresses the insulin signaling, but also elicits vascular inflammation. |
| 7893 | 15893134 | Among them, TNF-alpha has been most widely studied; it not only suppresses the insulin signaling, but also elicits vascular inflammation. |
| 7894 | 15893134 | Indeed, inhibition of TNF-alpha was found to improve insulin resistance in obese rats and reduce the progression of atherosclerosis in apolipoprotein E knockout mice, respectively. |
| 7895 | 15893134 | Indeed, inhibition of TNF-alpha was found to improve insulin resistance in obese rats and reduce the progression of atherosclerosis in apolipoprotein E knockout mice, respectively. |
| 7896 | 15893134 | Indeed, inhibition of TNF-alpha was found to improve insulin resistance in obese rats and reduce the progression of atherosclerosis in apolipoprotein E knockout mice, respectively. |
| 7897 | 15893134 | Indeed, inhibition of TNF-alpha was found to improve insulin resistance in obese rats and reduce the progression of atherosclerosis in apolipoprotein E knockout mice, respectively. |
| 7898 | 15893134 | These observations demonstrate that TNF-alpha could play a central role in the pathogenesis of insulin resistance and accelerated atherosclerosis in the metabolic syndrome. |
| 7899 | 15893134 | These observations demonstrate that TNF-alpha could play a central role in the pathogenesis of insulin resistance and accelerated atherosclerosis in the metabolic syndrome. |
| 7900 | 15893134 | These observations demonstrate that TNF-alpha could play a central role in the pathogenesis of insulin resistance and accelerated atherosclerosis in the metabolic syndrome. |
| 7901 | 15893134 | These observations demonstrate that TNF-alpha could play a central role in the pathogenesis of insulin resistance and accelerated atherosclerosis in the metabolic syndrome. |
| 7902 | 15893134 | In the process of the search for such a unique anti-hypertensive drug, we have recently found that azelnidipine, a newly developed and commercially used long-acting dihydropyridine-based calcium antagonist (DHP), inhibited TNF-alpha-induced activator protein-1 activation and interleukin-8 expression in human umbilical vein endothelial cells by suppressing NADPH oxidase-mediated reactive oxygen species generation. |
| 7903 | 15893134 | In the process of the search for such a unique anti-hypertensive drug, we have recently found that azelnidipine, a newly developed and commercially used long-acting dihydropyridine-based calcium antagonist (DHP), inhibited TNF-alpha-induced activator protein-1 activation and interleukin-8 expression in human umbilical vein endothelial cells by suppressing NADPH oxidase-mediated reactive oxygen species generation. |
| 7904 | 15893134 | In the process of the search for such a unique anti-hypertensive drug, we have recently found that azelnidipine, a newly developed and commercially used long-acting dihydropyridine-based calcium antagonist (DHP), inhibited TNF-alpha-induced activator protein-1 activation and interleukin-8 expression in human umbilical vein endothelial cells by suppressing NADPH oxidase-mediated reactive oxygen species generation. |
| 7905 | 15893134 | In the process of the search for such a unique anti-hypertensive drug, we have recently found that azelnidipine, a newly developed and commercially used long-acting dihydropyridine-based calcium antagonist (DHP), inhibited TNF-alpha-induced activator protein-1 activation and interleukin-8 expression in human umbilical vein endothelial cells by suppressing NADPH oxidase-mediated reactive oxygen species generation. |
| 7906 | 15892652 | The adipokines regulating insulin sensitivity are tumor necrosis factor alpha, adiponectin, interleukin-6, resistin and leptin. |
| 7907 | 15892652 | This review examines the mechanism how these adipokines influence insulin sensitivity, how the adipocyte production of the adipokines is regulated and if genetic variance in the genes encoding for adipokines is important for the development of type 2 diabetes mellitus. |
| 7908 | 15878720 | The increased interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in diabetic mice were significantly suppressed by the intake of histidine or carnosine (P < 0.05). |
| 7909 | 15877313 | Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). |
| 7910 | 15876977 | CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. |
| 7911 | 15868110 | Nitrite, IL-1beta and TNF-alpha were significantly higher in macrophage supernatants and sera of the acutely affected STZ-LETO rats either with or without LPS stimulation compared to corresponding controls. |
| 7912 | 15868110 | Nitrite, IL-1beta and TNF-alpha were significantly higher in macrophage supernatants and sera of the acutely affected STZ-LETO rats either with or without LPS stimulation compared to corresponding controls. |
| 7913 | 15868110 | On the other hand, chronically diabetic OLETF rats' macrophage supernatants showed significant decreases of IL-1beta and TNF-alpha levels upon LPS stimulation or even without stimulation (IL-1beta); and insignificant increase in nitrite concentration, which turned significant upon LPS stimulation. |
| 7914 | 15868110 | On the other hand, chronically diabetic OLETF rats' macrophage supernatants showed significant decreases of IL-1beta and TNF-alpha levels upon LPS stimulation or even without stimulation (IL-1beta); and insignificant increase in nitrite concentration, which turned significant upon LPS stimulation. |
| 7915 | 15867292 | Serum insulin, glucose, tumor necrosis factor (TNF)-alpha, and interleukin-6 were lower in CLA-fed mice than in controls (P < 0.05), whereas serum TNF-alpha was increased by exercise (P < 0.05). |
| 7916 | 15858601 | Does a central MHC gene in linkage disequilibrium with HLA-DRB1*0401 affect susceptibility to type 1 diabetes? |
| 7917 | 15858601 | Does a central MHC gene in linkage disequilibrium with HLA-DRB1*0401 affect susceptibility to type 1 diabetes? |
| 7918 | 15858601 | We addressed whether this reflects linkage disequilibrium with the true susceptibility locus by studying broader MHC haplotypes marked by alleles of HLA-B, IKBL (adjacent to TNFA) and complement C4. |
| 7919 | 15858601 | We addressed whether this reflects linkage disequilibrium with the true susceptibility locus by studying broader MHC haplotypes marked by alleles of HLA-B, IKBL (adjacent to TNFA) and complement C4. |
| 7920 | 15858601 | A gene between TNFA and HLA-B on the 8.1AH (HLA-A1,B8,;DR3,DQ2) modifies the effects of the class II alleles. |
| 7921 | 15858601 | A gene between TNFA and HLA-B on the 8.1AH (HLA-A1,B8,;DR3,DQ2) modifies the effects of the class II alleles. |
| 7922 | 15858601 | Here, alleles characteristic of the 62.1AH (C4B3, IKBL+446*T and HLA-A2,B15) were screened in donors preselected for HLA-DRB1*0401. |
| 7923 | 15858601 | Here, alleles characteristic of the 62.1AH (C4B3, IKBL+446*T and HLA-A2,B15) were screened in donors preselected for HLA-DRB1*0401. |
| 7924 | 15858601 | C4B3 was associated with diabetes, consistent with a diabetes gene telomeric of MHC class II. |
| 7925 | 15858601 | C4B3 was associated with diabetes, consistent with a diabetes gene telomeric of MHC class II. |
| 7926 | 15858601 | However, with these tools, selection of HLA-DRB1*0401, DQB1*0302 donors who are positive and negative for C4B3 will allow bidirectional mapping of diabetes genes in the central MHC. |
| 7927 | 15858601 | However, with these tools, selection of HLA-DRB1*0401, DQB1*0302 donors who are positive and negative for C4B3 will allow bidirectional mapping of diabetes genes in the central MHC. |
| 7928 | 15855330 | Sphingosine kinase (SPHK) and S1P were characterized in INS-1 insulinoma cells and isolated rat islets of Langerhans. |
| 7929 | 15855330 | Sphingosine kinase (SPHK) and S1P were characterized in INS-1 insulinoma cells and isolated rat islets of Langerhans. |
| 7930 | 15855330 | Sphingosine kinase (SPHK) and S1P were characterized in INS-1 insulinoma cells and isolated rat islets of Langerhans. |
| 7931 | 15855330 | Sphingosine kinase (SPHK) and S1P were characterized in INS-1 insulinoma cells and isolated rat islets of Langerhans. |
| 7932 | 15855330 | Sphingosine kinase (SPHK) and S1P were characterized in INS-1 insulinoma cells and isolated rat islets of Langerhans. |
| 7933 | 15855330 | SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. |
| 7934 | 15855330 | SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. |
| 7935 | 15855330 | SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. |
| 7936 | 15855330 | SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. |
| 7937 | 15855330 | SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. |
| 7938 | 15855330 | IL-1beta or TNF-alpha increased islet SPHK activity within 15 min to 1 h; activity remained elevated after 8 h. |
| 7939 | 15855330 | IL-1beta or TNF-alpha increased islet SPHK activity within 15 min to 1 h; activity remained elevated after 8 h. |
| 7940 | 15855330 | IL-1beta or TNF-alpha increased islet SPHK activity within 15 min to 1 h; activity remained elevated after 8 h. |
| 7941 | 15855330 | IL-1beta or TNF-alpha increased islet SPHK activity within 15 min to 1 h; activity remained elevated after 8 h. |
| 7942 | 15855330 | IL-1beta or TNF-alpha increased islet SPHK activity within 15 min to 1 h; activity remained elevated after 8 h. |
| 7943 | 15855330 | SPHK2 was the predominant active isoform in INS-1 cells; little or no SPHK1 activity was detected. |
| 7944 | 15855330 | SPHK2 was the predominant active isoform in INS-1 cells; little or no SPHK1 activity was detected. |
| 7945 | 15855330 | SPHK2 was the predominant active isoform in INS-1 cells; little or no SPHK1 activity was detected. |
| 7946 | 15855330 | SPHK2 was the predominant active isoform in INS-1 cells; little or no SPHK1 activity was detected. |
| 7947 | 15855330 | SPHK2 was the predominant active isoform in INS-1 cells; little or no SPHK1 activity was detected. |
| 7948 | 15855330 | Compared with basal values, IL-1beta and TNF-alpha induced increases in SPHK1a mRNA levels relative to 18S ribosomal RNA in INS-1 cells within 1 h; relative SPHK2 mRNA levels were unchanged after cytokine treatment. |
| 7949 | 15855330 | Compared with basal values, IL-1beta and TNF-alpha induced increases in SPHK1a mRNA levels relative to 18S ribosomal RNA in INS-1 cells within 1 h; relative SPHK2 mRNA levels were unchanged after cytokine treatment. |
| 7950 | 15855330 | Compared with basal values, IL-1beta and TNF-alpha induced increases in SPHK1a mRNA levels relative to 18S ribosomal RNA in INS-1 cells within 1 h; relative SPHK2 mRNA levels were unchanged after cytokine treatment. |
| 7951 | 15855330 | Compared with basal values, IL-1beta and TNF-alpha induced increases in SPHK1a mRNA levels relative to 18S ribosomal RNA in INS-1 cells within 1 h; relative SPHK2 mRNA levels were unchanged after cytokine treatment. |
| 7952 | 15855330 | Compared with basal values, IL-1beta and TNF-alpha induced increases in SPHK1a mRNA levels relative to 18S ribosomal RNA in INS-1 cells within 1 h; relative SPHK2 mRNA levels were unchanged after cytokine treatment. |
| 7953 | 15855330 | IL-1beta, but not TNF-alpha, induced relative SPHK1a mRNA expression levels within 1 h in islets, whereas SPHK2 mRNA levels were unchanged. |
| 7954 | 15855330 | IL-1beta, but not TNF-alpha, induced relative SPHK1a mRNA expression levels within 1 h in islets, whereas SPHK2 mRNA levels were unchanged. |
| 7955 | 15855330 | IL-1beta, but not TNF-alpha, induced relative SPHK1a mRNA expression levels within 1 h in islets, whereas SPHK2 mRNA levels were unchanged. |
| 7956 | 15855330 | IL-1beta, but not TNF-alpha, induced relative SPHK1a mRNA expression levels within 1 h in islets, whereas SPHK2 mRNA levels were unchanged. |
| 7957 | 15855330 | IL-1beta, but not TNF-alpha, induced relative SPHK1a mRNA expression levels within 1 h in islets, whereas SPHK2 mRNA levels were unchanged. |
| 7958 | 15855330 | Thus, IL-1beta and TNF-alpha induced an early and sustained increase in SPHK activity in INS-1 cells and isolated islets, suggesting that S1P plays a role in the pathological response of pancreatic beta-cells to cytokines. |
| 7959 | 15855330 | Thus, IL-1beta and TNF-alpha induced an early and sustained increase in SPHK activity in INS-1 cells and isolated islets, suggesting that S1P plays a role in the pathological response of pancreatic beta-cells to cytokines. |
| 7960 | 15855330 | Thus, IL-1beta and TNF-alpha induced an early and sustained increase in SPHK activity in INS-1 cells and isolated islets, suggesting that S1P plays a role in the pathological response of pancreatic beta-cells to cytokines. |
| 7961 | 15855330 | Thus, IL-1beta and TNF-alpha induced an early and sustained increase in SPHK activity in INS-1 cells and isolated islets, suggesting that S1P plays a role in the pathological response of pancreatic beta-cells to cytokines. |
| 7962 | 15855330 | Thus, IL-1beta and TNF-alpha induced an early and sustained increase in SPHK activity in INS-1 cells and isolated islets, suggesting that S1P plays a role in the pathological response of pancreatic beta-cells to cytokines. |
| 7963 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 7964 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 7965 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 7966 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 7967 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 7968 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 7969 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 7970 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 7971 | 15855326 | These included tumor necrosis factor-alpha, inducible nitric oxide synthase, monocyte chemoattractant protein-1, granzyme B, and Fas/Fas ligand, all of which contribute to the pathogenesis of the rejection of transplanted islets. |
| 7972 | 15850785 | Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-beta and tumor necrosis factor-alpha. |
| 7973 | 15850785 | Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-beta and tumor necrosis factor-alpha. |
| 7974 | 15850785 | Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-beta and tumor necrosis factor-alpha. |
| 7975 | 15850785 | Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-beta and tumor necrosis factor-alpha. |
| 7976 | 15850785 | Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitizing and has anti-atherosclerotic properties. |
| 7977 | 15850785 | Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitizing and has anti-atherosclerotic properties. |
| 7978 | 15850785 | Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitizing and has anti-atherosclerotic properties. |
| 7979 | 15850785 | Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitizing and has anti-atherosclerotic properties. |
| 7980 | 15850785 | Plasma levels of adiponectin are decreased in obese individuals and patients with type 2 diabetes with insulin resistance. |
| 7981 | 15850785 | Plasma levels of adiponectin are decreased in obese individuals and patients with type 2 diabetes with insulin resistance. |
| 7982 | 15850785 | Plasma levels of adiponectin are decreased in obese individuals and patients with type 2 diabetes with insulin resistance. |
| 7983 | 15850785 | Plasma levels of adiponectin are decreased in obese individuals and patients with type 2 diabetes with insulin resistance. |
| 7984 | 15850785 | Tumor necrosis factor-alpha (TNF-alpha) decreases the expression of adiponectin in adipocytes. |
| 7985 | 15850785 | Tumor necrosis factor-alpha (TNF-alpha) decreases the expression of adiponectin in adipocytes. |
| 7986 | 15850785 | Tumor necrosis factor-alpha (TNF-alpha) decreases the expression of adiponectin in adipocytes. |
| 7987 | 15850785 | Tumor necrosis factor-alpha (TNF-alpha) decreases the expression of adiponectin in adipocytes. |
| 7988 | 15850785 | The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. |
| 7989 | 15850785 | The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. |
| 7990 | 15850785 | The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. |
| 7991 | 15850785 | The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. |
| 7992 | 15850785 | Mutation analysis of putative response elements for sterol regulatory element binding protein (SREBP) (-431 to -423) and CCAAT/enhancer binding protein (C/EBP) (-230 to -224) showed that both elements were required for basal promoter activity. |
| 7993 | 15850785 | Mutation analysis of putative response elements for sterol regulatory element binding protein (SREBP) (-431 to -423) and CCAAT/enhancer binding protein (C/EBP) (-230 to -224) showed that both elements were required for basal promoter activity. |
| 7994 | 15850785 | Mutation analysis of putative response elements for sterol regulatory element binding protein (SREBP) (-431 to -423) and CCAAT/enhancer binding protein (C/EBP) (-230 to -224) showed that both elements were required for basal promoter activity. |
| 7995 | 15850785 | Mutation analysis of putative response elements for sterol regulatory element binding protein (SREBP) (-431 to -423) and CCAAT/enhancer binding protein (C/EBP) (-230 to -224) showed that both elements were required for basal promoter activity. |
| 7996 | 15850785 | Adiponectin transcription was increased 3-fold in cells that over-expressed constitutively active C/EBP-beta. |
| 7997 | 15850785 | Adiponectin transcription was increased 3-fold in cells that over-expressed constitutively active C/EBP-beta. |
| 7998 | 15850785 | Adiponectin transcription was increased 3-fold in cells that over-expressed constitutively active C/EBP-beta. |
| 7999 | 15850785 | Adiponectin transcription was increased 3-fold in cells that over-expressed constitutively active C/EBP-beta. |
| 8000 | 15850785 | The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta. |
| 8001 | 15850785 | The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta. |
| 8002 | 15850785 | The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta. |
| 8003 | 15850785 | The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta. |
| 8004 | 15850715 | GLUT-4 (glucose transporter) receptor, tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), daf-genes and PPARs (peroxisomal proliferation activator receptors) play a role in the development of insulin resistance syndrome and associated conditions. |
| 8005 | 15850715 | GLUT-4 (glucose transporter) receptor, tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), daf-genes and PPARs (peroxisomal proliferation activator receptors) play a role in the development of insulin resistance syndrome and associated conditions. |
| 8006 | 15850715 | GLUT-4 (glucose transporter) receptor, tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), daf-genes and PPARs (peroxisomal proliferation activator receptors) play a role in the development of insulin resistance syndrome and associated conditions. |
| 8007 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 8008 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 8009 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 8010 | 15850715 | In the nematode, Caenorhabditis elegans, the protein encoded by daf-2 is 35% identical to the human insulin receptor; daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 enhances superoxide dismutase (SOD) expression. |
| 8011 | 15850715 | In the nematode, Caenorhabditis elegans, the protein encoded by daf-2 is 35% identical to the human insulin receptor; daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 enhances superoxide dismutase (SOD) expression. |
| 8012 | 15850715 | In the nematode, Caenorhabditis elegans, the protein encoded by daf-2 is 35% identical to the human insulin receptor; daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 enhances superoxide dismutase (SOD) expression. |
| 8013 | 15850715 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 8014 | 15850715 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 8015 | 15850715 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 8016 | 15850715 | These evidences suggest that the activities of Delta6 and Delta5 enzymes play a critical role in the expression and regulation of GLUT-4, TNF-alpha, IL-6, MIF, daf-genes, melatonin, and leptin by modulating the synthesis and tissue concentrations of LCPUFAs. |
| 8017 | 15850715 | These evidences suggest that the activities of Delta6 and Delta5 enzymes play a critical role in the expression and regulation of GLUT-4, TNF-alpha, IL-6, MIF, daf-genes, melatonin, and leptin by modulating the synthesis and tissue concentrations of LCPUFAs. |
| 8018 | 15850715 | These evidences suggest that the activities of Delta6 and Delta5 enzymes play a critical role in the expression and regulation of GLUT-4, TNF-alpha, IL-6, MIF, daf-genes, melatonin, and leptin by modulating the synthesis and tissue concentrations of LCPUFAs. |
| 8019 | 15850715 | Both insulin and insulin-like growth factor-1 (IGF-1) attenuated this response. |
| 8020 | 15850715 | Both insulin and insulin-like growth factor-1 (IGF-1) attenuated this response. |
| 8021 | 15850715 | Both insulin and insulin-like growth factor-1 (IGF-1) attenuated this response. |
| 8022 | 15850715 | SIRT1 sequesters the proapoptotic factor Bax, prevents stress-induced apoptosis of cells, and thus, prolongs survival. |
| 8023 | 15850715 | SIRT1 sequesters the proapoptotic factor Bax, prevents stress-induced apoptosis of cells, and thus, prolongs survival. |
| 8024 | 15850715 | SIRT1 sequesters the proapoptotic factor Bax, prevents stress-induced apoptosis of cells, and thus, prolongs survival. |
| 8025 | 15850715 | In addition, SIRT1 repressed PPAR-gamma, and overexpression of SIRT1 attenuated adipogenesis, and upregulation of SIRT in differentiated fat cells triggered lipolysis and loss of fat, events that are known to attenuate insulin resistance and prolong life span. |
| 8026 | 15850715 | In addition, SIRT1 repressed PPAR-gamma, and overexpression of SIRT1 attenuated adipogenesis, and upregulation of SIRT in differentiated fat cells triggered lipolysis and loss of fat, events that are known to attenuate insulin resistance and prolong life span. |
| 8027 | 15850715 | In addition, SIRT1 repressed PPAR-gamma, and overexpression of SIRT1 attenuated adipogenesis, and upregulation of SIRT in differentiated fat cells triggered lipolysis and loss of fat, events that are known to attenuate insulin resistance and prolong life span. |
| 8028 | 15849359 | Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. |
| 8029 | 15849359 | Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. |
| 8030 | 15849359 | Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. |
| 8031 | 15849359 | Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. |
| 8032 | 15849359 | Mouse Pelle-like kinase (mPLK, homolog of human IL-1 receptor-associated kinase (IRAK)) participates in inflammatory signaling. |
| 8033 | 15849359 | Mouse Pelle-like kinase (mPLK, homolog of human IL-1 receptor-associated kinase (IRAK)) participates in inflammatory signaling. |
| 8034 | 15849359 | Mouse Pelle-like kinase (mPLK, homolog of human IL-1 receptor-associated kinase (IRAK)) participates in inflammatory signaling. |
| 8035 | 15849359 | Mouse Pelle-like kinase (mPLK, homolog of human IL-1 receptor-associated kinase (IRAK)) participates in inflammatory signaling. |
| 8036 | 15849359 | We evaluated IRS-1 as a novel substrate for mPLK that may contribute to linking inflammation with insulin resistance. |
| 8037 | 15849359 | We evaluated IRS-1 as a novel substrate for mPLK that may contribute to linking inflammation with insulin resistance. |
| 8038 | 15849359 | We evaluated IRS-1 as a novel substrate for mPLK that may contribute to linking inflammation with insulin resistance. |
| 8039 | 15849359 | We evaluated IRS-1 as a novel substrate for mPLK that may contribute to linking inflammation with insulin resistance. |
| 8040 | 15849359 | Wild-type mPLK, but not a kinase-inactive mutant (mPLK-KD), directly phosphorylated full-length IRS-1 in vitro. |
| 8041 | 15849359 | Wild-type mPLK, but not a kinase-inactive mutant (mPLK-KD), directly phosphorylated full-length IRS-1 in vitro. |
| 8042 | 15849359 | Wild-type mPLK, but not a kinase-inactive mutant (mPLK-KD), directly phosphorylated full-length IRS-1 in vitro. |
| 8043 | 15849359 | Wild-type mPLK, but not a kinase-inactive mutant (mPLK-KD), directly phosphorylated full-length IRS-1 in vitro. |
| 8044 | 15849359 | This in vitro phosphorylation was increased when mPLK was immunoprecipitated from tumor necrosis factor (TNF)-alpha-treated cells. |
| 8045 | 15849359 | This in vitro phosphorylation was increased when mPLK was immunoprecipitated from tumor necrosis factor (TNF)-alpha-treated cells. |
| 8046 | 15849359 | This in vitro phosphorylation was increased when mPLK was immunoprecipitated from tumor necrosis factor (TNF)-alpha-treated cells. |
| 8047 | 15849359 | This in vitro phosphorylation was increased when mPLK was immunoprecipitated from tumor necrosis factor (TNF)-alpha-treated cells. |
| 8048 | 15849359 | In NIH-3T3(IR) cells, wild-type mPLK (but not mPLK-KD) co-immunoprecipitated with IRS-1. |
| 8049 | 15849359 | In NIH-3T3(IR) cells, wild-type mPLK (but not mPLK-KD) co-immunoprecipitated with IRS-1. |
| 8050 | 15849359 | In NIH-3T3(IR) cells, wild-type mPLK (but not mPLK-KD) co-immunoprecipitated with IRS-1. |
| 8051 | 15849359 | In NIH-3T3(IR) cells, wild-type mPLK (but not mPLK-KD) co-immunoprecipitated with IRS-1. |
| 8052 | 15849359 | Using mass spectrometry, we identified Ser(24) in the pleckstrin homology (PH) domain of IRS-1 as a specific phosphorylation site for mPLK. |
| 8053 | 15849359 | Using mass spectrometry, we identified Ser(24) in the pleckstrin homology (PH) domain of IRS-1 as a specific phosphorylation site for mPLK. |
| 8054 | 15849359 | Using mass spectrometry, we identified Ser(24) in the pleckstrin homology (PH) domain of IRS-1 as a specific phosphorylation site for mPLK. |
| 8055 | 15849359 | Using mass spectrometry, we identified Ser(24) in the pleckstrin homology (PH) domain of IRS-1 as a specific phosphorylation site for mPLK. |
| 8056 | 15849359 | IRS-1 mutants S24D or S24E (mimicking phosphorylation at Ser(24)) had impaired ability to associate with insulin receptors resulting in diminished tyrosine phosphorylation of IRS-1 and impaired ability of IRS-1 to bind and activate PI-3 kinase in response to insulin. |
| 8057 | 15849359 | IRS-1 mutants S24D or S24E (mimicking phosphorylation at Ser(24)) had impaired ability to associate with insulin receptors resulting in diminished tyrosine phosphorylation of IRS-1 and impaired ability of IRS-1 to bind and activate PI-3 kinase in response to insulin. |
| 8058 | 15849359 | IRS-1 mutants S24D or S24E (mimicking phosphorylation at Ser(24)) had impaired ability to associate with insulin receptors resulting in diminished tyrosine phosphorylation of IRS-1 and impaired ability of IRS-1 to bind and activate PI-3 kinase in response to insulin. |
| 8059 | 15849359 | IRS-1 mutants S24D or S24E (mimicking phosphorylation at Ser(24)) had impaired ability to associate with insulin receptors resulting in diminished tyrosine phosphorylation of IRS-1 and impaired ability of IRS-1 to bind and activate PI-3 kinase in response to insulin. |
| 8060 | 15849359 | IRS-1-S24D also had an impaired ability to mediate insulin-stimulated translocation of GLUT4 in rat adipose cells. |
| 8061 | 15849359 | IRS-1-S24D also had an impaired ability to mediate insulin-stimulated translocation of GLUT4 in rat adipose cells. |
| 8062 | 15849359 | IRS-1-S24D also had an impaired ability to mediate insulin-stimulated translocation of GLUT4 in rat adipose cells. |
| 8063 | 15849359 | IRS-1-S24D also had an impaired ability to mediate insulin-stimulated translocation of GLUT4 in rat adipose cells. |
| 8064 | 15849359 | Importantly, endogenous mPLK/IRAK was activated in response to TNF-alpha or interleukin 1 treatment of primary adipose cells. |
| 8065 | 15849359 | Importantly, endogenous mPLK/IRAK was activated in response to TNF-alpha or interleukin 1 treatment of primary adipose cells. |
| 8066 | 15849359 | Importantly, endogenous mPLK/IRAK was activated in response to TNF-alpha or interleukin 1 treatment of primary adipose cells. |
| 8067 | 15849359 | Importantly, endogenous mPLK/IRAK was activated in response to TNF-alpha or interleukin 1 treatment of primary adipose cells. |
| 8068 | 15849359 | In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser(24), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser(24). |
| 8069 | 15849359 | In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser(24), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser(24). |
| 8070 | 15849359 | In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser(24), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser(24). |
| 8071 | 15849359 | In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser(24), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser(24). |
| 8072 | 15849359 | We conclude that IRS-1 is a novel physiological substrate for mPLK. |
| 8073 | 15849359 | We conclude that IRS-1 is a novel physiological substrate for mPLK. |
| 8074 | 15849359 | We conclude that IRS-1 is a novel physiological substrate for mPLK. |
| 8075 | 15849359 | We conclude that IRS-1 is a novel physiological substrate for mPLK. |
| 8076 | 15849359 | TNF-alpha-regulated phosphorylation at Ser(24) in the pleckstrin homology domain of IRS-1 by mPLK/IRAK represents an additional mechanism for cross-talk between inflammatory signaling and insulin signaling that may contribute to metabolic insulin resistance. |
| 8077 | 15849359 | TNF-alpha-regulated phosphorylation at Ser(24) in the pleckstrin homology domain of IRS-1 by mPLK/IRAK represents an additional mechanism for cross-talk between inflammatory signaling and insulin signaling that may contribute to metabolic insulin resistance. |
| 8078 | 15849359 | TNF-alpha-regulated phosphorylation at Ser(24) in the pleckstrin homology domain of IRS-1 by mPLK/IRAK represents an additional mechanism for cross-talk between inflammatory signaling and insulin signaling that may contribute to metabolic insulin resistance. |
| 8079 | 15849359 | TNF-alpha-regulated phosphorylation at Ser(24) in the pleckstrin homology domain of IRS-1 by mPLK/IRAK represents an additional mechanism for cross-talk between inflammatory signaling and insulin signaling that may contribute to metabolic insulin resistance. |
| 8080 | 15833265 | Most NKT cells express both an invariant T cell antigen receptor and the NK cell receptor NK1.1, and are referred to as invariant NKT cells. |
| 8081 | 15833265 | This invariant T cell receptor is restricted to interactions with glycolipids presented by the non-classical MHC, CD1d. |
| 8082 | 15833265 | These NKT cells rapidly produce high levels of interleukin (IL)-2, IFN-gamma, TNF-alpha, and IL-4 upon stimulation through their TCR. |
| 8083 | 15826820 | Using quantitative real-time PCR we could show that basal TGF-beta mRNA expression is about 2-fold decreased in end-stage renal failure patients, while expression of TNF-alpha becomes 2-fold increased, further doubling during hemodialysis. |
| 8084 | 15826373 | When injected into connective tissue of the scalp, purified FimA protein induced TNF-alpha and MIP-2 expression confirming that it is pro-inflammatory. |
| 8085 | 15821103 | The acquisition of an insulin-secreting phenotype by HGF-treated rat pancreatic ductal cells (ARIP) is associated with the development of susceptibility to cytokine-induced apoptosis. |
| 8086 | 15821103 | The present study had the following three aims: 1. to investigate whether pancreatic ductal epithelial cells can be induced to differentiate into insulin-producing cells by exposing them to hepatocyte growth factor (HGF); 2. to characterize some of the molecular events leading to their differentiation toward a beta-cell-like phenotype; 3. to evaluate the susceptibility of newly differentiated insulin-secreting cells to cytokine-induced apoptosis, a mechanism of beta-cell destruction occurring in type 1 diabetes. |
| 8087 | 15821103 | We demonstrated that HGF-treated rat pancreatic ductal cell line (ARIP) cells acquired the capability to transcribe the insulin gene and translate its counterpart protein. |
| 8088 | 15821103 | HGF-treated cells also exhibited a glucose-dependent capability to secrete insulin into the cultured medium. |
| 8089 | 15821103 | Expression analysis of some of the genes regulating pancreatic beta-cell differentiation revealed a time-dependent transcription of neurogenin-3 and Neuro-D in response to HGF. |
| 8090 | 15821103 | Finally, we determined the susceptibility to proinflammatory cytokine (PTh1)-induced apoptosis by incubating HGF-treated and untreated ARIP cells with a cocktail of interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). |
| 8091 | 15821103 | Such treatment induced apoptotic death, as determined by the TUNEL technique, in about 40% of HGF-treated, insulin-secreting ARIP cells, while untreated ARIP cells were resistant to PTh1-induced apoptosis. |
| 8092 | 15821103 | In conclusion, we showed that HGF promotes the differentiation of ARIP cells into pancreatic beta-cell-like cells, and that the differentiation toward an insulin-secreting phenotype is associated with the appearance of susceptibility to cytokine-induced apoptosis. |
| 8093 | 15803108 | Moreover, orlistat appears to have a favourable effect on some inflammatory markers, such as TNF-alpha and interleukin-6 and has a time-depended effect on some haemostatic factors. |
| 8094 | 15790730 | Neutralization of MIF also down-regulated the ex vivo secretion of the proinflammatory mediators, TNF-alpha, interferon-gamma, and nitric oxide, while augmenting that of the antiinflammatory cytokine, IL-10. |
| 8095 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 8096 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 8097 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 8098 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 8099 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 8100 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 8101 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 8102 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 8103 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 8104 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 8105 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 8106 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 8107 | 15784408 | Because the inflammatory cytokine, tumor necrosis factor-alpha (TNF alpha), is associated with insulin resistance in various models of obesity and diabetes, we sought to determine whether circulating concentrations of this cytokine and its soluble receptors are higher in MA than NHW, and also to determine if the TNF alpha system is related to the lower insulin sensitivity in MA. |
| 8108 | 15784408 | Because the inflammatory cytokine, tumor necrosis factor-alpha (TNF alpha), is associated with insulin resistance in various models of obesity and diabetes, we sought to determine whether circulating concentrations of this cytokine and its soluble receptors are higher in MA than NHW, and also to determine if the TNF alpha system is related to the lower insulin sensitivity in MA. |
| 8109 | 15784408 | Fasting blood samples were used to determine concentrations of TNF alpha, soluble TNF receptors 1 (sTNFR1) and 2 (sTNFR2) in the same 13 MA (7 women, 6 men, age=27.0+/-2.0 years, BMI=23.0+/-0.7) and 13 NHW (7 women, 6 men, age=24.8+/-1.5 years, BMI=22.8+/-0.6) previously shown to exhibit differences in insulin sensitivity. |
| 8110 | 15784408 | Fasting blood samples were used to determine concentrations of TNF alpha, soluble TNF receptors 1 (sTNFR1) and 2 (sTNFR2) in the same 13 MA (7 women, 6 men, age=27.0+/-2.0 years, BMI=23.0+/-0.7) and 13 NHW (7 women, 6 men, age=24.8+/-1.5 years, BMI=22.8+/-0.6) previously shown to exhibit differences in insulin sensitivity. |
| 8111 | 15779368 | [TNF-alpha gene polymorphism, insulin resistance and type 2 diabetes in humans]. |
| 8112 | 15772055 | Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. |
| 8113 | 15772055 | Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. |
| 8114 | 15772055 | Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. |
| 8115 | 15772055 | Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. |
| 8116 | 15772055 | Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. |
| 8117 | 15772055 | We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. |
| 8118 | 15772055 | We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. |
| 8119 | 15772055 | We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. |
| 8120 | 15772055 | We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. |
| 8121 | 15772055 | We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. |
| 8122 | 15772055 | During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. |
| 8123 | 15772055 | During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. |
| 8124 | 15772055 | During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. |
| 8125 | 15772055 | During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. |
| 8126 | 15772055 | During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. |
| 8127 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 8128 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 8129 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 8130 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 8131 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 8132 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 8133 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 8134 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 8135 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 8136 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 8137 | 15766512 | [Adiponectin: a new link between obesity, insulin resistance and cardiovascular disease]. |
| 8138 | 15766512 | Adiponectin stimulates fatty acids oxidation, reduces plasma triglycerides, and improves glucose metabolism by increasing the insulin sensitivity. |
| 8139 | 15766512 | In addition, adiponectin inhibits the inflammatory process that accompanies atherogenesis, as it reduces the expression of endothelial adhesion molecules, macrophage-to-foam cell transformation, tumor necrosis factor-alpha (TNF-alpha) expression in macrophages and adipocytes, and smooth muscle cell proliferation. |
| 8140 | 15766512 | Several insulin-resistant states, such as obesity and type 2 diabetes, or cardiovascular diseases, have been found to be associated with low levels of plasma adiponectin. |
| 8141 | 15766512 | Thus, therapeutic approaches aimed at increasing the adiponectin concentrations or the adiponectin tissue sensitivity and action could represent a novel treatment strategy for insulin resistance in type 2 diabetes and might have therapeutic implications as an anti-obesity drug or as an anti-atherogenic plasma protein. |
| 8142 | 15755259 | There were also pro-inflammatory and profibrotic responses, including increased IL-1beta (interleukin-1beta) expression in intact epidermis, TNF-alpha (tumour necrosis factor-alpha) in regions of angiogenesis, CTGF (connective tissue growth factor) in medial layers of arteries, and TGF-beta (transforming growth factor-beta) in glomerular tufts, tubular epithelial cells and interstitial endothelial cells. |
| 8143 | 15754849 | Lp(a), triglycerides, blood glucose, plasma insulin, malondialdehyde, diene conjugates, TBARS and TNF-alpha and IL-6 levels, which were significantly greater during the acute phase, showed a significant decline and serum nitrite and coenzyme Q demonstrated an increase at 4 weeks of follow-up when the acute reactions evoked by MI had been controlled. |
| 8144 | 15754848 | These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting in an increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotension-converting enzyme (ACE), interleukin (IL)-1, -2, -6, -18, and tumor necrosis factor-alpha (TNF-alpha), all of which are are proinflammatory agents. |
| 8145 | 15754848 | These triggering factors are known to enhance sympathetic activity and decrease vagal tone, resulting in an increased secretion of plasma cortisol, noradrenaline, aldosterone, angiotension-converting enzyme (ACE), interleukin (IL)-1, -2, -6, -18, and tumor necrosis factor-alpha (TNF-alpha), all of which are are proinflammatory agents. |
| 8146 | 15754848 | In our study, we found a decrease in magnesium, potassium, vitamin A, E, C and beta carotene combined with an increase in thiobarbituric acid-reactive substances (TBARS), MDA and diene conjugates, TNF-alpha and IL-6, all of which are indicators of oxidative damage and proinflammatory activity, respectively. |
| 8147 | 15754848 | In our study, we found a decrease in magnesium, potassium, vitamin A, E, C and beta carotene combined with an increase in thiobarbituric acid-reactive substances (TBARS), MDA and diene conjugates, TNF-alpha and IL-6, all of which are indicators of oxidative damage and proinflammatory activity, respectively. |
| 8148 | 15754841 | It is possible that a marginal deficiency of long-chain PUFAs, especially n-3 fatty acids, due to poor dietary intake during the critical period of brain growth and development in the fetus, and later in the infant and also possibly in the child, adolescent and adult may enhance the release of tumor necrosis factor-alpha (TNF-alpha) interleukin (IL)-1, 2 and 6 and cause neuronal dysfunction. |
| 8149 | 15754841 | Treatment with neuropeptide Y abolished hyperphagia and ob mRNA (leptin mRNA) in this animal model. |
| 8150 | 15754841 | Treatment with omega-3 fatty acids, beta blockers, ACE inhibitors, estrogen, and meditation may have a beneficial effect on insulin receptors and ventromedial hypothalamic dysfunction. |
| 8151 | 15753145 | Dietary micronutrients with anti-inflammatory properties, specially alpha-tocopherol, may play an important role with regard to the prevention and treatment of CVD. alpha-Tocopherol has been shown to have anti-inflammatory effects both in vitro and in vivo. alpha-Tocopherol therapy, especially at high doses, has been shown to decrease release of pro-inflammatory cytokines (such as interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha) and the chemokine interleukin-8, and to decrease adhesion of monocytes to endothelium. |
| 8152 | 15749853 | Heat shock protein 60 inhibits Th1-mediated hepatitis model via innate regulation of Th1/Th2 transcription factors and cytokines. |
| 8153 | 15749853 | Yet, HSP60 can also down-regulate experimental immune arthritis and diabetes models by specific inhibition of Th1-like responses. |
| 8154 | 15749853 | We now report that HSP60 in vitro differentially modulates the expression of Th1/Th2 transcription factors in human T cells: HSP60 down-regulates T-bet, NF-kappaB, and NFATp and up-regulates GATA-3, leading to decreased secretion of TNF-alpha and IFN-gamma and enhanced secretion of IL-10. |
| 8155 | 15749853 | In BALB/c mice, HSP60 in vivo inhibited the clinical, histological, and serological manifestations of Con A-induced hepatitis associated with up-regulated T cell expression of suppressor of cytokine signaling 3 and GATA-3 and down-regulated T-bet expression. |
| 8156 | 15748944 | The objective of present study was to determine whether leukocyte-endothelial cell adhesive molecule, intercellular cell adhesion molecule-1 (ICAM-1) was increased after ischemia in diabetic rats. |
| 8157 | 15748944 | Western analyses also showed that interlukin-1beta (IL-1beta), but not TNF-alpha, was increased at 3 days of the reperfusion in diabetic rats. |
| 8158 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8159 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8160 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8161 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8162 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8163 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8164 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8165 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8166 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8167 | 15746249 | Tumor necrosis factor-{alpha} decreases Akt protein levels in 3T3-L1 adipocytes via the caspase-dependent ubiquitination of Akt. |
| 8168 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8169 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8170 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8171 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8172 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8173 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8174 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8175 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8176 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8177 | 15746249 | TNF-alpha is a mediator of insulin resistance in sepsis, obesity, and type 2 diabetes and is known to impair insulin signaling in adipocytes. |
| 8178 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8179 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8180 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8181 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8182 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8183 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8184 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8185 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8186 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8187 | 15746249 | In the present study we examined the posttranslational mechanisms by which short-term (<6-h) exposure of 3T3-L1 adipocytes to TNF-alpha decreases Akt levels. |
| 8188 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8189 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8190 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8191 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8192 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8193 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8194 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8195 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8196 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8197 | 15746249 | TNF-alpha treatment both increased the ubiquitination of Akt and decreased its protein level. |
| 8198 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8199 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8200 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8201 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8202 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8203 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8204 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8205 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8206 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8207 | 15746249 | The decrease in protein was associated with the presence of an (immunoreactive) Akt fragment after TNF-alpha treatment, indicative of Akt cleavage. |
| 8208 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8209 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8210 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8211 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8212 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8213 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8214 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8215 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8216 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8217 | 15746249 | The caspase-6 inhibitor Z-Val-Glu(OMe)-Ile-Asp(OMe)-CH(2)F potently suppressed Akt ubiquitination, degradation, and fragment formation, whereas the proteasome inhibitor Z-Leu-Leu-Leu-CHO modestly attenuated the decline in Akt levels. |
| 8218 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8219 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8220 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8221 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8222 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8223 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8224 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8225 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8226 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8227 | 15746249 | Exposure to TNF-alpha also enhanced the association of Akt with an E3 ligase activity. |
| 8228 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8229 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8230 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8231 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8232 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8233 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8234 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8235 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8236 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8237 | 15746249 | Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. |
| 8238 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8239 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8240 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8241 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8242 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8243 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8244 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8245 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8246 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8247 | 15746249 | Collectively, our results suggest that TNF-alpha induces the caspase-dependent degradation of Akt via the cleavage and ubiquitination of Akt, which results in its degradation through the 26S proteasome. |
| 8248 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8249 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8250 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8251 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8252 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8253 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8254 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8255 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8256 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8257 | 15746249 | Furthermore, the caspase- and proteasome-mediated degradation of Akt due to TNF-alpha exposure leads to impaired Akt-dependent insulin signaling in adipocytes. |
| 8258 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8259 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8260 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8261 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8262 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8263 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8264 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8265 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8266 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8267 | 15746249 | These findings expand the mechanism by which TNF-alpha impairs insulin signaling. |
| 8268 | 15744804 | Plasma adiponectin and insulin resistance in Korean type 2 diabetes mellitus. |
| 8269 | 15744804 | Adipose tissue plays an important role in insulin resistance through the dysregulated production and secretion of adipose-derived proteins, including tumor necrosis factor-alpha, plasminogen activator inhibitor-1, leptin, resistin, angiotensinogen, and adiponectin. |
| 8270 | 15744804 | In this study, the relationship between fasting plasma adiponectin concentration and adiposity, body composition, insulin sensitivity (ITT, HOMAIR, QUICK), lipid profile, fasting insulin concentration were examined in Korean type 2 diabetes. |
| 8271 | 15744804 | Baseline blood samples were drawn for the determinations of fasting plasma glucose, insulin, adiponectin, total cholesterol, triglyceride, LDL-cholesterol, and HDL-cholesterol. |
| 8272 | 15744804 | In conclusion, the plasma adiponectin concentrations were closely related to the insulin resistance parameters in Korean type 2 diabetic patients. |
| 8273 | 15741250 | Resistin is a recently recognized adipocytokine thought to contribute to insulin resistance. |
| 8274 | 15741250 | We determined resistin levels and metabolic parameters in 24 HIV-infected men and women with lipoatrophy and hyperinsulinemia and studied the effect of 12 wk of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone (4-8 mg/d) on resistin in these subjects. |
| 8275 | 15741250 | Participants completed metabolic testing before and after rosiglitazone including fasting determination of resistin, adiponectin, and leptin levels, serum inflammatory markers, and hyperinsulinemic euglycemic clamp testing. |
| 8276 | 15741250 | Resistin concentration decreased significantly after rosiglitazone (12.17 +/- 1.15 ng/ml to 10.23 +/- 1.05 ng/ml; P = 0.02), in conjunction with significant increases in adiponectin- (P < 0.001) and insulin- stimulated glucose disposal (P = 0.004). |
| 8277 | 15741250 | Leptin levels, as well as TNF-alpha, did not change with rosiglitazone. |
| 8278 | 15741250 | In summary, among HIV-infected subjects with insulin resistance and lipoatrophy, resistin levels decreased significantly after rosiglitazone. |
| 8279 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 8280 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 8281 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 8282 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 8283 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 8284 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 8285 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 8286 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 8287 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 8288 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 8289 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 8290 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 8291 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 8292 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 8293 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 8294 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 8295 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 8296 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 8297 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 8298 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 8299 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 8300 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 8301 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 8302 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 8303 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 8304 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 8305 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 8306 | 15725700 | We found that combined treatment of PPARgamma and cytokines (IL-1 or TNF-alpha) inhibited adipogenesis and induced osteoblastgenesis in bone marrow-derived mesenchymal stem cells. |
| 8307 | 15725700 | We found that combined treatment of PPARgamma and cytokines (IL-1 or TNF-alpha) inhibited adipogenesis and induced osteoblastgenesis in bone marrow-derived mesenchymal stem cells. |
| 8308 | 15725700 | We found that combined treatment of PPARgamma and cytokines (IL-1 or TNF-alpha) inhibited adipogenesis and induced osteoblastgenesis in bone marrow-derived mesenchymal stem cells. |
| 8309 | 15725700 | Furthermore, we showed that the ligand dependent transactivation function of PPARgamma was suppressed by IL-1 and TNF-alpha. |
| 8310 | 15725700 | Furthermore, we showed that the ligand dependent transactivation function of PPARgamma was suppressed by IL-1 and TNF-alpha. |
| 8311 | 15725700 | Furthermore, we showed that the ligand dependent transactivation function of PPARgamma was suppressed by IL-1 and TNF-alpha. |
| 8312 | 15725700 | This suppression was mediated through NF-kappaB activated by the TAK1/TAB1-NIK cascade, a downstream cascade triggered with IL-1 or TNF-alpha signaling. |
| 8313 | 15725700 | This suppression was mediated through NF-kappaB activated by the TAK1/TAB1-NIK cascade, a downstream cascade triggered with IL-1 or TNF-alpha signaling. |
| 8314 | 15725700 | This suppression was mediated through NF-kappaB activated by the TAK1/TAB1-NIK cascade, a downstream cascade triggered with IL-1 or TNF-alpha signaling. |
| 8315 | 15718275 | Immunohistochemistry displayed a greater amount of TNF-related apoptosis-inducing ligand (TRAIL) and KILLER, a key murine ligand and receptor involved in the extrinsic pathway, expressed in cumulus cells from hyperglycemic mice compared with controls, suggesting that this apoptotic pathway may be up-regulated under diabetic stress. |
| 8316 | 15707402 | Inflammatory islet damage is mediated at least partially by pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) produced by resident islet macrophages. |
| 8317 | 15707402 | Inflammatory islet damage is mediated at least partially by pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) produced by resident islet macrophages. |
| 8318 | 15707402 | Our present study has demonstrated that inhibition of the p38 pathway by a chemical p38 inhibitor, SB203580, suppresses IL-1beta and TNF-alpha production in human islets exposed to lipopolysaccharide (LPS) and/or inflammatory cytokines. |
| 8319 | 15707402 | Our present study has demonstrated that inhibition of the p38 pathway by a chemical p38 inhibitor, SB203580, suppresses IL-1beta and TNF-alpha production in human islets exposed to lipopolysaccharide (LPS) and/or inflammatory cytokines. |
| 8320 | 15707402 | SB203580 also inhibited the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the treated islets. |
| 8321 | 15707402 | SB203580 also inhibited the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the treated islets. |
| 8322 | 15704741 | [Tumor necrosis factor alfa (TNFalpha) and insulin resistance]. |
| 8323 | 15700136 | Arterial osteoprotegerin: increased amounts in diabetes and modifiable synthesis from vascular smooth muscle cells by insulin and TNF-alpha. |
| 8324 | 15699496 | In this study, mRNA expression of cytokines IL-12, TNF-alpha, IL-1, and IL-6 was studied in monocytes from diabetic patients after in vitro immune stimulation. |
| 8325 | 15699496 | In this study, mRNA expression of cytokines IL-12, TNF-alpha, IL-1, and IL-6 was studied in monocytes from diabetic patients after in vitro immune stimulation. |
| 8326 | 15699496 | Whereas IL-12(p40) was highly expressed in type 1 diabetic patients, TNF-alpha, IL-1, and IL-6 transcripts were elevated in type 1 but especially type 2 diabetic patients compared with healthy controls, suggesting an important proinflammatory milieu. |
| 8327 | 15699496 | Whereas IL-12(p40) was highly expressed in type 1 diabetic patients, TNF-alpha, IL-1, and IL-6 transcripts were elevated in type 1 but especially type 2 diabetic patients compared with healthy controls, suggesting an important proinflammatory milieu. |
| 8328 | 15694007 | Troglitazone, a PPAR-gamma activator prevents endothelial cell adhesion molecule expression and lymphocyte adhesion mediated by TNF-alpha. |
| 8329 | 15690319 | Differential regulation of insulin action and tumor necrosis factor alpha system activity by metformin. |
| 8330 | 15685173 | Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF-kappaB. |
| 8331 | 15685173 | The hepatic production of proinflammatory cytokines, including IL-6, IL-1beta and TNF-alpha, was increased in LIKK mice to a similar extent as induced by HFD in in wild-type mice. |
| 8332 | 15685173 | Insulin resistance was improved by systemic neutralization of IL-6 or salicylate inhibition of IKK-beta. |
| 8333 | 15684477 | The CML-enhanced neovascularization activity is associated with the actions of tumor necrosis factor (TNF) alpha, vascular endothelial growth factor and platelet-derived growth factor released from the choroidal explant (Kobayashi et al., Biol. |
| 8334 | 15679072 | Serum levels of soluble tumor necrosis factor-alpha receptor 2 are linked to insulin resistance and glucose intolerance in children. |
| 8335 | 15677345 | Biochemical analysis of the pancreas showed that OGG-1(-/-) mice had greater insulin content, indicative of a greater beta-cell mass coupled with lower levels of the chemokine MIP-1alpha and Th1 cytokines IL-12 and TNF-alpha. |
| 8336 | 15677345 | Levels of protective Th2 cytokines, IL-4 and IL-10 were significantly higher in the pancreata of OGG-1(-/-) mice as compared with the levels measured in wild-type mice. |
| 8337 | 15671250 | Microarray analysis revealed increased transcripts of genes encoding inflammatory cytokines, particularly interleukin (IL)-17, and islet cell regenerating genes, Reg3alpha, Reg3beta, and Reg3gamma. |
| 8338 | 15671250 | Our data indicate that progression to insulitis was connected to marked changes in islet antigen expression, beta-cell differentiation, and T cell activation and signaling, all associated with tumor necrosis factor-alpha and IL-6 expression. |
| 8339 | 15663921 | Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. |
| 8340 | 15663921 | Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. |
| 8341 | 15663921 | Adipocytes secrete a variety of cytokines, including IL-6 and TNF-alpha, that promote inflammation. |
| 8342 | 15663921 | Adipocytes secrete a variety of cytokines, including IL-6 and TNF-alpha, that promote inflammation. |
| 8343 | 15657375 | Elevated serum interferon-gamma-inducible chemokine-10/CXC chemokine ligand-10 in autoimmune primary adrenal insufficiency and in vitro expression in human adrenal cells primary cultures after stimulation with proinflammatory cytokines. |
| 8344 | 15657375 | No relationship was found between serum CXCL10 levels and anti-21-hydroxylase or adrenal cortex autoantibody titers or between CXCL10 levels and duration of disease. |
| 8345 | 15657375 | CXCL10, although not basally detected in cultured hZFC, was strongly induced by interferon-gamma and synergistically increased by TNF-alpha addition. |
| 8346 | 15654920 | The main pathway involved in insulin induction of adipogenic differentiation, monitored by fatty acid synthase expression, is the cascade insulin receptor substrate (IRS)-1/phosphatidylinositol 3-kinase (PI3K)/Akt. |
| 8347 | 15654920 | The main pathway involved in insulin induction of adipogenic differentiation, monitored by fatty acid synthase expression, is the cascade insulin receptor substrate (IRS)-1/phosphatidylinositol 3-kinase (PI3K)/Akt. |
| 8348 | 15654920 | Acute insulin treatment stimulates glucose transport largely by mediating translocation of GLUT4 to the plasma membrane, involving the activation of IRS-2/PI3K, and the downstream targets Akt and protein kinase C zeta. |
| 8349 | 15654920 | Acute insulin treatment stimulates glucose transport largely by mediating translocation of GLUT4 to the plasma membrane, involving the activation of IRS-2/PI3K, and the downstream targets Akt and protein kinase C zeta. |
| 8350 | 15654920 | Tumour necrosis factor (TNF-alpha) caused insulin resistance on glucose uptake by impairing insulin signalling at the level of IRS-2. |
| 8351 | 15654920 | Tumour necrosis factor (TNF-alpha) caused insulin resistance on glucose uptake by impairing insulin signalling at the level of IRS-2. |
| 8352 | 15654920 | Furthermore, brown adipocytes are also target cells for rosiglitazone action since they show a high expression of peroxisome proliferator activated receptor gamma, and rosiglitazone increased the expression of the thermogenic uncoupling protein 1. |
| 8353 | 15654920 | Furthermore, brown adipocytes are also target cells for rosiglitazone action since they show a high expression of peroxisome proliferator activated receptor gamma, and rosiglitazone increased the expression of the thermogenic uncoupling protein 1. |
| 8354 | 15654920 | Rosiglitazone ameliorates insulin resistance provoked by TNF-alpha, completely restoring insulin-stimulated glucose uptake in parallel to the insulin signalling cascade. |
| 8355 | 15654920 | Rosiglitazone ameliorates insulin resistance provoked by TNF-alpha, completely restoring insulin-stimulated glucose uptake in parallel to the insulin signalling cascade. |
| 8356 | 15652754 | We examined the effect of Linomide on T cell adhesion to intact ECM, and separately to LN, and FN, and on the release and production of tumor necrosis factor (TNFalpha) and nitrogen oxide (NO) in relation to adhesive molecules in non-obese diabetic (NOD) female spleen cells, focusing on intracellular adhesion molecule-1 (ICAM-1) and CD44. |
| 8357 | 15652754 | We examined the effect of Linomide on T cell adhesion to intact ECM, and separately to LN, and FN, and on the release and production of tumor necrosis factor (TNFalpha) and nitrogen oxide (NO) in relation to adhesive molecules in non-obese diabetic (NOD) female spleen cells, focusing on intracellular adhesion molecule-1 (ICAM-1) and CD44. |
| 8358 | 15652754 | In addition, exposure of T cells to Linomide resulted in increased expression of CD44 and ICAM-1 molecules on spleen cells of Linomide-treated mice; such an increase in adhesion molecule expression may lead to more effective arrest of T cell migration in vivo. |
| 8359 | 15652754 | In addition, exposure of T cells to Linomide resulted in increased expression of CD44 and ICAM-1 molecules on spleen cells of Linomide-treated mice; such an increase in adhesion molecule expression may lead to more effective arrest of T cell migration in vivo. |
| 8360 | 15652754 | The regulation of T-cell adhesion, adhesion receptor expression, and inhibition of TNFalpha and NO secretion by Linomide may explain its beneficial role and provide a new tool for suppressing self-reactive T cell-dependent autoimmune diseases. |
| 8361 | 15652754 | The regulation of T-cell adhesion, adhesion receptor expression, and inhibition of TNFalpha and NO secretion by Linomide may explain its beneficial role and provide a new tool for suppressing self-reactive T cell-dependent autoimmune diseases. |
| 8362 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8363 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8364 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8365 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8366 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8367 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8368 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8369 | 15652492 | TNF-alpha induces interleukin-8 and endothelin-1 expression in human endothelial cells with different redox pathways. |
| 8370 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8371 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8372 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8373 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8374 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8375 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8376 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8377 | 15652492 | We investigated the effect of TNF-alpha on interleukin-8 (IL-8) and endothelin-1 (ET-1) expression, and their different signal transduction pathways. |
| 8378 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8379 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8380 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8381 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8382 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8383 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8384 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8385 | 15652492 | By Northern blot analysis, TNF-alpha at 50, 100, 200, and 400 U/ml significantly induced IL-8 mRNA expression by 206%, 252%, 211%, and 158%, respectively, as compared to controls (p < 0.05). |
| 8386 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8387 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8388 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8389 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8390 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8391 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8392 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8393 | 15652492 | Overexpression of human superoxide dismutase (SOD) by adenovirus-mediated gene transfer or addition of exogenous hydrogen peroxide (H(2)O(2)) significantly enhanced TNF-alpha-induced IL-8 mRNA expression. |
| 8394 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8395 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8396 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8397 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8398 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8399 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8400 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8401 | 15652492 | Furthermore, HMECs treated with TNF-alpha at 50, 100, and 200 U/ml significantly increased ET-1 mRNA expression by 71%, 82%, and 66%, respectively (p < 0.05). |
| 8402 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8403 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8404 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8405 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8406 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8407 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8408 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8409 | 15652492 | By contrast, SOD gene transfer and exogenous H(2)O(2) significantly inhibited TNF-alpha-induced ET-1 mRNA expression. |
| 8410 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8411 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8412 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8413 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8414 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8415 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8416 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8417 | 15652492 | Thus, TNF-alpha significantly induces both IL-8 and ET-1 gene expression in HMECs possibly through different redox signaling pathways. |
| 8418 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8419 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8420 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8421 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8422 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8423 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8424 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8425 | 15652492 | H(2)O(2) enhances TNF-alpha-induced IL-8 expression, but inhibits TNF-alpha-induced ET-1 expression. |
| 8426 | 15651716 | The characteristics evaluated included age, height, body weight, body mass index (BMI), systolic and diastolic blood pressure, duration of diabetes, haemoglobin A1C and blood lipid concentrations, urinary albumin excretion rate, circulating concentrations of leptin, tumour necrosis factor-alpha (TNF-alpha), TNF-alpha receptor 1 and genotypes of the angiotensin-converting enzyme (ACE) gene. |
| 8427 | 15651716 | The characteristics evaluated included age, height, body weight, body mass index (BMI), systolic and diastolic blood pressure, duration of diabetes, haemoglobin A1C and blood lipid concentrations, urinary albumin excretion rate, circulating concentrations of leptin, tumour necrosis factor-alpha (TNF-alpha), TNF-alpha receptor 1 and genotypes of the angiotensin-converting enzyme (ACE) gene. |
| 8428 | 15651716 | We found statistically significant negative correlations between circulating OB-Re concentration and body weight, BMI, diastolic blood pressure, concentrations of leptin and TNF-alpha receptor 1. |
| 8429 | 15651716 | We found statistically significant negative correlations between circulating OB-Re concentration and body weight, BMI, diastolic blood pressure, concentrations of leptin and TNF-alpha receptor 1. |
| 8430 | 15646011 | In the present study we measured interleukin-18 (IL-18) and tumour necrosis factor-alpha (TNF-alpha) levels by enzyme linked immunosorbent assay (ELISA) in sera from 65 diabetic [30 with type 1 insulin dependent diabetes mellitus (IDDM) and 35 with type 2 non-insulin dependent diabetes mellitus (NIDDM)] patients and 15 healthy volunteers, to investigate their associations with metabolic parameters and to elucidate their roles in the pathogenesis of diabetic complications especially diabetic nephropathy. |
| 8431 | 15646011 | In the present study we measured interleukin-18 (IL-18) and tumour necrosis factor-alpha (TNF-alpha) levels by enzyme linked immunosorbent assay (ELISA) in sera from 65 diabetic [30 with type 1 insulin dependent diabetes mellitus (IDDM) and 35 with type 2 non-insulin dependent diabetes mellitus (NIDDM)] patients and 15 healthy volunteers, to investigate their associations with metabolic parameters and to elucidate their roles in the pathogenesis of diabetic complications especially diabetic nephropathy. |
| 8432 | 15646011 | In the present study we measured interleukin-18 (IL-18) and tumour necrosis factor-alpha (TNF-alpha) levels by enzyme linked immunosorbent assay (ELISA) in sera from 65 diabetic [30 with type 1 insulin dependent diabetes mellitus (IDDM) and 35 with type 2 non-insulin dependent diabetes mellitus (NIDDM)] patients and 15 healthy volunteers, to investigate their associations with metabolic parameters and to elucidate their roles in the pathogenesis of diabetic complications especially diabetic nephropathy. |
| 8433 | 15646011 | In the present study we measured interleukin-18 (IL-18) and tumour necrosis factor-alpha (TNF-alpha) levels by enzyme linked immunosorbent assay (ELISA) in sera from 65 diabetic [30 with type 1 insulin dependent diabetes mellitus (IDDM) and 35 with type 2 non-insulin dependent diabetes mellitus (NIDDM)] patients and 15 healthy volunteers, to investigate their associations with metabolic parameters and to elucidate their roles in the pathogenesis of diabetic complications especially diabetic nephropathy. |
| 8434 | 15646011 | Levels of IL-18 and TNF-alpha were significantly higher in both IDDM and NIDDM individuals as compared to the control group. |
| 8435 | 15646011 | Levels of IL-18 and TNF-alpha were significantly higher in both IDDM and NIDDM individuals as compared to the control group. |
| 8436 | 15646011 | Levels of IL-18 and TNF-alpha were significantly higher in both IDDM and NIDDM individuals as compared to the control group. |
| 8437 | 15646011 | Levels of IL-18 and TNF-alpha were significantly higher in both IDDM and NIDDM individuals as compared to the control group. |
| 8438 | 15646011 | Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. |
| 8439 | 15646011 | Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. |
| 8440 | 15646011 | Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. |
| 8441 | 15646011 | Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. |
| 8442 | 15646011 | High serum levels of IL-18 and TNF-alpha suggested that they might play a role in the pathogenesis of DM and in the development of nephropathy in diabetic patients whether of type 1 or 2. |
| 8443 | 15646011 | High serum levels of IL-18 and TNF-alpha suggested that they might play a role in the pathogenesis of DM and in the development of nephropathy in diabetic patients whether of type 1 or 2. |
| 8444 | 15646011 | High serum levels of IL-18 and TNF-alpha suggested that they might play a role in the pathogenesis of DM and in the development of nephropathy in diabetic patients whether of type 1 or 2. |
| 8445 | 15646011 | High serum levels of IL-18 and TNF-alpha suggested that they might play a role in the pathogenesis of DM and in the development of nephropathy in diabetic patients whether of type 1 or 2. |
| 8446 | 15645885 | Bacteria or their products have an indirect role by stimulating inflammation, which is associated with the excessive production of inflammatory mediators, such as prostaglandins, or cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1. |
| 8447 | 15634497 | [Maternal serum tumor necrosis factor-alpha concentration and correlation with insulin resistance in gestational diabetes]. |
| 8448 | 15630637 | Particularly interesting seems to be the function of inflammation markers (CRP, TNF-alpha, IL-1 beta, ISPs) as potential risk factors. |
| 8449 | 15628321 | Serum levels of tumor necrosis factor-alpha and interleukin-1 beta, which are thought to be essential for granuloma formation and induction of EN, were markedly elevated. |
| 8450 | 15627478 | Thiazolidinediones (TZDs) are pharmacological ligands of the peroxisome proliferator-activated receptor (PPAR)-gamma that are extensively used in the treatment of type II diabetes. |
| 8451 | 15627478 | On the contrary, both RSG and TRO significantly potentiated TNF-alpha-induced production of granulocyte/macrophage-colony-stimulating factor, interleukin (IL)-6 and/or IL-8 in these cells. |
| 8452 | 15625348 | TNF-alpha is known to cause insulin resistance, with similar defects in the insulin signalling pathway to those described in HCV infection. |
| 8453 | 15625348 | TNF-alpha is known to cause insulin resistance, with similar defects in the insulin signalling pathway to those described in HCV infection. |
| 8454 | 15625348 | A model of mice transgenic for the HCV core protein demonstrated insulin resistance, glucose intolerance, and elevated intrahepatic TNF-alpha mRNA; all of which were ameliorated by anti-TNF-alpha antibodies. |
| 8455 | 15625348 | A model of mice transgenic for the HCV core protein demonstrated insulin resistance, glucose intolerance, and elevated intrahepatic TNF-alpha mRNA; all of which were ameliorated by anti-TNF-alpha antibodies. |
| 8456 | 15622443 | TNF-alpha, TGF-beta1, IL-10, IL-6, gene polymorphisms in latent autoimmune diabetes of adults (LADA) and type 2 diabetes mellitus. |
| 8457 | 15622443 | TNF-alpha, TGF-beta1, IL-10, IL-6, gene polymorphisms in latent autoimmune diabetes of adults (LADA) and type 2 diabetes mellitus. |
| 8458 | 15622443 | In this study, healthy individuals LADA and type 2 diabetic patients were genotyped for IL-6-174G/C, TNF-alpha-308A/G, TGF-beta1-codon10T/C, TGF-beta1-codon25G/C, IL-10-1082A/G, IL-10-819T/C, IL-10-592A/C gene polymorphisms, by sequence-specific-primer polymerase chain reaction methodology. |
| 8459 | 15622443 | In this study, healthy individuals LADA and type 2 diabetic patients were genotyped for IL-6-174G/C, TNF-alpha-308A/G, TGF-beta1-codon10T/C, TGF-beta1-codon25G/C, IL-10-1082A/G, IL-10-819T/C, IL-10-592A/C gene polymorphisms, by sequence-specific-primer polymerase chain reaction methodology. |
| 8460 | 15616624 | The evidence that human insulin-dependent diabetes mellitus (IDDM) is a T cell-mediated disease is well substantiated, and the use of transgenic technology to understand the Th1/Th2 paradigm will provide keys to attenuating pathogenic autoimmunity. |
| 8461 | 15616624 | Insofar as the role of Th1 cytokines in IDDM is concerned, interferon gamma is considered a critical player in the etiology, a proinflammatory role has been determined for IDDM, interleukin-2 is considered an "amplification" factor, and tumor necrosis factor-alpha presents dichotomous effects. |
| 8462 | 15616624 | Regarding the role of Th2 cytokines in IDDM, interleukin-4 is essential for immunoprotection and counterregulation of IDDM, and interleukin-10 plays immunoprotective and destructive roles. |
| 8463 | 15616624 | Of all the cytokines examined, IL-4 seems to be the likely candidate for preventing IDDM. |
| 8464 | 15613743 | Healing of chronic gastric ulcers in diabetic rats treated with native aspirin, nitric oxide (NO)-derivative of aspirin and cyclooxygenase (COX)-2 inhibitor. |
| 8465 | 15613743 | Healing of chronic gastric ulcers in diabetic rats treated with native aspirin, nitric oxide (NO)-derivative of aspirin and cyclooxygenase (COX)-2 inhibitor. |
| 8466 | 15613743 | Healing of chronic gastric ulcers in diabetic rats treated with native aspirin, nitric oxide (NO)-derivative of aspirin and cyclooxygenase (COX)-2 inhibitor. |
| 8467 | 15613743 | Healing of chronic gastric ulcers in diabetic rats treated with native aspirin, nitric oxide (NO)-derivative of aspirin and cyclooxygenase (COX)-2 inhibitor. |
| 8468 | 15613743 | Four weeks after STZ injection, gastric ulcers were induced using the acetic acid method and rats with gastric ulcers received the treatment with 1) aspirin (ASA, 30 mg/kg-d i.g.), 2) NO-ASA applied in equimolar dose of 50 mg/kg-d i.g., 3) rofecoxib (5 mg/kg-d i.g.), the selective cyclooxygenase-(COX)-2 inhibitor and 4) SNAP (5 mg/kg-d i.g.), a donor of NO, combined with ASA (30 mg/kg-d i.g.). |
| 8469 | 15613743 | Four weeks after STZ injection, gastric ulcers were induced using the acetic acid method and rats with gastric ulcers received the treatment with 1) aspirin (ASA, 30 mg/kg-d i.g.), 2) NO-ASA applied in equimolar dose of 50 mg/kg-d i.g., 3) rofecoxib (5 mg/kg-d i.g.), the selective cyclooxygenase-(COX)-2 inhibitor and 4) SNAP (5 mg/kg-d i.g.), a donor of NO, combined with ASA (30 mg/kg-d i.g.). |
| 8470 | 15613743 | Four weeks after STZ injection, gastric ulcers were induced using the acetic acid method and rats with gastric ulcers received the treatment with 1) aspirin (ASA, 30 mg/kg-d i.g.), 2) NO-ASA applied in equimolar dose of 50 mg/kg-d i.g., 3) rofecoxib (5 mg/kg-d i.g.), the selective cyclooxygenase-(COX)-2 inhibitor and 4) SNAP (5 mg/kg-d i.g.), a donor of NO, combined with ASA (30 mg/kg-d i.g.). |
| 8471 | 15613743 | Four weeks after STZ injection, gastric ulcers were induced using the acetic acid method and rats with gastric ulcers received the treatment with 1) aspirin (ASA, 30 mg/kg-d i.g.), 2) NO-ASA applied in equimolar dose of 50 mg/kg-d i.g., 3) rofecoxib (5 mg/kg-d i.g.), the selective cyclooxygenase-(COX)-2 inhibitor and 4) SNAP (5 mg/kg-d i.g.), a donor of NO, combined with ASA (30 mg/kg-d i.g.). |
| 8472 | 15613743 | Ten days after the induction of the ulcers, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively and the plasma cytokine such as IL-1beta, TNF-alpha and IL-10 were determined. |
| 8473 | 15613743 | Ten days after the induction of the ulcers, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively and the plasma cytokine such as IL-1beta, TNF-alpha and IL-10 were determined. |
| 8474 | 15613743 | Ten days after the induction of the ulcers, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively and the plasma cytokine such as IL-1beta, TNF-alpha and IL-10 were determined. |
| 8475 | 15613743 | Ten days after the induction of the ulcers, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively and the plasma cytokine such as IL-1beta, TNF-alpha and IL-10 were determined. |
| 8476 | 15613743 | The prolongation of the healing in diabetic animals was associated with an increase in the plasma cytokine (IL-1beta, TNF-alpha and IL-10) levels. |
| 8477 | 15613743 | The prolongation of the healing in diabetic animals was associated with an increase in the plasma cytokine (IL-1beta, TNF-alpha and IL-10) levels. |
| 8478 | 15613743 | The prolongation of the healing in diabetic animals was associated with an increase in the plasma cytokine (IL-1beta, TNF-alpha and IL-10) levels. |
| 8479 | 15613743 | The prolongation of the healing in diabetic animals was associated with an increase in the plasma cytokine (IL-1beta, TNF-alpha and IL-10) levels. |
| 8480 | 15613743 | ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals. |
| 8481 | 15613743 | ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals. |
| 8482 | 15613743 | ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals. |
| 8483 | 15613743 | ASA and rofecoxib, that significantly suppressed the mucosal prostaglandin (PG) E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin, while elevating plasma IL-1beta, TNF-alpha and IL-10 concentrations in non-diabetic rats and these alterations were significantly augmented in diabetic animals. |
| 8484 | 15613743 | In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals. |
| 8485 | 15613743 | In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals. |
| 8486 | 15613743 | In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals. |
| 8487 | 15613743 | In contrast to ASA, the treatment with NO-ASA failed to influence both, the ulcer healing and GBF at ulcer margin and significantly attenuated the plasma levels of IL-1beta, TNF-alpha and IL-10 as compared to those recorded in ASA- or rofecoxib-treated animals. |
| 8488 | 15613743 | We conclude that: 1) ulcer healing is dramatically impaired in experimental diabetes and this effect involves the fall in the gastric microcirculation at the ulcer margin and increased release of proinflammatory cytokines; 2) classic NSAID such as ASA and selective COX-2 inhibitors such as rofecoxib, prolong ulcer healing under diabetic conditions probably due to suppression of endogenous PG and the fall in the GBF at the ulcer margin suggesting that both COX isoforms, namely, COX-1 and COX-2, are important sources of PG during ulcer healing in diabetes; and 3) NO-ASA counteracts the impairment of ulcer healing in diabetic rats induced by ASA, mainly due to the release of NO that compensates for PG deficiency resulting in enhancement in the GBF at ulcer margin and suppression of cytokine release in the ulcer area. |
| 8489 | 15613743 | We conclude that: 1) ulcer healing is dramatically impaired in experimental diabetes and this effect involves the fall in the gastric microcirculation at the ulcer margin and increased release of proinflammatory cytokines; 2) classic NSAID such as ASA and selective COX-2 inhibitors such as rofecoxib, prolong ulcer healing under diabetic conditions probably due to suppression of endogenous PG and the fall in the GBF at the ulcer margin suggesting that both COX isoforms, namely, COX-1 and COX-2, are important sources of PG during ulcer healing in diabetes; and 3) NO-ASA counteracts the impairment of ulcer healing in diabetic rats induced by ASA, mainly due to the release of NO that compensates for PG deficiency resulting in enhancement in the GBF at ulcer margin and suppression of cytokine release in the ulcer area. |
| 8490 | 15613743 | We conclude that: 1) ulcer healing is dramatically impaired in experimental diabetes and this effect involves the fall in the gastric microcirculation at the ulcer margin and increased release of proinflammatory cytokines; 2) classic NSAID such as ASA and selective COX-2 inhibitors such as rofecoxib, prolong ulcer healing under diabetic conditions probably due to suppression of endogenous PG and the fall in the GBF at the ulcer margin suggesting that both COX isoforms, namely, COX-1 and COX-2, are important sources of PG during ulcer healing in diabetes; and 3) NO-ASA counteracts the impairment of ulcer healing in diabetic rats induced by ASA, mainly due to the release of NO that compensates for PG deficiency resulting in enhancement in the GBF at ulcer margin and suppression of cytokine release in the ulcer area. |
| 8491 | 15613743 | We conclude that: 1) ulcer healing is dramatically impaired in experimental diabetes and this effect involves the fall in the gastric microcirculation at the ulcer margin and increased release of proinflammatory cytokines; 2) classic NSAID such as ASA and selective COX-2 inhibitors such as rofecoxib, prolong ulcer healing under diabetic conditions probably due to suppression of endogenous PG and the fall in the GBF at the ulcer margin suggesting that both COX isoforms, namely, COX-1 and COX-2, are important sources of PG during ulcer healing in diabetes; and 3) NO-ASA counteracts the impairment of ulcer healing in diabetic rats induced by ASA, mainly due to the release of NO that compensates for PG deficiency resulting in enhancement in the GBF at ulcer margin and suppression of cytokine release in the ulcer area. |
| 8492 | 15613409 | Recombinant methionyl human leptin administration activates signal transducer and activator of transcription 3 signaling in peripheral blood mononuclear cells in vivo and regulates soluble tumor necrosis factor-alpha receptor levels in humans with relative leptin deficiency. |
| 8493 | 15613407 | Increasing leptin levels from low physiologic to high physiologic in lean men and from higher physiologic to low pharmacologic in obese men over 3 d did not alter serum interferon-gamma, IL-10, TNF-alpha, monocyte chemoattractant protein-1, or soluble intercellular adhesion molecule-1. |
| 8494 | 15613407 | Increasing leptin levels from low physiologic to high physiologic in lean men and from higher physiologic to low pharmacologic in obese men over 3 d did not alter serum interferon-gamma, IL-10, TNF-alpha, monocyte chemoattractant protein-1, or soluble intercellular adhesion molecule-1. |
| 8495 | 15613407 | In obese subjects with type 2 diabetes mellitus, the administration of r-metHuLeptin for 4 or 16 wk, resulting in high pharmacologic leptin levels, did not activate the TNF-alpha system or increase cytokines or inflammatory markers, including IL-10, IL-6, C-reactive protein, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1. |
| 8496 | 15613407 | In obese subjects with type 2 diabetes mellitus, the administration of r-metHuLeptin for 4 or 16 wk, resulting in high pharmacologic leptin levels, did not activate the TNF-alpha system or increase cytokines or inflammatory markers, including IL-10, IL-6, C-reactive protein, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1. |
| 8497 | 15600254 | Genetic determination of TNF and myeloperoxidase production in dialyzed patients with diabetic nephropathy. |
| 8498 | 15593124 | The leukocyte recruitment was studied from 1 to 7 days after injection of thioglycollate (peritoneum), C5a (peritoneum, air pouch), CCL2 and CCL3 (air pouch). |
| 8499 | 15593124 | Morphological and flow cytometric analysis of the recruited cells was performed, IL-1 beta, TNF-alpha, IL-6, IL-12 and IL-10 in exudates measured, and in vitro CCL2-chemotaxis of exudate M Phi (Boyden chamber) determined. |
| 8500 | 15593124 | Chemokine-injected air pouches of NOD mice showed an increased IL-10 and a decreased IL-1 beta level, while the other cytokines were normally or very lowly expressed. |
| 8501 | 15593124 | A raised IL-10/IL-1 beta ratio at these sites and a deficient migratory capacity of NOD monocytes are important determinants in this impairment. |
| 8502 | 15591634 | Effect of amlodipine on insulin resistance & tumor necrosis factor-alpha levels in hypertensive obese type 2 diabetic patients. |
| 8503 | 15584977 | Expression of HLA-DR, CD80/86 and CD11c and secretion of interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, IL-6 and IL-10 were measured using flow cytometry. |
| 8504 | 15570020 | In all diabetic mice, the intake of these agents reduced triglyceride levels in plasma and liver (P < 0.05); however, only NAC, SAC and SPC treatments reduced cholesterol level in liver (P < 0.05). |
| 8505 | 15570020 | The overexpression of interleukin-6 and tumor necrosis factor-alpha in diabetic mice was suppressed by the intake of the 5 cysteine-containing agents (P < 0.05). |
| 8506 | 15565861 | Cells were transduced using a Maloney murine leukemia virus (MLV) vector coding for yellow fluorescent protein (YFP) and for one of the following antiapoptotic genes: cFLIP, FADD-DN, BcL-2, PI-9, and ICAM-2. |
| 8507 | 15565861 | The data demonstrate that cFLIP, FADD-DN, and PI-9 are significantly more effective in protecting NIT-1 cells than BcL-2 and ICAM-2. |
| 8508 | 15565861 | Additionally, the data show that despite its weak in vitro inhibition of caspase-3, PI-9 affords significant protection against TNF-alpha-induced apoptosis in these cells. |
| 8509 | 15564564 | Regulation of vascular calcification by osteoclast regulatory factors RANKL and osteoprotegerin. |
| 8510 | 15564564 | One emerging area in vascular biology involves the RANKL/RANK/OPG system, molecules of the tumor necrosis factor-related family recently discovered to be critical regulators of immune and skeletal biology. |
| 8511 | 15564564 | Concerted research efforts are greatly needed to understand these potential roles, clarify whether RANKL (receptor activator of nuclear factor kappaB ligand) promotes and osteoprotegerin (OPG) protects against vascular calcification, define how OPG genetic polymorphisms relate to cardiovascular disease, and learn whether elevated serum OPG levels reflect endothelial dysfunction in patients. |
| 8512 | 15564564 | Overall, the RANKL/RANK/OPG system may mediate important and complex links between the vascular, skeletal, and immune systems. |
| 8513 | 15564333 | In experimental models, oral salicylates, through their ability to interfere with the nuclear factor-kappa B (NF-kappa B) transcription pathway, have been demonstrated to reverse insulin resistance. |
| 8514 | 15564333 | In experimental models, oral salicylates, through their ability to interfere with the nuclear factor-kappa B (NF-kappa B) transcription pathway, have been demonstrated to reverse insulin resistance. |
| 8515 | 15564333 | In experimental models, oral salicylates, through their ability to interfere with the nuclear factor-kappa B (NF-kappa B) transcription pathway, have been demonstrated to reverse insulin resistance. |
| 8516 | 15564333 | After an 18-h incubation, the tissues were collected, and NF-kappa B p65 DNA-binding activity and I kappa B kinase (IKK-beta) and insulin receptor-beta protein expression were assessed by ELISA and Western blotting, respectively. |
| 8517 | 15564333 | After an 18-h incubation, the tissues were collected, and NF-kappa B p65 DNA-binding activity and I kappa B kinase (IKK-beta) and insulin receptor-beta protein expression were assessed by ELISA and Western blotting, respectively. |
| 8518 | 15564333 | After an 18-h incubation, the tissues were collected, and NF-kappa B p65 DNA-binding activity and I kappa B kinase (IKK-beta) and insulin receptor-beta protein expression were assessed by ELISA and Western blotting, respectively. |
| 8519 | 15564333 | The incubation medium was collected, and the release of TNF-alpha, IL-6, IL-8, resistin, adiponectin, and leptin was quantified by ELISA. |
| 8520 | 15564333 | The incubation medium was collected, and the release of TNF-alpha, IL-6, IL-8, resistin, adiponectin, and leptin was quantified by ELISA. |
| 8521 | 15564333 | The incubation medium was collected, and the release of TNF-alpha, IL-6, IL-8, resistin, adiponectin, and leptin was quantified by ELISA. |
| 8522 | 15564333 | Treatment of adipose tissue and skeletal muscle with sulfasalazine and BAY 11-7082 significantly inhibited the release of IL-6, IL-8, and TNF-alpha; NF-kappa B p65 DNA-binding activity; and IKK-beta protein expression (P < 0.05, by Newman-Keuls test). |
| 8523 | 15564333 | Treatment of adipose tissue and skeletal muscle with sulfasalazine and BAY 11-7082 significantly inhibited the release of IL-6, IL-8, and TNF-alpha; NF-kappa B p65 DNA-binding activity; and IKK-beta protein expression (P < 0.05, by Newman-Keuls test). |
| 8524 | 15564333 | Treatment of adipose tissue and skeletal muscle with sulfasalazine and BAY 11-7082 significantly inhibited the release of IL-6, IL-8, and TNF-alpha; NF-kappa B p65 DNA-binding activity; and IKK-beta protein expression (P < 0.05, by Newman-Keuls test). |
| 8525 | 15564333 | There was no effect of sulfasalazine and BAY 11-7082 on resistin, adiponectin, or leptin release. |
| 8526 | 15564333 | There was no effect of sulfasalazine and BAY 11-7082 on resistin, adiponectin, or leptin release. |
| 8527 | 15564333 | There was no effect of sulfasalazine and BAY 11-7082 on resistin, adiponectin, or leptin release. |
| 8528 | 15564333 | The data presented in this study demonstrate that the IKK-beta/NF-kappa B transcription pathway is a key regulator of IL-6, IL-8, and TNF-alpha release from adipose tissue and skeletal muscle. |
| 8529 | 15564333 | The data presented in this study demonstrate that the IKK-beta/NF-kappa B transcription pathway is a key regulator of IL-6, IL-8, and TNF-alpha release from adipose tissue and skeletal muscle. |
| 8530 | 15564333 | The data presented in this study demonstrate that the IKK-beta/NF-kappa B transcription pathway is a key regulator of IL-6, IL-8, and TNF-alpha release from adipose tissue and skeletal muscle. |
| 8531 | 15564333 | Control of the IKK-beta/NF-kappa B pathway may therefore provide an alternative therapeutic strategy for regulating aberrant cytokine release and thereby alleviating insulin resistance in type 2 diabetes mellitus. |
| 8532 | 15564333 | Control of the IKK-beta/NF-kappa B pathway may therefore provide an alternative therapeutic strategy for regulating aberrant cytokine release and thereby alleviating insulin resistance in type 2 diabetes mellitus. |
| 8533 | 15564333 | Control of the IKK-beta/NF-kappa B pathway may therefore provide an alternative therapeutic strategy for regulating aberrant cytokine release and thereby alleviating insulin resistance in type 2 diabetes mellitus. |
| 8534 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8535 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8536 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8537 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8538 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8539 | 15563986 | TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC. |
| 8540 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8541 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8542 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8543 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8544 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8545 | 15563986 | Although tumor necrosis factor alpha (TNFalpha) decreases the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), its mechanism is not understood. |
| 8546 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8547 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8548 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8549 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8550 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8551 | 15563986 | We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes. |
| 8552 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8553 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8554 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8555 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8556 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8557 | 15563986 | PPARgamma mRNA and aP2 mRNA levels were measured with real-time PCR. |
| 8558 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8559 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8560 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8561 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8562 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8563 | 15563986 | The application of 1 microM C6-ceramide for 36 h reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 56.3%, 80.4% and 62.1%, respectively. |
| 8564 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8565 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8566 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8567 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8568 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8569 | 15563986 | Overexpression of wild type PKCzeta magnified and accelerated the effect of TNFalpha and C6-ceramide on PPARgamma mRNA levels, whereas overexpression of dominant negative PKCzeta abolished the effect. |
| 8570 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8571 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8572 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8573 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8574 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8575 | 15563986 | We also found that the overexpression of constitutive active PKCzeta reduced PPARgamma mRNA level, aP2 mRNA level, and PPARgamma protein level to 61.4%, 70.3% and 81.6%, respectively. |
| 8576 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8577 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8578 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8579 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8580 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8581 | 15563986 | Furthermore, TNFalpha activated nuclear factor-kappaB (NF-kappaB), known as a downstream effector of PKCzeta to 256.6%, which was enhanced with overexpression of wild-type PKCzeta. |
| 8582 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8583 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8584 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8585 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8586 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8587 | 15563986 | On the other hand, treatment with phorbol 12-myristate 13-acetate, another activator of NF-kappaB, also reduced the expression of PPARgamma to 57.8%. |
| 8588 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8589 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8590 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8591 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8592 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8593 | 15563986 | These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway. |
| 8594 | 15563975 | There are many molecules, including Fas ligand (FasL) and cytokines, such as IL-1, TNF-alpha and IFN-gamma that cause release of other cytokine-mediators that have potential to damage the beta cells. |
| 8595 | 15563975 | The beta cell-death appears to ultimately be caused by receptor (Fas/FasL)-mediated mechanisms and/or by secretion of cytotoxic molecules (e.g., granzymes, perforin). |
| 8596 | 15563975 | Transgenic mice with beta cell specific overexpression of copper, zinc superoxide dismutase, or thioredoxin are resistant to autoimmune and STZ-induced diabetes. |
| 8597 | 15563961 | To test the role of adipocytokines, that tend to be abnormal in IGT subjects, on diabetic neuropathy, we analyzed the relationship between plasma adipocytokine levels (TNFalpha, adiponectin, and leptin) and nerve conduction velocity in 105 type 2 diabetic subjects (M/F = 66/39, age = 60.8 +/- 11.8 years, BMI = 24.7 +/- 5.0kg/m2). |
| 8598 | 15563961 | To test the role of adipocytokines, that tend to be abnormal in IGT subjects, on diabetic neuropathy, we analyzed the relationship between plasma adipocytokine levels (TNFalpha, adiponectin, and leptin) and nerve conduction velocity in 105 type 2 diabetic subjects (M/F = 66/39, age = 60.8 +/- 11.8 years, BMI = 24.7 +/- 5.0kg/m2). |
| 8599 | 15563961 | To test the role of adipocytokines, that tend to be abnormal in IGT subjects, on diabetic neuropathy, we analyzed the relationship between plasma adipocytokine levels (TNFalpha, adiponectin, and leptin) and nerve conduction velocity in 105 type 2 diabetic subjects (M/F = 66/39, age = 60.8 +/- 11.8 years, BMI = 24.7 +/- 5.0kg/m2). |
| 8600 | 15563961 | Relationship between corrected MCV or corrected SCV as a dependent variable and the duration of diabetes, HbA1C, BMI, TNFalpha, adiponectin, and leptin concentrations as independent variables were analyzed by multiple regression. |
| 8601 | 15563961 | Relationship between corrected MCV or corrected SCV as a dependent variable and the duration of diabetes, HbA1C, BMI, TNFalpha, adiponectin, and leptin concentrations as independent variables were analyzed by multiple regression. |
| 8602 | 15563961 | Relationship between corrected MCV or corrected SCV as a dependent variable and the duration of diabetes, HbA1C, BMI, TNFalpha, adiponectin, and leptin concentrations as independent variables were analyzed by multiple regression. |
| 8603 | 15563961 | Only corrected SCV was related significantly with TNFalpha (P < 0.05), and close to significantly with leptin (P = 0.059) concentrations. |
| 8604 | 15563961 | Only corrected SCV was related significantly with TNFalpha (P < 0.05), and close to significantly with leptin (P = 0.059) concentrations. |
| 8605 | 15563961 | Only corrected SCV was related significantly with TNFalpha (P < 0.05), and close to significantly with leptin (P = 0.059) concentrations. |
| 8606 | 15562250 | We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-alpha, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 +/- 0.8 kg/m2; age, 57 +/- 1 yr). |
| 8607 | 15562250 | We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-alpha, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 +/- 0.8 kg/m2; age, 57 +/- 1 yr). |
| 8608 | 15562250 | In all women, visceral fat volume was negatively related to leptin (r = -0.46, P < 0.05) and tended to be negatively related to adiponectin (r = -0.38, P = 0.09) gene expression. |
| 8609 | 15562250 | In all women, visceral fat volume was negatively related to leptin (r = -0.46, P < 0.05) and tended to be negatively related to adiponectin (r = -0.38, P = 0.09) gene expression. |
| 8610 | 15562250 | Among the nondiabetic women, fasting insulin (r = 0.69, P < 0.01), 2-h insulin (r = 0.56, P < 0.05), and HOMA index (r = 0.59, P < 0.05) correlated positively with TNF-alpha gene expression; fasting insulin (r = 0.54, P < 0.05) was positively related to, and 2-h insulin (r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area (r = -0.56, P < 0.05) was negatively related to, and insulin area (r = -0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression. |
| 8611 | 15562250 | Among the nondiabetic women, fasting insulin (r = 0.69, P < 0.01), 2-h insulin (r = 0.56, P < 0.05), and HOMA index (r = 0.59, P < 0.05) correlated positively with TNF-alpha gene expression; fasting insulin (r = 0.54, P < 0.05) was positively related to, and 2-h insulin (r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area (r = -0.56, P < 0.05) was negatively related to, and insulin area (r = -0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression. |
| 8612 | 15562250 | Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-beta-actin ratio, 2.26 +/- 0.46 vs. 3.31 +/- 0.33, P < 0.05). |
| 8613 | 15562250 | Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-beta-actin ratio, 2.26 +/- 0.46 vs. 3.31 +/- 0.33, P < 0.05). |
| 8614 | 15555051 | After this treatment, cell proliferation, activation of mitogen-activated protein kinase (MAPK), the level of apoptosis, and caspase-3 activation induced by removal of growth factors or tumor necrosis factor-alpha treatment were studied. |
| 8615 | 15555051 | After this treatment, cell proliferation, activation of mitogen-activated protein kinase (MAPK), the level of apoptosis, and caspase-3 activation induced by removal of growth factors or tumor necrosis factor-alpha treatment were studied. |
| 8616 | 15555051 | On the other hand, MCI-186 did not alter the level of apoptosis and caspase-3 activation induced by TNF-alpha treatment. |
| 8617 | 15555051 | On the other hand, MCI-186 did not alter the level of apoptosis and caspase-3 activation induced by TNF-alpha treatment. |
| 8618 | 15553663 | We have previously shown that nifedipine, one of the most popular dihydropyridine-based calcium antagonists, blocked tumor necrosis factor-alpha-induced monocyte chemoattractant protein-1 expression in endothelial cells (ECs) through its antioxidative properties. |
| 8619 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 8620 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 8621 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 8622 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 8623 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 8624 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 8625 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 8626 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 8627 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 8628 | 15540536 | The most important mediators and markers of this inflammation cascade are NF-kappaB, TNF-alpha, IL-6, CRP and PAI-1. |
| 8629 | 15531521 | The aim of this study was to 1) profile the basal release of TNF-alpha, IL-6, IL-8, and 8-isoprostane (a marker of oxidative stress); and 2) investigate the effect of stimulation on the release of cytokines from sc adipose tissue and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus (GDM). |
| 8630 | 15531521 | The aim of this study was to 1) profile the basal release of TNF-alpha, IL-6, IL-8, and 8-isoprostane (a marker of oxidative stress); and 2) investigate the effect of stimulation on the release of cytokines from sc adipose tissue and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus (GDM). |
| 8631 | 15531521 | The aim of this study was to 1) profile the basal release of TNF-alpha, IL-6, IL-8, and 8-isoprostane (a marker of oxidative stress); and 2) investigate the effect of stimulation on the release of cytokines from sc adipose tissue and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus (GDM). |
| 8632 | 15531521 | The aim of this study was to 1) profile the basal release of TNF-alpha, IL-6, IL-8, and 8-isoprostane (a marker of oxidative stress); and 2) investigate the effect of stimulation on the release of cytokines from sc adipose tissue and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus (GDM). |
| 8633 | 15531521 | The aim of this study was to 1) profile the basal release of TNF-alpha, IL-6, IL-8, and 8-isoprostane (a marker of oxidative stress); and 2) investigate the effect of stimulation on the release of cytokines from sc adipose tissue and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus (GDM). |
| 8634 | 15531521 | Placenta, sc adipose tissue, and skeletal muscle were incubated in the absence (control) or presence of lipopolysaccharide (LPS; 10 microg/ml), TNF-alpha (10 ng/ml), IL-6 (10 ng/ml), or IL-8 (10 ng/ml). |
| 8635 | 15531521 | Placenta, sc adipose tissue, and skeletal muscle were incubated in the absence (control) or presence of lipopolysaccharide (LPS; 10 microg/ml), TNF-alpha (10 ng/ml), IL-6 (10 ng/ml), or IL-8 (10 ng/ml). |
| 8636 | 15531521 | Placenta, sc adipose tissue, and skeletal muscle were incubated in the absence (control) or presence of lipopolysaccharide (LPS; 10 microg/ml), TNF-alpha (10 ng/ml), IL-6 (10 ng/ml), or IL-8 (10 ng/ml). |
| 8637 | 15531521 | Placenta, sc adipose tissue, and skeletal muscle were incubated in the absence (control) or presence of lipopolysaccharide (LPS; 10 microg/ml), TNF-alpha (10 ng/ml), IL-6 (10 ng/ml), or IL-8 (10 ng/ml). |
| 8638 | 15531521 | Placenta, sc adipose tissue, and skeletal muscle were incubated in the absence (control) or presence of lipopolysaccharide (LPS; 10 microg/ml), TNF-alpha (10 ng/ml), IL-6 (10 ng/ml), or IL-8 (10 ng/ml). |
| 8639 | 15531521 | After an 18-h incubation, the medium was collected, and the release of TNF-alpha, IL-6, IL-8, and 8-isoprostane was quantified by ELISA. |
| 8640 | 15531521 | After an 18-h incubation, the medium was collected, and the release of TNF-alpha, IL-6, IL-8, and 8-isoprostane was quantified by ELISA. |
| 8641 | 15531521 | After an 18-h incubation, the medium was collected, and the release of TNF-alpha, IL-6, IL-8, and 8-isoprostane was quantified by ELISA. |
| 8642 | 15531521 | After an 18-h incubation, the medium was collected, and the release of TNF-alpha, IL-6, IL-8, and 8-isoprostane was quantified by ELISA. |
| 8643 | 15531521 | After an 18-h incubation, the medium was collected, and the release of TNF-alpha, IL-6, IL-8, and 8-isoprostane was quantified by ELISA. |
| 8644 | 15531521 | Their was no difference in the release of TNF-alpha, IL-6, and IL-8 from placenta, adipose tissue, and skeletal muscle obtained from normal pregnant women and women with GDM. |
| 8645 | 15531521 | Their was no difference in the release of TNF-alpha, IL-6, and IL-8 from placenta, adipose tissue, and skeletal muscle obtained from normal pregnant women and women with GDM. |
| 8646 | 15531521 | Their was no difference in the release of TNF-alpha, IL-6, and IL-8 from placenta, adipose tissue, and skeletal muscle obtained from normal pregnant women and women with GDM. |
| 8647 | 15531521 | Their was no difference in the release of TNF-alpha, IL-6, and IL-8 from placenta, adipose tissue, and skeletal muscle obtained from normal pregnant women and women with GDM. |
| 8648 | 15531521 | Their was no difference in the release of TNF-alpha, IL-6, and IL-8 from placenta, adipose tissue, and skeletal muscle obtained from normal pregnant women and women with GDM. |
| 8649 | 15531521 | Stimulation of placenta, adipose tissue, and skeletal muscle with LPS and TNF-alpha resulted in greater release of IL-6 and IL-8, whereas only LPS increased TNF-alpha release from all three tissues. |
| 8650 | 15531521 | Stimulation of placenta, adipose tissue, and skeletal muscle with LPS and TNF-alpha resulted in greater release of IL-6 and IL-8, whereas only LPS increased TNF-alpha release from all three tissues. |
| 8651 | 15531521 | Stimulation of placenta, adipose tissue, and skeletal muscle with LPS and TNF-alpha resulted in greater release of IL-6 and IL-8, whereas only LPS increased TNF-alpha release from all three tissues. |
| 8652 | 15531521 | Stimulation of placenta, adipose tissue, and skeletal muscle with LPS and TNF-alpha resulted in greater release of IL-6 and IL-8, whereas only LPS increased TNF-alpha release from all three tissues. |
| 8653 | 15531521 | Stimulation of placenta, adipose tissue, and skeletal muscle with LPS and TNF-alpha resulted in greater release of IL-6 and IL-8, whereas only LPS increased TNF-alpha release from all three tissues. |
| 8654 | 15531184 | One component of inflammation that has reported to be increased in patients with diabetes only and CVD only are proinflammatory cytokines, particularly interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and interleukin-1 (IL-1beta). |
| 8655 | 15531184 | One component of inflammation that has reported to be increased in patients with diabetes only and CVD only are proinflammatory cytokines, particularly interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and interleukin-1 (IL-1beta). |
| 8656 | 15531184 | These results indicate that both IL-6 and TNF-alpha are chronically increased in diabetic women with and without CVD compared to nondiabetic women. |
| 8657 | 15531184 | These results indicate that both IL-6 and TNF-alpha are chronically increased in diabetic women with and without CVD compared to nondiabetic women. |
| 8658 | 15525583 | Rat islets treated with a cytokine combination (interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma) displayed a significant increase in islet cell apoptosis when the islets were incubated in 24.4 mM glucose compared with untreated islets at the same glucose concentration (13.07 +/- 1.78% vs 6.09 +/- 0.78%; P < 0.01) or islets incubated in 5.5 mM glucose concentration and cytokines (13.07 +/- 1.78% vs 8.04 +/- 1.56%; P < 0.05). |
| 8659 | 15525583 | However, the expression of anti-apoptotic mediators such as bcl-2 and bcl-xL did not show any significant change. |
| 8660 | 15525583 | These results suggest that cytokine- and STZ-mediated apoptotic effects on islet cells might be mediated by a glucose-induced hyperfunctional status and associated with an increase in Fas (Apo-1, CD-95) expression and no changes in the expression of the anti-apoptotic proteins bcl-xL and bcl-2. |
| 8661 | 15523649 | The region spanning the tumor necrosis factor (TNF) cluster in the human major histocompatibility complex (MHC) has been implicated in susceptibility to numerous immunopathological diseases, including type 1 diabetes mellitus and rheumatoid arthritis. |
| 8662 | 15523649 | The region spanning the tumor necrosis factor (TNF) cluster in the human major histocompatibility complex (MHC) has been implicated in susceptibility to numerous immunopathological diseases, including type 1 diabetes mellitus and rheumatoid arthritis. |
| 8663 | 15523649 | To this end, we genotyped 32 human leukocyte antigen (HLA)-homozygous workshop cell lines and 300 healthy control samples for 19 coding and promoter region SNPs spanning 45 kb in the central MHC near the TNF genes. |
| 8664 | 15523649 | To this end, we genotyped 32 human leukocyte antigen (HLA)-homozygous workshop cell lines and 300 healthy control samples for 19 coding and promoter region SNPs spanning 45 kb in the central MHC near the TNF genes. |
| 8665 | 15522996 | Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia. |
| 8666 | 15522996 | Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia. |
| 8667 | 15522996 | Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia. |
| 8668 | 15522996 | Resistin is an adipocyte-secreted hormone proposed to link obesity with insulin resistance and diabetes, but no previous study has performed a joint quantitative evaluation of white adipose tissue (WAT) resistin mRNA expression and serum levels in relation to insulinemia and glycemia in mice. |
| 8669 | 15522996 | Resistin is an adipocyte-secreted hormone proposed to link obesity with insulin resistance and diabetes, but no previous study has performed a joint quantitative evaluation of white adipose tissue (WAT) resistin mRNA expression and serum levels in relation to insulinemia and glycemia in mice. |
| 8670 | 15522996 | Resistin is an adipocyte-secreted hormone proposed to link obesity with insulin resistance and diabetes, but no previous study has performed a joint quantitative evaluation of white adipose tissue (WAT) resistin mRNA expression and serum levels in relation to insulinemia and glycemia in mice. |
| 8671 | 15522996 | We have thus comparatively assessed WAT resistin mRNA expression and serum resistin levels in lean C57BL/6J mice and various mouse models of obesity, including diet-induced obese (DIO) C57BL/6J mice, high fat-fed TNF-alpha-/- mice, and brown adipose tissue (BAT)-deficient uncoupling protein-diphtheria toxin A chain (UCP1-DTA) mice. |
| 8672 | 15522996 | We have thus comparatively assessed WAT resistin mRNA expression and serum resistin levels in lean C57BL/6J mice and various mouse models of obesity, including diet-induced obese (DIO) C57BL/6J mice, high fat-fed TNF-alpha-/- mice, and brown adipose tissue (BAT)-deficient uncoupling protein-diphtheria toxin A chain (UCP1-DTA) mice. |
| 8673 | 15522996 | We have thus comparatively assessed WAT resistin mRNA expression and serum resistin levels in lean C57BL/6J mice and various mouse models of obesity, including diet-induced obese (DIO) C57BL/6J mice, high fat-fed TNF-alpha-/- mice, and brown adipose tissue (BAT)-deficient uncoupling protein-diphtheria toxin A chain (UCP1-DTA) mice. |
| 8674 | 15522996 | We also studied whether treatment with the weight-reducing and insulin-sensitizing compounds, MTII, an alpha-melanocyte-stimulating hormone analog, or CNTF(Ax15), a ciliary neurotrophic factor analog, alters resistin mRNA expression and/or circulating levels in lean and DIO C57BL/6J mice. |
| 8675 | 15522996 | We also studied whether treatment with the weight-reducing and insulin-sensitizing compounds, MTII, an alpha-melanocyte-stimulating hormone analog, or CNTF(Ax15), a ciliary neurotrophic factor analog, alters resistin mRNA expression and/or circulating levels in lean and DIO C57BL/6J mice. |
| 8676 | 15522996 | We also studied whether treatment with the weight-reducing and insulin-sensitizing compounds, MTII, an alpha-melanocyte-stimulating hormone analog, or CNTF(Ax15), a ciliary neurotrophic factor analog, alters resistin mRNA expression and/or circulating levels in lean and DIO C57BL/6J mice. |
| 8677 | 15522996 | We find that resistin mRNA expression is similar in DIO and lean C57BL/6J mice, as well as in TNF-alpha-/- and wild-type (WT) mice. |
| 8678 | 15522996 | We find that resistin mRNA expression is similar in DIO and lean C57BL/6J mice, as well as in TNF-alpha-/- and wild-type (WT) mice. |
| 8679 | 15522996 | We find that resistin mRNA expression is similar in DIO and lean C57BL/6J mice, as well as in TNF-alpha-/- and wild-type (WT) mice. |
| 8680 | 15522996 | Circulating resistin levels, however, are higher in DIO C57BL/6J, high fat-fed TNF-alpha-/-, and UCP1-DTA mice compared with lean controls. |
| 8681 | 15522996 | Circulating resistin levels, however, are higher in DIO C57BL/6J, high fat-fed TNF-alpha-/-, and UCP1-DTA mice compared with lean controls. |
| 8682 | 15522996 | Circulating resistin levels, however, are higher in DIO C57BL/6J, high fat-fed TNF-alpha-/-, and UCP1-DTA mice compared with lean controls. |
| 8683 | 15522996 | Moreover, although resistin mRNA expression is upregulated by MTII treatment for 24 h and downregulated by CNTF(Ax15) treatment for 3 or 7 days, circulating resistin levels are not altered by MTII or CNTF(Ax15) treatment. |
| 8684 | 15522996 | Moreover, although resistin mRNA expression is upregulated by MTII treatment for 24 h and downregulated by CNTF(Ax15) treatment for 3 or 7 days, circulating resistin levels are not altered by MTII or CNTF(Ax15) treatment. |
| 8685 | 15522996 | Moreover, although resistin mRNA expression is upregulated by MTII treatment for 24 h and downregulated by CNTF(Ax15) treatment for 3 or 7 days, circulating resistin levels are not altered by MTII or CNTF(Ax15) treatment. |
| 8686 | 15522996 | In addition, serum resistin levels, but not resistin mRNA expression levels, are correlated with body weight, and neither resistin mRNA expression nor serum resistin levels are correlated with serum insulin or glucose levels. |
| 8687 | 15522996 | In addition, serum resistin levels, but not resistin mRNA expression levels, are correlated with body weight, and neither resistin mRNA expression nor serum resistin levels are correlated with serum insulin or glucose levels. |
| 8688 | 15522996 | In addition, serum resistin levels, but not resistin mRNA expression levels, are correlated with body weight, and neither resistin mRNA expression nor serum resistin levels are correlated with serum insulin or glucose levels. |
| 8689 | 15522996 | We conclude that transcriptional regulation of resistin in WAT does not correlate with circulating resistin levels and that circulating resistin is unlikely to play a major endocrine role in insulin resistance or glycemia in mice. |
| 8690 | 15522996 | We conclude that transcriptional regulation of resistin in WAT does not correlate with circulating resistin levels and that circulating resistin is unlikely to play a major endocrine role in insulin resistance or glycemia in mice. |
| 8691 | 15522996 | We conclude that transcriptional regulation of resistin in WAT does not correlate with circulating resistin levels and that circulating resistin is unlikely to play a major endocrine role in insulin resistance or glycemia in mice. |
| 8692 | 15522953 | This enhanced engraftment potential maps to the insulin-dependent diabetes locus 9 (Idd9) locus, and as such the tumor necrosis factor (TNF) receptor family as well as ski/sno genes may be involved in the mechanism underlying the autonomy of NOD HSCs. |
| 8693 | 15522914 | Intramyocardial lipid deposition was associated with an up-regulation of peroxisome proliferator-activated receptor alpha (PPARalpha) -regulated genes, myosin heavy chain beta (MHC-beta), and tumor necrosis factor alpha (TNF-alpha). |
| 8694 | 15504342 | AMPK inhibits fatty acid-induced increases in NF-kappaB transactivation in cultured human umbilical vein endothelial cells. |
| 8695 | 15504342 | AMPK inhibits fatty acid-induced increases in NF-kappaB transactivation in cultured human umbilical vein endothelial cells. |
| 8696 | 15504342 | AMPK inhibits fatty acid-induced increases in NF-kappaB transactivation in cultured human umbilical vein endothelial cells. |
| 8697 | 15504342 | We report here a novel role of AMPK, to prevent the activation of NF-kappaB in endothelial cells exposed to the fatty acid palmitate or the cytokine TNF-alpha. |
| 8698 | 15504342 | We report here a novel role of AMPK, to prevent the activation of NF-kappaB in endothelial cells exposed to the fatty acid palmitate or the cytokine TNF-alpha. |
| 8699 | 15504342 | We report here a novel role of AMPK, to prevent the activation of NF-kappaB in endothelial cells exposed to the fatty acid palmitate or the cytokine TNF-alpha. |
| 8700 | 15504342 | Incubation of cultured human umbilical vein endothelial cells (HUVEC) with elevated levels of palmitate (0.4mM) increased NF-kappaB reporter gene expression by 2- to 4-fold within 8h and caused a 7-fold increase in VCAM-1 mRNA expression at 24h. |
| 8701 | 15504342 | Incubation of cultured human umbilical vein endothelial cells (HUVEC) with elevated levels of palmitate (0.4mM) increased NF-kappaB reporter gene expression by 2- to 4-fold within 8h and caused a 7-fold increase in VCAM-1 mRNA expression at 24h. |
| 8702 | 15504342 | Incubation of cultured human umbilical vein endothelial cells (HUVEC) with elevated levels of palmitate (0.4mM) increased NF-kappaB reporter gene expression by 2- to 4-fold within 8h and caused a 7-fold increase in VCAM-1 mRNA expression at 24h. |
| 8703 | 15504342 | Similar increases in NF-kappaB activation and VCAM-1 expression were not observed in cells incubated with an elevated concentration of glucose (25mM). |
| 8704 | 15504342 | Similar increases in NF-kappaB activation and VCAM-1 expression were not observed in cells incubated with an elevated concentration of glucose (25mM). |
| 8705 | 15504342 | Similar increases in NF-kappaB activation and VCAM-1 expression were not observed in cells incubated with an elevated concentration of glucose (25mM). |
| 8706 | 15504342 | The increases in NF-kappaB activation and VCAM-1 expression caused by palmitate were markedly inhibited by co-incubation with the AMPK activator AICAR and, where studied, by expression of a constitutively active AMPK. |
| 8707 | 15504342 | The increases in NF-kappaB activation and VCAM-1 expression caused by palmitate were markedly inhibited by co-incubation with the AMPK activator AICAR and, where studied, by expression of a constitutively active AMPK. |
| 8708 | 15504342 | The increases in NF-kappaB activation and VCAM-1 expression caused by palmitate were markedly inhibited by co-incubation with the AMPK activator AICAR and, where studied, by expression of a constitutively active AMPK. |
| 8709 | 15504342 | Likewise, AMPK activation inhibited the increase in NF-kappaB reporter gene expression observed in HUVEC incubated with TNF-alpha. |
| 8710 | 15504342 | Likewise, AMPK activation inhibited the increase in NF-kappaB reporter gene expression observed in HUVEC incubated with TNF-alpha. |
| 8711 | 15504342 | Likewise, AMPK activation inhibited the increase in NF-kappaB reporter gene expression observed in HUVEC incubated with TNF-alpha. |
| 8712 | 15504342 | The results suggest that AMPK inhibits the activation of NF-kappaB caused by both palmitate and TNF-alpha. |
| 8713 | 15504342 | The results suggest that AMPK inhibits the activation of NF-kappaB caused by both palmitate and TNF-alpha. |
| 8714 | 15504342 | The results suggest that AMPK inhibits the activation of NF-kappaB caused by both palmitate and TNF-alpha. |
| 8715 | 15504342 | The mechanism responsible for this action, as well as its relevance to the reported anti-atherogenic actions of exercise, metformin, thiazolidinediones, and adiponectin, all of which have been shown to activate AMPK, remains to be determined. |
| 8716 | 15504342 | The mechanism responsible for this action, as well as its relevance to the reported anti-atherogenic actions of exercise, metformin, thiazolidinediones, and adiponectin, all of which have been shown to activate AMPK, remains to be determined. |
| 8717 | 15504342 | The mechanism responsible for this action, as well as its relevance to the reported anti-atherogenic actions of exercise, metformin, thiazolidinediones, and adiponectin, all of which have been shown to activate AMPK, remains to be determined. |
| 8718 | 15492021 | In vivo apoptosis of diabetogenic T cells in NOD mice by IFN-gamma/TNF-alpha. |
| 8719 | 15492021 | In vivo apoptosis of diabetogenic T cells in NOD mice by IFN-gamma/TNF-alpha. |
| 8720 | 15492021 | In vivo apoptosis of diabetogenic T cells in NOD mice by IFN-gamma/TNF-alpha. |
| 8721 | 15492021 | In vivo apoptosis of diabetogenic T cells in NOD mice by IFN-gamma/TNF-alpha. |
| 8722 | 15492021 | In vivo apoptosis of diabetogenic T cells in NOD mice by IFN-gamma/TNF-alpha. |
| 8723 | 15492021 | BCG immunization sequentially induced the production of TNF-alpha, IFN-gamma and IL-4 by splenocytes, increased the expression of Fas(high) (Apo-1/CD95), Fas ligand (FasL, CD95L) and TNF receptor (TNFR) on T cells leading to T cell apoptosis. |
| 8724 | 15492021 | BCG immunization sequentially induced the production of TNF-alpha, IFN-gamma and IL-4 by splenocytes, increased the expression of Fas(high) (Apo-1/CD95), Fas ligand (FasL, CD95L) and TNF receptor (TNFR) on T cells leading to T cell apoptosis. |
| 8725 | 15492021 | BCG immunization sequentially induced the production of TNF-alpha, IFN-gamma and IL-4 by splenocytes, increased the expression of Fas(high) (Apo-1/CD95), Fas ligand (FasL, CD95L) and TNF receptor (TNFR) on T cells leading to T cell apoptosis. |
| 8726 | 15492021 | BCG immunization sequentially induced the production of TNF-alpha, IFN-gamma and IL-4 by splenocytes, increased the expression of Fas(high) (Apo-1/CD95), Fas ligand (FasL, CD95L) and TNF receptor (TNFR) on T cells leading to T cell apoptosis. |
| 8727 | 15492021 | BCG immunization sequentially induced the production of TNF-alpha, IFN-gamma and IL-4 by splenocytes, increased the expression of Fas(high) (Apo-1/CD95), Fas ligand (FasL, CD95L) and TNF receptor (TNFR) on T cells leading to T cell apoptosis. |
| 8728 | 15492021 | The primary role of IFN-gamma and TNF-alpha in BCG-immunotherapy was demonstrated by (i) reversing the immune regulatory effect of BCG by in vivo treatment with neutralizing anti-cytokine antibodies, (ii) inducing effect similar to BCG by treatment with these cytokines. |
| 8729 | 15492021 | The primary role of IFN-gamma and TNF-alpha in BCG-immunotherapy was demonstrated by (i) reversing the immune regulatory effect of BCG by in vivo treatment with neutralizing anti-cytokine antibodies, (ii) inducing effect similar to BCG by treatment with these cytokines. |
| 8730 | 15492021 | The primary role of IFN-gamma and TNF-alpha in BCG-immunotherapy was demonstrated by (i) reversing the immune regulatory effect of BCG by in vivo treatment with neutralizing anti-cytokine antibodies, (ii) inducing effect similar to BCG by treatment with these cytokines. |
| 8731 | 15492021 | The primary role of IFN-gamma and TNF-alpha in BCG-immunotherapy was demonstrated by (i) reversing the immune regulatory effect of BCG by in vivo treatment with neutralizing anti-cytokine antibodies, (ii) inducing effect similar to BCG by treatment with these cytokines. |
| 8732 | 15492021 | The primary role of IFN-gamma and TNF-alpha in BCG-immunotherapy was demonstrated by (i) reversing the immune regulatory effect of BCG by in vivo treatment with neutralizing anti-cytokine antibodies, (ii) inducing effect similar to BCG by treatment with these cytokines. |
| 8733 | 15492021 | We show that Fas and TNF are two pathways in BCG-induced apoptosis of diabetogenic T cells, since in vitro blocking FasL or TNFR1 with antibody reduced T cell apoptosis and increased T cell proliferative response. |
| 8734 | 15492021 | We show that Fas and TNF are two pathways in BCG-induced apoptosis of diabetogenic T cells, since in vitro blocking FasL or TNFR1 with antibody reduced T cell apoptosis and increased T cell proliferative response. |
| 8735 | 15492021 | We show that Fas and TNF are two pathways in BCG-induced apoptosis of diabetogenic T cells, since in vitro blocking FasL or TNFR1 with antibody reduced T cell apoptosis and increased T cell proliferative response. |
| 8736 | 15492021 | We show that Fas and TNF are two pathways in BCG-induced apoptosis of diabetogenic T cells, since in vitro blocking FasL or TNFR1 with antibody reduced T cell apoptosis and increased T cell proliferative response. |
| 8737 | 15492021 | We show that Fas and TNF are two pathways in BCG-induced apoptosis of diabetogenic T cells, since in vitro blocking FasL or TNFR1 with antibody reduced T cell apoptosis and increased T cell proliferative response. |
| 8738 | 15492021 | Our results suggest that BCG down-regulates destructive autoimmunity by TNF-alpha/IFN-gamma-induced apoptosis of diabetogenic T cells through both Fas and TNF pathways. |
| 8739 | 15492021 | Our results suggest that BCG down-regulates destructive autoimmunity by TNF-alpha/IFN-gamma-induced apoptosis of diabetogenic T cells through both Fas and TNF pathways. |
| 8740 | 15492021 | Our results suggest that BCG down-regulates destructive autoimmunity by TNF-alpha/IFN-gamma-induced apoptosis of diabetogenic T cells through both Fas and TNF pathways. |
| 8741 | 15492021 | Our results suggest that BCG down-regulates destructive autoimmunity by TNF-alpha/IFN-gamma-induced apoptosis of diabetogenic T cells through both Fas and TNF pathways. |
| 8742 | 15492021 | Our results suggest that BCG down-regulates destructive autoimmunity by TNF-alpha/IFN-gamma-induced apoptosis of diabetogenic T cells through both Fas and TNF pathways. |
| 8743 | 15486052 | The Inflammation Score was composed of: white blood cell count, erythrocyte sedimentation rate, C-reactive protein, and soluble fraction of TNF-alpha receptors 1 and 2. |
| 8744 | 15481803 | The latter, in turn, lead to the formation, within the brain, of proinflammatory cytokines including interleukin (IL)-1alpha, IL-1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and one or more antinflammatory cytokines including tumor growth factor beta (TGF-beta), and IL-10. |
| 8745 | 15481803 | The latter, in turn, lead to the formation, within the brain, of proinflammatory cytokines including interleukin (IL)-1alpha, IL-1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and one or more antinflammatory cytokines including tumor growth factor beta (TGF-beta), and IL-10. |
| 8746 | 15481803 | De Simoni et al. were the first to show that the intracerebroventricular (icv) injection of IL-1beta in rats induced a dramatic increase in the concentration of circulating IL-6 that was much greater and more prolonged than that induced by intravenous bolus injection of the same dose of cytokine. |
| 8747 | 15481803 | De Simoni et al. were the first to show that the intracerebroventricular (icv) injection of IL-1beta in rats induced a dramatic increase in the concentration of circulating IL-6 that was much greater and more prolonged than that induced by intravenous bolus injection of the same dose of cytokine. |
| 8748 | 15481803 | Although IL-6, TNF-alpha and LPS are passively transferred from brain to blood (as shown by radioiodine-labeled tracer studies) peripheral cytokine responses to central injection differ from responses to IL-1beta. |
| 8749 | 15481803 | Although IL-6, TNF-alpha and LPS are passively transferred from brain to blood (as shown by radioiodine-labeled tracer studies) peripheral cytokine responses to central injection differ from responses to IL-1beta. |
| 8750 | 15472209 | Inverse correlations between indexes of insulin sensitivity and serum markers of inflammation have been observed and, particularly, TNF-alpha has been shown to be associated with the appearance of insulin resistance in pregnancy. |
| 8751 | 15471850 | Cytokines such as interleukin-1 (IL-1), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) mediate beta-cell dysfunction and islet degeneration, in part, through the induction of the inducible isoform of nitric-oxide synthase and the production of nitric oxide by beta-cells. |
| 8752 | 15471850 | Cytokines such as interleukin-1 (IL-1), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) mediate beta-cell dysfunction and islet degeneration, in part, through the induction of the inducible isoform of nitric-oxide synthase and the production of nitric oxide by beta-cells. |
| 8753 | 15471850 | In this study, we have shown that treatment of rat islets with IL-1beta or human islets with a cytokine mixture containing IL-1beta + IFN-gamma +/- TNF-alpha stimulates COX-2 expression and PGE(2) formation in a time-dependent manner. |
| 8754 | 15471850 | In this study, we have shown that treatment of rat islets with IL-1beta or human islets with a cytokine mixture containing IL-1beta + IFN-gamma +/- TNF-alpha stimulates COX-2 expression and PGE(2) formation in a time-dependent manner. |
| 8755 | 15470906 | What are the effects of peroxisome proliferator-activated receptor agonists on adiponectin, tumor necrosis factor-alpha, and other cytokines in insulin resistance? |
| 8756 | 15470906 | What are the effects of peroxisome proliferator-activated receptor agonists on adiponectin, tumor necrosis factor-alpha, and other cytokines in insulin resistance? |
| 8757 | 15470906 | Tumor necrosis factor-alpha (TNF-alpha) and adiponectin are believed to be important in the development of insulin resistance and atherosclerosis. |
| 8758 | 15470906 | Tumor necrosis factor-alpha (TNF-alpha) and adiponectin are believed to be important in the development of insulin resistance and atherosclerosis. |
| 8759 | 15470276 | Exposure to HAART increased intercellular adhesion molecule-1 (ICAM-1) gene expression and concomitant exposure to TNF-alpha further increased ICAM-1, vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule cell surface protein levels. |
| 8760 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 8761 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 8762 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 8763 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 8764 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 8765 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 8766 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 8767 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 8768 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 8769 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 8770 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 8771 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 8772 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 8773 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 8774 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 8775 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 8776 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 8777 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 8778 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 8779 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 8780 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 8781 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 8782 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 8783 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 8784 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 8785 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 8786 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 8787 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 8788 | 15464423 | Perforin, FasL, TNFalpha, IL-1, IFNgamma, and NO have been claimed as the effector molecules; however, they, as a single agent, might explain only part of beta-cell death in type 1 diabetes. |
| 8789 | 15464423 | Perforin, FasL, TNFalpha, IL-1, IFNgamma, and NO have been claimed as the effector molecules; however, they, as a single agent, might explain only part of beta-cell death in type 1 diabetes. |
| 8790 | 15464423 | Combinations or synergism between IFNgamma and TNFalpha or IL-1beta are being revisited as the death effectors, and molecular mechanism explaining such a synergism was addressed in several recent papers. |
| 8791 | 15464423 | Combinations or synergism between IFNgamma and TNFalpha or IL-1beta are being revisited as the death effectors, and molecular mechanism explaining such a synergism was addressed in several recent papers. |
| 8792 | 15383694 | Expression levels of interferon-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 mRNA were lower in GK/Jcl diabetic rats than those in control Wistar rats. |
| 8793 | 15383694 | Expression levels of interferon-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 mRNA were lower in GK/Jcl diabetic rats than those in control Wistar rats. |
| 8794 | 15383694 | Alveolar macrophages from GK/Jcl rats secreted less TNF-alpha and IL-12, and produced less NO compared with those from Wistar rats. |
| 8795 | 15383694 | Alveolar macrophages from GK/Jcl rats secreted less TNF-alpha and IL-12, and produced less NO compared with those from Wistar rats. |
| 8796 | 15379764 | Improvement of insulin sensitivity in insulin resistant subjects during prolonged treatment with the anti-TNF-alpha antibody infliximab. |
| 8797 | 15374883 | The prevention of GVHD in those recipients was associated with low-level production of inflammatory cytokines (ie, tumor necrosis factor alpha [TNF-alpha]), high-level production of anti-inflammatory cytokines (ie, interleukin 4 [IL-4] and IL-10), and confining of the donor CD8+ T-cell expansion to lymphohematopoietic tissues. |
| 8798 | 15365619 | Rosiglitazone ameliorates insulin resistance in brown adipocytes of Wistar rats by impairing TNF-alpha induction of p38 and p42/p44 mitogen-activated protein kinases. |
| 8799 | 15356076 | Plasma adiponectin (7.1 +/- 1.0 to 7.2 +/- 1.1 microg/ml), resistin (4.0 +/- 0.3 to 3.8 +/- 0.3 ng/ml), IL-6 (1.4 +/- 0.3 to 1.6 +/- 0.4 pg/ml), and TNFalpha (2.3 +/- 0.3 to 2.4 +/- 0.3 pg/ml) did not change after acipimox treatment. |
| 8800 | 15356076 | We concluded that sustained reduction in plasma FFA concentration in subjects with a strong family history of T2DM increases peripheral (muscle) and hepatic insulin sensitivity without increasing adiponectin levels or altering the secretion of other adipocytokines by the adipocyte. |
| 8801 | 15356026 | Before and after treatment, subjects received a 75-g oral glucose tolerance test (OGTT); euglycemic insulin clamp (40 mU/m(2).min) with 3-(3)H-glucose; determination of fat mass ((3)H(2)O); and measurement of fasting glucose, free fatty acids (FFAs), leptin, adiponectin, and TNFalpha concentrations. |
| 8802 | 15356026 | Before and after treatment, subjects received a 75-g oral glucose tolerance test (OGTT); euglycemic insulin clamp (40 mU/m(2).min) with 3-(3)H-glucose; determination of fat mass ((3)H(2)O); and measurement of fasting glucose, free fatty acids (FFAs), leptin, adiponectin, and TNFalpha concentrations. |
| 8803 | 15356026 | After 4 months of PIO, fasting plasma glucose concentration (Delta = -2.7 mol/liter), mean plasma glucose during OGTT (Delta = -3.8 mol/liter), and hemoglobin A(1c) (Delta = 1.7%) decreased (P < 0.05 vs. placebo) without change in fasting or post-OGTT plasma insulin levels. |
| 8804 | 15356026 | After 4 months of PIO, fasting plasma glucose concentration (Delta = -2.7 mol/liter), mean plasma glucose during OGTT (Delta = -3.8 mol/liter), and hemoglobin A(1c) (Delta = 1.7%) decreased (P < 0.05 vs. placebo) without change in fasting or post-OGTT plasma insulin levels. |
| 8805 | 15356026 | Fasting FFAs (Delta = 168 micromol/liter) and TNFalpha (Delta = 0.7 pg/ml) concentrations decreased (P < 0.05 vs. placebo), whereas adiponectin (Delta = 8.7 microg/ml) increased (P < 0.01 vs. placebo). |
| 8806 | 15356026 | Fasting FFAs (Delta = 168 micromol/liter) and TNFalpha (Delta = 0.7 pg/ml) concentrations decreased (P < 0.05 vs. placebo), whereas adiponectin (Delta = 8.7 microg/ml) increased (P < 0.01 vs. placebo). |
| 8807 | 15356026 | These results suggest that the direct effects of PIO on adipose tissue to decrease plasma FFA levels and increase plasma adiponectin contribute to the improvements in hepatic and peripheral insulin sensitivity and glucose tolerance in patients with T2DM. |
| 8808 | 15356026 | These results suggest that the direct effects of PIO on adipose tissue to decrease plasma FFA levels and increase plasma adiponectin contribute to the improvements in hepatic and peripheral insulin sensitivity and glucose tolerance in patients with T2DM. |
| 8809 | 15351728 | A novel IKKbeta inhibitor stimulates adiponectin levels and ameliorates obesity-linked insulin resistance. |
| 8810 | 15351728 | A novel insulin sensitizer, IkappaB kinase beta (IKKbeta) inhibitor, ameliorated insulin resistance and up-regulated plasma levels of adiponectin without producing a significant change in body weight in KKAy mice that were fed a high-fat diet. |
| 8811 | 15351728 | The IKKbeta inhibitor cancelled the TNFalpha-mediated down-regulation of adiponectin secretion and simultaneously up-regulated the phosphorylation of Akt in 3T3-L1 adipocytes. |
| 8812 | 15351728 | Using dominant-negative mutants of Akt or PKClambda (downstream effectors of phosphoinositide 3-kinase), insulin-stimulated Akt activity was found to be important in the regulation of adiponectin secretion by insulin in 3T3-L1 adipocytes. |
| 8813 | 15351728 | These observations suggest that "insulin-stimulated Akt activity in adipocytes" may play an important role in the regulation of adiponectin secretion. |
| 8814 | 15334371 | Fat-derived tumor necrosis factor alpha (TNF-alpha) and the acute-phase response protein, C-reactive protein (CRP), may also have a role in the development of obesity-related insulin resistance and type 2 diabetes mellitus. |
| 8815 | 15334371 | Fat-derived tumor necrosis factor alpha (TNF-alpha) and the acute-phase response protein, C-reactive protein (CRP), may also have a role in the development of obesity-related insulin resistance and type 2 diabetes mellitus. |
| 8816 | 15334371 | Fat-derived tumor necrosis factor alpha (TNF-alpha) and the acute-phase response protein, C-reactive protein (CRP), may also have a role in the development of obesity-related insulin resistance and type 2 diabetes mellitus. |
| 8817 | 15334371 | In this study, a group of 14 naturally occurring, insulin-requiring, type 2 diabetic cynomolgus monkeys were used to evaluate the effects of the PPAR-gamma agonist, rosiglitazone, on glycemic and lipid parameters and serum levels of TNF-alpha and CRP. |
| 8818 | 15334371 | In this study, a group of 14 naturally occurring, insulin-requiring, type 2 diabetic cynomolgus monkeys were used to evaluate the effects of the PPAR-gamma agonist, rosiglitazone, on glycemic and lipid parameters and serum levels of TNF-alpha and CRP. |
| 8819 | 15334371 | In this study, a group of 14 naturally occurring, insulin-requiring, type 2 diabetic cynomolgus monkeys were used to evaluate the effects of the PPAR-gamma agonist, rosiglitazone, on glycemic and lipid parameters and serum levels of TNF-alpha and CRP. |
| 8820 | 15334371 | No significant differences were noted in TNF-alpha and CRP serum levels during the treatment period. |
| 8821 | 15334371 | No significant differences were noted in TNF-alpha and CRP serum levels during the treatment period. |
| 8822 | 15334371 | No significant differences were noted in TNF-alpha and CRP serum levels during the treatment period. |
| 8823 | 15331536 | Mitochondrial catalase overexpression protects insulin-producing cells against toxicity of reactive oxygen species and proinflammatory cytokines. |
| 8824 | 15331536 | Mitochondrial catalase overexpression protects insulin-producing cells against toxicity of reactive oxygen species and proinflammatory cytokines. |
| 8825 | 15331536 | Therefore, catalase was stably overexpressed in mitochondria and for comparison in the cytoplasmic compartment of insulin-producing RINm5F cells and analyzed for its protective effect against toxicity of reactive oxygen species (ROS) and proinflammatory cytokines. |
| 8826 | 15331536 | Therefore, catalase was stably overexpressed in mitochondria and for comparison in the cytoplasmic compartment of insulin-producing RINm5F cells and analyzed for its protective effect against toxicity of reactive oxygen species (ROS) and proinflammatory cytokines. |
| 8827 | 15331536 | Mitochondrial catalase overexpression also preferentially protected against the toxicity of interleukin-1beta (IL-1beta) and a proinflammatory cytokine mixture (IL-1beta, tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) that is more toxic than IL-1beta alone. |
| 8828 | 15331536 | Mitochondrial catalase overexpression also preferentially protected against the toxicity of interleukin-1beta (IL-1beta) and a proinflammatory cytokine mixture (IL-1beta, tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) that is more toxic than IL-1beta alone. |
| 8829 | 15331536 | The observed higher rate of cell death after exposure to a cytokine mixture in comparison with the weaker effect of IL-1beta alone may be due to an additive toxicity of TNF-alpha through ROS formation in mitochondria. |
| 8830 | 15331536 | The observed higher rate of cell death after exposure to a cytokine mixture in comparison with the weaker effect of IL-1beta alone may be due to an additive toxicity of TNF-alpha through ROS formation in mitochondria. |
| 8831 | 15327404 | Effect of advanced glycation end-products on gene expression and synthesis of TNF-alpha and endothelial nitric oxide synthase by endothelial cells. |
| 8832 | 15322087 | Guggulsterone inhibits NF-kappaB and IkappaBalpha kinase activation, suppresses expression of anti-apoptotic gene products, and enhances apoptosis. |
| 8833 | 15322087 | Guggulsterone inhibits NF-kappaB and IkappaBalpha kinase activation, suppresses expression of anti-apoptotic gene products, and enhances apoptosis. |
| 8834 | 15322087 | Guggulsterone inhibits NF-kappaB and IkappaBalpha kinase activation, suppresses expression of anti-apoptotic gene products, and enhances apoptosis. |
| 8835 | 15322087 | Guggulsterone suppressed DNA binding of NF-kappaB induced by tumor necrosis factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and interleukin-1. |
| 8836 | 15322087 | Guggulsterone suppressed DNA binding of NF-kappaB induced by tumor necrosis factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and interleukin-1. |
| 8837 | 15322087 | Guggulsterone suppressed DNA binding of NF-kappaB induced by tumor necrosis factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and interleukin-1. |
| 8838 | 15322087 | NF-kappaB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, NIK, and IKK was also blocked by guggulsterone but without affecting p65-mediated gene transcription. |
| 8839 | 15322087 | NF-kappaB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, NIK, and IKK was also blocked by guggulsterone but without affecting p65-mediated gene transcription. |
| 8840 | 15322087 | NF-kappaB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, NIK, and IKK was also blocked by guggulsterone but without affecting p65-mediated gene transcription. |
| 8841 | 15322087 | In addition, guggulsterone decreased the expression of gene products involved in anti-apoptosis (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP, and survivin), proliferation (cyclin D1 and c-Myc), and metastasis (MMP-9, COX-2, and VEGF); this correlated with enhancement of apoptosis induced by TNF and chemotherapeutic agents. |
| 8842 | 15322087 | In addition, guggulsterone decreased the expression of gene products involved in anti-apoptosis (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP, and survivin), proliferation (cyclin D1 and c-Myc), and metastasis (MMP-9, COX-2, and VEGF); this correlated with enhancement of apoptosis induced by TNF and chemotherapeutic agents. |
| 8843 | 15322087 | In addition, guggulsterone decreased the expression of gene products involved in anti-apoptosis (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP, and survivin), proliferation (cyclin D1 and c-Myc), and metastasis (MMP-9, COX-2, and VEGF); this correlated with enhancement of apoptosis induced by TNF and chemotherapeutic agents. |
| 8844 | 15319185 | Unstimulated islet endothelium showed constitutive levels of ICAM-1 counter-ligand expression with minimal VCAM-1 expression; however, TNF-alpha stimulation increased cell surface density of both molecules. |
| 8845 | 15306563 | TNFalpha-induced insulin resistance in adipocytes as a membrane microdomain disorder: involvement of ganglioside GM3. |
| 8846 | 15306563 | TNFalpha-induced insulin resistance in adipocytes as a membrane microdomain disorder: involvement of ganglioside GM3. |
| 8847 | 15306563 | TNFalpha-induced insulin resistance in adipocytes as a membrane microdomain disorder: involvement of ganglioside GM3. |
| 8848 | 15306563 | Tumor necrosis factor alpha (TNFalpha) induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 8849 | 15306563 | Tumor necrosis factor alpha (TNFalpha) induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 8850 | 15306563 | Tumor necrosis factor alpha (TNFalpha) induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 8851 | 15306563 | In the DRMs from TNFalpha-treated 3T3-L1 adipocytes, GM3 levels were doubled compared with results in normal adipocytes. |
| 8852 | 15306563 | In the DRMs from TNFalpha-treated 3T3-L1 adipocytes, GM3 levels were doubled compared with results in normal adipocytes. |
| 8853 | 15306563 | In the DRMs from TNFalpha-treated 3T3-L1 adipocytes, GM3 levels were doubled compared with results in normal adipocytes. |
| 8854 | 15306563 | Furthermore, insulin-dependent IR internalization and intracellular movement of the IR substrate 1(IRS-1) were both greatly suppressed in the treated cells, leading to an uncoupling of IR-IRS-1 signaling. |
| 8855 | 15306563 | Furthermore, insulin-dependent IR internalization and intracellular movement of the IR substrate 1(IRS-1) were both greatly suppressed in the treated cells, leading to an uncoupling of IR-IRS-1 signaling. |
| 8856 | 15306563 | Furthermore, insulin-dependent IR internalization and intracellular movement of the IR substrate 1(IRS-1) were both greatly suppressed in the treated cells, leading to an uncoupling of IR-IRS-1 signaling. |
| 8857 | 15297438 | The aims of this study were to clarify whether common mechanisms are involved in FFA- and cytokine-induced beta-cell apoptosis and determine whether TNFalpha, an adipocyte-derived cytokine, potentiates FFA toxicity through enhanced NF-kappaB activation. |
| 8858 | 15297438 | The aims of this study were to clarify whether common mechanisms are involved in FFA- and cytokine-induced beta-cell apoptosis and determine whether TNFalpha, an adipocyte-derived cytokine, potentiates FFA toxicity through enhanced NF-kappaB activation. |
| 8859 | 15297438 | The aims of this study were to clarify whether common mechanisms are involved in FFA- and cytokine-induced beta-cell apoptosis and determine whether TNFalpha, an adipocyte-derived cytokine, potentiates FFA toxicity through enhanced NF-kappaB activation. |
| 8860 | 15297438 | Apoptosis was induced in insulinoma (INS)-1E cells, rat islets, and fluorescence-activated cell sorting-purified beta-cells by oleate, palmitate, and/or cytokines (IL-1beta, interferon-gamma, TNFalpha). |
| 8861 | 15297438 | Apoptosis was induced in insulinoma (INS)-1E cells, rat islets, and fluorescence-activated cell sorting-purified beta-cells by oleate, palmitate, and/or cytokines (IL-1beta, interferon-gamma, TNFalpha). |
| 8862 | 15297438 | Apoptosis was induced in insulinoma (INS)-1E cells, rat islets, and fluorescence-activated cell sorting-purified beta-cells by oleate, palmitate, and/or cytokines (IL-1beta, interferon-gamma, TNFalpha). |
| 8863 | 15297438 | The NF-kappaB-dependent genes inducible nitric oxide synthase and monocyte chemoattractant protein-1 were induced by IL-1beta but not by FFAs. |
| 8864 | 15297438 | The NF-kappaB-dependent genes inducible nitric oxide synthase and monocyte chemoattractant protein-1 were induced by IL-1beta but not by FFAs. |
| 8865 | 15297438 | The NF-kappaB-dependent genes inducible nitric oxide synthase and monocyte chemoattractant protein-1 were induced by IL-1beta but not by FFAs. |
| 8866 | 15297438 | Moreover, FFAs did not enhance NF-kappaB activation by TNFalpha. |
| 8867 | 15297438 | Moreover, FFAs did not enhance NF-kappaB activation by TNFalpha. |
| 8868 | 15297438 | Moreover, FFAs did not enhance NF-kappaB activation by TNFalpha. |
| 8869 | 15297438 | Palmitate and oleate induced C/EBP homologous protein, activating transcription factor-4, and immunoglobulin heavy chain binding protein mRNAs, X-box binding protein-1 alternative splicing, and activation of the activating transcription factor-6 promoter in INS-1E cells, suggesting that FFAs trigger an endoplasmic reticulum (ER) stress response. |
| 8870 | 15297438 | Palmitate and oleate induced C/EBP homologous protein, activating transcription factor-4, and immunoglobulin heavy chain binding protein mRNAs, X-box binding protein-1 alternative splicing, and activation of the activating transcription factor-6 promoter in INS-1E cells, suggesting that FFAs trigger an endoplasmic reticulum (ER) stress response. |
| 8871 | 15297438 | Palmitate and oleate induced C/EBP homologous protein, activating transcription factor-4, and immunoglobulin heavy chain binding protein mRNAs, X-box binding protein-1 alternative splicing, and activation of the activating transcription factor-6 promoter in INS-1E cells, suggesting that FFAs trigger an endoplasmic reticulum (ER) stress response. |
| 8872 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 8873 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 8874 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 8875 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 8876 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 8877 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 8878 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 8879 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 8880 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 8881 | 15292331 | Soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, C-reactive protein, TNFalpha, von Willebrand factor, and tissue plasminogen activator were measured at baseline and at the end of the trial. |
| 8882 | 15292331 | Soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, C-reactive protein, TNFalpha, von Willebrand factor, and tissue plasminogen activator were measured at baseline and at the end of the trial. |
| 8883 | 15292331 | A significant reduction in weight, fasting plasma glucose, soluble intercellular adhesion molecule (306 +/- 75 vs. 268 +/- 61 ng/ml, P = 0.029), soluble vascular cell adhesion molecule (595 +/- 114 vs. 508 +/- 126 ng/ml, P = 0.006), and von Willebrand factor (124 +/- 34 vs. 94 +/- 34%, P = 0.001) was seen in the treatment group, whereas tissue plasminogen activator, TNFalpha, and C-reactive protein levels did not change. |
| 8884 | 15292331 | A significant reduction in weight, fasting plasma glucose, soluble intercellular adhesion molecule (306 +/- 75 vs. 268 +/- 61 ng/ml, P = 0.029), soluble vascular cell adhesion molecule (595 +/- 114 vs. 508 +/- 126 ng/ml, P = 0.006), and von Willebrand factor (124 +/- 34 vs. 94 +/- 34%, P = 0.001) was seen in the treatment group, whereas tissue plasminogen activator, TNFalpha, and C-reactive protein levels did not change. |
| 8885 | 15283163 | Urinary PAI-1 concentrations (ng/gCr) were directly correlated with urinary N-acetyl glucosaminidase (NAG) levels (r=0.58, p<0.05). |
| 8886 | 15283163 | Exposure of growth-arrested HRCs with hypoxia (1% O2) or TNF-alpha (10 ng/ml) for 24 hours increased the secretion rate of PAI-1 protein by about 2.0-fold, while 24-hour treatment with high glucose (450 mg/dl) did not increase PAI-1 secretion at all, compared with that of the control cells under normal glucose (100 mg/dl) and normoxia (18% O2). |
| 8887 | 15277389 | We measured 1) proinflammatory cytokines (tumor necrosis factor-alpha, interleukin [IL]-6, IL1-beta, and IL-8), 2) markers of cardiovascular risk (C-reactive protein [CRP], homocysteine, and plasminogen activator inhibitor-1 [PAI-1]), 3) products of reactive oxygen species (ROS; thiobarbituric acid [TBA]-reacting material, and dichlorofluorescein [DCF]), and 4) cortisol, growth hormone (GH), and free fatty acids (FFAs) on admission (before insulin therapy) and after insulin therapy and resolution of hyperglycemia and/or ketoacidosis. |
| 8888 | 15277389 | Circulating levels of cytokines, TBA, DCF, PAI-1, FFAs, cortisol, and GH on admission were significantly increased two- to fourfold in patients with hyperglycemic crises compared with control subjects, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises. |
| 8889 | 15277389 | Changes in CRP and homocysteine in response to insulin therapy did not reach control levels after resolution of hyperglycemia. |
| 8890 | 15277374 | The secretion rate of leptin decreased by approximately 40%, as did that of tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6 and -8 decreased by 25-30%, whereas the secretion of plasminogen activator inhibitor 1 (PAI-1) and adiponectin did not show any changes. |
| 8891 | 15277374 | The secretion rate of leptin decreased by approximately 40%, as did that of tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6 and -8 decreased by 25-30%, whereas the secretion of plasminogen activator inhibitor 1 (PAI-1) and adiponectin did not show any changes. |
| 8892 | 15277374 | Regarding mRNA expression (by real-time PCR), only that of leptin and IL-6 decreased significantly. |
| 8893 | 15277374 | Regarding mRNA expression (by real-time PCR), only that of leptin and IL-6 decreased significantly. |
| 8894 | 15277374 | Circulating levels of leptin and PAI-1 decreased by 30 and 40%, respectively, but there were only minor changes in circulating TNF-alpha, IL-6, or adiponectin. |
| 8895 | 15277374 | Circulating levels of leptin and PAI-1 decreased by 30 and 40%, respectively, but there were only minor changes in circulating TNF-alpha, IL-6, or adiponectin. |
| 8896 | 15277374 | In conclusion, moderate caloric restriction but not macronutrient composition influences the production and secretion of adipose tissue-derived proteins during weight reduction, leptin being the most sensitive and adiponectin and PAI-1 the least sensitive. |
| 8897 | 15277374 | In conclusion, moderate caloric restriction but not macronutrient composition influences the production and secretion of adipose tissue-derived proteins during weight reduction, leptin being the most sensitive and adiponectin and PAI-1 the least sensitive. |
| 8898 | 15270782 | C-reactive protein, its role in inflammation, Type 2 diabetes and cardiovascular disease, and the effects of insulin-sensitizing treatment with thiazolidinediones. |
| 8899 | 15270782 | Increased concentrations of the marker of inflammation, C-reactive protein (CRP), are associated with insulin resistance, Type 2 diabetes and the development of cardiovascular disease. |
| 8900 | 15270782 | Treatment with these agents has a range of anti-atherogenic effects, including reduced levels of CRP, plasminogen activator inhibitor-1 (PAI-1), TNF-alpha and reactive oxygen species. |
| 8901 | 15258755 | All the PDCL showed resistance to Fas-mediated apoptosis but were significantly sensitive to the pro-apoptotic effect of inflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and interferon gamma]. |
| 8902 | 15258755 | All the PDCL showed resistance to Fas-mediated apoptosis but were significantly sensitive to the pro-apoptotic effect of inflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and interferon gamma]. |
| 8903 | 15258755 | Vascular endothelial growth factor, CCL2, CCL5 and transforming growth factor beta were the factors most frequently released; less frequent was the secretion of CXCL8, CCL22, IL-6 and sporadically CXCL12, IL-10 and hepatocyte growth factor. |
| 8904 | 15258755 | Vascular endothelial growth factor, CCL2, CCL5 and transforming growth factor beta were the factors most frequently released; less frequent was the secretion of CXCL8, CCL22, IL-6 and sporadically CXCL12, IL-10 and hepatocyte growth factor. |
| 8905 | 15258755 | The cytokines IL-1beta and TNFalpha were always undetectable. |
| 8906 | 15258755 | The cytokines IL-1beta and TNFalpha were always undetectable. |
| 8907 | 15256772 | We report the case of a 74-year-old woman with acquired generalized lipodystrophy who presented with low-normal serum concentrations of leptin, low adiponectin and resistin levels, and high serum levels of TNF alpha. |
| 8908 | 15256362 | We examined the induction of steatohepatitis and liver fibrosis in obese and type 2 diabetic db/db mice in a nutritional model of NASH and determined the relationship of the expressions of osteopontin (OPN) and leptin receptors to the pathogenesis of NASH. db/db mice and the corresponding lean and nondiabetic db/m mice were fed a diet deficient in methionine and choline (MCD diet) or control diet for 4 wk. |
| 8909 | 15256362 | Collagen I mRNA expression was increased 10-fold in db/db mice, 4-fold in db/m mice, and was unchanged in ob/ob mice. mRNA expressions of OPN, TNF-alpha, TGF-beta, and short-form leptin receptors (Ob-Ra) were significantly increased in db/db mice compared with db/m or ob/ob mice. |
| 8910 | 15256362 | Cultured hepatocytes expressed only Ob-Ra, and leptin stimulated OPN mRNA and protein expression in these cells. |
| 8911 | 15240727 | The expression of IL-1beta, TNF-alpha, and IL-12 was significantly decreased in the spleen of AG-treated, KRV-infected DR-BB rats compared with PBS-treated, KRV-infected control rats. |
| 8912 | 15240727 | Subsequent experiments revealed that AG treatment exerted its preventive effect in KRV-infected rats by maintaining the finely tuned immune balance normally disrupted by KRV, evidenced by a significant decrease in the expression of IFN-gamma, but not IL-4, and a decrease in Th1-type chemokine receptors CCR5, CXCR3, and CXCR4. |
| 8913 | 15240727 | We also found that iNOS inhibition by AG decreased the KRV-induced expression of MHC class II molecules and IL-2R alpha-chain, resulting in the suppression of T cell activation, evidenced by the decreased cytolytic activity of CD8(+) T cells. |
| 8914 | 15240650 | The proinflammatory cytokines TNFalpha, IL-6, and IL-8 are released from the placenta at term and have been implicated in and/or associated with various metabolic events, including decreased insulin sensitivity. |
| 8915 | 15240650 | The proinflammatory cytokines TNFalpha, IL-6, and IL-8 are released from the placenta at term and have been implicated in and/or associated with various metabolic events, including decreased insulin sensitivity. |
| 8916 | 15240650 | The proinflammatory cytokines TNFalpha, IL-6, and IL-8 are released from the placenta at term and have been implicated in and/or associated with various metabolic events, including decreased insulin sensitivity. |
| 8917 | 15240650 | The proinflammatory cytokines TNFalpha, IL-6, and IL-8 are released from the placenta at term and have been implicated in and/or associated with various metabolic events, including decreased insulin sensitivity. |
| 8918 | 15240650 | Under basal conditions, release of TNFalpha, IL-6, and IL-8 was similar in both control and GDM groups. |
| 8919 | 15240650 | Under basal conditions, release of TNFalpha, IL-6, and IL-8 was similar in both control and GDM groups. |
| 8920 | 15240650 | Under basal conditions, release of TNFalpha, IL-6, and IL-8 was similar in both control and GDM groups. |
| 8921 | 15240650 | Under basal conditions, release of TNFalpha, IL-6, and IL-8 was similar in both control and GDM groups. |
| 8922 | 15240650 | In response to oxidative stress, TNFalpha and 8-isoprostane release and nuclear factor-kappaB (NF-kappaB) DNA-binding activity were significantly increased in normal tissues (20-fold, 2-fold, and 35%, respectively, P < 0.01). |
| 8923 | 15240650 | In response to oxidative stress, TNFalpha and 8-isoprostane release and nuclear factor-kappaB (NF-kappaB) DNA-binding activity were significantly increased in normal tissues (20-fold, 2-fold, and 35%, respectively, P < 0.01). |
| 8924 | 15240650 | In response to oxidative stress, TNFalpha and 8-isoprostane release and nuclear factor-kappaB (NF-kappaB) DNA-binding activity were significantly increased in normal tissues (20-fold, 2-fold, and 35%, respectively, P < 0.01). |
| 8925 | 15240650 | In response to oxidative stress, TNFalpha and 8-isoprostane release and nuclear factor-kappaB (NF-kappaB) DNA-binding activity were significantly increased in normal tissues (20-fold, 2-fold, and 35%, respectively, P < 0.01). |
| 8926 | 15240650 | In contrast, the response of GDM tissues to oxidant stress was blunted, with no change in 8-isoprostane release, a 4-fold increase in TNFalpha release, and a 40% reduction in NF-kappaB DNA-binding activity. |
| 8927 | 15240650 | In contrast, the response of GDM tissues to oxidant stress was blunted, with no change in 8-isoprostane release, a 4-fold increase in TNFalpha release, and a 40% reduction in NF-kappaB DNA-binding activity. |
| 8928 | 15240650 | In contrast, the response of GDM tissues to oxidant stress was blunted, with no change in 8-isoprostane release, a 4-fold increase in TNFalpha release, and a 40% reduction in NF-kappaB DNA-binding activity. |
| 8929 | 15240650 | In contrast, the response of GDM tissues to oxidant stress was blunted, with no change in 8-isoprostane release, a 4-fold increase in TNFalpha release, and a 40% reduction in NF-kappaB DNA-binding activity. |
| 8930 | 15236748 | In contrast to the limited response of macrophages from C57BL/6 or NOR mice, NOD macrophages reacted aberrantly to both necrotic and apoptotic cells, with secretion of inappropriately high amounts of IL1beta and TNFalpha. |
| 8931 | 15231994 | Biochemical, genetic, and animal studies in recent years have established a critical role for the adipokine Acrp30/adiponectin in controlling whole-body metabolism, particularly by enhancing insulin sensitivity in muscle and liver, and by increasing fatty acid oxidation in muscle. |
| 8932 | 15231994 | We describe a widely expressed and highly conserved family of adiponectin paralogs designated as C1q/tumor necrosis factor-alpha-related proteins (CTRPs) 1-7. |
| 8933 | 15231994 | In the present study, we focus on mCTRP2, the mouse paralog most similar to adiponectin. |
| 8934 | 15231994 | At nanomolar concentrations, bacterially produced mCTRP2 rapidly induced phosphorylation of AMP-activated protein kinase, acetyl-CoA carboxylase, and mitogen-activated protein kinase in C2C12 myotubes, which resulted in increased glycogen accumulation and fatty acid oxidation. |
| 8935 | 15225809 | Expression of calbindin-D(28k) in neural cell suppressed the proapoptotic actions of presenilin-1, which is causally linked to familial Alzheimer's disease, by preventing calcium mediated mitochondrial damage and the subsequent release of cytochrome c. |
| 8936 | 15225809 | Calbindin, by buffering intracellular calcium can also protect HEK 293 kidney cells from parathyroid hormone induced apoptosis that was found to be mediated by a phospholipase C dependent increase in intracellular calcium. |
| 8937 | 15225809 | Our findings suggest that calbindin is capable of directly inhibiting the activity of caspase-3, a common downstream effector of multiple apoptotic signaling pathways, and that this inhibition results in an inhibition of tumor necrosis factor (TNFalpha) and glucocorticoid induced apoptosis in bone cells. |
| 8938 | 15223984 | Finally, ROS and lipid peroxidation increase the generation of several cytokines (TNF-alpha, TGF-B, Fas ligand) that play sundry roles in the pathogenesis of NASH. |
| 8939 | 15223973 | These signals mainly originate, either from the adipose tissue, like leptin and to a lesser extent interleukin 6, or from the pancreas, like insulin and amylin. |
| 8940 | 15223973 | It is well established, at least for leptin and insulin, that they enter the brain from the plasma where they induce/repress a network of important neuropeptide regulators of energy intake and expenditure. |
| 8941 | 15223973 | Beside these endocrine signals, a growing amount of literature show data relative to adipocyte-derived molecules, most of them belonging to the cytokine family, like IL6, TNFalpha, IL8, IL10 whose secretion also correlates with body fat mass and that may locally regulate fat mass expansion. |
| 8942 | 15223973 | In this review, we will synthesize data relative to the role played by insulin, leptin and amylin, either alone or through a cross talk, in "energy level sensing" at the brain level. |
| 8943 | 15217754 | In this study we analyze the mRNA expression levels of TNFalpha and its receptors (TNFR1 and TNFR2), in peripheral blood mononuclear cells (PBMC) from eleven, non-morbid, obese and 14, obese, type 2 DM women, by real-time quantitative PCR. |
| 8944 | 15217754 | We show an increase in the TNFR2 to TNFR1 ratio (mTNFR2/mTNFR1) in type 2 DM (r = 0.63; p = 0.021, after adjusting for age). |
| 8945 | 15217754 | Likewise, a positive correlation between mTNFR2/mTNFR1 and glucose was observed (r = 0.5; p = 0.029) in the whole group. |
| 8946 | 15217754 | We show that except for a positive association of mTNFR1 with body mass index at 60 min and of mTNFR2 with plasmatic triglycerids levels, no other significant differences were elicited by acute glucose in obese, non-diabetic women. |
| 8947 | 15213278 | Strongly positive statistical correlations were observed in patients with CKD between monocyte RAGE and plasma levels of tumor necrosis factor alpha (TNF-alpha) (r = 0.61), the monocyte activation marker, neopterin (r = 0.65), and the systemic acute phase reactant, C-reactive protein (r = 0.44). |
| 8948 | 15206145 | These include plasminogen activator inhibitor 1(PAI-1), tumor necrosis factor(TNF-alpha), leptin and adiponectin. |
| 8949 | 15206145 | These include plasminogen activator inhibitor 1(PAI-1), tumor necrosis factor(TNF-alpha), leptin and adiponectin. |
| 8950 | 15206145 | Increased productions of PAI-1 and TNF-alpha from accumulated fat contribute to the formation of thrombosis and insulin resistance in obesity, respectively. |
| 8951 | 15206145 | Increased productions of PAI-1 and TNF-alpha from accumulated fat contribute to the formation of thrombosis and insulin resistance in obesity, respectively. |
| 8952 | 15206145 | Adiponectin exerts insulin-sensitizing and anti-atherogenic effects, hence decrease of plasma adiponectin is causative for insulin resistance and atherosclerosis in obesity. |
| 8953 | 15206145 | Adiponectin exerts insulin-sensitizing and anti-atherogenic effects, hence decrease of plasma adiponectin is causative for insulin resistance and atherosclerosis in obesity. |
| 8954 | 15203128 | Freshly isolated islets or MIN6 beta cells, when pre-incubated with IL-6, showed significantly higher viabilities measured by MTT assay and FACS analysis of PI stained cells against pro-apoptotic signaling delivered by IL-1beta, TNF-alpha and IFN-gamma. |
| 8955 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8956 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8957 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8958 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8959 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8960 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 8961 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8962 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8963 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8964 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8965 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8966 | 15201277 | We challenged human endothelial cells simultaneously with tumor necrosis factor alpha (TNFalpha) and thrombin because many pathophysiological conditions, such as sepsis, diabetes, and coronary artery disease, result in the concurrent presence of circulating inflammatory mediators and activated thrombin. |
| 8967 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8968 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8969 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8970 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8971 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8972 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 8973 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8974 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8975 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8976 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8977 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8978 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 8979 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8980 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8981 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8982 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8983 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8984 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 8985 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8986 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8987 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8988 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8989 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8990 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 8991 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8992 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8993 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8994 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8995 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8996 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 8997 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 8998 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 8999 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 9000 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 9001 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 9002 | 15201277 | Transcription factors downstream of the extracellular signal-regulated kinases as well as changes in NFkappaB regulation were not involved in the synergistic increase in tissue factor expression by thrombin and TNFalpha. |
| 9003 | 15192149 | CD154 is a negative regulator of autoaggressive CD8+ T cells in type 1 diabetes. |
| 9004 | 15192149 | CD154 is a negative regulator of autoaggressive CD8+ T cells in type 1 diabetes. |
| 9005 | 15192149 | CD154 is a negative regulator of autoaggressive CD8+ T cells in type 1 diabetes. |
| 9006 | 15192149 | TNF/CD80 mice, a CD8(+) T cell-mediated model for type 1 diabetes, transgenically express tumor necrosis factor alpha (TNF-alpha) and the costimulatory molecule CD80 in their pancreatic islets. |
| 9007 | 15192149 | TNF/CD80 mice, a CD8(+) T cell-mediated model for type 1 diabetes, transgenically express tumor necrosis factor alpha (TNF-alpha) and the costimulatory molecule CD80 in their pancreatic islets. |
| 9008 | 15192149 | TNF/CD80 mice, a CD8(+) T cell-mediated model for type 1 diabetes, transgenically express tumor necrosis factor alpha (TNF-alpha) and the costimulatory molecule CD80 in their pancreatic islets. |
| 9009 | 15192149 | TNF/CD80 CD154-deficient mice rapidly develop diabetes, whereas CD154-sufficient mice do not. |
| 9010 | 15192149 | TNF/CD80 CD154-deficient mice rapidly develop diabetes, whereas CD154-sufficient mice do not. |
| 9011 | 15192149 | TNF/CD80 CD154-deficient mice rapidly develop diabetes, whereas CD154-sufficient mice do not. |
| 9012 | 15192149 | This finding correlates with the decreased numbers of CD4(+)CD25(+) T regulatory (T(R)) cells in the islets and pancreatic lymph nodes, in comparison to disease-protected CD154-sufficient mice. |
| 9013 | 15192149 | This finding correlates with the decreased numbers of CD4(+)CD25(+) T regulatory (T(R)) cells in the islets and pancreatic lymph nodes, in comparison to disease-protected CD154-sufficient mice. |
| 9014 | 15192149 | This finding correlates with the decreased numbers of CD4(+)CD25(+) T regulatory (T(R)) cells in the islets and pancreatic lymph nodes, in comparison to disease-protected CD154-sufficient mice. |
| 9015 | 15192149 | Adoptive transfer studies show that CD8(+) T cells from TNF/CD80 CD154-deficient, but not CD154-sufficient, mice are resistant to regulation in vivo. |
| 9016 | 15192149 | Adoptive transfer studies show that CD8(+) T cells from TNF/CD80 CD154-deficient, but not CD154-sufficient, mice are resistant to regulation in vivo. |
| 9017 | 15192149 | Adoptive transfer studies show that CD8(+) T cells from TNF/CD80 CD154-deficient, but not CD154-sufficient, mice are resistant to regulation in vivo. |
| 9018 | 15192149 | This study provides evidence that CD40-transduced signals initiate T(R) cell increase in vivo and that CD154-transduced signals sensitize autoaggressive CD8(+) T cells to suppression. |
| 9019 | 15192149 | This study provides evidence that CD40-transduced signals initiate T(R) cell increase in vivo and that CD154-transduced signals sensitize autoaggressive CD8(+) T cells to suppression. |
| 9020 | 15192149 | This study provides evidence that CD40-transduced signals initiate T(R) cell increase in vivo and that CD154-transduced signals sensitize autoaggressive CD8(+) T cells to suppression. |
| 9021 | 15191547 | Similar results were noted at the molecular level by the persistent expression of tumor necrosis factor-alpha (TNF-alpha) and the chemokines MCP-1 and MIP-2. |
| 9022 | 15190958 | Hyperglycemia at admission to the intensive care unit is associated with elevated serum concentrations of interleukin-6 and reduced ex vivo secretion of tumor necrosis factor-alpha. |
| 9023 | 15181049 | We have recently demonstrated a potent antiinflammatory effect of troglitazone, an agonist of peroxisome proliferator-activated receptor gamma (PPARgamma) and a partial agonist of PPARalpha in both the nondiabetic obese and diabetic obese subjects. |
| 9024 | 15181049 | We have recently demonstrated a potent antiinflammatory effect of troglitazone, an agonist of peroxisome proliferator-activated receptor gamma (PPARgamma) and a partial agonist of PPARalpha in both the nondiabetic obese and diabetic obese subjects. |
| 9025 | 15181049 | We have recently demonstrated a potent antiinflammatory effect of troglitazone, an agonist of peroxisome proliferator-activated receptor gamma (PPARgamma) and a partial agonist of PPARalpha in both the nondiabetic obese and diabetic obese subjects. |
| 9026 | 15181049 | Nuclear factor kappaB (NFkappaB)-binding activity in mononuclear cells, plasma monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, soluble intercellular adhesion molecule-1, C-reactive protein (CRP), and serum amyloid A (SAA) were measured. |
| 9027 | 15181049 | Nuclear factor kappaB (NFkappaB)-binding activity in mononuclear cells, plasma monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, soluble intercellular adhesion molecule-1, C-reactive protein (CRP), and serum amyloid A (SAA) were measured. |
| 9028 | 15181049 | Nuclear factor kappaB (NFkappaB)-binding activity in mononuclear cells, plasma monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, soluble intercellular adhesion molecule-1, C-reactive protein (CRP), and serum amyloid A (SAA) were measured. |
| 9029 | 15181049 | Rosiglitazone treatment resulted in a reduction in plasma MCP-1 and CRP in both groups (P < 0.05). |
| 9030 | 15181049 | Rosiglitazone treatment resulted in a reduction in plasma MCP-1 and CRP in both groups (P < 0.05). |
| 9031 | 15181049 | Rosiglitazone treatment resulted in a reduction in plasma MCP-1 and CRP in both groups (P < 0.05). |
| 9032 | 15181049 | Plasma TNF-alpha and SAA concentrations were inhibited significantly in the obese group (P < 0.05) but not in the obese diabetic subjects. |
| 9033 | 15181049 | Plasma TNF-alpha and SAA concentrations were inhibited significantly in the obese group (P < 0.05) but not in the obese diabetic subjects. |
| 9034 | 15181049 | Plasma TNF-alpha and SAA concentrations were inhibited significantly in the obese group (P < 0.05) but not in the obese diabetic subjects. |
| 9035 | 15181049 | NFkappaB-binding activity and plasma MCP-1, CRP, SAA, and TNF-alpha did not change in the obese and obese diabetic control groups. |
| 9036 | 15181049 | NFkappaB-binding activity and plasma MCP-1, CRP, SAA, and TNF-alpha did not change in the obese and obese diabetic control groups. |
| 9037 | 15181049 | NFkappaB-binding activity and plasma MCP-1, CRP, SAA, and TNF-alpha did not change in the obese and obese diabetic control groups. |
| 9038 | 15181044 | Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. |
| 9039 | 15181044 | Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. |
| 9040 | 15181044 | Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. |
| 9041 | 15181044 | Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. |
| 9042 | 15181044 | We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. |
| 9043 | 15181044 | We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. |
| 9044 | 15181044 | We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. |
| 9045 | 15181044 | We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. |
| 9046 | 15181044 | MS+ subjects had significantly lower adiponectin (7.6 +/- 0.6 vs. 10.4 +/- 0.6 microg/ml; P = 0.003) and significantly higher TNF-alpha (3.3 +/- 0.2 vs. 2.8 +/- 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. |
| 9047 | 15181044 | MS+ subjects had significantly lower adiponectin (7.6 +/- 0.6 vs. 10.4 +/- 0.6 microg/ml; P = 0.003) and significantly higher TNF-alpha (3.3 +/- 0.2 vs. 2.8 +/- 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. |
| 9048 | 15181044 | MS+ subjects had significantly lower adiponectin (7.6 +/- 0.6 vs. 10.4 +/- 0.6 microg/ml; P = 0.003) and significantly higher TNF-alpha (3.3 +/- 0.2 vs. 2.8 +/- 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. |
| 9049 | 15181044 | MS+ subjects had significantly lower adiponectin (7.6 +/- 0.6 vs. 10.4 +/- 0.6 microg/ml; P = 0.003) and significantly higher TNF-alpha (3.3 +/- 0.2 vs. 2.8 +/- 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. |
| 9050 | 15181044 | Plasma adiponectin and TNF-alpha levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. |
| 9051 | 15181044 | Plasma adiponectin and TNF-alpha levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. |
| 9052 | 15181044 | Plasma adiponectin and TNF-alpha levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. |
| 9053 | 15181044 | Plasma adiponectin and TNF-alpha levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. |
| 9054 | 15181044 | After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-alpha concentrations did not change. |
| 9055 | 15181044 | After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-alpha concentrations did not change. |
| 9056 | 15181044 | After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-alpha concentrations did not change. |
| 9057 | 15181044 | After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-alpha concentrations did not change. |
| 9058 | 15181044 | Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss. |
| 9059 | 15181044 | Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss. |
| 9060 | 15181044 | Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss. |
| 9061 | 15181044 | Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss. |
| 9062 | 15181014 | Suppressor of cytokine signaling 3 is a physiological regulator of adipocyte insulin signaling. |
| 9063 | 15181014 | Suppressor of cytokine signaling 3 is a physiological regulator of adipocyte insulin signaling. |
| 9064 | 15181014 | We observed that several cytokines and hormones that induce insulin resistance also stimulate SOCS3 expression in 3T3-L1 adipocytes and that SOCS3 mRNA is increased in adipose tissue of obese/diabetic mice. |
| 9065 | 15181014 | We observed that several cytokines and hormones that induce insulin resistance also stimulate SOCS3 expression in 3T3-L1 adipocytes and that SOCS3 mRNA is increased in adipose tissue of obese/diabetic mice. |
| 9066 | 15181014 | We then hypothesized that SOCS3 may mediate cytokine- and hormone-induced insulin resistance. |
| 9067 | 15181014 | We then hypothesized that SOCS3 may mediate cytokine- and hormone-induced insulin resistance. |
| 9068 | 15181014 | By using SOCS3-deficient adipocytes differentiated from mouse embryonic fibroblasts, we found that SOCS3 deficiency increases insulin-stimulated IRS1 and IRS2 phosphorylation, IRS-associated phosphatidylinositol 3-kinase activity, and insulin-stimulated glucose uptake. |
| 9069 | 15181014 | By using SOCS3-deficient adipocytes differentiated from mouse embryonic fibroblasts, we found that SOCS3 deficiency increases insulin-stimulated IRS1 and IRS2 phosphorylation, IRS-associated phosphatidylinositol 3-kinase activity, and insulin-stimulated glucose uptake. |
| 9070 | 15181014 | Moreover, lack of SOCS3 substantially limits the inhibitory effects of tumor necrosis factor-alpha to suppress IRS1 and IRS2 tyrosine phosphorylation, phosphatidylinositol 3-kinase activity, and glucose uptake in adipocytes. |
| 9071 | 15181014 | Moreover, lack of SOCS3 substantially limits the inhibitory effects of tumor necrosis factor-alpha to suppress IRS1 and IRS2 tyrosine phosphorylation, phosphatidylinositol 3-kinase activity, and glucose uptake in adipocytes. |
| 9072 | 15181014 | The ameliorated insulin signaling in SOCS3-deficient adipocytes is mainly due to the suppression of tumor necrosis factor-alpha-induced IRS1 and IRS2 protein degradation. |
| 9073 | 15181014 | The ameliorated insulin signaling in SOCS3-deficient adipocytes is mainly due to the suppression of tumor necrosis factor-alpha-induced IRS1 and IRS2 protein degradation. |
| 9074 | 15181014 | Therefore, our data suggest that endogenous SOCS3 expression is a key determinant of basal insulin signaling and is an important molecular mediator of cytokine-induced insulin resistance in adipocytes. |
| 9075 | 15181014 | Therefore, our data suggest that endogenous SOCS3 expression is a key determinant of basal insulin signaling and is an important molecular mediator of cytokine-induced insulin resistance in adipocytes. |
| 9076 | 15181014 | We conclude that SOCS3 plays an important role in mediating insulin resistance and may be an excellent target for therapeutic intervention in insulin resistance and type II diabetes. |
| 9077 | 15181014 | We conclude that SOCS3 plays an important role in mediating insulin resistance and may be an excellent target for therapeutic intervention in insulin resistance and type II diabetes. |
| 9078 | 15178645 | Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells. |
| 9079 | 15178645 | PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not. |
| 9080 | 15178645 | Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels. |
| 9081 | 15178645 | PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478. |
| 9082 | 15178645 | Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF. |
| 9083 | 15178645 | Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA. |
| 9084 | 15178645 | PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas. |
| 9085 | 15178645 | Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF. |
| 9086 | 15171690 | In samples of quadriceps femoris muscle, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitrite, nitrate and nitrotyrosine were determined. |
| 9087 | 15171690 | In samples of quadriceps femoris muscle, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitrite, nitrate and nitrotyrosine were determined. |
| 9088 | 15171690 | In samples of quadriceps femoris muscle, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitrite, nitrate and nitrotyrosine were determined. |
| 9089 | 15171690 | The macrophage-specific antigen CD163, the T-cell membrane factor CD154 and tumour necrosis factor-alpha (TNF-alpha) were also assayed. |
| 9090 | 15171690 | The macrophage-specific antigen CD163, the T-cell membrane factor CD154 and tumour necrosis factor-alpha (TNF-alpha) were also assayed. |
| 9091 | 15171690 | The macrophage-specific antigen CD163, the T-cell membrane factor CD154 and tumour necrosis factor-alpha (TNF-alpha) were also assayed. |
| 9092 | 15171690 | Nitrotyrosine levels were higher in the patient than in the control group (42.1+/-24.4 vs 10.3+/-2.5 ng/mg protein, P<0.00002), as were CD163 (10-fold) and TNF-alpha (fourfold) levels. |
| 9093 | 15171690 | Nitrotyrosine levels were higher in the patient than in the control group (42.1+/-24.4 vs 10.3+/-2.5 ng/mg protein, P<0.00002), as were CD163 (10-fold) and TNF-alpha (fourfold) levels. |
| 9094 | 15171690 | Nitrotyrosine levels were higher in the patient than in the control group (42.1+/-24.4 vs 10.3+/-2.5 ng/mg protein, P<0.00002), as were CD163 (10-fold) and TNF-alpha (fourfold) levels. |
| 9095 | 15171690 | The increased levels of CD163, CD154 and TNF-alpha indicate that an inflammatory process occurs in skeletal muscle of type 2 diabetic patients. |
| 9096 | 15171690 | The increased levels of CD163, CD154 and TNF-alpha indicate that an inflammatory process occurs in skeletal muscle of type 2 diabetic patients. |
| 9097 | 15171690 | The increased levels of CD163, CD154 and TNF-alpha indicate that an inflammatory process occurs in skeletal muscle of type 2 diabetic patients. |
| 9098 | 15171690 | This may contribute to iNOS induction, muscle damage and insulin resistance. |
| 9099 | 15171690 | This may contribute to iNOS induction, muscle damage and insulin resistance. |
| 9100 | 15171690 | This may contribute to iNOS induction, muscle damage and insulin resistance. |
| 9101 | 15171689 | Relationship of plasma extracellular-superoxide dismutase level with insulin resistance in type 2 diabetic patients. |
| 9102 | 15171689 | Relationship of plasma extracellular-superoxide dismutase level with insulin resistance in type 2 diabetic patients. |
| 9103 | 15171689 | The aim of this study was to assess plasma levels of EC-SOD and to evaluate the relationship of the EC-SOD level with insulin resistance in type 2 diabetic patients. |
| 9104 | 15171689 | The aim of this study was to assess plasma levels of EC-SOD and to evaluate the relationship of the EC-SOD level with insulin resistance in type 2 diabetic patients. |
| 9105 | 15171689 | We determined plasma EC-SOD in 122 patients and found for the first time that the EC-SOD level was strongly and positively related to adiponectin (r=0.503, P < 0.001), and significantly and inversely related to fasting plasma glucose (FPG) (r=-0.209, P=0.022), body-mass index (BMI) (r=-0.187, P=0.040) and homeostasis model assessment-insulin resistance index (HOMA-R) (r=-0.190, P=0.039). |
| 9106 | 15171689 | We determined plasma EC-SOD in 122 patients and found for the first time that the EC-SOD level was strongly and positively related to adiponectin (r=0.503, P < 0.001), and significantly and inversely related to fasting plasma glucose (FPG) (r=-0.209, P=0.022), body-mass index (BMI) (r=-0.187, P=0.040) and homeostasis model assessment-insulin resistance index (HOMA-R) (r=-0.190, P=0.039). |
| 9107 | 15171689 | Stepwise-multiple regression analysis also showed a significant influence of adiponectin (F=33.27) on the EC-SOD level. |
| 9108 | 15171689 | Stepwise-multiple regression analysis also showed a significant influence of adiponectin (F=33.27) on the EC-SOD level. |
| 9109 | 15171689 | Administration of pioglitazone to 19 diabetic patients significantly increased the plasma levels of EC-SOD (69.9+/-19.3 ng/ml to 97.4+/-25.9 ng/ml; P < 0.0001) and adiponectin, while it decreased tumor necrosis factor-alpha (TNF-alpha). |
| 9110 | 15171689 | Administration of pioglitazone to 19 diabetic patients significantly increased the plasma levels of EC-SOD (69.9+/-19.3 ng/ml to 97.4+/-25.9 ng/ml; P < 0.0001) and adiponectin, while it decreased tumor necrosis factor-alpha (TNF-alpha). |
| 9111 | 15171689 | The present observations suggest that factors related to the pathogenesis of insulin resistance play an important role in the regulation of the plasma EC-SOD concentration. |
| 9112 | 15171689 | The present observations suggest that factors related to the pathogenesis of insulin resistance play an important role in the regulation of the plasma EC-SOD concentration. |
| 9113 | 15171689 | It is possible that the increase in the EC-SOD level by pioglitazone administration in diabetic patients is due to a decline of TNF-alpha, which is known to suppress EC-SOD expression. |
| 9114 | 15171689 | It is possible that the increase in the EC-SOD level by pioglitazone administration in diabetic patients is due to a decline of TNF-alpha, which is known to suppress EC-SOD expression. |
| 9115 | 15169905 | Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 cause insulin resistance through inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms. |
| 9116 | 15169905 | Here we show that in both obesity and lipopolysaccharide (LPS)-induced endotoxemia there is an increase in suppressor of cytokine signaling (SOCS) proteins, SOCS-1 and SOCS-3, in liver, muscle, and, to a lesser extent, fat. |
| 9117 | 15169905 | Direct overexpression of SOCS-3 in liver by adenoviral-mediated gene transfer markedly decreases tyrosine phosphorylation of both IRS-1 and IRS-2, while SOCS-1 overexpression preferentially inhibits IRS-2 phosphorylation. |
| 9118 | 15169905 | Neither affects IR phosphorylation, although both SOCS-1 and SOCS-3 bind to the insulin receptor in vivo in an insulin-dependent fashion. |
| 9119 | 15169905 | Experiments with cultured cells expressing mutant insulin receptors reveal that SOCS-3 binds to Tyr960 of IR, a key residue for the recognition of IRS-1 and IRS-2, whereas SOCS-1 binds to the domain in the catalytic loop essential for IRS-2 recognition in vitro. |
| 9120 | 15169905 | Moreover, overexpression of either SOCS-1 or SOCS-3 attenuates insulin-induced glycogen synthesis in L6 myotubes and activation of glucose uptake in 3T3L1 adipocytes. |
| 9121 | 15169905 | By contrast, a reduction of SOCS-1 or SOCS-3 by antisense treatment partially restores tumor necrosis factor alpha-induced downregulation of tyrosine phosphorylation of IRS proteins in 3T3L1 adipocytes. |
| 9122 | 15169905 | These data indicate that SOCS-1 and SOCS-3 act as negative regulators in insulin signaling and serve as one of the missing links between insulin resistance and cytokine signaling. |
| 9123 | 15168015 | Interleukin-6 and tumor necrosis factor-alpha are not increased in patients with Type 2 diabetes: evidence that plasma interleukin-6 is related to fat mass and not insulin responsiveness. |
| 9124 | 15163543 | On the other hand, arsenite has high affinity for sulfhydryl groups and thus can form covalent bonds with the disulfide bridges in the molecules of insulin, insulin receptors, glucose transporters (GLUTs), and enzymes involved in glucose metabolism (e.g., pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase). |
| 9125 | 15163543 | Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated. |
| 9126 | 15163543 | Arsenite at physiologically relevant concentration also shows inhibitory effect on the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear hormone receptor important for activating insulin action. |
| 9127 | 15163543 | Oxidative stress has been suggested as a major pathogenic link to both insulin resistance and beta cell dysfunction through mechanisms involving activation of nuclear factor-kappaB (NF-kappaB), which is also activated by low levels of arsenic. |
| 9128 | 15163543 | Although without supportive data, superoxide production induced by arsenic exposure can theoretically impair insulin secretion by interaction with uncoupling protein 2 (UCP2), and oxidative stress can also cause amyloid formation in the pancreas, which could progressively destroy the insulin-secreting beta cells. |
| 9129 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9130 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9131 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9132 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9133 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9134 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9135 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9136 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9137 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9138 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9139 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9140 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9141 | 15153522 | Role of calcium in pancreatic islet cell death by IFN-gamma/TNF-alpha. |
| 9142 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9143 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9144 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9145 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9146 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9147 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9148 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9149 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9150 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9151 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9152 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9153 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9154 | 15153522 | We studied the intracellular events associated with pancreatic beta cell apoptosis by IFN-gamma/TNF-alpha synergism. |
| 9155 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9156 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9157 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9158 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9159 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9160 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9161 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9162 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9163 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9164 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9165 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9166 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9167 | 15153522 | IFN-gamma/TNF-alpha treatment of MIN6N8 insulinoma cells increased the amplitude of high voltage-activated Ca(2+) currents, while treatment with IFN-gamma or TNF-alpha alone did not. |
| 9168 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9169 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9170 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9171 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9172 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9173 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9174 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9175 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9176 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9177 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9178 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9179 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9180 | 15153522 | Cytosolic Ca(2+) concentration ([Ca(2+)](c)) was also increased by IFN-gamma/TNF-alpha treatment. |
| 9181 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9182 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9183 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9184 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9185 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9186 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9187 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9188 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9189 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9190 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9191 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9192 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9193 | 15153522 | Blockade of L-type Ca(2+) channel by nifedipine abrogated death of insulinoma cells by IFN-gamma/TNF-alpha. |
| 9194 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9195 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9196 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9197 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9198 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9199 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9200 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9201 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9202 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9203 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9204 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9205 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9206 | 15153522 | Diazoxide that attenuates voltage-activated Ca(2+) currents inhibited MIN6N8 cell death by IFN-gamma/TNF-alpha, while glibenclamide that accentuates voltage-activated Ca(2+) currents augmented insulinoma cell death. |
| 9207 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9208 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9209 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9210 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9211 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9212 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9213 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9214 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9215 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9216 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9217 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9218 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9219 | 15153522 | A protein kinase C inhibitor attenuated MIN6N8 cell death and the increase in [Ca(2+)](c) by IFN-gamma/TNF-alpha. |
| 9220 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9221 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9222 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9223 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9224 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9225 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9226 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9227 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9228 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9229 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9230 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9231 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9232 | 15153522 | Following the increase in [Ca(2+)](c), calpain was activated, and calpain inhibitors decreased insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9233 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9234 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9235 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9236 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9237 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9238 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9239 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9240 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9241 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9242 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9243 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9244 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9245 | 15153522 | As a downstream of calpain, calcineurin was activated and the inhibition of calcineurin activation by FK506 diminished insulinoma cell death by IFN-gamma/TNF-alpha. |
| 9246 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9247 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9248 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9249 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9250 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9251 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9252 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9253 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9254 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9255 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9256 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9257 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9258 | 15153522 | BAD phosphorylation was decreased by IFN-gamma/TNF-alpha because of the increased calcineurin activity, which was reversed by FK506. |
| 9259 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9260 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9261 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9262 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9263 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9264 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9265 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9266 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9267 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9268 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9269 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9270 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9271 | 15153522 | IFN-gamma/TNF-alpha induced cytochrome c translocation from mitochondria to cytoplasm and activation of caspase-9. |
| 9272 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9273 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9274 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9275 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9276 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9277 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9278 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9279 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9280 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9281 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9282 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9283 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9284 | 15153522 | Effector caspases such as caspase-3 or -7 were also activated by IFN-gamma/TNF-alpha treatment. |
| 9285 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9286 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9287 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9288 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9289 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9290 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9291 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9292 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9293 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9294 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9295 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9296 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9297 | 15153522 | These results indicate that IFN-gamma/TNF-alpha synergism induces pancreatic beta cell apoptosis by Ca(2+) channel activation followed by downstream intracellular events such as mitochondrial events and caspase activation and also suggest the therapeutic potential of Ca(2+) modulation in type 1 diabetes. |
| 9298 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9299 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9300 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9301 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9302 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9303 | 15149950 | Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-alpha. |
| 9304 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9305 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9306 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9307 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9308 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9309 | 15149950 | IL-6 and TNF-alpha have been associated with insulin resistance and type 2 diabetes. |
| 9310 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9311 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9312 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9313 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9314 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9315 | 15149950 | However, few studies have directly examined the effects of either IL-6 or TNF-alpha on skeletal muscle FA metabolism. |
| 9316 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9317 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9318 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9319 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9320 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9321 | 15149950 | Here, we used a pulse-chase technique to determine the effect of IL-6 (50-5,000 pg/ml) and TNF-alpha (50-5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. |
| 9322 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9323 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9324 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9325 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9326 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9327 | 15149950 | When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). |
| 9328 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9329 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9330 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9331 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9332 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9333 | 15149950 | Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). |
| 9334 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9335 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9336 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9337 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9338 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9339 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 9340 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9341 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9342 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9343 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9344 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9345 | 15149950 | In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. |
| 9346 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9347 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9348 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9349 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9350 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9351 | 15149950 | In contrast, TNF-alpha had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-alpha-induced insulin resistance in skeletal muscle. |
| 9352 | 15149866 | Adiponectin plays a crucial role in the association between obesity, type 2 diabetes, and insulin resistance. |
| 9353 | 15149866 | Mechanisms explaining the relationship between adiponectin and insulin resistance suggest that adiponectin and tumor necrosis factor (TNF)-alpha inhibited each other's expression and production in adipocytes. |
| 9354 | 15149866 | Thiazolidinediones, which are insulin-sensitizing agents, increased the production of adiponectin through directly enhancing its gene expression. |
| 9355 | 15149866 | Adiponectin receptors 1 (AdipoR1) and 2 (AdipoR2) are expressed ubiquitously in most organs, especially in skeletal muscle in AdipoR1, and liver in AdipoR2. |
| 9356 | 15147359 | We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. |
| 9357 | 15147359 | Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. |
| 9358 | 15147359 | Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. |
| 9359 | 15147359 | In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. |
| 9360 | 15147359 | In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. |
| 9361 | 15147359 | Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. |
| 9362 | 15146098 | The role of TNF-alpha in insulin resistance. |
| 9363 | 15146098 | The role of TNF-alpha in insulin resistance. |
| 9364 | 15146098 | The role of TNF-alpha in insulin resistance. |
| 9365 | 15146098 | Among the latter are tumor necrosis factor-alpha (TNF-alpha), adiponectin, IL-6, resistin and free fatty acids. |
| 9366 | 15146098 | Among the latter are tumor necrosis factor-alpha (TNF-alpha), adiponectin, IL-6, resistin and free fatty acids. |
| 9367 | 15146098 | Among the latter are tumor necrosis factor-alpha (TNF-alpha), adiponectin, IL-6, resistin and free fatty acids. |
| 9368 | 15146098 | This review will discuss the regulation of insulin responses by TNF-alpha and evidence supporting the hypothesis that over expression of TNF-alpha plays a role in the pathophysiology of insulin resistance. |
| 9369 | 15146098 | This review will discuss the regulation of insulin responses by TNF-alpha and evidence supporting the hypothesis that over expression of TNF-alpha plays a role in the pathophysiology of insulin resistance. |
| 9370 | 15146098 | This review will discuss the regulation of insulin responses by TNF-alpha and evidence supporting the hypothesis that over expression of TNF-alpha plays a role in the pathophysiology of insulin resistance. |
| 9371 | 15135803 | We examined the hypothesis that progesterone but not 17beta-estradiol (E) increases the secretion of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 9372 | 15135803 | We examined the hypothesis that progesterone but not 17beta-estradiol (E) increases the secretion of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 9373 | 15135803 | Results show that estrogen inhibits IL-6 but not TNF-alpha secretion (p < 0.05) in monocytes activated by lipopolysaccharide (LPS) or high glucose. |
| 9374 | 15135803 | Results show that estrogen inhibits IL-6 but not TNF-alpha secretion (p < 0.05) in monocytes activated by lipopolysaccharide (LPS) or high glucose. |
| 9375 | 15122091 | Alteration in insulin action: role of IRS-1 serine phosphorylation in the retroregulation of insulin signalling. |
| 9376 | 15122091 | Tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) and its binding to phosphatidylinositol 3-kinase (PI 3-kinase) are critical events in the insulin signalling cascade leading to insulin-stimulated glucose transport. |
| 9377 | 15122091 | Recent findings demonstrate that "diabetogenic" factors such as FFA, TNFalpha, hyperinsulinemia and cellular stress, increase the serine phosphorylation of IRS-1 and identified Ser307/612/632 as phosphorylated sites. |
| 9378 | 15122091 | These exciting results suggest that serine phosphorylation of IRS-1 is a possible hallmark of insulin resistance in biologically insulin responsive cells or tIssues. |
| 9379 | 15120750 | In addition, BHA markedly attenuated the production of proinflammatory cytokines IL-1beta and TNF-alpha by both islets of pancreas and peritoneal macrophages. |
| 9380 | 15115315 | Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. |
| 9381 | 15115315 | Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. |
| 9382 | 15115315 | Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. |
| 9383 | 15115315 | Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. |
| 9384 | 15115315 | PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. |
| 9385 | 15115315 | PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. |
| 9386 | 15114276 | LCPUFAs suppress the production of tumor necrosis factor-alpha (TNF-alpha) (and so also of OX40, since it belongs to the family of TNFR) and the expression of Bcl-2, suggesting that these fatty acids have the ability to prevent/suppress autoimmune diseases. |
| 9387 | 15114276 | This indicates that LCPUFAs present in human breast milk suppress the levels of OX40 and decrease the expression of Bcl-xL and Bcl-2 on exposure to self-antigens and thus, protects against the development of autoimmune diseases in later life. |
| 9388 | 15100317 | Suppressor of cytokine signaling-1 overexpression protects pancreatic beta cells from CD8+ T cell-mediated autoimmune destruction. |
| 9389 | 15100317 | Suppressor of cytokine signaling-1 overexpression protects pancreatic beta cells from CD8+ T cell-mediated autoimmune destruction. |
| 9390 | 15100317 | SOCS-1 appeared to protect at least in part by inhibiting TNF- and IFN-gamma-induced Fas expression on beta cells. |
| 9391 | 15100317 | SOCS-1 appeared to protect at least in part by inhibiting TNF- and IFN-gamma-induced Fas expression on beta cells. |
| 9392 | 15100317 | Fas expression was up-regulated on beta cells in vivo in prediabetic NOD8.3 mice, and this was inhibited by SOCS-1. |
| 9393 | 15100317 | Fas expression was up-regulated on beta cells in vivo in prediabetic NOD8.3 mice, and this was inhibited by SOCS-1. |
| 9394 | 15100317 | Additionally, IFN-gamma-induced class I MHC up-regulation and TNF- and IFN-gamma-induced IL-15 expression by beta cells were inhibited by SOCS-1, which correlated with suppressed 8.3 T cell proliferation in vitro. |
| 9395 | 15100317 | Additionally, IFN-gamma-induced class I MHC up-regulation and TNF- and IFN-gamma-induced IL-15 expression by beta cells were inhibited by SOCS-1, which correlated with suppressed 8.3 T cell proliferation in vitro. |
| 9396 | 15100317 | Our findings suggest that increasing SOCS-1 expression may be useful as a strategy to block CD8(+) T cell-mediated type 1 diabetes as well as to more generally prevent cytokine-dependent tissue destruction in inflammatory diseases. |
| 9397 | 15100317 | Our findings suggest that increasing SOCS-1 expression may be useful as a strategy to block CD8(+) T cell-mediated type 1 diabetes as well as to more generally prevent cytokine-dependent tissue destruction in inflammatory diseases. |
| 9398 | 15096655 | Interleukin-11 inhibits NF-kappaB and AP-1 activation in islets and prevents diabetes induced with streptozotocin in mice. |
| 9399 | 15096655 | Interleukin-11 inhibits NF-kappaB and AP-1 activation in islets and prevents diabetes induced with streptozotocin in mice. |
| 9400 | 15096655 | This laboratory has reported that multiple low doses of streptozotocin (MLD-STZ) similarly upregulate the T helper (Th)1-type proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in islets of both the diabetes-susceptible male and the diabetes-resistant female C57BL/6 mice and that MLD-STZ downregulates the anti-inflammatory Th2-type cytokines interleukin (IL)-4 and IL-10, as well as the anti-inflammatory Th3-type cytokine-transforming growth factor (TGF)-ss1 in islets of male, but not female, mice. |
| 9401 | 15096655 | This laboratory has reported that multiple low doses of streptozotocin (MLD-STZ) similarly upregulate the T helper (Th)1-type proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in islets of both the diabetes-susceptible male and the diabetes-resistant female C57BL/6 mice and that MLD-STZ downregulates the anti-inflammatory Th2-type cytokines interleukin (IL)-4 and IL-10, as well as the anti-inflammatory Th3-type cytokine-transforming growth factor (TGF)-ss1 in islets of male, but not female, mice. |
| 9402 | 15096655 | Here, we investigated the effects of MLD-STZ on the anti-inflammatory cytokine IL-11 and the transcription factors nuclear factor (NF)-kappaB and activator protein (AP)-1, which are involved in gene activation of proinflammatory cytokines, and on the cytosolic kinase (IKK-alpha) of NF-kappaB inhibitor (IkappaB). |
| 9403 | 15096655 | Here, we investigated the effects of MLD-STZ on the anti-inflammatory cytokine IL-11 and the transcription factors nuclear factor (NF)-kappaB and activator protein (AP)-1, which are involved in gene activation of proinflammatory cytokines, and on the cytosolic kinase (IKK-alpha) of NF-kappaB inhibitor (IkappaB). |
| 9404 | 15096655 | Furthermore, the effect of recombinant human (rh)IL-11 on MLD-STZ diabetes, insulitis, cytokines, IKK-alpha, NF-kappaB, and AP-1 was analyzed in islets. |
| 9405 | 15096655 | Furthermore, the effect of recombinant human (rh)IL-11 on MLD-STZ diabetes, insulitis, cytokines, IKK-alpha, NF-kappaB, and AP-1 was analyzed in islets. |
| 9406 | 15096655 | Interleukin-11 prevented diabetes without affecting insulitis; attenuated TNF-alpha and IFN-gamma response; and stimulated IL-4 production and inhibited activation of IKK-alpha, NF-kappaB, and AP-1. |
| 9407 | 15096655 | Interleukin-11 prevented diabetes without affecting insulitis; attenuated TNF-alpha and IFN-gamma response; and stimulated IL-4 production and inhibited activation of IKK-alpha, NF-kappaB, and AP-1. |
| 9408 | 15096655 | In this process, the transcription factors NF-kappaB and AP-1 might play a key role. |
| 9409 | 15096655 | In this process, the transcription factors NF-kappaB and AP-1 might play a key role. |
| 9410 | 15093669 | While vanadium deficiency accounts for several physiological malfunctionings including thyroid, glucose and lipid metabolism, etc., several genes are regulated by this element or by its compounds, which include genes for tumor necrosis factor-alpha (TNF-alpha), Interleukin-8 (IL-8), activator protein-1 (AP-1), ras, c-raf-1, mitogen activated protein kinase (MAPK), p53, nuclear factors-kappaB, etc. |
| 9411 | 15081318 | Regulation of monocyte chemoattractant protein-1 by the oxidized lipid, 13-hydroperoxyoctadecadienoic acid, in vascular smooth muscle cells via nuclear factor-kappa B (NF-kappa B). |
| 9412 | 15081318 | We also observed reduced activation of the transcription factor, NF-kappa B and reduced expression of MCP-1/JE mRNA in VSMC from 12/15-LO knock-out mice relative to WT. |
| 9413 | 15081318 | To confirm the role of NF-kappa B in 13-HPODE-induced MCP-1 expression and to selectively block the induction of such inflammatory genes in VSMC, we designed novel molecular approaches to knockdown NF-kappa B with short interfering RNAs (siRNAs). |
| 9414 | 15081318 | We designed siRNAs to human NF-kappa B p65 transcriptionally active subunit by using a rapid PCR-based approach that generates sense and antisense siRNA separated by a hairpin loop downstream of the U6 promoter. siRNA PCR products targeting seven different sites on p65 cDNA could induce upto 92% reduction in HA-p65 protein levels. |
| 9415 | 15081318 | We cloned the PCR products into a pCR3.1 vector and these p65 siRNA expressing plasmids very effectively blocked 13-HPODE-induced expression of both MCP-1 and TNF-alpha genes. |
| 9416 | 15081318 | These results show for the first time that 13-HPODE can induce MCP-1 in the vasculature via activation of NF-kappa B. |
| 9417 | 15071491 | We investigated the hypothesis that low-penetrance mutations in genes (TNFRSF1A, MEFV and NALP3/CIAS1) associated with hereditary periodic fever syndromes (HPFs) might be risk factors for AA amyloidosis among patients with chronic inflammatory disorders, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), Crohn's disease, undiagnosed recurrent fevers and HPFs themselves. |
| 9418 | 15071491 | Four of 67 patients with RA plus amyloidosis had MEFV variants compared with none of 34 RA patients without amyloid (P value=0.03). |
| 9419 | 15071491 | The E148Q variant of MEFV was present in two of the three patients with TNF receptor-associated periodic syndrome (TRAPS) complicated by amyloid in two separate multiplex TRAPS families containing 5 and 16 affected members respectively, and the single patient with Muckle-Wells syndrome who had amyloidosis was homozygous for this variant. |
| 9420 | 15071491 | Although allelic variants in HPFs genes are not major susceptibility factors for AA amyloidosis in chronic inflammatory disease, low-penetrance variants of MEFV and TNFRSF1A may have clinically significant proinflammatory effects. |
| 9421 | 15068125 | Although the predominant paradigm used to explain this link is the portal/visceral hypothesis giving a key role in elevated non-esterified fatty acid concentrations, two new emerging paradigms are the ectopic fat storage syndrome (deposition of triglycerides in muscle, liver and pancreatic cells) and the adipose tissue as endocrine organ hypothesis (secretion of various adipocytokins, i.e. leptin, TNF-alpha, resistin, adiponectin, implicated in insulin resistance and possibly beta-cell dysfunction). |
| 9422 | 15063602 | Comparison of serum concentrations of C-reactive protein, TNF-alpha, and interleukin 6 between elderly Korean women with normal and impaired glucose tolerance. |
| 9423 | 15063602 | Comparison of serum concentrations of C-reactive protein, TNF-alpha, and interleukin 6 between elderly Korean women with normal and impaired glucose tolerance. |
| 9424 | 15063602 | Comparison of serum concentrations of C-reactive protein, TNF-alpha, and interleukin 6 between elderly Korean women with normal and impaired glucose tolerance. |
| 9425 | 15063602 | This study was performed to compare concentrations of pro-inflammatory cytokines, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) as well as acute-phase protein, such as C-reactive protein (CRP) between subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). |
| 9426 | 15063602 | This study was performed to compare concentrations of pro-inflammatory cytokines, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) as well as acute-phase protein, such as C-reactive protein (CRP) between subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). |
| 9427 | 15063602 | This study was performed to compare concentrations of pro-inflammatory cytokines, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) as well as acute-phase protein, such as C-reactive protein (CRP) between subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). |
| 9428 | 15063602 | Serum pro-inflammatory cytokine IL-6 or TNF-alpha concentrations, however, were neither increased in subjects with IGT nor closely correlated with the components of the metabolic syndrome. |
| 9429 | 15063602 | Serum pro-inflammatory cytokine IL-6 or TNF-alpha concentrations, however, were neither increased in subjects with IGT nor closely correlated with the components of the metabolic syndrome. |
| 9430 | 15063602 | Serum pro-inflammatory cytokine IL-6 or TNF-alpha concentrations, however, were neither increased in subjects with IGT nor closely correlated with the components of the metabolic syndrome. |
| 9431 | 15059968 | Here, we investigated whether the expression of Grb14 and its binding partner ZIP (PKC zeta interacting protein) is regulated during insulin resistance in type 2 diabetic rodents and humans. |
| 9432 | 15059968 | Hormonal regulation of Grb14 and ZIP expression was then investigated in 3T3-F442A adipocytes. |
| 9433 | 15059968 | In this model, insulin stimulated Grb14 expression, while TNF-alpha increased ZIP expression. |
| 9434 | 15059615 | Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, hypertension, hypercholesterolemia, and hyperuricemia revealed that the following polymorphisms were significantly (P < 0.005) associated with CAD: the 1019C -->T of the connexin 37 gene for men with type 2 diabetes; the 2445G -->A in the fatty acid-binding protein 2 gene for women with this condition; the -863C-->A in the tumor necrosis factor-alpha gene, the -219G-->T in the apolipoprotein E gene, the 1019C-->T in the connexin 37 gene for men without type 2 diabetes; and the -482C-->T in the apolipoprotein C-III gene for women without this condition. |
| 9435 | 15047607 | Here we report novel protective effects of 11 beta-HSD-1 deficiency on adipose function, distribution, and gene expression in vivo in 11 beta-HSD-1 nullizygous (11 beta-HSD-1(-/-)) mice. 11 beta-HSD-1(-/-) mice expressed lower resistin and tumor necrosis factor-alpha, but higher peroxisome proliferator-activated receptor-gamma, adiponectin, and uncoupling protein-2 mRNA levels in adipose, indicating insulin sensitization. |
| 9436 | 15047607 | Isolated 11 beta-HSD-1(-/-) adipocytes exhibited higher basal and insulin-stimulated glucose uptake. 11 beta-HSD-1(-/-) mice also exhibited reduced visceral fat accumulation upon high-fat feeding. |
| 9437 | 15041043 | IL10 resistant PGS2 expression in at-risk/Type 1 diabetic human monocytes. |
| 9438 | 15041043 | Aberrant prostaglandin synthase 2 (PGS2/COX2) expression constitutes an antigen presenting cell (APC) dysfunction seen in monocytes of humans at risk for or with Type 1 diabetes. |
| 9439 | 15041043 | During endotoxin activation of PGS2 expression in healthy monocytes, granulocyte-monocyte colony stimulating factor (GM-CSF) is activated and, in turn, promotes PGS2 gene activation. |
| 9440 | 15041043 | GM-CSF is considered a major target the action for IL10 in its suppression of PGS2. |
| 9441 | 15041043 | We found that the PGS2 expression in monocytes from 47% of at-risk and diabetic humans tested were highly resistant to suppression by IL10 (maintaining > or =50% of their untreated expression), and had significantly increased GM-CSF production in vitro (1043+/-SD2798 pg/10(6)cells, subject n=35, vs 29.7+/-SD91 pg/10(6)cells, control n=20; P=0.0165). |
| 9442 | 15041043 | The PGS2 insensitivity to IL10 of these cells was not due to a lack of IL10 functionality or its suppression of GM-CSF. |
| 9443 | 15041043 | In contrast to its effects on PGS2, IL10 regulation of GM-CSF and other monocyte factors (i.e., DR, IL1beta, TNFalpha, IL12, CD54, and CD64) remained intact. |
| 9444 | 15041043 | These findings suggest that the inability of IL10 to properly downregulate PGS2 gene expression may contribute to its dysregulation in Type 1 diabetes. |
| 9445 | 15037212 | Type 1, or cellular, immune response is characterized by overproduction of TNF-alpha, IFN-gamma, IL-1, IL-2 and IL-8 and is the underlying immune mechanism of psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis (EAU). |
| 9446 | 15037212 | Type 1, or cellular, immune response is characterized by overproduction of TNF-alpha, IFN-gamma, IL-1, IL-2 and IL-8 and is the underlying immune mechanism of psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis (EAU). |
| 9447 | 15037212 | Cetirizine, supposed to inhibit DNA binding activity of NF-kappa B, inhibits the expression of adhesion molecules on immunocytes and endothelial cells and the production of IL-8 and LTB4, two potent chemoattractants, by immune cells. |
| 9448 | 15037212 | Cetirizine, supposed to inhibit DNA binding activity of NF-kappa B, inhibits the expression of adhesion molecules on immunocytes and endothelial cells and the production of IL-8 and LTB4, two potent chemoattractants, by immune cells. |
| 9449 | 15037212 | Tryptase is a chemoattractant, generates kinins from kininogen, activates mast cells, triggers maturation of dendritic cells and stimulates the release of IL-8 from endothelial cells and the production of Th1 lymphokines by mononuclear immunocytes. |
| 9450 | 15037212 | Tryptase is a chemoattractant, generates kinins from kininogen, activates mast cells, triggers maturation of dendritic cells and stimulates the release of IL-8 from endothelial cells and the production of Th1 lymphokines by mononuclear immunocytes. |
| 9451 | 15037212 | Allopurinol is a free radical scavenger, suppresses the production of TNF-alpha and downregulates the expression of ICAM-1 and P2X(7) receptors on monocyte/macrophages. |
| 9452 | 15037212 | Allopurinol is a free radical scavenger, suppresses the production of TNF-alpha and downregulates the expression of ICAM-1 and P2X(7) receptors on monocyte/macrophages. |
| 9453 | 15037212 | ICAM-1 serves as a ligand for LFA-1 (on T lymphocytes), allowing proper antigen presentation. |
| 9454 | 15037212 | ICAM-1 serves as a ligand for LFA-1 (on T lymphocytes), allowing proper antigen presentation. |
| 9455 | 15037212 | P2X(7) receptors are thought to be involved in IL-1beta release, mitogenic stimulation of T lymphocytes and the probable cytoplasmic communication between macrophages and lymphocytes at inflammation sites. |
| 9456 | 15037212 | P2X(7) receptors are thought to be involved in IL-1beta release, mitogenic stimulation of T lymphocytes and the probable cytoplasmic communication between macrophages and lymphocytes at inflammation sites. |
| 9457 | 15033908 | Fas ligand down-regulates cytokine-induced Fas receptor expression on insulinoma (NIT-1), but not islet cells, from autoimmune nonobese diabetic mice. |
| 9458 | 15033908 | In the pathogenesis of autoimmune type 1 diabetes, the apoptosis receptor Fas appears de novo on the surface of insulin-producing beta-cells. |
| 9459 | 15033908 | Fas expression is thought to be induced by proinflammatory cytokines, such as IL-1beta, interferon-gamma (IFNgamma), and TNFalpha, released by islet-infiltrating mononuclear cells. |
| 9460 | 15033908 | To determine whether beta-cells can modulate their sensitivity to apoptosis at the level of Fas, we investigated the effect of Fas ligand (FasL) on surface expression of Fas in NIT-1 insulinoma cells from nonobese diabetic (NOD) mice prone to autoimmune diabetes and islet cells from NOD and nonautoimmune BALB/c mice. |
| 9461 | 15033908 | In NIT-1 insulinoma cells, Fas expression induced by the cytokine combination IL-1beta and IFNgamma was reduced in the presence of FasL, whereas in islet cells Fas expression was unaffected by FasL. |
| 9462 | 15033908 | The effect of FasL on NIT-1 cells was evident during and after the induction of Fas expression by IL-1beta and IFNgamma. |
| 9463 | 15033908 | Thus, FasL down-regulates cytokine-induced Fas expression in NOD mouse-derived NIT-1 cells, but not in NOD or BALB/c mouse islets. |
| 9464 | 15033908 | Islets apparently cannot protect themselves against FasL-induced apoptosis by down-regulating the Fas receptor. |
| 9465 | 15033908 | Understanding how NIT-1 insulinoma cells down-regulate Fas receptor in response to ligation by FasL has therapeutic implications for protecting normal beta-cells in autoimmune type 1 diabetes. |
| 9466 | 15029093 | Several adipokines are increased in the obese state and have been implicated in hypertension (angiotensinogen), impaired fibrinolysis (PAI-1) and insulin resistance (ASP, TNFalpha, IL-6, resistin). |
| 9467 | 15029093 | Conversely, leptin and adiponectin both exert an insulin-sensitizing effect, at least in part, by favoring tIssue fatty-acId oxIdation through activation of AMP-activated kinase. |
| 9468 | 15029093 | In obesity, insulin resistance has been linked to leptin resistance and decreased plasma adiponectin. |
| 9469 | 15029093 | In lipoatrophic mice, where leptin and adiponectin circulating levels are low, administration of the two adipokines synergistically reverses insulin resistance. |
| 9470 | 15029093 | Leptin and adiponectin also have distinct properties: leptin, as a long-term integrative signal of energy store and adiponectin, as a potent anti-atherogenic agent. |
| 9471 | 15029093 | The thiazolIdinedione anti-diabetic drugs increase endogenous adiponectin production in rodents and humans, supporting the Idea that the development of new drugs targeting adipokines might represent a promising therapeutic approach to protect obese patients from insulin resistance and atherosclerosis. |
| 9472 | 15028669 | BAT1 (D6S81E, UAP56) lies in the central MHC between TNF and HLA-B, a region containing genes that affect susceptibility to immunopathologic disorders. |
| 9473 | 15026281 | Acanthoic acid inhibits IL-8 production via MAPKs and NF-kappaB in a TNF-alpha-stimulated human intestinal epithelial cell line. |
| 9474 | 15025838 | The molecular mechanisms underlying the metabolic abnormalities induced by visceral adiposity have yet to be fully elucidated; however, adipocytokines such as adiponectin, tumor necrosis factor-alpha and resistin seem to play an important role in this process. |
| 9475 | 15024185 | The expression of cytokine genes in the peritoneal macrophages and splenic CD4- and CD8-positive lymphocytes of the nonobese diabetic mice. |
| 9476 | 15024185 | In this study, we showed that the mRNA expression of the pro-inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and GM-CSF, were increased while the anti-inflammatory cytokine, TGF-beta, decreased in the peritoneal macrophages of nonobese diabetic (NOD) mice. |
| 9477 | 15024185 | Surprisingly the expression of IFN-gamma and IL-2 by splenic CD4+ cells were lower in 5-week-old NOD mice as compared to the nonobese diabetic resistant (NOR) control mice, but their expression was higher in older NOD mice. |
| 9478 | 15024185 | The expression of IL-4 and IL-10 decreased in splenic CD4-positive lymphocytes. |
| 9479 | 15024185 | Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred. |
| 9480 | 14988260 | However, our previous work revealed that RAGE-binding AGEs free of endotoxin were incapable of inducing vascular cell adhesion molecule-1 (VCAM-1) or tumor necrosis factor-alpha (TNF-alpha) expression. |
| 9481 | 14988254 | Baseline levels of tumor necrosis factor (TNF)-alpha receptor 2, interleukin (IL)-6, and C-reactive protein (CRP) were significantly higher among case than control subjects (all P </= 0.001). |
| 9482 | 14988254 | After adjusting for BMI and other lifestyle factors, all three biomarkers significantly predicted diabetes risk; the odds ratios (ORs) comparing extreme quintiles were 1.64 (95% CI 1.10-2.45) for TNF-alphaR2, 1.91 (1.27-2.86) for IL-6, and 4.36 (2.80-6.80) for CRP (P for trend <0.001 for all biomarkers). |
| 9483 | 14988254 | Elevated CRP levels are a strong independent predictor of type 2 diabetes and may mediate associations of TNF-alphaR2 and IL-6 with type 2 diabetes. |
| 9484 | 14984317 | Effect of high glucose concentrations on expression of ELAM-1, VCAM-1 and ICAM-1 in HUVEC with and without cytokine activation. |
| 9485 | 14984317 | Incubation of human umbilical vein endothelial cells (HUVEC) in a culture medium with 11.0 mM, 16.5 mM and 22.0 mM glucose concentrations induced the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1). |
| 9486 | 14984317 | The effect of high glucose concentration on TNF-alpha induced expression of ELAM-1, VCAM-1 and ICAM-1 was negligible, if at all. |
| 9487 | 14984317 | These results show that even a short-term exposure of endothelial cells (ECs) to high glucose concentration leads to their activation associated with increased expression of adhesion molecules such as ELAM-1, VCAM-1 and ICAM-1. |
| 9488 | 14983034 | The adipose tissue produces several growth factors/hormones including leptin, tumor necrosis factor alpha, and adiponectin. |
| 9489 | 14981264 | The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity. |
| 9490 | 14981264 | The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity. |
| 9491 | 14981264 | Channel inhibition improves experimental autoimmune encephalitis, in part by reducing IL-2 and tumor necrosis factor production by peripheral T lymphocytes. |
| 9492 | 14981264 | Channel inhibition improves experimental autoimmune encephalitis, in part by reducing IL-2 and tumor necrosis factor production by peripheral T lymphocytes. |
| 9493 | 14981264 | Interestingly, although Kv1.3-/- mice on the high-calorie diet gain weight, they remain euglycemic, with low blood insulin levels. |
| 9494 | 14981264 | Interestingly, although Kv1.3-/- mice on the high-calorie diet gain weight, they remain euglycemic, with low blood insulin levels. |
| 9495 | 14981264 | This observation prompted us to examine the effect of Kv1.3 gene inactivation and inhibition on peripheral glucose homeostasis and insulin sensitivity. |
| 9496 | 14981264 | This observation prompted us to examine the effect of Kv1.3 gene inactivation and inhibition on peripheral glucose homeostasis and insulin sensitivity. |
| 9497 | 14981264 | Here we show that Kv1.3 gene deletion and channel inhibition increase peripheral insulin sensitivity in vivo. |
| 9498 | 14981264 | Here we show that Kv1.3 gene deletion and channel inhibition increase peripheral insulin sensitivity in vivo. |
| 9499 | 14981264 | Baseline and insulin-stimulated glucose uptake are increased in adipose tissue and skeletal muscle of Kv1.3-/- mice. |
| 9500 | 14981264 | Baseline and insulin-stimulated glucose uptake are increased in adipose tissue and skeletal muscle of Kv1.3-/- mice. |
| 9501 | 14981264 | Inhibition of Kv1.3 activity facilitates the translocation of the glucose transporter, GLUT4, to the plasma membrane. |
| 9502 | 14981264 | Inhibition of Kv1.3 activity facilitates the translocation of the glucose transporter, GLUT4, to the plasma membrane. |
| 9503 | 14981264 | It also suppresses c-JUN terminal kinase activity in fat and skeletal muscle and decreases IL-6 and tumor necrosis factor secretion by adipose tissue. |
| 9504 | 14981264 | It also suppresses c-JUN terminal kinase activity in fat and skeletal muscle and decreases IL-6 and tumor necrosis factor secretion by adipose tissue. |
| 9505 | 14981264 | We conclude that Kv1.3 inhibition improves insulin sensitivity by increasing the amount of GLUT4 at the plasma membrane. |
| 9506 | 14981264 | We conclude that Kv1.3 inhibition improves insulin sensitivity by increasing the amount of GLUT4 at the plasma membrane. |
| 9507 | 14976218 | Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF. |
| 9508 | 14976218 | Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF. |
| 9509 | 14976218 | Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF. |
| 9510 | 14976218 | Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF. |
| 9511 | 14976218 | Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF. |
| 9512 | 14976218 | We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process. |
| 9513 | 14976218 | We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process. |
| 9514 | 14976218 | We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process. |
| 9515 | 14976218 | We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process. |
| 9516 | 14976218 | We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process. |
| 9517 | 14976218 | HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF. |
| 9518 | 14976218 | HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF. |
| 9519 | 14976218 | HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF. |
| 9520 | 14976218 | HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF. |
| 9521 | 14976218 | HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF. |
| 9522 | 14976218 | ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters. |
| 9523 | 14976218 | ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters. |
| 9524 | 14976218 | ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters. |
| 9525 | 14976218 | ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters. |
| 9526 | 14976218 | ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters. |
| 9527 | 14976218 | Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters. |
| 9528 | 14976218 | Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters. |
| 9529 | 14976218 | Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters. |
| 9530 | 14976218 | Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters. |
| 9531 | 14976218 | Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters. |
| 9532 | 14976218 | Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription. |
| 9533 | 14976218 | Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription. |
| 9534 | 14976218 | Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription. |
| 9535 | 14976218 | Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription. |
| 9536 | 14976218 | Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription. |
| 9537 | 14976218 | Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic. |
| 9538 | 14976218 | Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic. |
| 9539 | 14976218 | Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic. |
| 9540 | 14976218 | Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic. |
| 9541 | 14976218 | Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic. |
| 9542 | 14972097 | Obesity, atherosclerosis, insulin resistance and hyperinsulinemia, hyperlipidemia, essential hypertension, type 2 diabetes mellitus, and coronary heart disease (CHD) are the components of metabolic syndrome X and are associated with elevated plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-alpha, which are markers of inflammation. |
| 9543 | 14965324 | Our initial studies on renal cyclooxygenase (COX)-2 expression and activity addressed the critical role of angiotensin II (Ang II) in increasing tumor necrosis factor alpha (TNF) that eventuated in expression of COX-2 in the medullary thick ascending limb (mTAL) of the nephron. |
| 9544 | 14965324 | COX-2 supplanted the dominant oxygenase, the cytochrome P450 (CYP) enzyme, omega-hydroxylase, that synthesized 20-hydroxyeicosatetraenoic acid (20-HETE). |
| 9545 | 14965001 | Content of different cytokines (IF alpha, TNF alpha, IL-1 alpha, IL-4, IL-6 and IL-10) was examined in the blood serum in two groups of healthy children-siblings with type 1 diabetes mellitus with and without revealed insulin autoantibodies against pancreatic islets (GADA, IA-2A and IAA) by enzyme-like immunosorbent assay (ELISA). |
| 9546 | 14965001 | Content of different cytokines (IF alpha, TNF alpha, IL-1 alpha, IL-4, IL-6 and IL-10) was examined in the blood serum in two groups of healthy children-siblings with type 1 diabetes mellitus with and without revealed insulin autoantibodies against pancreatic islets (GADA, IA-2A and IAA) by enzyme-like immunosorbent assay (ELISA). |
| 9547 | 14965001 | In the group of patients with two and more revealed autoantibodies the higher indices in the number of IF alpha, TNF alpha and IL-6, and the decrease in the level of IL-4 comparing with the group of children with negative reaction to diabetes associated autoantibodies were more often observed. |
| 9548 | 14965001 | In the group of patients with two and more revealed autoantibodies the higher indices in the number of IF alpha, TNF alpha and IL-6, and the decrease in the level of IL-4 comparing with the group of children with negative reaction to diabetes associated autoantibodies were more often observed. |
| 9549 | 14962280 | APIs, cultured for 1, 4, 8 and 11 days post-isolation, expressed mRNA for monocyte chemoattractant protein-1 (MCP-1), IL-1beta and TNF-alpha. |
| 9550 | 14962280 | APIs, cultured for 1, 4, 8 and 11 days post-isolation, expressed mRNA for monocyte chemoattractant protein-1 (MCP-1), IL-1beta and TNF-alpha. |
| 9551 | 14962280 | APIs, cultured for 1, 4, 8 and 11 days post-isolation, expressed mRNA for monocyte chemoattractant protein-1 (MCP-1), IL-1beta and TNF-alpha. |
| 9552 | 14962280 | However, APIs or their supernatants were not able to activate human aortic endothelial cells (HAECs) in vitro, and neither IL-1beta nor TNF-alpha were detected by enzyme-linked immunosorbent assay (ELISA) in API culture supernatants. |
| 9553 | 14962280 | However, APIs or their supernatants were not able to activate human aortic endothelial cells (HAECs) in vitro, and neither IL-1beta nor TNF-alpha were detected by enzyme-linked immunosorbent assay (ELISA) in API culture supernatants. |
| 9554 | 14962280 | However, APIs or their supernatants were not able to activate human aortic endothelial cells (HAECs) in vitro, and neither IL-1beta nor TNF-alpha were detected by enzyme-linked immunosorbent assay (ELISA) in API culture supernatants. |
| 9555 | 14962280 | Both recombinant porcine IL-1beta and TNF-alpha were able to activate human endothelial cells (ECs) inducing CD62E and CD106 expression as analyzed by flow cytometry. |
| 9556 | 14962280 | Both recombinant porcine IL-1beta and TNF-alpha were able to activate human endothelial cells (ECs) inducing CD62E and CD106 expression as analyzed by flow cytometry. |
| 9557 | 14962280 | Both recombinant porcine IL-1beta and TNF-alpha were able to activate human endothelial cells (ECs) inducing CD62E and CD106 expression as analyzed by flow cytometry. |
| 9558 | 14768049 | However, in vivo neutralization of IL-4, IL-10 or TGF-beta using monoclonal antibodies did not prevent the inhibition whereas treatment with an antibody against the glucocorticoid-induced TNF receptor abrogated the protection from disease. |
| 9559 | 14764813 | Soluble VCAM-1, E-selectin, and C-reactive protein concentrations were measured before and after treatment in 25 healthy subjects and 25 adult GH-deficient (GHD) patients randomized to GH treatment or placebo. |
| 9560 | 14764813 | Furthermore, we studied the direct effect of GH and IGF-I and serum from GH-treated subjects on basal and TNF alpha-stimulated expression of VCAM-1 and E-selectin on cultured human umbilical vein endothelial cells. |
| 9561 | 14764813 | In human umbilical vein endothelial cells, there was no direct stimulatory effect of either GH or IGF-I on the expression of VCAM-1 and E-selectin, but serum from GH-treated healthy subjects significantly increased the expression of VCAM-1 (P < 0.01). |
| 9562 | 14764790 | In the at-risk group, there was a decrease in the C-reactive protein [median (25-75 percentile), 0.12 mg/dl (0.07-0.27 mg/dl) at exit visit vs. 0.24 mg/dl (0.07-0.35 mg/dl) at baseline; P < 0.05] and TNF alpha [median (25-75 percentile), 2.6 pg/ml (1.8-4.1 pg/ml) at exit visit vs. 4.4 pg/ml (3.6-6.0 pg/ml) at baseline; P < 0.05] in the atorvastatin-treated patients, whereas in the diabetes group, a decrease in endothelin-1 (mean +/- SD, 0.97 +/- 0.29 pg/ml at exit visit vs. 1.19 +/- 0.42 pg/ml at baseline; P < 0.05) and plasminogen activator inhibitor-1 [median (25-75 percentile), 18 ng/ml (9-24 ng/ml) at exit visit vs. 27 ng/ml (7-41 ng/ml) at baseline; P < 0.05] were observed. |
| 9563 | 14758566 | Major secretagogues are cytokines such as TNF-alpha or IL-1. |
| 9564 | 14747392 | Associations were examined between tHcy level and markers of malnutrition-inflammation complex syndrome and 12-mo prospective hospitalization and mortality in 367 MHD patients, aged 54.5 +/- 14.7 (mean +/- SD) years, who included 199 men and 55% individuals with diabetes. tHcy was 24.4 +/- 11.8 micro mol/L, and 94% of the patients had hyperhomocysteinemia (tHcy >13.5 micro mol/L). tHcy had weak to moderate but statistically significant bivariate and multivariate correlations with some laboratory markers of nutrition (serum albumin, prealbumin, creatinine, and urea nitrogen) but no significant correlation with serum C-reactive protein or two proinflammatory cytokines (IL-6 and TNF-alpha). |
| 9565 | 14747298 | Myocardial infarct size (P < 0.05), apoptotic index (P < 0.005), and tissue levels of tumor necrosis factor (P < 0.01), interleukin-6 (P < 0.01), and interleukin-18 (P < 0.01) were higher in nondiabetic iNOS(-/-) mice compared with nondiabetic iNOS(+/+) mice. |
| 9566 | 14744635 | Catalytic antioxidants prevented the initiation of the innate immune response in LPS-stimulated macrophages as evidenced by the suppression of proinflammatory cytokines (TNF-alpha, IL-1beta) and ROS (NO2- and O2-). |
| 9567 | 14744635 | Catalytic antioxidants prevented the initiation of the innate immune response in LPS-stimulated macrophages as evidenced by the suppression of proinflammatory cytokines (TNF-alpha, IL-1beta) and ROS (NO2- and O2-). |
| 9568 | 14744635 | The coupling of the innate with the adaptive immune response is dependent on TNF-alpha, IL-1beta, NO2-, and O2- generation; therefore, agents like catalytic antioxidants that decrease proinflammatory cytokines and ROS may provide protective effects in diseases in which chronic inflammation plays a pathogenic role. |
| 9569 | 14744635 | The coupling of the innate with the adaptive immune response is dependent on TNF-alpha, IL-1beta, NO2-, and O2- generation; therefore, agents like catalytic antioxidants that decrease proinflammatory cytokines and ROS may provide protective effects in diseases in which chronic inflammation plays a pathogenic role. |
| 9570 | 14743439 | The expression of cytokines such as tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in the fetal brain of normal and diabetic embryos was induced in the neural tubes after CP treatment. |
| 9571 | 14742654 | We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. |
| 9572 | 14742654 | In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). |
| 9573 | 14734853 | The effects of tacrolimus on insulin-dependent diabetes mellitus (IDDM) induced by the D-variant of encephalomyocarditis virus (D-EMCV) have been investigated. |
| 9574 | 14734853 | The effects of tacrolimus on insulin-dependent diabetes mellitus (IDDM) induced by the D-variant of encephalomyocarditis virus (D-EMCV) have been investigated. |
| 9575 | 14734853 | Expressions of TNF-alpha and IFN-gamma mRNA in spleens of tacrolimus-treated D-EMCV-infected mice were lower than that of non-treated tacrolimus DEMCV-infected mice on 7 DPI. |
| 9576 | 14734853 | Expressions of TNF-alpha and IFN-gamma mRNA in spleens of tacrolimus-treated D-EMCV-infected mice were lower than that of non-treated tacrolimus DEMCV-infected mice on 7 DPI. |
| 9577 | 14734853 | The results suggest that tacrolimus suppresses expressions of TNF-alpha and IFN-gamma mRNAs to prevent the onset of D-EMCV-induced IDDM. |
| 9578 | 14734853 | The results suggest that tacrolimus suppresses expressions of TNF-alpha and IFN-gamma mRNAs to prevent the onset of D-EMCV-induced IDDM. |
| 9579 | 14734833 | Serum and cardiac tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. |
| 9580 | 14734833 | Serum and cardiac tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. |
| 9581 | 14734833 | Serum and cardiac tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. |
| 9582 | 14734833 | Lipopolysaccharide treatment significantly increased serum and cardiac TNF-alpha and IL-6 concentrations. |
| 9583 | 14734833 | Lipopolysaccharide treatment significantly increased serum and cardiac TNF-alpha and IL-6 concentrations. |
| 9584 | 14734833 | Lipopolysaccharide treatment significantly increased serum and cardiac TNF-alpha and IL-6 concentrations. |
| 9585 | 14734833 | Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-alpha elevation, but it significantly enhanced lipopolysaccharideinduced cardiac IL-6 production. |
| 9586 | 14734833 | Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-alpha elevation, but it significantly enhanced lipopolysaccharideinduced cardiac IL-6 production. |
| 9587 | 14734833 | Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-alpha elevation, but it significantly enhanced lipopolysaccharideinduced cardiac IL-6 production. |
| 9588 | 14732803 | The presence of systemic inflammation, characterized by elevated levels of certain potent pro-inflammatory mediators, such as C-reactive protein, leptin, TNF-alpha, IL-1beta, IL-6, reactive oxygen species and adhesion molecules, may predispose to the development of cardiovascular complications observed in patients with OSAS. |
| 9589 | 14722654 | We review how circulating factors such as insulin itself, TNF-alpha, interleukins, fatty acids and glycation products influence insulin action through insulin signalling molecules themselves or through other pathways ultimately impinging on the insulin-signalling pathway. |
| 9590 | 14714889 | Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), are upregulated and activate the inflammatory process. |
| 9591 | 14714889 | In MS, gelatinase B or MMP-9 is a pathogenic glycoprotein of which the sugars contribute to its interactions with the tissue inhibitor of metalloproteinases-1 (TIMP-1) and thus assist in the determination of the enzyme activity. |
| 9592 | 14714889 | In RA, gelatinase B cleaves denatured type II collagen into remnant epitopes, some of which constitute immunodominant glycopeptides. |
| 9593 | 14714889 | The most efficient cleavage by gelatinase B leads to a major insulin remnant epitope. |
| 9594 | 14711793 | At early time points, we measured organ histology, leukocyte accumulation, myeloperoxidase activity, activation of nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, in addition to messenger RNA for intracellular adhesion molecule-1 and tumor necrosis factor-alpha. |
| 9595 | 14711793 | At early time points, we measured organ histology, leukocyte accumulation, myeloperoxidase activity, activation of nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, in addition to messenger RNA for intracellular adhesion molecule-1 and tumor necrosis factor-alpha. |
| 9596 | 14711793 | Renal ischemia rapidly activated kidney and lung nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, and distant lung injury. |
| 9597 | 14711793 | Renal ischemia rapidly activated kidney and lung nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, and distant lung injury. |
| 9598 | 14711793 | Alpha-MSH administration immediately before reperfusion significantly decreased kidney and lung injury and prevented activation of kidney and lung transcription factors and stress response genes, and lung intracellular adhesion molecule-1 and tumor necrosis factor-alpha at early time points after renal ischemia/reperfusion. |
| 9599 | 14711793 | Alpha-MSH administration immediately before reperfusion significantly decreased kidney and lung injury and prevented activation of kidney and lung transcription factors and stress response genes, and lung intracellular adhesion molecule-1 and tumor necrosis factor-alpha at early time points after renal ischemia/reperfusion. |
| 9600 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9601 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9602 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9603 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9604 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9605 | 14709837 | The effect of leptin, tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) production on insulin resistance in Otsuka Long-Evans fatty rats. |
| 9606 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9607 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9608 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9609 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9610 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9611 | 14709837 | After 4 weeks the blood levels of leptin, tumor necrosis factor-alpha (TNF-alpha), and NO were measured. |
| 9612 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9613 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9614 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9615 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9616 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9617 | 14709837 | Leptin and TNF-alpha levels were significantly higher in the OLETF rats than in the LETO rats, while NO levels did not change between the two groups. |
| 9618 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9619 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9620 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9621 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9622 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9623 | 14709837 | The high-fat diet elevated blood leptin levels, but not TNF-alpha and NO levels. |
| 9624 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9625 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9626 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9627 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9628 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9629 | 14709837 | The HOMA-R in the OLETF rats was correlated with leptin, but not with BP, BW, TNF-alpha or NO. |
| 9630 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9631 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9632 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9633 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9634 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9635 | 14709837 | In conclusion, leptin, TNF-alpha, and NO may each regulate insulin sensitivity through their own unique pathways. |
| 9636 | 14704746 | When TNF-alpha activity is blocked in obesity, either biochemically or genetically, the result is improved insulin sensitivity. |
| 9637 | 14704746 | When TNF-alpha activity is blocked in obesity, either biochemically or genetically, the result is improved insulin sensitivity. |
| 9638 | 14704746 | These include the discovery of c-Jun N-terminal kinase (JNK) and I kappa beta kinase (I kappa K) as critical regulators of insulin action activated by TNF-alpha and other inflammatory and stress signals, and the identification of potential targets. |
| 9639 | 14704746 | These include the discovery of c-Jun N-terminal kinase (JNK) and I kappa beta kinase (I kappa K) as critical regulators of insulin action activated by TNF-alpha and other inflammatory and stress signals, and the identification of potential targets. |
| 9640 | 14704746 | Here, the role of the JNK pathway in insulin receptor signaling, the impact of blocking this pathway in obesity and the mechanisms underlying JNK-induced insulin resistance will be discussed. |
| 9641 | 14704746 | Here, the role of the JNK pathway in insulin receptor signaling, the impact of blocking this pathway in obesity and the mechanisms underlying JNK-induced insulin resistance will be discussed. |
| 9642 | 14704737 | This involves infiltration of T-cells and macrophages into the islets and local production of inflammatory cytokines such as interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. |
| 9643 | 14704737 | These include a cytokine selection strategy that results in cell lines that are resistant to the combined effects of IL-1 beta+IFN-gamma. |
| 9644 | 14702111 | In RIP-LCMV mice, blockade of TNF-alpha or IFN-gamma in vivo abolished the prevention of T1D. |
| 9645 | 14698276 | Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. |
| 9646 | 14698276 | Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. |
| 9647 | 14698276 | Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. |
| 9648 | 14698276 | Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. |
| 9649 | 14693987 | Effect of moderate alcohol consumption on adiponectin, tumor necrosis factor-alpha, and insulin sensitivity. |
| 9650 | 14693705 | IL-1 receptor deficiency slows progression to diabetes in the NOD mouse. |
| 9651 | 14693705 | IL-1 receptor deficiency slows progression to diabetes in the NOD mouse. |
| 9652 | 14693705 | They act by upregulation of genes including Fas and inducible nitric oxide synthase (iNOS), which have both been shown to lead to beta-cell death in vitro. |
| 9653 | 14693705 | They act by upregulation of genes including Fas and inducible nitric oxide synthase (iNOS), which have both been shown to lead to beta-cell death in vitro. |
| 9654 | 14693705 | We used mice deficient in the interleukin (IL)-1 receptor (IL-1R) to assess the contribution of IL-1 to different models of diabetes. |
| 9655 | 14693705 | We used mice deficient in the interleukin (IL)-1 receptor (IL-1R) to assess the contribution of IL-1 to different models of diabetes. |
| 9656 | 14693705 | IL-1R-deficient islets were protected from the damaging effects of tumor necrosis factor (TNF) and interferon (IFN)-gamma in vitro, and beta-cell expression of iNOS was reduced, suggesting that IL-1 mediates the induction of iNOS by TNF and IFN-gamma. |
| 9657 | 14693705 | IL-1R-deficient islets were protected from the damaging effects of tumor necrosis factor (TNF) and interferon (IFN)-gamma in vitro, and beta-cell expression of iNOS was reduced, suggesting that IL-1 mediates the induction of iNOS by TNF and IFN-gamma. |
| 9658 | 14693705 | IL-1 action was not required for induction of class I major histocompatibility complex or Fas by TNF and IFN-gamma. |
| 9659 | 14693705 | IL-1 action was not required for induction of class I major histocompatibility complex or Fas by TNF and IFN-gamma. |
| 9660 | 14693700 | Tumor necrosis factor-alpha (TNF-alpha) and hyperglycemia both impair insulin sensitivity in vivo. |
| 9661 | 14693700 | Tumor necrosis factor-alpha (TNF-alpha) and hyperglycemia both impair insulin sensitivity in vivo. |
| 9662 | 14693700 | Tumor necrosis factor-alpha (TNF-alpha) and hyperglycemia both impair insulin sensitivity in vivo. |
| 9663 | 14693700 | The ability of TNF-alpha to phosphorylate extracellular signal-regulated kinase 1 (ERK1) and ERK2 and to downregulate perilipin (which has been implicated in the lipolytic effect of TNF-alpha) was not affected by glucose. |
| 9664 | 14693700 | The ability of TNF-alpha to phosphorylate extracellular signal-regulated kinase 1 (ERK1) and ERK2 and to downregulate perilipin (which has been implicated in the lipolytic effect of TNF-alpha) was not affected by glucose. |
| 9665 | 14693700 | The ability of TNF-alpha to phosphorylate extracellular signal-regulated kinase 1 (ERK1) and ERK2 and to downregulate perilipin (which has been implicated in the lipolytic effect of TNF-alpha) was not affected by glucose. |
| 9666 | 14693700 | These findings suggest novel mechanisms by which TNF-alpha and hyperglycemia raise FFA levels and induce insulin resistance. |
| 9667 | 14693700 | These findings suggest novel mechanisms by which TNF-alpha and hyperglycemia raise FFA levels and induce insulin resistance. |
| 9668 | 14693700 | These findings suggest novel mechanisms by which TNF-alpha and hyperglycemia raise FFA levels and induce insulin resistance. |
| 9669 | 14687828 | Tumor necrosis factor-alpha-induced insulin resistance may mediate the hepatitis C virus-diabetes association. |
| 9670 | 14684612 | During the clamp, there is no alteration in the expression or activation in the insulin signaling molecules involved in glucose transport through the phosphoinositide 3-kinase/Akt and CAP/Cbl pathways in WAT from MIRKO. |
| 9671 | 14684612 | There is a 39.5% increase in serum adiponectin (P < 0.01) without modification in serum leptin, resistin, and TNF-alpha. |
| 9672 | 14684612 | There is an accelerated differentiation of small insulin sensitive adipocytes, an increased secretion of the insulin sensitizer adiponectin, and maintenance of leptin sensitivity. |
| 9673 | 14683455 | Decreased expression of one of these molecules, adiponectin/Acrp30, correlates strongly with insulin resistance. |
| 9674 | 14683455 | Interestingly, adiponectin was decreased in insulin resistant rodent models both of obesity and lipoatrophy, and replenishment of adiponectin ameliorated their insulin resistance. |
| 9675 | 14683455 | Moreover, adiponectin transgenic mice ameliorated insulin resistance and diabetes Adiponectin knockout mice showed insulin resistance and glucose intolerance. |
| 9676 | 14683455 | In muscle and liver, adiponectin activated AMP kinase and PPARalpha pathways thereby increasing beta-oxidation of lipids, leading to decreased TG content, which ameliorated insulin resistance under a high-fat diet. |
| 9677 | 14683455 | Despite similar plasma glucose and lipid levels on an apoE deficient background, adiponectin transgenic apoE deficient mice showed amelioration of atherosclerosis, which was associated with decreased expressions of class A scavenger receptor and tumor necrosis factor alpha. |
| 9678 | 14683455 | Finally, cDNA encoding adiponectin receptors (AdipoR1 and R2) have been identified by expression cloning, which facilitates the understanding of molecular mechanisms of adiponectin actions and obesity-linked diseases such as diabetes and atherosclerosis and the designing of novel antidiabetic and anti-atherogenic drugs with AdipoR1 and R2 as molecular targets. |
| 9679 | 14678864 | These chemical messengers include adiponectin, resistin, leptin, plasminogen activator inhibitor-1, tumor necrosis factor-alpha, and interleukin-6. |
| 9680 | 14668051 | Neuropoietic cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta (TGF-beta), exhibit pleiotrophic effects on homeostasis of glia and neurons in central, peripheral, and autonomic nervous system. |
| 9681 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9682 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9683 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9684 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9685 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9686 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9687 | 14656685 | Ex vivo lipopolysaccharide (LPS)-induced TNF-alpha, IL-1beta, IL-6 and PGE2 secretion in whole blood from Type 1 diabetes mellitus patients with or without aggressive periodontitis. |
| 9688 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9689 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9690 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9691 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9692 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9693 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9694 | 14656685 | Progression to severe periodontitis with loss of supporting structures is mediated by several factors, including secretion of a broad spectrum of inflammatory and destructive (PGE2). mediators such as cytokines (TNF-alpha, IL-1b and IL-6), chemokines (IL-8) and prostaglandin E2. |
| 9695 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9696 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9697 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9698 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9699 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9700 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9701 | 14656685 | The aim of this work is to investigate differences in the TNF-a, IL-1b and IL-6 expression and prostaglandin E2 (PGE2) release in blood from diabetic patients with and without aggressive periodontitis (AP) stimulated with lipopolysaccharide (LPS). |
| 9702 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9703 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9704 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9705 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9706 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9707 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9708 | 14656685 | A wide range of inter-individual variability in spontaneous and LPS-induced TNF-alpha, IL-1b and IL-6 levels in patient groups and controls was found. |
| 9709 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9710 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9711 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9712 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9713 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9714 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9715 | 14656685 | The mean of spontaneous and LPS-induced TNF-alpha and IL-1b levels did not differ significantly (p > 0.5) when patients were compared to control individuals. |
| 9716 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9717 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9718 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9719 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9720 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9721 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9722 | 14656685 | Although not significant, the spontaneous TNF-alpha, IL-1b and IL-6 levels in the group of Type 1 DM with AP were higher than in controls, while in diabetic patients without AP, these values were depressed in comparison with controls. |
| 9723 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9724 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9725 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9726 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9727 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9728 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9729 | 14656685 | Finally, we conclude that Type 1 diabetic patients with or without AP did not express higher LPS-induced TNF-a, IL-1b and IL-6 levels than controls. |
| 9730 | 14642793 | Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. |
| 9731 | 14642793 | Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. |
| 9732 | 14642793 | Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. |
| 9733 | 14642793 | Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. |
| 9734 | 14642793 | The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). |
| 9735 | 14642793 | The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). |
| 9736 | 14642793 | The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). |
| 9737 | 14642793 | The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). |
| 9738 | 14642793 | Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. |
| 9739 | 14642793 | Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. |
| 9740 | 14642793 | Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. |
| 9741 | 14642793 | Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. |
| 9742 | 14642793 | We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes. |
| 9743 | 14642793 | We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes. |
| 9744 | 14642793 | We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes. |
| 9745 | 14642793 | We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes. |
| 9746 | 14641043 | Down-regulation of insulin receptor tyrosine phosphorylation and subsequent steps in the insulin signalling pathway, including insulin receptor substrate-1 (IRS-1)-associated phosphoinositide 3-kinase (PI3K), Akt kinase serine phosphorylation and activity and glucose transporter (GLUT-4) protein content, are evident in skeletal muscle after eccentric exercise. |
| 9747 | 14641043 | Down-regulation of insulin receptor tyrosine phosphorylation and subsequent steps in the insulin signalling pathway, including insulin receptor substrate-1 (IRS-1)-associated phosphoinositide 3-kinase (PI3K), Akt kinase serine phosphorylation and activity and glucose transporter (GLUT-4) protein content, are evident in skeletal muscle after eccentric exercise. |
| 9748 | 14641043 | Down-regulation of insulin receptor tyrosine phosphorylation and subsequent steps in the insulin signalling pathway, including insulin receptor substrate-1 (IRS-1)-associated phosphoinositide 3-kinase (PI3K), Akt kinase serine phosphorylation and activity and glucose transporter (GLUT-4) protein content, are evident in skeletal muscle after eccentric exercise. |
| 9749 | 14641043 | Down-regulation of insulin receptor tyrosine phosphorylation and subsequent steps in the insulin signalling pathway, including insulin receptor substrate-1 (IRS-1)-associated phosphoinositide 3-kinase (PI3K), Akt kinase serine phosphorylation and activity and glucose transporter (GLUT-4) protein content, are evident in skeletal muscle after eccentric exercise. |
| 9750 | 14641043 | Furthermore, increased tumour necrosis factor alpha (TNF-alpha) secretion from monocytes is associated with the decrease in PI3K activity after this type of exercise. |
| 9751 | 14641043 | Furthermore, increased tumour necrosis factor alpha (TNF-alpha) secretion from monocytes is associated with the decrease in PI3K activity after this type of exercise. |
| 9752 | 14641043 | Furthermore, increased tumour necrosis factor alpha (TNF-alpha) secretion from monocytes is associated with the decrease in PI3K activity after this type of exercise. |
| 9753 | 14641043 | Furthermore, increased tumour necrosis factor alpha (TNF-alpha) secretion from monocytes is associated with the decrease in PI3K activity after this type of exercise. |
| 9754 | 14641043 | Recent studies have shown that TNF-alpha can increase IRS-1 serine/threonine phosphorylation, which impairs IRS-1 docking to the insulin receptor, and this inhibits insulin signalling. |
| 9755 | 14641043 | Recent studies have shown that TNF-alpha can increase IRS-1 serine/threonine phosphorylation, which impairs IRS-1 docking to the insulin receptor, and this inhibits insulin signalling. |
| 9756 | 14641043 | Recent studies have shown that TNF-alpha can increase IRS-1 serine/threonine phosphorylation, which impairs IRS-1 docking to the insulin receptor, and this inhibits insulin signalling. |
| 9757 | 14641043 | Recent studies have shown that TNF-alpha can increase IRS-1 serine/threonine phosphorylation, which impairs IRS-1 docking to the insulin receptor, and this inhibits insulin signalling. |
| 9758 | 14641043 | Thus a unifying hypothesis to explain insulin resistance after eccentric exercise may include inflammation arising from the disruption of muscle-cell integrity, leading to an acute-phase response that includes TNF-alpha, with the latter inhibiting insulin signalling and subsequent metabolic events. |
| 9759 | 14641043 | Thus a unifying hypothesis to explain insulin resistance after eccentric exercise may include inflammation arising from the disruption of muscle-cell integrity, leading to an acute-phase response that includes TNF-alpha, with the latter inhibiting insulin signalling and subsequent metabolic events. |
| 9760 | 14641043 | Thus a unifying hypothesis to explain insulin resistance after eccentric exercise may include inflammation arising from the disruption of muscle-cell integrity, leading to an acute-phase response that includes TNF-alpha, with the latter inhibiting insulin signalling and subsequent metabolic events. |
| 9761 | 14641043 | Thus a unifying hypothesis to explain insulin resistance after eccentric exercise may include inflammation arising from the disruption of muscle-cell integrity, leading to an acute-phase response that includes TNF-alpha, with the latter inhibiting insulin signalling and subsequent metabolic events. |
| 9762 | 14641043 | In contrast, exercise training increases insulin signalling and GLUT-4 expression, decreases TNF-alpha expression in skeletal muscle, and is associated with enhanced insulin sensitivity. |
| 9763 | 14641043 | In contrast, exercise training increases insulin signalling and GLUT-4 expression, decreases TNF-alpha expression in skeletal muscle, and is associated with enhanced insulin sensitivity. |
| 9764 | 14641043 | In contrast, exercise training increases insulin signalling and GLUT-4 expression, decreases TNF-alpha expression in skeletal muscle, and is associated with enhanced insulin sensitivity. |
| 9765 | 14641043 | In contrast, exercise training increases insulin signalling and GLUT-4 expression, decreases TNF-alpha expression in skeletal muscle, and is associated with enhanced insulin sensitivity. |
| 9766 | 14634066 | Expression of CD11c, CD40, CD54, and major histocompatibility complex I-A(g7) was reduced in cells cultured with additional DcR3.Fc, compared with DCs incubated with granulocyte macrophage-colony stimulating factor and interleukin (IL)-4, indicating that DcR3 interferes with the differentiation and maturation of BM-DCs. |
| 9767 | 14634066 | One of the most striking effects of DcR3.Fc on the differentiation of DCs was the up-regulation of CD86 and down-regulation of CD80, suggesting a modulatory potential to skew the T cell response toward the T helper cell type 2 (Th2) phenotype. |
| 9768 | 14634066 | Moreover, the secretion of interferon-gamma from T cells cocultured with DcR3.Fc-treated DCs was profoundly suppressed, indicating that DcR3 exerts a Th1-suppressing effect on differentiating DCs. |
| 9769 | 14634066 | Data from two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization-time-of-flight analysis show an up-regulation of some proteins-such as mitogen-activated protein kinase p38 beta, cyclin-dependent kinase 6, and signal-induced proliferation-associated gene 1-and a down-regulation of the IL-17 precursor; tumor necrosis factor-related apoptosis-inducing ligand family member-associated nuclear factor-kappaB activator-binding kinase 1; and Golgi S-nitroso-N-acetylpenicillamine in cells treated with DcR3, further demonstrating its effect on DC differentiation and function. |
| 9770 | 14633856 | Upregulation of interleukins, leptin, and tumor necrosis factor-alpha receptors and their downstream molecular adaptors indicated an activation of pathways recruiting stress-activated protein/c-Jun NH(2)-terminal kinases. |
| 9771 | 14633854 | Shortly after brain death induction, a significant increase in serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 was demonstrated in a time-dependent manner. |
| 9772 | 14633854 | Shortly after brain death induction, a significant increase in serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 was demonstrated in a time-dependent manner. |
| 9773 | 14633854 | Upregulation of TNF-alpha, IL-1beta, and IL-6 mRNA was noted in the pancreas. |
| 9774 | 14633854 | Upregulation of TNF-alpha, IL-1beta, and IL-6 mRNA was noted in the pancreas. |
| 9775 | 14633854 | Islet viability assessed in dissociated islet cells and in intact cultured islets was reduced in islets recovered from brain death donors, an effect associated with higher nuclear activities of NF-kappaB p50, c-Jun, and ATF-2. |
| 9776 | 14633854 | Islet viability assessed in dissociated islet cells and in intact cultured islets was reduced in islets recovered from brain death donors, an effect associated with higher nuclear activities of NF-kappaB p50, c-Jun, and ATF-2. |
| 9777 | 14630568 | Enhanced TNF-alpha production may also promote atherosclerosis due to increased insulin resistance and the expression of adhesion molecules. |
| 9778 | 14626649 | These include tumor necrosis factor (TNF-alpha), plasminogen activator inhibitor type 1 (PAI-1), leptin, resistine and adiponectin. |
| 9779 | 14626649 | These include tumor necrosis factor (TNF-alpha), plasminogen activator inhibitor type 1 (PAI-1), leptin, resistine and adiponectin. |
| 9780 | 14626649 | Adiponectin (also referred to as AdipoQ, Acrp 30, apM1 or GBP28) is a novel adipose-specific protein. |
| 9781 | 14626649 | Adiponectin (also referred to as AdipoQ, Acrp 30, apM1 or GBP28) is a novel adipose-specific protein. |
| 9782 | 14626649 | Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of many others, as leptin or TNF-alpha, its level is reduced in obesity and type 2 diabetes. |
| 9783 | 14626649 | Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of many others, as leptin or TNF-alpha, its level is reduced in obesity and type 2 diabetes. |
| 9784 | 14626649 | The administration of thiazolidinediones, which are synthetic PPARs-gamma ligands, significantly increases the plasma adiponectin concentrations, an effect that could improve insulin sensitivity. |
| 9785 | 14626649 | The administration of thiazolidinediones, which are synthetic PPARs-gamma ligands, significantly increases the plasma adiponectin concentrations, an effect that could improve insulin sensitivity. |
| 9786 | 14626649 | Thus, the administration of adiponectin may provide a novel treatment modality for insulin resistance and type 2 diabetes. |
| 9787 | 14626649 | Thus, the administration of adiponectin may provide a novel treatment modality for insulin resistance and type 2 diabetes. |
| 9788 | 14624957 | I investigated whether metabolism of essential fatty acids and the concentrations of their long-chain metabolites (long-chain polyunsaturated fatty acids [LCPUFAs]) are altered in fetal or perinatal growth retardation, maternal hypercholesterolemia, low-grade systemic inflammation, insulin resistance, and atherosclerosis, conditions that predispose to the development of coronary heart disease (CHD).I critically reviewed the literature pertaining to the metabolism of essential fatty acids in CHD and conditions that predispose to it.LCPUFAs enhance endothelial nitric oxide synthesis, suppress the production of the proinflammatory cytokines tumor necrosis factor and interleukin-6, attenuate insulin resistance, and have antiatherosclerotic properties. |
| 9789 | 14621575 | We discuss the method to select cases for chemoprophylaxis as to the cases of diabetes, collagen diseases and lung cancer administered corticosteroid preparations as well as the cases of Crohn's disease and rheumatoid arthritis administered anti-TNF-alpha among compromised hosts. |
| 9790 | 14609223 | CD4+ lymphocytes with specificity for insulin can be induced by immunization with the insulin B chain via the oral route or by DNA vaccination. |
| 9791 | 14609223 | In comparison to non-regulatory insulin B-specific cell lines, they produce high amounts of interleukin (IL)4 and IL10, whereas interferon (IFN)gamma and tumour necrosis factor (TNF)alpha levels are comparable. |
| 9792 | 14609223 | We propose that this is achieved by modulation of antigen presenting cells that lose the ability to propagate aggressive responses after exposure to IL4 or IL10 in vitro. |
| 9793 | 14609223 | In order to avoid induction of insulin B-specific autoaggressive T cells we have demonstrated that administration of IL4 or IL10 at the time of immunization is beneficial and therefore should be part of a potential future clinical application. |
| 9794 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 9795 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 9796 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 9797 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 9798 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 9799 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 9800 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 9801 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 9802 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 9803 | 14593614 | The two main transduction pathways are the phosphatidylinositol 3 kinase pathway activating protein kinase B which is involved in priority in metabolic effects, and the MAP kinase pathway involved in nuclear effects, proliferation and differentiation. |
| 9804 | 14593614 | This phosphorylation is activated in response to different signals involved in insulin resistance, hyperinsulinism, TNFalpha or increased free fatty acids from adipose tissue, which are transformed inside the cell in acyl-CoA. |
| 9805 | 14593611 | Here, we review new advances in our understanding of mechanisms leading to insulin resistance and type 2 diabetes from the perspective of the role and interactions of recently identified adipocyte-specific chemical messengers, the adipocytokines, such as adiponectin, tumor necrosis factor-alpha, interleukin 6, and resistin. |
| 9806 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 9807 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 9808 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 9809 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 9810 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 9811 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 9812 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 9813 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 9814 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 9815 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 9816 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 9817 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 9818 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 9819 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 9820 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 9821 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 9822 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 9823 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 9824 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 9825 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 9826 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 9827 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 9828 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 9829 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 9830 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 9831 | 14584758 | Elevated plasma levels of C-reactive protein (CRP) and IL-6 have been reported to be sensitive indicators of infection in adults with diabetic ketoacidosis (DKA). |
| 9832 | 14584758 | Elevated plasma levels of C-reactive protein (CRP) and IL-6 have been reported to be sensitive indicators of infection in adults with diabetic ketoacidosis (DKA). |
| 9833 | 14584758 | In 7 patients with severe DKA without infection, we measured plasma CRP, IL-6, IL-1beta and TNF-alpha levels prior to, during, and following correction of DKA. |
| 9834 | 14584758 | In 7 patients with severe DKA without infection, we measured plasma CRP, IL-6, IL-1beta and TNF-alpha levels prior to, during, and following correction of DKA. |
| 9835 | 14584758 | There were significant positive relationships between CRP and both IL-6 and IL-1beta prior to treatment (p <0.05); between CRP and IL-6, IL-1beta, and TNF-alpha at 6 hr (p <0.05); and between CRP and IL-1beta at 24 hr (p <0.05). |
| 9836 | 14584758 | There were significant positive relationships between CRP and both IL-6 and IL-1beta prior to treatment (p <0.05); between CRP and IL-6, IL-1beta, and TNF-alpha at 6 hr (p <0.05); and between CRP and IL-1beta at 24 hr (p <0.05). |
| 9837 | 14584587 | This controls many aspects of IRS-1, including its interaction with the insulin receptor and subsequent tyrosine phosphorylation, as well as its subcellular distribution and targeting for degradation by the proteasome. |
| 9838 | 14584587 | Emerging evidence indicates that 'diabetogenic factors' associated with insulin resistance, such as TNFalpha and elevated circulating fatty acids, impact on insulin signalling at the level of IRS-1 serine/threonine phosphorylation. |
| 9839 | 14584587 | The expression and/or activity of several kinases, such as IkappaB kinase beta (IKKbeta) and salt-induced kinase 2 (SIK2), and the phosphorylation of IRS-1 at key sites, such as Ser307 and Ser789, are increased in states of insulin resistance. |
| 9840 | 14583341 | F2-isoprostanes, measured using gas chromatography-mass spectrometry in 24 h urines and C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha), were measured before and after intervention. |
| 9841 | 14583341 | F2-isoprostanes, measured using gas chromatography-mass spectrometry in 24 h urines and C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha), were measured before and after intervention. |
| 9842 | 14583341 | There were no significant changes in CRP, IL-6, and TNF-alpha following EPA or DHA supplementation. |
| 9843 | 14583341 | There were no significant changes in CRP, IL-6, and TNF-alpha following EPA or DHA supplementation. |
| 9844 | 14583341 | There were no associations with Delta CRP or Delta IL-6. |
| 9845 | 14583341 | There were no associations with Delta CRP or Delta IL-6. |
| 9846 | 14581470 | Tumor necrosis factor-alpha inhibits endothelial nitric-oxide synthase gene promoter activity in bovine aortic endothelial cells. |
| 9847 | 14581470 | Tumor necrosis factor-alpha inhibits endothelial nitric-oxide synthase gene promoter activity in bovine aortic endothelial cells. |
| 9848 | 14581470 | Tumor necrosis factor-alpha inhibits endothelial nitric-oxide synthase gene promoter activity in bovine aortic endothelial cells. |
| 9849 | 14581470 | Tumor necrosis factor-alpha inhibits endothelial nitric-oxide synthase gene promoter activity in bovine aortic endothelial cells. |
| 9850 | 14581470 | Tumor necrosis factor-alpha inhibits endothelial nitric-oxide synthase gene promoter activity in bovine aortic endothelial cells. |
| 9851 | 14581470 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to reduce endothelial nitric-oxide synthase (eNOS) gene expression through post-transcriptional regulation of mRNA stability. |
| 9852 | 14581470 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to reduce endothelial nitric-oxide synthase (eNOS) gene expression through post-transcriptional regulation of mRNA stability. |
| 9853 | 14581470 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to reduce endothelial nitric-oxide synthase (eNOS) gene expression through post-transcriptional regulation of mRNA stability. |
| 9854 | 14581470 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to reduce endothelial nitric-oxide synthase (eNOS) gene expression through post-transcriptional regulation of mRNA stability. |
| 9855 | 14581470 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to reduce endothelial nitric-oxide synthase (eNOS) gene expression through post-transcriptional regulation of mRNA stability. |
| 9856 | 14581470 | TNF-alpha effected a time- and dose-dependent reduction in activity of a transiently transfected human -1197 eNOS-luciferase reporter. |
| 9857 | 14581470 | TNF-alpha effected a time- and dose-dependent reduction in activity of a transiently transfected human -1197 eNOS-luciferase reporter. |
| 9858 | 14581470 | TNF-alpha effected a time- and dose-dependent reduction in activity of a transiently transfected human -1197 eNOS-luciferase reporter. |
| 9859 | 14581470 | TNF-alpha effected a time- and dose-dependent reduction in activity of a transiently transfected human -1197 eNOS-luciferase reporter. |
| 9860 | 14581470 | TNF-alpha effected a time- and dose-dependent reduction in activity of a transiently transfected human -1197 eNOS-luciferase reporter. |
| 9861 | 14581470 | Electrophoretic mobility shift analysis and immunoperturbation studies showed evidence for Sp1 and Sp3 binding to each element. |
| 9862 | 14581470 | Electrophoretic mobility shift analysis and immunoperturbation studies showed evidence for Sp1 and Sp3 binding to each element. |
| 9863 | 14581470 | Electrophoretic mobility shift analysis and immunoperturbation studies showed evidence for Sp1 and Sp3 binding to each element. |
| 9864 | 14581470 | Electrophoretic mobility shift analysis and immunoperturbation studies showed evidence for Sp1 and Sp3 binding to each element. |
| 9865 | 14581470 | Electrophoretic mobility shift analysis and immunoperturbation studies showed evidence for Sp1 and Sp3 binding to each element. |
| 9866 | 14581470 | TNF-alpha treatment had no effect on the binding pattern to the downstream (-81 to -67) site but did suppress association of Sp1 and Sp3 to the upstream (-109 to -95) site. |
| 9867 | 14581470 | TNF-alpha treatment had no effect on the binding pattern to the downstream (-81 to -67) site but did suppress association of Sp1 and Sp3 to the upstream (-109 to -95) site. |
| 9868 | 14581470 | TNF-alpha treatment had no effect on the binding pattern to the downstream (-81 to -67) site but did suppress association of Sp1 and Sp3 to the upstream (-109 to -95) site. |
| 9869 | 14581470 | TNF-alpha treatment had no effect on the binding pattern to the downstream (-81 to -67) site but did suppress association of Sp1 and Sp3 to the upstream (-109 to -95) site. |
| 9870 | 14581470 | TNF-alpha treatment had no effect on the binding pattern to the downstream (-81 to -67) site but did suppress association of Sp1 and Sp3 to the upstream (-109 to -95) site. |
| 9871 | 14581470 | Collectively, these data indicate that TNF-alpha exerts transcriptional, as well as post-transcriptional, effects on eNOS gene expression and suggest a potential mechanism to account for the endothelial dysfunction that accompanies disorders such as diabetes mellitus and heart failure. |
| 9872 | 14581470 | Collectively, these data indicate that TNF-alpha exerts transcriptional, as well as post-transcriptional, effects on eNOS gene expression and suggest a potential mechanism to account for the endothelial dysfunction that accompanies disorders such as diabetes mellitus and heart failure. |
| 9873 | 14581470 | Collectively, these data indicate that TNF-alpha exerts transcriptional, as well as post-transcriptional, effects on eNOS gene expression and suggest a potential mechanism to account for the endothelial dysfunction that accompanies disorders such as diabetes mellitus and heart failure. |
| 9874 | 14581470 | Collectively, these data indicate that TNF-alpha exerts transcriptional, as well as post-transcriptional, effects on eNOS gene expression and suggest a potential mechanism to account for the endothelial dysfunction that accompanies disorders such as diabetes mellitus and heart failure. |
| 9875 | 14581470 | Collectively, these data indicate that TNF-alpha exerts transcriptional, as well as post-transcriptional, effects on eNOS gene expression and suggest a potential mechanism to account for the endothelial dysfunction that accompanies disorders such as diabetes mellitus and heart failure. |
| 9876 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 9877 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 9878 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 9879 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 9880 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 9881 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 9882 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 9883 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 9884 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 9885 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 9886 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 9887 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 9888 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 9889 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 9890 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 9891 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 9892 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 9893 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 9894 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 9895 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 9896 | 14572792 | Balance of tumor necrosis factor alpha and interleukin-10 in a buccal infection in a streptozotocin-induced diabetic rat model. |
| 9897 | 14572792 | Balance of tumor necrosis factor alpha and interleukin-10 in a buccal infection in a streptozotocin-induced diabetic rat model. |
| 9898 | 14572792 | Balance of tumor necrosis factor alpha and interleukin-10 in a buccal infection in a streptozotocin-induced diabetic rat model. |
| 9899 | 14572792 | Balance of tumor necrosis factor alpha and interleukin-10 in a buccal infection in a streptozotocin-induced diabetic rat model. |
| 9900 | 14572792 | This study evaluates the local levels of proinflammatory cytokine, tumor necrosis factor alpha (TNF-alpha), and anti-inflammatory cytokine, interleukin-10 (IL-10), in an experimental buccal abscess of a diabetic rat model. |
| 9901 | 14572792 | This study evaluates the local levels of proinflammatory cytokine, tumor necrosis factor alpha (TNF-alpha), and anti-inflammatory cytokine, interleukin-10 (IL-10), in an experimental buccal abscess of a diabetic rat model. |
| 9902 | 14572792 | This study evaluates the local levels of proinflammatory cytokine, tumor necrosis factor alpha (TNF-alpha), and anti-inflammatory cytokine, interleukin-10 (IL-10), in an experimental buccal abscess of a diabetic rat model. |
| 9903 | 14572792 | This study evaluates the local levels of proinflammatory cytokine, tumor necrosis factor alpha (TNF-alpha), and anti-inflammatory cytokine, interleukin-10 (IL-10), in an experimental buccal abscess of a diabetic rat model. |
| 9904 | 14572792 | The mean ratio of TNF-alpha to IL-10 levels was 1.17-1.67 in the diabetic group, which was higher than the 0.26-0.69 of the control group. |
| 9905 | 14572792 | The mean ratio of TNF-alpha to IL-10 levels was 1.17-1.67 in the diabetic group, which was higher than the 0.26-0.69 of the control group. |
| 9906 | 14572792 | The mean ratio of TNF-alpha to IL-10 levels was 1.17-1.67 in the diabetic group, which was higher than the 0.26-0.69 of the control group. |
| 9907 | 14572792 | The mean ratio of TNF-alpha to IL-10 levels was 1.17-1.67 in the diabetic group, which was higher than the 0.26-0.69 of the control group. |
| 9908 | 14572792 | These results suggest that the elevated proinflammatory TNF-alpha levels and decreased anti-inflammatory IL-10 levels, which are produced at local infection sites, may at least in part be related to the severity of inflammation in this rat model with diabetes induced by STZ. |
| 9909 | 14572792 | These results suggest that the elevated proinflammatory TNF-alpha levels and decreased anti-inflammatory IL-10 levels, which are produced at local infection sites, may at least in part be related to the severity of inflammation in this rat model with diabetes induced by STZ. |
| 9910 | 14572792 | These results suggest that the elevated proinflammatory TNF-alpha levels and decreased anti-inflammatory IL-10 levels, which are produced at local infection sites, may at least in part be related to the severity of inflammation in this rat model with diabetes induced by STZ. |
| 9911 | 14572792 | These results suggest that the elevated proinflammatory TNF-alpha levels and decreased anti-inflammatory IL-10 levels, which are produced at local infection sites, may at least in part be related to the severity of inflammation in this rat model with diabetes induced by STZ. |
| 9912 | 14567106 | The pathogenesis is related to metabolic alterations of the adipocytes with cellular insulin resistance and enhanced apoptosis of these cells caused by adipocytic cytokines such as adiponectin, leptin, TNF-alpha and interleukin 2. |
| 9913 | 14566971 | Age-related differences in MAP kinase activity in VSMC in response to glucose or TNF-alpha. |
| 9914 | 14566971 | Age-related differences in MAP kinase activity in VSMC in response to glucose or TNF-alpha. |
| 9915 | 14566971 | Activator protein-1 (AP-1) binding to DNA increased more in VSMC from old versus young rats (P < 0.02) and was related to increased expression of its components, c-Fos, Fra-1, and JunD. |
| 9916 | 14566971 | Activator protein-1 (AP-1) binding to DNA increased more in VSMC from old versus young rats (P < 0.02) and was related to increased expression of its components, c-Fos, Fra-1, and JunD. |
| 9917 | 14566971 | The relationship to upstream signals, i.e., activities of mitogen-activated protein kinases (MAPK), was studied using antibodies to total and phosphorylated forms of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK) and p38. |
| 9918 | 14566971 | The relationship to upstream signals, i.e., activities of mitogen-activated protein kinases (MAPK), was studied using antibodies to total and phosphorylated forms of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK) and p38. |
| 9919 | 14566971 | High glucose and TNF-alpha increased ERK phosphorylation more in old (P < 0.05); whereas only TNF-alpha induced JNK activation in young (P < 0.04). |
| 9920 | 14566971 | High glucose and TNF-alpha increased ERK phosphorylation more in old (P < 0.05); whereas only TNF-alpha induced JNK activation in young (P < 0.04). |
| 9921 | 14566971 | PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old. |
| 9922 | 14566971 | PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old. |
| 9923 | 14563014 | Islets of Langerhans isolated from diabetes-prone BB/OK rats were exposed to interleukin-1beta (IL-1beta) or to a combination of tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) under hypoglycemia at glucose concentrations of 2.2 and 3.2 mmol/l or in the presence of stimulatory conditions at 6.0 and 11 mmol/l glucose. |
| 9924 | 14563014 | Islets of Langerhans isolated from diabetes-prone BB/OK rats were exposed to interleukin-1beta (IL-1beta) or to a combination of tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) under hypoglycemia at glucose concentrations of 2.2 and 3.2 mmol/l or in the presence of stimulatory conditions at 6.0 and 11 mmol/l glucose. |
| 9925 | 14563014 | Islets of Langerhans isolated from diabetes-prone BB/OK rats were exposed to interleukin-1beta (IL-1beta) or to a combination of tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) under hypoglycemia at glucose concentrations of 2.2 and 3.2 mmol/l or in the presence of stimulatory conditions at 6.0 and 11 mmol/l glucose. |
| 9926 | 14563014 | Islets of Langerhans isolated from diabetes-prone BB/OK rats were exposed to interleukin-1beta (IL-1beta) or to a combination of tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) under hypoglycemia at glucose concentrations of 2.2 and 3.2 mmol/l or in the presence of stimulatory conditions at 6.0 and 11 mmol/l glucose. |
| 9927 | 14563014 | Islets of Langerhans isolated from diabetes-prone BB/OK rats were exposed to interleukin-1beta (IL-1beta) or to a combination of tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) under hypoglycemia at glucose concentrations of 2.2 and 3.2 mmol/l or in the presence of stimulatory conditions at 6.0 and 11 mmol/l glucose. |
| 9928 | 14563014 | Pancreatic islets exposed for 24 h to IL-1beta at a glucose concentration of 6.0 mmol/l exhibited a reduced insulin secretion following a 48h recovery period compared to islets which were cytokine treated at 2.2 or 3.2mmol/l glucose, respectively. |
| 9929 | 14563014 | Pancreatic islets exposed for 24 h to IL-1beta at a glucose concentration of 6.0 mmol/l exhibited a reduced insulin secretion following a 48h recovery period compared to islets which were cytokine treated at 2.2 or 3.2mmol/l glucose, respectively. |
| 9930 | 14563014 | Pancreatic islets exposed for 24 h to IL-1beta at a glucose concentration of 6.0 mmol/l exhibited a reduced insulin secretion following a 48h recovery period compared to islets which were cytokine treated at 2.2 or 3.2mmol/l glucose, respectively. |
| 9931 | 14563014 | Pancreatic islets exposed for 24 h to IL-1beta at a glucose concentration of 6.0 mmol/l exhibited a reduced insulin secretion following a 48h recovery period compared to islets which were cytokine treated at 2.2 or 3.2mmol/l glucose, respectively. |
| 9932 | 14563014 | Pancreatic islets exposed for 24 h to IL-1beta at a glucose concentration of 6.0 mmol/l exhibited a reduced insulin secretion following a 48h recovery period compared to islets which were cytokine treated at 2.2 or 3.2mmol/l glucose, respectively. |
| 9933 | 14563014 | Islets pre-exposed for 24h to TNF-alpha plus IFN-gamma at 2.2, 3.2 or 6.0 mmol/l glucose displayed no alterations of insulin secretion following a 48 h regeneration. |
| 9934 | 14563014 | Islets pre-exposed for 24h to TNF-alpha plus IFN-gamma at 2.2, 3.2 or 6.0 mmol/l glucose displayed no alterations of insulin secretion following a 48 h regeneration. |
| 9935 | 14563014 | Islets pre-exposed for 24h to TNF-alpha plus IFN-gamma at 2.2, 3.2 or 6.0 mmol/l glucose displayed no alterations of insulin secretion following a 48 h regeneration. |
| 9936 | 14563014 | Islets pre-exposed for 24h to TNF-alpha plus IFN-gamma at 2.2, 3.2 or 6.0 mmol/l glucose displayed no alterations of insulin secretion following a 48 h regeneration. |
| 9937 | 14563014 | Islets pre-exposed for 24h to TNF-alpha plus IFN-gamma at 2.2, 3.2 or 6.0 mmol/l glucose displayed no alterations of insulin secretion following a 48 h regeneration. |
| 9938 | 14563014 | A temporary (3 h) influence of IL-1beta under hyperglycemic conditions at 11 mmol/l glucose caused a reduction of the subsequent insulin secretion of Langerhans' islets prior incubated for 24 h at 6.0 mmol/l glucose without cytokines, but not of islets precultured at 2.2 mmol/l glucose. |
| 9939 | 14563014 | A temporary (3 h) influence of IL-1beta under hyperglycemic conditions at 11 mmol/l glucose caused a reduction of the subsequent insulin secretion of Langerhans' islets prior incubated for 24 h at 6.0 mmol/l glucose without cytokines, but not of islets precultured at 2.2 mmol/l glucose. |
| 9940 | 14563014 | A temporary (3 h) influence of IL-1beta under hyperglycemic conditions at 11 mmol/l glucose caused a reduction of the subsequent insulin secretion of Langerhans' islets prior incubated for 24 h at 6.0 mmol/l glucose without cytokines, but not of islets precultured at 2.2 mmol/l glucose. |
| 9941 | 14563014 | A temporary (3 h) influence of IL-1beta under hyperglycemic conditions at 11 mmol/l glucose caused a reduction of the subsequent insulin secretion of Langerhans' islets prior incubated for 24 h at 6.0 mmol/l glucose without cytokines, but not of islets precultured at 2.2 mmol/l glucose. |
| 9942 | 14563014 | A temporary (3 h) influence of IL-1beta under hyperglycemic conditions at 11 mmol/l glucose caused a reduction of the subsequent insulin secretion of Langerhans' islets prior incubated for 24 h at 6.0 mmol/l glucose without cytokines, but not of islets precultured at 2.2 mmol/l glucose. |
| 9943 | 14563014 | In contrast, a 3 h treatment with TNF-alpha plus IFN-gamma at 11 mmol/l glucose did not affect insulin secretion of islets prior held at 6.0 mmol/l glucose, whereas a transient exposure for 6h to IL-1beta as well as TNF-alpha plus IFN-gamma under similar conditions diminished insulin secretion of islets preincubated at 2.2 or 6.0 mmol/l glucose. |
| 9944 | 14563014 | In contrast, a 3 h treatment with TNF-alpha plus IFN-gamma at 11 mmol/l glucose did not affect insulin secretion of islets prior held at 6.0 mmol/l glucose, whereas a transient exposure for 6h to IL-1beta as well as TNF-alpha plus IFN-gamma under similar conditions diminished insulin secretion of islets preincubated at 2.2 or 6.0 mmol/l glucose. |
| 9945 | 14563014 | In contrast, a 3 h treatment with TNF-alpha plus IFN-gamma at 11 mmol/l glucose did not affect insulin secretion of islets prior held at 6.0 mmol/l glucose, whereas a transient exposure for 6h to IL-1beta as well as TNF-alpha plus IFN-gamma under similar conditions diminished insulin secretion of islets preincubated at 2.2 or 6.0 mmol/l glucose. |
| 9946 | 14563014 | In contrast, a 3 h treatment with TNF-alpha plus IFN-gamma at 11 mmol/l glucose did not affect insulin secretion of islets prior held at 6.0 mmol/l glucose, whereas a transient exposure for 6h to IL-1beta as well as TNF-alpha plus IFN-gamma under similar conditions diminished insulin secretion of islets preincubated at 2.2 or 6.0 mmol/l glucose. |
| 9947 | 14563014 | In contrast, a 3 h treatment with TNF-alpha plus IFN-gamma at 11 mmol/l glucose did not affect insulin secretion of islets prior held at 6.0 mmol/l glucose, whereas a transient exposure for 6h to IL-1beta as well as TNF-alpha plus IFN-gamma under similar conditions diminished insulin secretion of islets preincubated at 2.2 or 6.0 mmol/l glucose. |
| 9948 | 14563014 | TNF-alpha plus IFN-gamma at concentrations capable to decrease insulin secretion of islets during hyperglycemia do not affect the insulin output in a range between 2.2 and 6.0 mmol/l glucose. |
| 9949 | 14563014 | TNF-alpha plus IFN-gamma at concentrations capable to decrease insulin secretion of islets during hyperglycemia do not affect the insulin output in a range between 2.2 and 6.0 mmol/l glucose. |
| 9950 | 14563014 | TNF-alpha plus IFN-gamma at concentrations capable to decrease insulin secretion of islets during hyperglycemia do not affect the insulin output in a range between 2.2 and 6.0 mmol/l glucose. |
| 9951 | 14563014 | TNF-alpha plus IFN-gamma at concentrations capable to decrease insulin secretion of islets during hyperglycemia do not affect the insulin output in a range between 2.2 and 6.0 mmol/l glucose. |
| 9952 | 14563014 | TNF-alpha plus IFN-gamma at concentrations capable to decrease insulin secretion of islets during hyperglycemia do not affect the insulin output in a range between 2.2 and 6.0 mmol/l glucose. |
| 9953 | 14563014 | During glucose stimulation at 11 mmol/l islets' insulin secretory machinery is protected from IL-1beta as well as TNF-alpha plus IFN-gamma for 3 h by a preceding 24 h hypoglycemia, but its vulnerability is restored within additional 3 h. |
| 9954 | 14563014 | During glucose stimulation at 11 mmol/l islets' insulin secretory machinery is protected from IL-1beta as well as TNF-alpha plus IFN-gamma for 3 h by a preceding 24 h hypoglycemia, but its vulnerability is restored within additional 3 h. |
| 9955 | 14563014 | During glucose stimulation at 11 mmol/l islets' insulin secretory machinery is protected from IL-1beta as well as TNF-alpha plus IFN-gamma for 3 h by a preceding 24 h hypoglycemia, but its vulnerability is restored within additional 3 h. |
| 9956 | 14563014 | During glucose stimulation at 11 mmol/l islets' insulin secretory machinery is protected from IL-1beta as well as TNF-alpha plus IFN-gamma for 3 h by a preceding 24 h hypoglycemia, but its vulnerability is restored within additional 3 h. |
| 9957 | 14563014 | During glucose stimulation at 11 mmol/l islets' insulin secretory machinery is protected from IL-1beta as well as TNF-alpha plus IFN-gamma for 3 h by a preceding 24 h hypoglycemia, but its vulnerability is restored within additional 3 h. |
| 9958 | 14561180 | All the cytokines of the TNF superfamily mediate their effects through the activation of the transcription factor NF-kappaB, c-Jun N-terminal kinase, apoptosis, and proliferation. |
| 9959 | 14555286 | MLDSTZ treatment in vivo caused increased IFNgamma secretion, a decreased/retarded rate of increased TNFalpha accumulation, whereas IL-10 production was not altered compared to vehicle-treated mice. |
| 9960 | 14555286 | MLDSTZ treatment in vivo caused increased IFNgamma secretion, a decreased/retarded rate of increased TNFalpha accumulation, whereas IL-10 production was not altered compared to vehicle-treated mice. |
| 9961 | 14555286 | Production of TNFalpha, IFNgamma and IL-10 was all suppressed by the drug. |
| 9962 | 14555286 | Production of TNFalpha, IFNgamma and IL-10 was all suppressed by the drug. |
| 9963 | 14555218 | In type 2 diabetes, the metabolic derangement is associated with production of inflammatory mediators in insulin-sensitive tissues leading elevated levels of circulating inflammatory mediators such as IL-6 and TNF. |
| 9964 | 14555214 | Although distinct receptors, all members share a common cell signaling pathway that mediates the activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases (e.g. c-jun N-terminal kinase). |
| 9965 | 14555214 | Regulation of cell growth and activation of NF-kappaB and of c-jun N-terminal kinase by the TNF super family is mediated through sequential activation/association of a set of cell signaling proteins named TNF receptor-associated factors, Fas-associated death domain and FADD-like ICE, caspases, receptor-interacting protein, NF-kappaB-inducing kinases, and IkappaBalpha kinases. |
| 9966 | 14550286 | Adipokines such as Plasminogen activator inhibitor-1 (PAI-1), interleukin (IL)-8, and tumor necrosis factor (TNF)-alpha are elevated in patients with obesity, insulin resistance, and type 2 diabetes. |
| 9967 | 14550286 | Adipokines such as Plasminogen activator inhibitor-1 (PAI-1), interleukin (IL)-8, and tumor necrosis factor (TNF)-alpha are elevated in patients with obesity, insulin resistance, and type 2 diabetes. |
| 9968 | 14550286 | Glucose (up to 35mM) increased secretion of PAI-1 (p<0.01) and IL-8 (p<0.01), but not TNF-alpha, in a dose- and time-dependent manner. |
| 9969 | 14550286 | Glucose (up to 35mM) increased secretion of PAI-1 (p<0.01) and IL-8 (p<0.01), but not TNF-alpha, in a dose- and time-dependent manner. |
| 9970 | 14550286 | Glucosamine (5mM) decreased production of PAI-1 (p<0.05) and IL-8 (p<0.05), indicating that the hexosamine biosynthesis pathway is not involved in the glucose-induced increment in adipokine secretion. |
| 9971 | 14550286 | Glucosamine (5mM) decreased production of PAI-1 (p<0.05) and IL-8 (p<0.05), indicating that the hexosamine biosynthesis pathway is not involved in the glucose-induced increment in adipokine secretion. |
| 9972 | 14550286 | The present data demonstrate that glucose increases PAI-1 and IL-8 secretion. |
| 9973 | 14550286 | The present data demonstrate that glucose increases PAI-1 and IL-8 secretion. |
| 9974 | 14530283 | Expression profiling identifies genes that continue to respond to insulin in adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha. |
| 9975 | 14530283 | Expression profiling identifies genes that continue to respond to insulin in adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha. |
| 9976 | 14530283 | We have employed microarray technology using RNA from normal 3T3-L1 adipocytes and from 3T3-L1 adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha to identify a new class of insulin-responsive genes. |
| 9977 | 14530283 | We have employed microarray technology using RNA from normal 3T3-L1 adipocytes and from 3T3-L1 adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha to identify a new class of insulin-responsive genes. |
| 9978 | 14530283 | Socs-3, junB, and matrix metalloproteinase-11). |
| 9979 | 14530283 | Socs-3, junB, and matrix metalloproteinase-11). |
| 9980 | 14530283 | Glut-1 and beta3-adrenergic receptor), other novel insulin-sensitive genes were also identified (e.g. |
| 9981 | 14530283 | Glut-1 and beta3-adrenergic receptor), other novel insulin-sensitive genes were also identified (e.g. |
| 9982 | 14530283 | Egr-1, epiregulin, Fra-1, and ABCA1). |
| 9983 | 14530283 | Egr-1, epiregulin, Fra-1, and ABCA1). |
| 9984 | 14530283 | Using an antisense strategy, we show that tissue factor and macrophage colony-stimulating factor, two cardiovascular risk factors, are downstream EGR-1 target genes in the adipocyte. |
| 9985 | 14530283 | Using an antisense strategy, we show that tissue factor and macrophage colony-stimulating factor, two cardiovascular risk factors, are downstream EGR-1 target genes in the adipocyte. |
| 9986 | 14530204 | Tumor necrosis factor-alpha inhibits insulin's stimulating effect on glucose uptake and endothelium-dependent vasodilation in humans. |
| 9987 | 14514632 | Variations in IB1/JIP1 expression regulate susceptibility of beta-cells to cytokine-induced apoptosis irrespective of C-Jun NH2-terminal kinase signaling. |
| 9988 | 14514632 | Variations in IB1/JIP1 expression regulate susceptibility of beta-cells to cytokine-induced apoptosis irrespective of C-Jun NH2-terminal kinase signaling. |
| 9989 | 14514632 | Variations in IB1/JIP1 expression regulate susceptibility of beta-cells to cytokine-induced apoptosis irrespective of C-Jun NH2-terminal kinase signaling. |
| 9990 | 14514632 | Variations in IB1/JIP1 expression regulate susceptibility of beta-cells to cytokine-induced apoptosis irrespective of C-Jun NH2-terminal kinase signaling. |
| 9991 | 14514632 | Variations in IB1/JIP1 expression regulate susceptibility of beta-cells to cytokine-induced apoptosis irrespective of C-Jun NH2-terminal kinase signaling. |
| 9992 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 9993 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 9994 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 9995 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 9996 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 9997 | 14514632 | Studies in beta-cell lines indicated that IL-1beta reduced expression of islet brain (IB)-1/JNK interacting protein (JIP)-1, a JNK scaffold protein with antiapoptotic action. |
| 9998 | 14514632 | Studies in beta-cell lines indicated that IL-1beta reduced expression of islet brain (IB)-1/JNK interacting protein (JIP)-1, a JNK scaffold protein with antiapoptotic action. |
| 9999 | 14514632 | Studies in beta-cell lines indicated that IL-1beta reduced expression of islet brain (IB)-1/JNK interacting protein (JIP)-1, a JNK scaffold protein with antiapoptotic action. |
| 10000 | 14514632 | Studies in beta-cell lines indicated that IL-1beta reduced expression of islet brain (IB)-1/JNK interacting protein (JIP)-1, a JNK scaffold protein with antiapoptotic action. |
| 10001 | 14514632 | Studies in beta-cell lines indicated that IL-1beta reduced expression of islet brain (IB)-1/JNK interacting protein (JIP)-1, a JNK scaffold protein with antiapoptotic action. |
| 10002 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 10003 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 10004 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 10005 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 10006 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 10007 | 14514632 | Addition of IL-1beta to TNF-alpha + IFN-gamma increased apoptosis from 20 +/- 2% to 59 +/- 5%. |
| 10008 | 14514632 | Addition of IL-1beta to TNF-alpha + IFN-gamma increased apoptosis from 20 +/- 2% to 59 +/- 5%. |
| 10009 | 14514632 | Addition of IL-1beta to TNF-alpha + IFN-gamma increased apoptosis from 20 +/- 2% to 59 +/- 5%. |
| 10010 | 14514632 | Addition of IL-1beta to TNF-alpha + IFN-gamma increased apoptosis from 20 +/- 2% to 59 +/- 5%. |
| 10011 | 14514632 | Addition of IL-1beta to TNF-alpha + IFN-gamma increased apoptosis from 20 +/- 2% to 59 +/- 5%. |
| 10012 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 10013 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 10014 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 10015 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 10016 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 10017 | 14514632 | However, adenovirally mediated overexpression of IB1/JIP-1 also potentiated TNF-alpha + IFN-gamma-induced apoptosis, suggesting that the antiapoptotic effect of IB1/JIP-1 depends on well-defined cellular levels. |
| 10018 | 14514632 | However, adenovirally mediated overexpression of IB1/JIP-1 also potentiated TNF-alpha + IFN-gamma-induced apoptosis, suggesting that the antiapoptotic effect of IB1/JIP-1 depends on well-defined cellular levels. |
| 10019 | 14514632 | However, adenovirally mediated overexpression of IB1/JIP-1 also potentiated TNF-alpha + IFN-gamma-induced apoptosis, suggesting that the antiapoptotic effect of IB1/JIP-1 depends on well-defined cellular levels. |
| 10020 | 14514632 | However, adenovirally mediated overexpression of IB1/JIP-1 also potentiated TNF-alpha + IFN-gamma-induced apoptosis, suggesting that the antiapoptotic effect of IB1/JIP-1 depends on well-defined cellular levels. |
| 10021 | 14514632 | However, adenovirally mediated overexpression of IB1/JIP-1 also potentiated TNF-alpha + IFN-gamma-induced apoptosis, suggesting that the antiapoptotic effect of IB1/JIP-1 depends on well-defined cellular levels. |
| 10022 | 14514632 | We conclude that the IB1/JIP-1 level in beta-cells can control their susceptibility to apoptosis independent of JNK signaling. |
| 10023 | 14514632 | We conclude that the IB1/JIP-1 level in beta-cells can control their susceptibility to apoptosis independent of JNK signaling. |
| 10024 | 14514632 | We conclude that the IB1/JIP-1 level in beta-cells can control their susceptibility to apoptosis independent of JNK signaling. |
| 10025 | 14514632 | We conclude that the IB1/JIP-1 level in beta-cells can control their susceptibility to apoptosis independent of JNK signaling. |
| 10026 | 14514632 | We conclude that the IB1/JIP-1 level in beta-cells can control their susceptibility to apoptosis independent of JNK signaling. |
| 10027 | 14514596 | Fasting plasma leptin, tumor necrosis factor-alpha receptor 2, and monocyte chemoattracting protein 1 concentration in a population of glucose-tolerant and glucose-intolerant women: impact on cardiovascular mortality. |
| 10028 | 14508150 | The insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha, interleukin-6, macrophage migration inhibitory factor and other pro-inflammatory cytokines, and free radicals; and enhances the synthesis of endothelial nitric oxide and anti-inflammatory cytokines interleukin-4 and interleukin-10. |
| 10029 | 14501946 | With increased complexity (antibiotic and G-CSF prophylaxis) the survival rate was increased from 50% in Wistar rats to 89% in SHR (P<0.01) and the mRNA expression of IL-6 was decreased in the kidney of SHR (P<0.05). |
| 10030 | 14501946 | The mRNA expression of tumor necrosis factor-alpha and IL-10 was reduced (P<0.01) by pretreatment in the liver of DS rats with PCI. |
| 10031 | 14501946 | G-CSF and antibiotic prophylaxis increases only in SHR survival and decreases IL-6 mRNA expression in the kidney significantly. |
| 10032 | 14501164 | [The mechanisms by which PPARgamma and adiponectin regulate glucose and lipid metabolism]. |
| 10033 | 14501164 | Heterozygous PPARgamma knockout mice and KKA(y) mice administered with a PPARgamma antagonist were protected from high-fat diet-induced adipocyte hypertrophy and insulin resistance. |
| 10034 | 14501164 | Moderate reduction of PPARgamma activity prevented adipocyte hypertrophy, thereby diminution of TNFalpha, resistin, and FFA and upregulation of adiponectin and leptin. |
| 10035 | 14501164 | Insulin resistance in the lipoatrophic mice and KKA(y) mice were ameliorated by replenishment of adiponectin. |
| 10036 | 14501164 | Moreover, adiponectin transgenic mice ameliorated insulin resistance and diabetes, but not the obesity of ob/ob mice. |
| 10037 | 14501164 | Furthermore, targeted disruption of the adiponectin gene caused moderate insulin resistance and glucose intolerance. |
| 10038 | 14501164 | In muscle, adiponectin activated AMP kinase and PPARgamma pathways, thereby increasing beta-oxidation of lipids, leading to decreased TG content, which ameliorated muscle insulin resistance. |
| 10039 | 14501164 | In the liver, adiponectin also activated AMPK, thereby downregulating PEPCK and G6Pase, leading to decreased glucose output from the liver. |
| 10040 | 14501164 | In conclusion, PPARgamma plays a central role in the regulation of adipocyte hypertrophy and insulin sensitivity. |
| 10041 | 14501164 | The upregulation of the adiponectin pathway by PPARgamma may play a role in the increased insulin sensitivity of heterozygous PPARgamma knockout mice, and activation of adiponectin pathway may provide novel therapeutic strategies for obesity-linked disorders such as type 2 diabetes and metabolic syndrome. |
| 10042 | 14499240 | Plasma IL-10, IL-1beta, TNF-alpha, IL-6, IL-8 and IL-2 cytokine levels were assayed by ELISA at each of the time points. |
| 10043 | 14499240 | Plasma IL-10, IL-1beta, TNF-alpha, IL-6, IL-8 and IL-2 cytokine levels were assayed by ELISA at each of the time points. |
| 10044 | 14499240 | Treatment of DKA resulted in a significant decrease of IL-10 at 6-8 h (p = 0.0062), and further increases in the inflammatory cytokines at 6-8 h and/or 24 h vs 120 h (baseline): IL-1beta (p =.0048); TNF-alpha (p =.0188) and IL-8 (p =.0048). |
| 10045 | 14499240 | Treatment of DKA resulted in a significant decrease of IL-10 at 6-8 h (p = 0.0062), and further increases in the inflammatory cytokines at 6-8 h and/or 24 h vs 120 h (baseline): IL-1beta (p =.0048); TNF-alpha (p =.0188) and IL-8 (p =.0048). |
| 10046 | 13679655 | TNF pathway and TGFb play an important role in the regulation of PAI-1 synthesis in the adipose tissue and the liver with steatosis. |
| 10047 | 12974762 | Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. |
| 10048 | 12974762 | Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. |
| 10049 | 12974762 | Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. |
| 10050 | 12974762 | Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. |
| 10051 | 12974762 | In contrast, tumour necrosis factor (TNF)-alpha, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. |
| 10052 | 12974762 | In contrast, tumour necrosis factor (TNF)-alpha, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. |
| 10053 | 12974762 | In contrast, tumour necrosis factor (TNF)-alpha, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. |
| 10054 | 12974762 | In contrast, tumour necrosis factor (TNF)-alpha, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. |
| 10055 | 12974762 | However, adiponectin also negatively regulates TNF-alpha levels. |
| 10056 | 12974762 | However, adiponectin also negatively regulates TNF-alpha levels. |
| 10057 | 12974762 | However, adiponectin also negatively regulates TNF-alpha levels. |
| 10058 | 12974762 | However, adiponectin also negatively regulates TNF-alpha levels. |
| 10059 | 12974762 | Plasma levels of adiponectin, TNF-alpha and interleukin-6 were measured at 0, 1.5, 2, 4, 8 and 24 h. |
| 10060 | 12974762 | Plasma levels of adiponectin, TNF-alpha and interleukin-6 were measured at 0, 1.5, 2, 4, 8 and 24 h. |
| 10061 | 12974762 | Plasma levels of adiponectin, TNF-alpha and interleukin-6 were measured at 0, 1.5, 2, 4, 8 and 24 h. |
| 10062 | 12974762 | Plasma levels of adiponectin, TNF-alpha and interleukin-6 were measured at 0, 1.5, 2, 4, 8 and 24 h. |
| 10063 | 12974762 | TNF-alpha and interleukin-6 levels peaked at 1.5 h and 2 h, respectively. |
| 10064 | 12974762 | TNF-alpha and interleukin-6 levels peaked at 1.5 h and 2 h, respectively. |
| 10065 | 12974762 | TNF-alpha and interleukin-6 levels peaked at 1.5 h and 2 h, respectively. |
| 10066 | 12974762 | TNF-alpha and interleukin-6 levels peaked at 1.5 h and 2 h, respectively. |
| 10067 | 12966666 | Among these factors, the inflammatory process has been pointed out in which acute stage reactants participate, such as C-reactive protein, leukocyte count, globular sedimentation, multiple cytokines, alpha tumor necrosis factor, vascular and cellular adhesion molecules, some metalloproteinases, pregnancy-associated plasma protein A, lipoprotein-associated phospholipase A2, angiotensin II, and very probably infection. |
| 10068 | 12957321 | The central role of fat and effect of peroxisome proliferator-activated receptor-gamma on progression of insulin resistance and cardiovascular disease. |
| 10069 | 12957321 | The balance of adipose-derived substances, including free fatty acids, tumor necrosis factor-alpha, leptin, adiponectin, and plasminogen activator inhibitor-1, determine both insulin action and the state of vascular inflammation. |
| 10070 | 12957321 | Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands promote the balance of these substances to enhance insulin-mediated glucose uptake and decrease inflammation. |
| 10071 | 12957321 | PPAR-gamma ligands reverse the major defect of the insulin resistance syndrome and have important effects that inhibit atherosclerosis, improve endothelial cell function, and attenuate inflammation. |
| 10072 | 12957321 | Although more research is needed, data suggest that PPAR-gamma ligands may prevent the progression of insulin resistance to diabetes and endothelial dysfunction to atherosclerosis. |
| 10073 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10074 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10075 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10076 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10077 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10078 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10079 | 12952969 | Interleukin-6 (IL-6) induces insulin resistance in 3T3-L1 adipocytes and is, like IL-8 and tumor necrosis factor-alpha, overexpressed in human fat cells from insulin-resistant subjects. |
| 10080 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10081 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10082 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10083 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10084 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10085 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10086 | 12952969 | Several studies have shown a relationship between interleukin (IL) 6 levels and insulin resistance. |
| 10087 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10088 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10089 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10090 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10091 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10092 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10093 | 12952969 | To examine putative mechanisms and cross-talk with insulin, 3T3-L1 adipocytes were cultured for different times with IL-6 and tumor necrosis factor alpha (TNF-alpha). |
| 10094 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10095 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10096 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10097 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10098 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10099 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10100 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 10101 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10102 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10103 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10104 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10105 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10106 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10107 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 10108 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10109 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10110 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10111 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10112 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10113 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10114 | 12952969 | This effect of IL-6 was accompanied by a marked reduction in IRS-1, but not IRS-2, protein expression, and insulin-stimulated tyrosine phosphorylation, whereas no inhibitory effect was seen on the insulin receptor tyrosine phosphorylation. |
| 10115 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10116 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10117 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10118 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10119 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10120 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10121 | 12952969 | Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. |
| 10122 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10123 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10124 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10125 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10126 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10127 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10128 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 10129 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10130 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10131 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10132 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10133 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10134 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10135 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 10136 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10137 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10138 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10139 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10140 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10141 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10142 | 12952969 | The link between IL-6 and insulin resistance in man was further corroborated by the finding that the expression of IL-6, like that of TNF-alpha and IL-8, was markedly increased ( approximately 15-fold) in human fat cells from insulin-resistant individuals. |
| 10143 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10144 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10145 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10146 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10147 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10148 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10149 | 12952969 | We conclude that IL-6 can play an important role in insulin resistance in man and, furthermore, that it may act in concert with other cytokines that also are up-regulated in adipose cells in insulin resistance. |
| 10150 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 10151 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 10152 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 10153 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 10154 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 10155 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 10156 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 10157 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 10158 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 10159 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 10160 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 10161 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 10162 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 10163 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 10164 | 12948526 | Insulin resistance in adipose tissue: direct and indirect effects of tumor necrosis factor-alpha. |
| 10165 | 12948526 | Insulin resistance in adipose tissue: direct and indirect effects of tumor necrosis factor-alpha. |
| 10166 | 12948526 | Insulin resistance in adipose tissue: direct and indirect effects of tumor necrosis factor-alpha. |
| 10167 | 12948526 | Insulin resistance in adipose tissue: direct and indirect effects of tumor necrosis factor-alpha. |
| 10168 | 12948526 | Tumor necrosis factor-alpha (TNF-alpha), a paracrine/autocrine factor highly expressed in adipose tissues of obese animals and human subjects, is implicated in the induction of insulin resistance seen in obesity and type 2 diabetes. |
| 10169 | 12948526 | Tumor necrosis factor-alpha (TNF-alpha), a paracrine/autocrine factor highly expressed in adipose tissues of obese animals and human subjects, is implicated in the induction of insulin resistance seen in obesity and type 2 diabetes. |
| 10170 | 12948526 | Tumor necrosis factor-alpha (TNF-alpha), a paracrine/autocrine factor highly expressed in adipose tissues of obese animals and human subjects, is implicated in the induction of insulin resistance seen in obesity and type 2 diabetes. |
| 10171 | 12948526 | Tumor necrosis factor-alpha (TNF-alpha), a paracrine/autocrine factor highly expressed in adipose tissues of obese animals and human subjects, is implicated in the induction of insulin resistance seen in obesity and type 2 diabetes. |
| 10172 | 12948526 | Here, we review several molecular aspects of adipose tissue physiology, and highlight the direct effects of TNF-alpha on the functions of adipose tissue including induction of lipolysis, inhibition of insulin signaling, and alterations in expression of adipocyte important genes through activation of NF-kappaB, as well as their pertinence to insulin sensitivity of adipocytes. |
| 10173 | 12948526 | Here, we review several molecular aspects of adipose tissue physiology, and highlight the direct effects of TNF-alpha on the functions of adipose tissue including induction of lipolysis, inhibition of insulin signaling, and alterations in expression of adipocyte important genes through activation of NF-kappaB, as well as their pertinence to insulin sensitivity of adipocytes. |
| 10174 | 12948526 | Here, we review several molecular aspects of adipose tissue physiology, and highlight the direct effects of TNF-alpha on the functions of adipose tissue including induction of lipolysis, inhibition of insulin signaling, and alterations in expression of adipocyte important genes through activation of NF-kappaB, as well as their pertinence to insulin sensitivity of adipocytes. |
| 10175 | 12948526 | Here, we review several molecular aspects of adipose tissue physiology, and highlight the direct effects of TNF-alpha on the functions of adipose tissue including induction of lipolysis, inhibition of insulin signaling, and alterations in expression of adipocyte important genes through activation of NF-kappaB, as well as their pertinence to insulin sensitivity of adipocytes. |
| 10176 | 12948526 | We also review the ability of TNF-alpha to inhibit synthesis of several adipocyte-specific proteins including Acrp30 (adiponectin) and enhance release of free fatty acids (FFAs) from adipose tissue, and discuss how these factors may act as systemic mediators of TNF-alpha and affect whole body energy homeostasis and overall insulin sensitivity. |
| 10177 | 12948526 | We also review the ability of TNF-alpha to inhibit synthesis of several adipocyte-specific proteins including Acrp30 (adiponectin) and enhance release of free fatty acids (FFAs) from adipose tissue, and discuss how these factors may act as systemic mediators of TNF-alpha and affect whole body energy homeostasis and overall insulin sensitivity. |
| 10178 | 12948526 | We also review the ability of TNF-alpha to inhibit synthesis of several adipocyte-specific proteins including Acrp30 (adiponectin) and enhance release of free fatty acids (FFAs) from adipose tissue, and discuss how these factors may act as systemic mediators of TNF-alpha and affect whole body energy homeostasis and overall insulin sensitivity. |
| 10179 | 12948526 | We also review the ability of TNF-alpha to inhibit synthesis of several adipocyte-specific proteins including Acrp30 (adiponectin) and enhance release of free fatty acids (FFAs) from adipose tissue, and discuss how these factors may act as systemic mediators of TNF-alpha and affect whole body energy homeostasis and overall insulin sensitivity. |
| 10180 | 12941768 | In addition, the densities of IL-1 alpha- and IL-4-positive cells detected by immunohistochemistry and IL-4 mRNA-expressing cells evaluated by in situ hybridization were increased in the lamina propria in patients with type 1 diabetes and normal mucosa. |
| 10181 | 12941768 | Instead, the densities of IL-2, gamma-interferon (IFN-gamma), and tumor necrosis factor alpha-positive cells, the density of IFN-gamma mRNA positive cells, and the amounts of IFN-gamma mRNA detected by RT-PCR correlated with the degree of celiac disease in patients with type 1 diabetes. |
| 10182 | 12941767 | DcR3/TR6 is a soluble death decoy receptor belonging to the tumor necrosis factor (TNF) receptor family, and it can block apoptosis mediated by several TNF receptor family members such as Fas and LT beta R. |
| 10183 | 12941767 | In vitro experiments showed an increased apoptosis among islets that were treated with FasL and gamma-interferon (IFN-gamma) in combination. |
| 10184 | 12941767 | Functional study showed that insulin release was compromised after FasL and IFN-gamma treatment, and the compromise could be prevented with TR6-Fc. |
| 10185 | 12941767 | This indicates that TR6 indeed protected beta-cells from damage caused by FasL and IFN-gamma. |
| 10186 | 12941766 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of tumor cells but not most normal cells. |
| 10187 | 12934668 | VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-I 2 h after TNF-alpha administration. |
| 10188 | 12934668 | VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-I 2 h after TNF-alpha administration. |
| 10189 | 12934668 | VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-I 2 h after TNF-alpha administration. |
| 10190 | 12934668 | Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. |
| 10191 | 12934668 | Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. |
| 10192 | 12934668 | Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. |
| 10193 | 12934668 | The present results demonstrated that TNF-alpha can amplify or antagonize the effects of EFAD on lipid profile, lipoprotein composition, and LPL activity. |
| 10194 | 12934668 | The present results demonstrated that TNF-alpha can amplify or antagonize the effects of EFAD on lipid profile, lipoprotein composition, and LPL activity. |
| 10195 | 12934668 | The present results demonstrated that TNF-alpha can amplify or antagonize the effects of EFAD on lipid profile, lipoprotein composition, and LPL activity. |
| 10196 | 12930356 | Critical roles of CD30/CD30L interactions in murine autoimmune diabetes. |
| 10197 | 12930356 | CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. |
| 10198 | 12930356 | In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. |
| 10199 | 12930356 | Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. |
| 10200 | 12930356 | In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. |
| 10201 | 12930356 | In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. |
| 10202 | 12930356 | These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice. |
| 10203 | 12928786 | Intact pgrn is anti-inflammatory through the inhibition of some of the actions of tumor necrosis factor, while the proteolytic peptides may stimulate the production of proinflammatory cytokines such as interleukin 8. |
| 10204 | 12927809 | Adiponectin gene activation by thiazolidinediones requires PPAR gamma 2, but not C/EBP alpha-evidence for differential regulation of the aP2 and adiponectin genes. |
| 10205 | 12927809 | We examined the role of PPAR gamma 2 and C/EBP alpha for adiponectin and aP2 gene activation in C/EBP alpha(-/-) fibroblasts by stably expressing PPAR gamma 2 or C/EBP alpha. |
| 10206 | 12927809 | PPAR gamma 2, but not PPAR gamma 1, mRNA markedly increased during the differentiation to adipocytes in cells expressing C/EBP alpha. |
| 10207 | 12927809 | Both infected cell lines differentiated to an adipocyte phenotype and the mRNA for both aP2 and adiponectin increased in parallel. |
| 10208 | 12927809 | Thiazolidinediones markedly activated the gene in PPAR gamma 2-expressing cells in the absence of C/EBP alpha, suggesting that the adiponectin promoter may have functional PPAR gamma-response elements. |
| 10209 | 12927809 | Several observations showed that the adiponectin and aP2 genes can be differentially regulated in adipocytes: (1) Topiramate, an anti-epileptic agent with weight-reducing properties, increased adiponectin mRNA levels and secretion, but did not, like the thiazolidinediones, increase aP2 expression; (2) IL-6 reduced adiponectin, but significantly increased, aP2 expression; and (3) TNFalpha inhibited adiponectin, but paradoxically increased, aP2 expression in PPAR gamma 2-infected C/EBP alpha null cells. |
| 10210 | 12925533 | Adipocyte-selective reduction of the leptin receptors induced by antisense RNA leads to increased adiposity, dyslipidemia, and insulin resistance. |
| 10211 | 12925533 | Despite a normal level of leptin receptors in the hypothalamus and normal food intake, mutant mice developed increased adiposity, decreased body temperature, hyperinsulinemia, hypertriglyceridemia, impaired glucose tolerance and insulin sensitivity, as well as elevated hepatic and skeletal muscle triglyceride levels. |
| 10212 | 12925533 | These include tumor necrosis factor-alpha, adiponectin, leptin, fatty acid synthase, sterol regulatory element-binding protein 1, glycerol kinase, and beta3-adrenergic receptor. |
| 10213 | 12925533 | Importantly, this suggests the possibility that leptin resistance at the adipocyte level might be a molecular link between obesity and type 2 diabetes. |
| 10214 | 12924619 | Chinese medicine, Jiang-Tang-Ke-Li, improves insulin resistance by modulating muscle fiber composition and muscle tumor necrosis factor-alpha in fructose-fed rats. |
| 10215 | 12924619 | Chinese medicine, Jiang-Tang-Ke-Li, improves insulin resistance by modulating muscle fiber composition and muscle tumor necrosis factor-alpha in fructose-fed rats. |
| 10216 | 12924619 | The results suggest that the Chinese medicine JTKL, which contains PG as one of its valid components, improves insulin resistance by modulating muscle fiber composition and TNF-alpha in skeletal muscles in hypertensive and insulin-resistant FFR. |
| 10217 | 12924619 | The results suggest that the Chinese medicine JTKL, which contains PG as one of its valid components, improves insulin resistance by modulating muscle fiber composition and TNF-alpha in skeletal muscles in hypertensive and insulin-resistant FFR. |
| 10218 | 12923954 | [Selected cytokines (Il-6, Il-8, Il-10, MCP-1, TNF-alpha) in children and adolescents with atherosclerosis risk factors: obesity, hypertension, diabetes]. |
| 10219 | 12914718 | The visceral fat accumulation is characterised by the increased, abundant secretion of a number of peptides such as leptin, insulin-like growth factor (IGF), adiponectin and the recently reported resistin and visfatin hormones. |
| 10220 | 12914718 | Elevated resistin and tumour necrosis factor (TNF-alpha) levels and low levels of adiponectin secretion may have implications for the risk of development of type 2 diabetes and cardiovascular disease. |
| 10221 | 12898475 | Lower rate of tumor necrosis factor-alpha -863A allele and higher concentration of tumor necrosis factor-alpha receptor 2 in first-degree relatives of subjects with type 2 diabetes. |
| 10222 | 12898475 | Lower rate of tumor necrosis factor-alpha -863A allele and higher concentration of tumor necrosis factor-alpha receptor 2 in first-degree relatives of subjects with type 2 diabetes. |
| 10223 | 12898475 | Lower rate of tumor necrosis factor-alpha -863A allele and higher concentration of tumor necrosis factor-alpha receptor 2 in first-degree relatives of subjects with type 2 diabetes. |
| 10224 | 12898475 | Allelic variants of the tumor necrosis factor-alpha (TNF-alpha) gene seem to contribute to insulin resistance increasing the transcription rate of TNF-alpha. |
| 10225 | 12898475 | Allelic variants of the tumor necrosis factor-alpha (TNF-alpha) gene seem to contribute to insulin resistance increasing the transcription rate of TNF-alpha. |
| 10226 | 12898475 | Allelic variants of the tumor necrosis factor-alpha (TNF-alpha) gene seem to contribute to insulin resistance increasing the transcription rate of TNF-alpha. |
| 10227 | 12898475 | To investigate whether an abnormal TNF-alpha system regulation may contribute to early impairment of insulin action in first-degree relatives of patients with type 2 diabetes mellitus (DM), we studied the TNF-alpha -863C/A polymorphism and the soluble fraction of TNF-alpha receptor-2 (sTNFR2) concentration in these subjects in comparison to a control group. |
| 10228 | 12898475 | To investigate whether an abnormal TNF-alpha system regulation may contribute to early impairment of insulin action in first-degree relatives of patients with type 2 diabetes mellitus (DM), we studied the TNF-alpha -863C/A polymorphism and the soluble fraction of TNF-alpha receptor-2 (sTNFR2) concentration in these subjects in comparison to a control group. |
| 10229 | 12898475 | To investigate whether an abnormal TNF-alpha system regulation may contribute to early impairment of insulin action in first-degree relatives of patients with type 2 diabetes mellitus (DM), we studied the TNF-alpha -863C/A polymorphism and the soluble fraction of TNF-alpha receptor-2 (sTNFR2) concentration in these subjects in comparison to a control group. |
| 10230 | 12890914 | A secondary aim was to determine the effect of this treatment on plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and to investigate the relationships between this adipocytokine and insulin resistance. |
| 10231 | 12890914 | A secondary aim was to determine the effect of this treatment on plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and to investigate the relationships between this adipocytokine and insulin resistance. |
| 10232 | 12890914 | A secondary aim was to determine the effect of this treatment on plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and to investigate the relationships between this adipocytokine and insulin resistance. |
| 10233 | 12890914 | A secondary aim was to determine the effect of this treatment on plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and to investigate the relationships between this adipocytokine and insulin resistance. |
| 10234 | 12890914 | Insulin resistance determined using the Homeostatic Model Assessment (HOMA), echocardiographic measurements and analysis of plasma TNF-alpha concentration were carried out in 47 patients with DCM without diabetes mellitus before and after 6 months of beta-blocker therapy. |
| 10235 | 12890914 | Insulin resistance determined using the Homeostatic Model Assessment (HOMA), echocardiographic measurements and analysis of plasma TNF-alpha concentration were carried out in 47 patients with DCM without diabetes mellitus before and after 6 months of beta-blocker therapy. |
| 10236 | 12890914 | Insulin resistance determined using the Homeostatic Model Assessment (HOMA), echocardiographic measurements and analysis of plasma TNF-alpha concentration were carried out in 47 patients with DCM without diabetes mellitus before and after 6 months of beta-blocker therapy. |
| 10237 | 12890914 | Insulin resistance determined using the Homeostatic Model Assessment (HOMA), echocardiographic measurements and analysis of plasma TNF-alpha concentration were carried out in 47 patients with DCM without diabetes mellitus before and after 6 months of beta-blocker therapy. |
| 10238 | 12890914 | Beta-blockade was also associated with a decrease in plasma TNF-alpha concentration although no significant relationship between this change and the improvement in insulin resistance was observed. |
| 10239 | 12890914 | Beta-blockade was also associated with a decrease in plasma TNF-alpha concentration although no significant relationship between this change and the improvement in insulin resistance was observed. |
| 10240 | 12890914 | Beta-blockade was also associated with a decrease in plasma TNF-alpha concentration although no significant relationship between this change and the improvement in insulin resistance was observed. |
| 10241 | 12890914 | Beta-blockade was also associated with a decrease in plasma TNF-alpha concentration although no significant relationship between this change and the improvement in insulin resistance was observed. |
| 10242 | 12890914 | The mechanism of the change in insulin function remains unclear, but may be related to improvements in left ventricular function or an attenuation of the inhibitory effect of reduction in TNF-alpha on insulin signaling. |
| 10243 | 12890914 | The mechanism of the change in insulin function remains unclear, but may be related to improvements in left ventricular function or an attenuation of the inhibitory effect of reduction in TNF-alpha on insulin signaling. |
| 10244 | 12890914 | The mechanism of the change in insulin function remains unclear, but may be related to improvements in left ventricular function or an attenuation of the inhibitory effect of reduction in TNF-alpha on insulin signaling. |
| 10245 | 12890914 | The mechanism of the change in insulin function remains unclear, but may be related to improvements in left ventricular function or an attenuation of the inhibitory effect of reduction in TNF-alpha on insulin signaling. |
| 10246 | 12885274 | Cellular FLIP (c-FLIP), also known as FLICE-inhibitory protein, has been identified as an inhibitor of apoptosis triggered by engagement of death receptors (DRs) such as Fas or TRAIL (TNF-related apoptosis-inducing ligand). cFLIP is recruited to DR signalling complexes, where it prevents caspase activation. |
| 10247 | 12882935 | The majority of these genes fall into four signaling pathways: insulin, transforming growth factor-beta, tumor necrosis factor-alpha, and peroxisome proliferator-activated receptor. |
| 10248 | 12882915 | Our results demonstrate that direct, in vivo administration of tumor necrosis factor-alpha (1,000 units), interleukin-1beta (1,000 units), and interferon-gamma (2,000 units) into the rat pancreas through a bile duct cannula leads to the formation of lipid-derived free radicals in this tissue. |
| 10249 | 12882915 | Inhibition of the enzyme inducible cyclooxygenase (COX-2) and the transcription factor nuclear factor-kappaB (NF-kappaB) significantly diminished the free radicals' signal intensity, implicating these factors in the formation of free radicals. |
| 10250 | 12882912 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is expressed in different tissues and cells, including pancreas and lymphocytes, and can induce apoptosis in various tumor cells but not in most normal cells. |
| 10251 | 12882912 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is expressed in different tissues and cells, including pancreas and lymphocytes, and can induce apoptosis in various tumor cells but not in most normal cells. |
| 10252 | 12882912 | Here we show by cDNA array analyses that TRAIL gene expression is upregulated in pancreatic islets during the development of autoimmune type 1 diabetes in nonobese diabetic (NOD) mice and in Min6 islet beta-cells activated by TNF-alpha + interferon-gamma. |
| 10253 | 12882912 | Here we show by cDNA array analyses that TRAIL gene expression is upregulated in pancreatic islets during the development of autoimmune type 1 diabetes in nonobese diabetic (NOD) mice and in Min6 islet beta-cells activated by TNF-alpha + interferon-gamma. |
| 10254 | 12882912 | TRAIL inhibits the proliferation of NOD diabetogenic T-cells by suppressing interleukin (IL)-2 production and cell cycle progression, and this inhibition can be rescued in the presence of exogenous IL-2. cDNA array and Western blot analyses indicate that TRAIL upregulates the expression of the cdk inhibitor p27(kip1). |
| 10255 | 12882912 | TRAIL inhibits the proliferation of NOD diabetogenic T-cells by suppressing interleukin (IL)-2 production and cell cycle progression, and this inhibition can be rescued in the presence of exogenous IL-2. cDNA array and Western blot analyses indicate that TRAIL upregulates the expression of the cdk inhibitor p27(kip1). |
| 10256 | 12878589 | Here we demonstrate that LDL(-) increases tumor necrosis factor alpha (TNFalpha)-induced inflammatory responses through NF kappa B and AP-1 activation with corresponding increases in vascular cell adhesion molecule-1 (VCAM1) expression. |
| 10257 | 12878589 | Here we demonstrate that LDL(-) increases tumor necrosis factor alpha (TNFalpha)-induced inflammatory responses through NF kappa B and AP-1 activation with corresponding increases in vascular cell adhesion molecule-1 (VCAM1) expression. |
| 10258 | 12878589 | In contrast, exposing LDL(-) to the key lipolytic enzyme lipoprotein lipase (LPL) reversed these responses, inhibiting VCAM1 below levels seen with TNFalpha alone. |
| 10259 | 12878589 | In contrast, exposing LDL(-) to the key lipolytic enzyme lipoprotein lipase (LPL) reversed these responses, inhibiting VCAM1 below levels seen with TNFalpha alone. |
| 10260 | 12878589 | LPL is known to act on lipoproteins to generate endogenous peroxisomal proliferator-activated receptor alpha (PPAR alpha) ligand, thus limiting inflammation. |
| 10261 | 12878589 | LPL is known to act on lipoproteins to generate endogenous peroxisomal proliferator-activated receptor alpha (PPAR alpha) ligand, thus limiting inflammation. |
| 10262 | 12878589 | As compared with LDL(-) alone, LPL-treated LDL(-) increased PPAR alpha activation 20-fold in either cell-based transfection or radioligand displacement assays. |
| 10263 | 12878589 | As compared with LDL(-) alone, LPL-treated LDL(-) increased PPAR alpha activation 20-fold in either cell-based transfection or radioligand displacement assays. |
| 10264 | 12878589 | LPL-treated LDL(-) suppressed NF kappa B and AP-1 activation, increasing expression of the PPAR alpha target gene I kappa B alpha, although only in the genetic presence of PPAR alpha and with intact LPL hydrolysis. |
| 10265 | 12878589 | LPL-treated LDL(-) suppressed NF kappa B and AP-1 activation, increasing expression of the PPAR alpha target gene I kappa B alpha, although only in the genetic presence of PPAR alpha and with intact LPL hydrolysis. |
| 10266 | 12878589 | Mass spectrometry reveals that LPL-treatment of either LDL or LDL(-) releases hydroxy-octadecadienoic acids (HODEs), potent PPAR alpha activators. |
| 10267 | 12878589 | Mass spectrometry reveals that LPL-treatment of either LDL or LDL(-) releases hydroxy-octadecadienoic acids (HODEs), potent PPAR alpha activators. |
| 10268 | 12878589 | These findings suggest LPL-mediated PPAR alpha activation as an alternative catabolic pathway that may limit inflammatory responses to LDL(-). |
| 10269 | 12878589 | These findings suggest LPL-mediated PPAR alpha activation as an alternative catabolic pathway that may limit inflammatory responses to LDL(-). |
| 10270 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10271 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10272 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10273 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10274 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10275 | 12870175 | Skeletal muscle interleukin-6 and tumor necrosis factor-alpha release in healthy subjects and patients with type 2 diabetes at rest and during exercise. |
| 10276 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10277 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10278 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10279 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10280 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10281 | 12870175 | Blood samples were obtained from a femoral artery and vein from 1 limb, and plasma was analyzed for glucose and the cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. |
| 10282 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10283 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10284 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10285 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10286 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10287 | 12870175 | Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and net leg IL-6, TNF-alpha, and glucose balance were calculated as the product of LBF and femoral arteriovenous (fa-v) glucose, IL-6, and TNF-alpha difference. |
| 10288 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10289 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10290 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10291 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10292 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10293 | 12870175 | Arterial plasma glucose and IL-6 were higher (P<.05) at rest in D compared with C, but there were no differences in arterial TNF-alpha concentrations at rest when comparing groups. |
| 10294 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10295 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10296 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10297 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10298 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10299 | 12870175 | Despite measurable arterial levels of both IL-6 and TNF-alpha in both groups at rest, there was not net leg release of either cytokine at rest. |
| 10300 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10301 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10302 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10303 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10304 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10305 | 12870175 | In contrast with IL-6, exercise does not result in the release of TNF-alpha from the contracting limbs of either healthy subjects or patients with type 2 diabetes. |
| 10306 | 12866991 | Because visceral and subcutaneous adipose tissues are the major sources of cytokines (adipokines), increased adipose tissue mass is associated with alteration in adipokine production (eg, overexpression of tumor necrosis factor-a, interleukin-6, plasminogen activator inhibitor-1, and underexpression of adiponectin in adipose tissue). |
| 10307 | 12866991 | Because visceral and subcutaneous adipose tissues are the major sources of cytokines (adipokines), increased adipose tissue mass is associated with alteration in adipokine production (eg, overexpression of tumor necrosis factor-a, interleukin-6, plasminogen activator inhibitor-1, and underexpression of adiponectin in adipose tissue). |
| 10308 | 12866991 | Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-a, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. |
| 10309 | 12866991 | Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-a, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. |
| 10310 | 12866663 | Inflammatory markers like CRP, PAI-1, IL-6 are present in higher concentrations in insulin resistant people than in normal people. |
| 10311 | 12866663 | TNFalpha has been shown to be responsible for insulin resistance in obese subjects. |
| 10312 | 12861268 | Some recent discoveries have made it evident that this is a very active endocrine tissue that secretes important molecules related to different processes such as the immune response (TNF alpha) the regulation of food intake and expenditure of energy (leptin, Acrp30/adipoQ) and the vascular function (angiotensin and plasminogen activator inhibitor type 1). |
| 10313 | 12849705 | Hypoglycaemia downregulates endotoxin-induced production of tumour necrosis factor-alpha, but does not affect IL-1beta, IL-6, or IL-10. |
| 10314 | 12849705 | Hypoglycaemia downregulates endotoxin-induced production of tumour necrosis factor-alpha, but does not affect IL-1beta, IL-6, or IL-10. |
| 10315 | 12849705 | Hypoglycaemia downregulates endotoxin-induced production of tumour necrosis factor-alpha, but does not affect IL-1beta, IL-6, or IL-10. |
| 10316 | 12849705 | Hypoglycaemia downregulates endotoxin-induced production of tumour necrosis factor-alpha, but does not affect IL-1beta, IL-6, or IL-10. |
| 10317 | 12849705 | The aim of the present study was to investigate the effect of hypoglycaemia on the production capacity of the proinflammatory cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) in subjects with and without diabetes. |
| 10318 | 12849705 | The aim of the present study was to investigate the effect of hypoglycaemia on the production capacity of the proinflammatory cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) in subjects with and without diabetes. |
| 10319 | 12849705 | The aim of the present study was to investigate the effect of hypoglycaemia on the production capacity of the proinflammatory cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) in subjects with and without diabetes. |
| 10320 | 12849705 | The aim of the present study was to investigate the effect of hypoglycaemia on the production capacity of the proinflammatory cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) in subjects with and without diabetes. |
| 10321 | 12849705 | Circulating levels of cytokines and endotoxin-induced production of TNFalpha, IL-1beta, IL-6, and IL-10 were assessed. |
| 10322 | 12849705 | Circulating levels of cytokines and endotoxin-induced production of TNFalpha, IL-1beta, IL-6, and IL-10 were assessed. |
| 10323 | 12849705 | Circulating levels of cytokines and endotoxin-induced production of TNFalpha, IL-1beta, IL-6, and IL-10 were assessed. |
| 10324 | 12849705 | Circulating levels of cytokines and endotoxin-induced production of TNFalpha, IL-1beta, IL-6, and IL-10 were assessed. |
| 10325 | 12849705 | In non-diabetic subjects, hypoglycaemia downregulated the production capacity of TNFalpha in a concentration-dependent fashion (P=0.007), but not of IL-1beta, IL-6, or IL-10. |
| 10326 | 12849705 | In non-diabetic subjects, hypoglycaemia downregulated the production capacity of TNFalpha in a concentration-dependent fashion (P=0.007), but not of IL-1beta, IL-6, or IL-10. |
| 10327 | 12849705 | In non-diabetic subjects, hypoglycaemia downregulated the production capacity of TNFalpha in a concentration-dependent fashion (P=0.007), but not of IL-1beta, IL-6, or IL-10. |
| 10328 | 12849705 | In non-diabetic subjects, hypoglycaemia downregulated the production capacity of TNFalpha in a concentration-dependent fashion (P=0.007), but not of IL-1beta, IL-6, or IL-10. |
| 10329 | 12849705 | The downregulation of TNFalpha could not be explained by increased insulin or adrenaline levels. |
| 10330 | 12849705 | The downregulation of TNFalpha could not be explained by increased insulin or adrenaline levels. |
| 10331 | 12849705 | The downregulation of TNFalpha could not be explained by increased insulin or adrenaline levels. |
| 10332 | 12849705 | The downregulation of TNFalpha could not be explained by increased insulin or adrenaline levels. |
| 10333 | 12833656 | Bristol-Myers Squibb Pharma Co is developing the tumor necrosis factor-alpha (TNF alpha) converting enzyme inhibitor BMS-561392 (DPC-333) for the potential treatment of diseases characterized by overproduction of TNF alpha, such as rheumatoid arthritis (RA). |
| 10334 | 12829659 | Promoter polymorphisms of the TNF-alpha (G-308A) and IL-6 (C-174G) genes predict the conversion from impaired glucose tolerance to type 2 diabetes: the Finnish Diabetes Prevention Study. |
| 10335 | 12829659 | Promoter polymorphisms of the TNF-alpha (G-308A) and IL-6 (C-174G) genes predict the conversion from impaired glucose tolerance to type 2 diabetes: the Finnish Diabetes Prevention Study. |
| 10336 | 12829659 | Promoter polymorphisms of the TNF-alpha (G-308A) and IL-6 (C-174G) genes predict the conversion from impaired glucose tolerance to type 2 diabetes: the Finnish Diabetes Prevention Study. |
| 10337 | 12829659 | Therefore, we investigated whether the promoter polymorphisms of the tumor necrosis factor-alpha (TNF-alpha; G-308A) and interleukin 6 (IL-6; C-174G) genes predict the conversion from impaired glucose tolerance (IGT) to type 2 diabetes in the Finnish Diabetes Prevention Study. |
| 10338 | 12829659 | Therefore, we investigated whether the promoter polymorphisms of the tumor necrosis factor-alpha (TNF-alpha; G-308A) and interleukin 6 (IL-6; C-174G) genes predict the conversion from impaired glucose tolerance (IGT) to type 2 diabetes in the Finnish Diabetes Prevention Study. |
| 10339 | 12829659 | Therefore, we investigated whether the promoter polymorphisms of the tumor necrosis factor-alpha (TNF-alpha; G-308A) and interleukin 6 (IL-6; C-174G) genes predict the conversion from impaired glucose tolerance (IGT) to type 2 diabetes in the Finnish Diabetes Prevention Study. |
| 10340 | 12829659 | Subjects with both the A allele of the TNF-alpha gene and the C-174C genotype of the IL-6 gene had a 2.2-fold (CI 1.02-4.85, P = 0.045) higher risk of developing type 2 diabetes than subjects without the risk genotypes. |
| 10341 | 12829659 | Subjects with both the A allele of the TNF-alpha gene and the C-174C genotype of the IL-6 gene had a 2.2-fold (CI 1.02-4.85, P = 0.045) higher risk of developing type 2 diabetes than subjects without the risk genotypes. |
| 10342 | 12829659 | Subjects with both the A allele of the TNF-alpha gene and the C-174C genotype of the IL-6 gene had a 2.2-fold (CI 1.02-4.85, P = 0.045) higher risk of developing type 2 diabetes than subjects without the risk genotypes. |
| 10343 | 12829646 | Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. |
| 10344 | 12829646 | Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. |
| 10345 | 12829646 | Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. |
| 10346 | 12829646 | Adiponectin is a 29-kDa adipocyte protein that has been linked to the insulin resistance of obesity and lipodystrophy. |
| 10347 | 12829646 | Adiponectin is a 29-kDa adipocyte protein that has been linked to the insulin resistance of obesity and lipodystrophy. |
| 10348 | 12829646 | Adiponectin is a 29-kDa adipocyte protein that has been linked to the insulin resistance of obesity and lipodystrophy. |
| 10349 | 12829646 | To better understand the regulation of adiponectin expression, we measured plasma adiponectin and adipose tissue adiponectin mRNA levels in nondiabetic subjects with varying degrees of obesity and insulin resistance. |
| 10350 | 12829646 | To better understand the regulation of adiponectin expression, we measured plasma adiponectin and adipose tissue adiponectin mRNA levels in nondiabetic subjects with varying degrees of obesity and insulin resistance. |
| 10351 | 12829646 | To better understand the regulation of adiponectin expression, we measured plasma adiponectin and adipose tissue adiponectin mRNA levels in nondiabetic subjects with varying degrees of obesity and insulin resistance. |
| 10352 | 12829646 | Plasma adiponectin had a strong association with insulin sensitivity index (S(I)) (r = 0.67, P < 0.0001, n = 51) that was not affected by sex, but no relation with insulin secretion. |
| 10353 | 12829646 | Plasma adiponectin had a strong association with insulin sensitivity index (S(I)) (r = 0.67, P < 0.0001, n = 51) that was not affected by sex, but no relation with insulin secretion. |
| 10354 | 12829646 | Plasma adiponectin had a strong association with insulin sensitivity index (S(I)) (r = 0.67, P < 0.0001, n = 51) that was not affected by sex, but no relation with insulin secretion. |
| 10355 | 12829646 | Using this approach, insulin-sensitive subjects demonstrated a twofold higher plasma level of adiponectin (5.6 +/- 0.6 and 11.2 +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005). |
| 10356 | 12829646 | Using this approach, insulin-sensitive subjects demonstrated a twofold higher plasma level of adiponectin (5.6 +/- 0.6 and 11.2 +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005). |
| 10357 | 12829646 | Using this approach, insulin-sensitive subjects demonstrated a twofold higher plasma level of adiponectin (5.6 +/- 0.6 and 11.2 +/- 1.1 micro g/ml in insulin-resistant and insulin-sensitive subjects, respectively; P < 0.0005). |
| 10358 | 12829646 | Adiponectin expression was not related to plasma levels of leptin or interleukin-6. |
| 10359 | 12829646 | Adiponectin expression was not related to plasma levels of leptin or interleukin-6. |
| 10360 | 12829646 | Adiponectin expression was not related to plasma levels of leptin or interleukin-6. |
| 10361 | 12829646 | However, there was a significant inverse correlation between plasma adiponectin and tumor necrosis factor (TNF)-alpha mRNA expression (r = -0.47, P < 0.005), and subjects with the highest levels of adiponectin mRNA expression secreted the lowest levels of TNF-alpha from their adipose tissue in vitro. |
| 10362 | 12829646 | However, there was a significant inverse correlation between plasma adiponectin and tumor necrosis factor (TNF)-alpha mRNA expression (r = -0.47, P < 0.005), and subjects with the highest levels of adiponectin mRNA expression secreted the lowest levels of TNF-alpha from their adipose tissue in vitro. |
| 10363 | 12829646 | However, there was a significant inverse correlation between plasma adiponectin and tumor necrosis factor (TNF)-alpha mRNA expression (r = -0.47, P < 0.005), and subjects with the highest levels of adiponectin mRNA expression secreted the lowest levels of TNF-alpha from their adipose tissue in vitro. |
| 10364 | 12829646 | Thus, adiponectin expression from adipose tissue is higher in lean subjects and women, and is associated with higher degrees of insulin sensitivity and lower TNF-alpha expression. |
| 10365 | 12829646 | Thus, adiponectin expression from adipose tissue is higher in lean subjects and women, and is associated with higher degrees of insulin sensitivity and lower TNF-alpha expression. |
| 10366 | 12829646 | Thus, adiponectin expression from adipose tissue is higher in lean subjects and women, and is associated with higher degrees of insulin sensitivity and lower TNF-alpha expression. |
| 10367 | 12825835 | P2Y6 nucleotide receptor activates PKC to protect 1321N1 astrocytoma cells against tumor necrosis factor-induced apoptosis. |
| 10368 | 12825835 | P2Y6 nucleotide receptor activates PKC to protect 1321N1 astrocytoma cells against tumor necrosis factor-induced apoptosis. |
| 10369 | 12825835 | P2Y6 nucleotide receptor activates PKC to protect 1321N1 astrocytoma cells against tumor necrosis factor-induced apoptosis. |
| 10370 | 12825835 | P2Y6 nucleotide receptor activates PKC to protect 1321N1 astrocytoma cells against tumor necrosis factor-induced apoptosis. |
| 10371 | 12825835 | We recently reported that the activation by UDP of rat P2Y6 nucleotide receptors expressed in 1321N1 astrocytoma cells protected them from TNFalpha-induced apoptosis by suppressing activation of caspase 3 and 8. |
| 10372 | 12825835 | We recently reported that the activation by UDP of rat P2Y6 nucleotide receptors expressed in 1321N1 astrocytoma cells protected them from TNFalpha-induced apoptosis by suppressing activation of caspase 3 and 8. |
| 10373 | 12825835 | We recently reported that the activation by UDP of rat P2Y6 nucleotide receptors expressed in 1321N1 astrocytoma cells protected them from TNFalpha-induced apoptosis by suppressing activation of caspase 3 and 8. |
| 10374 | 12825835 | We recently reported that the activation by UDP of rat P2Y6 nucleotide receptors expressed in 1321N1 astrocytoma cells protected them from TNFalpha-induced apoptosis by suppressing activation of caspase 3 and 8. |
| 10375 | 12825835 | Cell death was induced in 1321N1 astrocytoma cells permanently expressing the rat P2Y6 receptor by exposure to TNFalpha in the presence of cycloheximide. |
| 10376 | 12825835 | Cell death was induced in 1321N1 astrocytoma cells permanently expressing the rat P2Y6 receptor by exposure to TNFalpha in the presence of cycloheximide. |
| 10377 | 12825835 | Cell death was induced in 1321N1 astrocytoma cells permanently expressing the rat P2Y6 receptor by exposure to TNFalpha in the presence of cycloheximide. |
| 10378 | 12825835 | Cell death was induced in 1321N1 astrocytoma cells permanently expressing the rat P2Y6 receptor by exposure to TNFalpha in the presence of cycloheximide. |
| 10379 | 12825835 | The activation of P2Y6 receptors by UDP both protected the astrocytes from TNF-alpha induced apoptosis and activated protein kinase C (PKC) isotypes. |
| 10380 | 12825835 | The activation of P2Y6 receptors by UDP both protected the astrocytes from TNF-alpha induced apoptosis and activated protein kinase C (PKC) isotypes. |
| 10381 | 12825835 | The activation of P2Y6 receptors by UDP both protected the astrocytes from TNF-alpha induced apoptosis and activated protein kinase C (PKC) isotypes. |
| 10382 | 12825835 | The activation of P2Y6 receptors by UDP both protected the astrocytes from TNF-alpha induced apoptosis and activated protein kinase C (PKC) isotypes. |
| 10383 | 12825835 | The antiapoptotic protein, Akt, was not affected by P2Y6 receptor activation. |
| 10384 | 12825835 | The antiapoptotic protein, Akt, was not affected by P2Y6 receptor activation. |
| 10385 | 12825835 | The antiapoptotic protein, Akt, was not affected by P2Y6 receptor activation. |
| 10386 | 12825835 | The antiapoptotic protein, Akt, was not affected by P2Y6 receptor activation. |
| 10387 | 12825835 | The addition of phospholipase C (PLC) inhibitors, D609 or U73122, partially antagonized both UDP-induced protection and PKC activation. |
| 10388 | 12825835 | The addition of phospholipase C (PLC) inhibitors, D609 or U73122, partially antagonized both UDP-induced protection and PKC activation. |
| 10389 | 12825835 | The addition of phospholipase C (PLC) inhibitors, D609 or U73122, partially antagonized both UDP-induced protection and PKC activation. |
| 10390 | 12825835 | The addition of phospholipase C (PLC) inhibitors, D609 or U73122, partially antagonized both UDP-induced protection and PKC activation. |
| 10391 | 12823641 | In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 10392 | 12823641 | In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 10393 | 12823641 | In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. |
| 10394 | 12823641 | Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). |
| 10395 | 12823641 | Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). |
| 10396 | 12823641 | Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). |
| 10397 | 12823641 | In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. |
| 10398 | 12823641 | In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. |
| 10399 | 12823641 | In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. |
| 10400 | 12818128 | [Polymorphism of TNF-alpha (308 A/G), IL-10 (1082 A/G, 819 C/T 592 A/C), IL-6 (174 G/C), and IFN-gamma (874 A/T); genetically conditioned cytokine synthesis level in children with diabetes type 1]. |
| 10401 | 12795417 | In murine models of autoimmune lupus, for example, mutations in the death receptor Fas (CD95) or in its ligand, FasL (CD95L), have been identified and shown to render lymphoid cells resistant to apoptosis. |
| 10402 | 12795417 | In contrast, select lymphoid subpopulations of mice with autoimmune diabetes manifest an increased susceptibility to apoptosis as a result of impaired activation of the transcription factor nuclear factor-kappa B (NF-kappaB), which normally protects cells against tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis. |
| 10403 | 12795417 | The genetic basis of this defect in NF-kappaB activation is a mutation in the promoter-enhancer region of a gene that encodes an essential subunit (LMP2) of the proteasome. |
| 10404 | 12791316 | IL-1beta, IFN-gamma and TNF-alpha increase vulnerability of pancreatic beta cells to autoimmune destruction. |
| 10405 | 12791316 | IL-1beta, IFN-gamma and TNF-alpha increase vulnerability of pancreatic beta cells to autoimmune destruction. |
| 10406 | 12791316 | IL-1beta, IFN-gamma and TNF-alpha increase vulnerability of pancreatic beta cells to autoimmune destruction. |
| 10407 | 12791316 | Islets from diabetes-prone and congenic diabetes-resistant BB rats were exposed to interleukin (IL)-1beta alone or in combination with interferon (IFN)-gamma plus tumour necrosis factor (TNF)-alpha. |
| 10408 | 12791316 | Islets from diabetes-prone and congenic diabetes-resistant BB rats were exposed to interleukin (IL)-1beta alone or in combination with interferon (IFN)-gamma plus tumour necrosis factor (TNF)-alpha. |
| 10409 | 12791316 | Islets from diabetes-prone and congenic diabetes-resistant BB rats were exposed to interleukin (IL)-1beta alone or in combination with interferon (IFN)-gamma plus tumour necrosis factor (TNF)-alpha. |
| 10410 | 12791316 | Independent of diabetes susceptibility IL-1beta treated islet beta-cells expressed a significantly increased amount of ICAM-1 on their surfaces which was not further increased by IFN-gamma+TNF-alpha. |
| 10411 | 12791316 | Independent of diabetes susceptibility IL-1beta treated islet beta-cells expressed a significantly increased amount of ICAM-1 on their surfaces which was not further increased by IFN-gamma+TNF-alpha. |
| 10412 | 12791316 | Independent of diabetes susceptibility IL-1beta treated islet beta-cells expressed a significantly increased amount of ICAM-1 on their surfaces which was not further increased by IFN-gamma+TNF-alpha. |
| 10413 | 12791316 | However, IL-1beta induced Fas expression was significantly enhanced only on beta-cells from diabetes-prone BB rats. |
| 10414 | 12791316 | However, IL-1beta induced Fas expression was significantly enhanced only on beta-cells from diabetes-prone BB rats. |
| 10415 | 12791316 | However, IL-1beta induced Fas expression was significantly enhanced only on beta-cells from diabetes-prone BB rats. |
| 10416 | 12791316 | From these results we suggest that IL-1beta mediates the major stimulus for ICAM-1 induction which is possibly a necessary but not sufficient step in the process of beta-cell destruction. |
| 10417 | 12791316 | From these results we suggest that IL-1beta mediates the major stimulus for ICAM-1 induction which is possibly a necessary but not sufficient step in the process of beta-cell destruction. |
| 10418 | 12791316 | From these results we suggest that IL-1beta mediates the major stimulus for ICAM-1 induction which is possibly a necessary but not sufficient step in the process of beta-cell destruction. |
| 10419 | 12788886 | A combination of human leukocyte antigen DQB1*02 and the tumor necrosis factor alpha promoter G308A polymorphism predisposes to an insulin-deficient phenotype in patients with type 2 diabetes. |
| 10420 | 12788886 | A combination of human leukocyte antigen DQB1*02 and the tumor necrosis factor alpha promoter G308A polymorphism predisposes to an insulin-deficient phenotype in patients with type 2 diabetes. |
| 10421 | 12788886 | To study whether the TNF alpha gene could be such a modifying gene, we studied TNF alpha promoter polymorphisms (G-->A substitution at positions -308 and -238) in relation to HLA-DQB1 genotypes in type 2 patients from mixed type 1/2 families or common type 2 diabetes families as well as in patients with adult-onset type 1 diabetes and control subjects. |
| 10422 | 12788886 | To study whether the TNF alpha gene could be such a modifying gene, we studied TNF alpha promoter polymorphisms (G-->A substitution at positions -308 and -238) in relation to HLA-DQB1 genotypes in type 2 patients from mixed type 1/2 families or common type 2 diabetes families as well as in patients with adult-onset type 1 diabetes and control subjects. |
| 10423 | 12788878 | We aimed to study the interaction of adiponectin with chronic inflammation and known components of the insulin resistance syndrome. |
| 10424 | 12788878 | Insulin sensitivity (minimal model analysis) and plasma soluble fractions of TNF-alpha receptor 1 (sTNFR1) and 2 (sTNFR2), adrenal and thyroid function, and adiponectin were evaluated in 68 apparently healthy subjects. |
| 10425 | 12788878 | As expected also, circulating adiponectin was significantly associated with waist to hip ratio (r = -0.28; P = 0.013), diastolic blood pressure (r = -0.25; P = 0.027), fasting plasma high-density lipoprotein cholesterol (r = 0.35; P = 0.001), triglycerides (r = -0.37; P = 0.001), and insulin sensitivity (r = 0.30; P = 0.011). |
| 10426 | 12788878 | Predictive variables in these models included insulin sensitivity, waist to hip ratio and free T(4), contributing to 17%, 10%, and 8% of adiponectin variance, respectively, These findings suggest that circulating adiponectin differentially modulates insulin action and that thyroid-axis, inflammatory cytokines, and the adrenal cortex might intervene in this modulation. |
| 10427 | 12788833 | Other accompanying abnormalities may include elevated levels of leptin, TNFalpha, tissue plasminogen activator, plasminogen activator inhibitor-1, and testosterone. |
| 10428 | 12788800 | Atherosclerosis and insulin resistance share similar pathophysiological mechanisms, mainly due to the actions of the two major proinflammatory cytokines, TNF-alpha and IL-6. |
| 10429 | 12767912 | Heme oxygenase-1 fused to a TAT peptide transduces and protects pancreatic beta-cells. |
| 10430 | 12767912 | We have generated a fusion protein composed of HO-1 and TAT protein transduction domain (TAT/PTD), an 11-aa cell penetrating peptide from the human immunodeficiency virus TAT protein. |
| 10431 | 12767912 | Transduction of TAT/PTD-HO-1 to insulin-producing cells protects against TNF-alpha-mediated cytotoxicity. |
| 10432 | 12767912 | TAT/PTD-HO-1 transduction to islets does not impair islet physiology, as assessed by reversion of chemically induced diabetes in immunodeficient mice. |
| 10433 | 12765944 | Involvement of AMP-activated protein kinase in glucose uptake stimulated by the globular domain of adiponectin in primary rat adipocytes. |
| 10434 | 12765944 | Adiponectin is an abundant adipocyte-derived plasma protein with anti-atherosclerotic and insulin-sensitizing properties that suppresses hepatic glucose production and enhances glucose uptake into skeletal muscle. |
| 10435 | 12765944 | Globular adiponectin increased glucose uptake in adipocytes without stimulating tyrosine phosphorylation of the insulin receptor or insulin receptor substrate-1, and without enhancing phosphorylation of Akt on Ser-473. |
| 10436 | 12765944 | Globular adiponectin further enhanced insulin-stimulated glucose uptake at submaximal insulin concentrations and reversed the inhibitory effect of tumor necrosis factor-alpha on insulin-stimulated glucose uptake. |
| 10437 | 12765944 | Cellular treatment with globular adiponectin increased the Thr-172 phosphorylation and catalytic activity of AMP-activated protein kinase and enhanced the Ser-79 phosphorylation of acetyl CoA carboxylase, an enzyme downstream of AMP kinase in adipose cells. |
| 10438 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10439 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10440 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10441 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10442 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10443 | 12759891 | Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. |
| 10444 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10445 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10446 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10447 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10448 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10449 | 12759891 | To compare levels of interleukin (IL)-18, tumor necrosis factor-alpha (TNF-alpha), and IL-6 in serum, we studied 151 type 2 diabetes mellitus patients with various degrees of nephropathy, as well as 80 healthy volunteers. |
| 10450 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10451 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10452 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10453 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10454 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10455 | 12759891 | IL-18, TNF-alpha, and IL-6 in serum were measured using an enzyme-linked immunosorbent assay (ELISA) with the respective mouse monoclonal antibodies. |
| 10456 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10457 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10458 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10459 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10460 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10461 | 12759891 | Significant differences in serum levels of IL-18 and TNF-alpha were observed between the patients and control subjects (IL-18, 278.0 +/- 11.9 pg/mL v 172.8 +/- 7.7 pg/mL, P <.0001; TNF-alpha, 2.41 +/- 0.18 pg/mL v 0.46 +/- 0.18 pg/mL, P <.0001), whereas that of IL-6 was not different between the two groups (0.73 +/- 0.10 pg/mL v 0.65 +/- 0.08 pg/mL, difference not significant [NS]), although patients with nephropathy showed higher levels. |
| 10462 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10463 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10464 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10465 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10466 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10467 | 12759891 | In addition, IL-18 levels were increased in diabetic patients with the development of urinary albumin excretion, with the highest found in those with microalbuminuria (<30 micro g/mg creatinine, 252.7 +/- 16.4 pg/mL; 30 to >300 micro g/mg creatinine, 352.7 +/- 35.2 pg/mL; >>300 micro g/mg creatinine, 350.0 +/- 16.0 pg/mL). |
| 10468 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10469 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10470 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10471 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10472 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10473 | 12759891 | Similarly, TNF-alpha and IL-6 in diabetic patients with microalbuminuria or clinical albuminuria were significantly increased as compared with those without albuminuria (TNF-alpha, 3.20 +/- 0.41 pg/mL v 1.94 +/- 0.18 pg/mL; IL-6, 1.64 +/- 1.11 pg/mL v 0.51 +/- 0.05 pg/mL, P <.05, respectively). |
| 10474 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10475 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10476 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10477 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10478 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10479 | 12759891 | These results suggest that serum levels of IL-18, TNF-alpha, and IL-6 may have some etiopathogenic roles in diabetic nephropathy. |
| 10480 | 12759426 | IL-12 administration accelerates autoimmune diabetes in both wild-type and IFN-gamma-deficient nonobese diabetic mice, revealing pathogenic and protective effects of IL-12-induced IFN-gamma. |
| 10481 | 12759426 | IL-12 administration to nonobese diabetic (NOD) mice induces IFN-gamma-secreting type 1 T cells and high circulating IFN-gamma levels and accelerates insulin-dependent diabetes mellitus (IDDM). |
| 10482 | 12759426 | Here we show that IL-12-induced IFN-gamma production is dispensable for diabetes acceleration, because exogenous IL-12 could enhance IDDM development in IFN-gamma-deficient as well as in IFN-gamma-sufficient NOD mice. |
| 10483 | 12759426 | Both in IFN-gamma(+/-) and IFN-gamma(-/-) NOD mice, IL-12 administration generates a massive and destructive insulitis characterized by T cells, macrophages, and CD11c(+) dendritic cells, and increases the number of pancreatic CD4(+) cells secreting IL-2 and TNF-alpha. |
| 10484 | 12759426 | Surprisingly, IL-12-induced IFN-gamma hinders pancreatic B cell infiltration and inhibits the capacity of APCs to activate T cells. |
| 10485 | 12759426 | Although pancreatic CD4(+) T cells from IL-12-treated IFN-gamma(-/-) mice fail to up-regulate the P-selectin ligand, suggesting that their entry into the pancreas may be impaired, T cell expansion is favored in these mice compared with IL-12-treated IFN-gamma(+/-) mice because IL-12 administration in the absence of IFN-gamma leads to enhanced cell proliferation and reduced T cell apoptosis. |
| 10486 | 12759426 | NO, an effector molecule in beta cell destruction, is produced ex vivo in high quantity by pancreas-infiltrating cells through a mechanism involving IL-12-induced IFN-gamma. |
| 10487 | 12759426 | Conversely, in IL-12-treated IFN-gamma-deficient mice, other pathways of beta cell death appear to be increased, as indicated by the up-regulated expression of Fas ligand on Th1 cells in the absence of IFN-gamma. |
| 10488 | 12759426 | These data demonstrate that IFN-gamma has a dual role, pathogenic and protective, in IDDM development, and its deletion allows IL-12 to establish alternative pathways leading to diabetes acceleration. |
| 10489 | 12753658 | Tumor necrosis factor-alpha (TNF-alpha) expression is linked with insulin resistance, and is under strong genetic control. |
| 10490 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10491 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10492 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10493 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10494 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10495 | 12746279 | The angiotensin II type 1 receptor mediates renal interstitial content of tumor necrosis factor-alpha in diabetic rats. |
| 10496 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10497 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10498 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10499 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10500 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10501 | 12746279 | A unique microdialysis technique was used to demonstrate that increased levels of angiotensin II (Ang II) and consequent stimulation of the Ang II type 1 (AT(1)) receptor increase the renal content of TNF-alpha in diabetes. |
| 10502 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10503 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10504 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10505 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10506 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10507 | 12746279 | Recovery of Ang II and TNF-alpha in renal interstitial fluid (RIF) was measured in conscious rats before and weekly for 12 wk after induction of diabetes with streptozocin and in response to oral valsartan (10 mg/kg.d). |
| 10508 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10509 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10510 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10511 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10512 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10513 | 12746279 | AT(1) receptor blockade with valsartan prevented the increase in TNF-alpha in the diabetic group. |
| 10514 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10515 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10516 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10517 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10518 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10519 | 12746279 | This study shows that diabetes is associated with an increase in the vasoconstrictive hormone Ang II and the inflammatory cytokine TNF-alpha, both of which play a role in accelerating renal function decline in diabetic nephropathy. |
| 10520 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10521 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10522 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10523 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10524 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10525 | 12746279 | The study also confirms that valsartan reduces intrarenal level of TNF-alpha by acting on Ang II at the AT(1) receptor level. |
| 10526 | 12742378 | We have recently described an impaired proliferative response of CD4(+) T-cells to primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. |
| 10527 | 12742378 | In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the immune response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). |
| 10528 | 12742378 | Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the immune response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). |
| 10529 | 12742378 | Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). |
| 10530 | 12742378 | When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. |
| 10531 | 12741355 | The following parameters were examined: cardiohaemodynamics, the content of cortisol, insulin, ACTH, TTH and thyroxin in blood, of transport proteins and of the concentration of IL-1 and TNF-alpha in blood. |
| 10532 | 12734774 | Interleukin (IL)-6 mRNA expression is stimulated by insulin, isoproterenol, tumour necrosis factor alpha, growth hormone, and IL-6 in 3T3-L1 adipocytes. |
| 10533 | 12734774 | Interleukin (IL)-6 mRNA expression is stimulated by insulin, isoproterenol, tumour necrosis factor alpha, growth hormone, and IL-6 in 3T3-L1 adipocytes. |
| 10534 | 12734774 | Interleukin (IL)-6 mRNA expression is stimulated by insulin, isoproterenol, tumour necrosis factor alpha, growth hormone, and IL-6 in 3T3-L1 adipocytes. |
| 10535 | 12734774 | For further evaluation of IL-6 gene expression regulation, fully differentiated 3T3-L1 adipocytes were treated with various hormones known to induce insulin resistance. |
| 10536 | 12734774 | For further evaluation of IL-6 gene expression regulation, fully differentiated 3T3-L1 adipocytes were treated with various hormones known to induce insulin resistance. |
| 10537 | 12734774 | For further evaluation of IL-6 gene expression regulation, fully differentiated 3T3-L1 adipocytes were treated with various hormones known to induce insulin resistance. |
| 10538 | 12734774 | Interestingly, treatment of adipocytes with 100 nM insulin, 10 micro M isoproterenol, 10 ng/ml tumour necrosis factor alpha (TNFalpha), and 500 ng/ml growth hormone (GH) for 16 h stimulated IL-6 mRNA expression 2.3-fold, 47-fold, 74-fold, and 1.4-fold, respectively (p < 0.01). |
| 10539 | 12734774 | Interestingly, treatment of adipocytes with 100 nM insulin, 10 micro M isoproterenol, 10 ng/ml tumour necrosis factor alpha (TNFalpha), and 500 ng/ml growth hormone (GH) for 16 h stimulated IL-6 mRNA expression 2.3-fold, 47-fold, 74-fold, and 1.4-fold, respectively (p < 0.01). |
| 10540 | 12734774 | Interestingly, treatment of adipocytes with 100 nM insulin, 10 micro M isoproterenol, 10 ng/ml tumour necrosis factor alpha (TNFalpha), and 500 ng/ml growth hormone (GH) for 16 h stimulated IL-6 mRNA expression 2.3-fold, 47-fold, 74-fold, and 1.4-fold, respectively (p < 0.01). |
| 10541 | 12734774 | Furthermore, stimulation of IL-6 expression was time-dependent with maximal stimulatory effects detectable after 1 h of insulin, isoproterenol, and GH addition and 12 h of TNFalpha, respectively. |
| 10542 | 12734774 | Furthermore, stimulation of IL-6 expression was time-dependent with maximal stimulatory effects detectable after 1 h of insulin, isoproterenol, and GH addition and 12 h of TNFalpha, respectively. |
| 10543 | 12734774 | Furthermore, stimulation of IL-6 expression was time-dependent with maximal stimulatory effects detectable after 1 h of insulin, isoproterenol, and GH addition and 12 h of TNFalpha, respectively. |
| 10544 | 12734774 | Taken together, our results demonstrate that IL-6 expression in adipocytes is governed by an autocrine positive feedback loop and upregulated by insulin, isoproterenol, TNFalpha, and GH. |
| 10545 | 12734774 | Taken together, our results demonstrate that IL-6 expression in adipocytes is governed by an autocrine positive feedback loop and upregulated by insulin, isoproterenol, TNFalpha, and GH. |
| 10546 | 12734774 | Taken together, our results demonstrate that IL-6 expression in adipocytes is governed by an autocrine positive feedback loop and upregulated by insulin, isoproterenol, TNFalpha, and GH. |
| 10547 | 12734774 | In concert with this adipocytokine's upregulation in states of decreased insulin sensitivity such as obesity and diabetes, the data support a possible role of IL-6 as a selectively regulated mediator of insulin resistance. |
| 10548 | 12734774 | In concert with this adipocytokine's upregulation in states of decreased insulin sensitivity such as obesity and diabetes, the data support a possible role of IL-6 as a selectively regulated mediator of insulin resistance. |
| 10549 | 12734774 | In concert with this adipocytokine's upregulation in states of decreased insulin sensitivity such as obesity and diabetes, the data support a possible role of IL-6 as a selectively regulated mediator of insulin resistance. |
| 10550 | 12734773 | Reports have suggested that adipose tissue-derived cytokines such as tumor necrosis factor-alpha, interleukin-6 and interleukin-8 could be involved in the development of these health complications. |
| 10551 | 12734773 | Ovariectomy significantly increased interleukin-6 gene expression (p < 0.05) as well as interleukin-8 protein levels (p < 0.05) and gene expression (p < 0.05) in the adipose tissue, and estrogen replacement significantly reversed this increase (p < 0.05). |
| 10552 | 12734773 | In conclusion, estrogen-deficient rats were found to have increased production of interleukin-6 and interleukin-8, which could be attenuated by estrogen-replacement. |
| 10553 | 12732648 | Troglitazone antagonizes tumor necrosis factor-alpha-induced reprogramming of adipocyte gene expression by inhibiting the transcriptional regulatory functions of NF-kappaB. |
| 10554 | 12732648 | Troglitazone antagonizes tumor necrosis factor-alpha-induced reprogramming of adipocyte gene expression by inhibiting the transcriptional regulatory functions of NF-kappaB. |
| 10555 | 12732648 | Troglitazone antagonizes tumor necrosis factor-alpha-induced reprogramming of adipocyte gene expression by inhibiting the transcriptional regulatory functions of NF-kappaB. |
| 10556 | 12732648 | Troglitazone (TGZ), a member of the thiazolidinedione class of anti-diabetic compounds and a peroxisome proliferator activator receptor-gamma (PPAR-gamma) agonist, restores systemic insulin sensitivity and improves the full insulin resistance syndrome in vivo. |
| 10557 | 12732648 | Troglitazone (TGZ), a member of the thiazolidinedione class of anti-diabetic compounds and a peroxisome proliferator activator receptor-gamma (PPAR-gamma) agonist, restores systemic insulin sensitivity and improves the full insulin resistance syndrome in vivo. |
| 10558 | 12732648 | Troglitazone (TGZ), a member of the thiazolidinedione class of anti-diabetic compounds and a peroxisome proliferator activator receptor-gamma (PPAR-gamma) agonist, restores systemic insulin sensitivity and improves the full insulin resistance syndrome in vivo. |
| 10559 | 12732648 | Here we investigated the potential functional interaction between PPAR-gamma and NF-kappaB in adipocytes. |
| 10560 | 12732648 | Here we investigated the potential functional interaction between PPAR-gamma and NF-kappaB in adipocytes. |
| 10561 | 12732648 | Here we investigated the potential functional interaction between PPAR-gamma and NF-kappaB in adipocytes. |
| 10562 | 12732648 | We show that TGZ selectively blocked tumor necrosis factor-alpha-induced and NF-kappaB-dependent repression of multiple adipocyte-specific genes and induction of growth phase and other genes. |
| 10563 | 12732648 | We show that TGZ selectively blocked tumor necrosis factor-alpha-induced and NF-kappaB-dependent repression of multiple adipocyte-specific genes and induction of growth phase and other genes. |
| 10564 | 12732648 | We show that TGZ selectively blocked tumor necrosis factor-alpha-induced and NF-kappaB-dependent repression of multiple adipocyte-specific genes and induction of growth phase and other genes. |
| 10565 | 12732648 | Notably, the expressions of some tumor necrosis factor-alpha-induced genes in adipocytes were unaffected by PPAR-gamma activation. |
| 10566 | 12732648 | Notably, the expressions of some tumor necrosis factor-alpha-induced genes in adipocytes were unaffected by PPAR-gamma activation. |
| 10567 | 12732648 | Notably, the expressions of some tumor necrosis factor-alpha-induced genes in adipocytes were unaffected by PPAR-gamma activation. |
| 10568 | 12732648 | In reporter gene assays in HeLa cells, ectopic expression of PPAR-gamma abolished induction of a NF-kappaB-responsive reporter gene by the p65 subunit (RelA) of NF-kappaB, and the inhibition was further enhanced in the presence of TGZ. |
| 10569 | 12732648 | In reporter gene assays in HeLa cells, ectopic expression of PPAR-gamma abolished induction of a NF-kappaB-responsive reporter gene by the p65 subunit (RelA) of NF-kappaB, and the inhibition was further enhanced in the presence of TGZ. |
| 10570 | 12732648 | In reporter gene assays in HeLa cells, ectopic expression of PPAR-gamma abolished induction of a NF-kappaB-responsive reporter gene by the p65 subunit (RelA) of NF-kappaB, and the inhibition was further enhanced in the presence of TGZ. |
| 10571 | 12732648 | Conversely, overexpression of p65 inhibited induction of a PPAR-gamma-responsive reporter gene by activated PPAR-gamma in a dose-dependent manner. |
| 10572 | 12732648 | Conversely, overexpression of p65 inhibited induction of a PPAR-gamma-responsive reporter gene by activated PPAR-gamma in a dose-dependent manner. |
| 10573 | 12732648 | Conversely, overexpression of p65 inhibited induction of a PPAR-gamma-responsive reporter gene by activated PPAR-gamma in a dose-dependent manner. |
| 10574 | 12732648 | Other NF-kappaB family members, p50 and c-Rel as well as the S276A mutant of p65, blocked PPAR-gamma-mediated gene transcription less effectively. |
| 10575 | 12732648 | Other NF-kappaB family members, p50 and c-Rel as well as the S276A mutant of p65, blocked PPAR-gamma-mediated gene transcription less effectively. |
| 10576 | 12732648 | Other NF-kappaB family members, p50 and c-Rel as well as the S276A mutant of p65, blocked PPAR-gamma-mediated gene transcription less effectively. |
| 10577 | 12732648 | Thus, p65 antagonizes the transcriptional regulatory activity of PPAR-gamma in adipocytes, and PPAR-gamma activation can at least partially override the inhibitory effects of p65 on the expression of key adipocyte genes. |
| 10578 | 12732648 | Thus, p65 antagonizes the transcriptional regulatory activity of PPAR-gamma in adipocytes, and PPAR-gamma activation can at least partially override the inhibitory effects of p65 on the expression of key adipocyte genes. |
| 10579 | 12732648 | Thus, p65 antagonizes the transcriptional regulatory activity of PPAR-gamma in adipocytes, and PPAR-gamma activation can at least partially override the inhibitory effects of p65 on the expression of key adipocyte genes. |
| 10580 | 12732648 | Our data suggest that inhibition of NF-kappaB activity is a mechanism by which PPAR-gamma agonists improve insulin sensitivity in vivo and that adipocyte NF-kappaB is a potential therapeutic target for obesity-linked type 2 diabetes. |
| 10581 | 12732648 | Our data suggest that inhibition of NF-kappaB activity is a mechanism by which PPAR-gamma agonists improve insulin sensitivity in vivo and that adipocyte NF-kappaB is a potential therapeutic target for obesity-linked type 2 diabetes. |
| 10582 | 12732648 | Our data suggest that inhibition of NF-kappaB activity is a mechanism by which PPAR-gamma agonists improve insulin sensitivity in vivo and that adipocyte NF-kappaB is a potential therapeutic target for obesity-linked type 2 diabetes. |
| 10583 | 12716761 | RT-PCR analysis further confirmed that HG significantly increased the expression of monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, beta(2)-integrin, interleukin-1beta, and others. |
| 10584 | 12716761 | HG-induced MCP-1 mRNA expression and monocyte adhesion were blocked by specific inhibitors of oxidant stress, protein kinase C, ERK1/2, and p38 mitogen-activated protein kinases. |
| 10585 | 12716748 | Recent studies incriminating tumor necrosis factor (TNF)-alpha as the final effector in pancreatic beta-cell death in type 1 diabetes underscore the potential role of TNF-alpha-dependent NF-kappaB activation as an important modulator of pancreatic beta-cell death in autoimmune diabetes. |
| 10586 | 12716748 | Recent studies incriminating tumor necrosis factor (TNF)-alpha as the final effector in pancreatic beta-cell death in type 1 diabetes underscore the potential role of TNF-alpha-dependent NF-kappaB activation as an important modulator of pancreatic beta-cell death in autoimmune diabetes. |
| 10587 | 12716748 | Recent studies incriminating tumor necrosis factor (TNF)-alpha as the final effector in pancreatic beta-cell death in type 1 diabetes underscore the potential role of TNF-alpha-dependent NF-kappaB activation as an important modulator of pancreatic beta-cell death in autoimmune diabetes. |
| 10588 | 12716748 | Recent studies incriminating tumor necrosis factor (TNF)-alpha as the final effector in pancreatic beta-cell death in type 1 diabetes underscore the potential role of TNF-alpha-dependent NF-kappaB activation as an important modulator of pancreatic beta-cell death in autoimmune diabetes. |
| 10589 | 12716748 | Recent studies incriminating tumor necrosis factor (TNF)-alpha as the final effector in pancreatic beta-cell death in type 1 diabetes underscore the potential role of TNF-alpha-dependent NF-kappaB activation as an important modulator of pancreatic beta-cell death in autoimmune diabetes. |
| 10590 | 12716748 | We studied the role of NF-kappaB activation in pancreatic islet cell death by using a gamma-interferon (IFN-gamma)/TNF-alpha synergism model we had previously reported. |
| 10591 | 12716748 | We studied the role of NF-kappaB activation in pancreatic islet cell death by using a gamma-interferon (IFN-gamma)/TNF-alpha synergism model we had previously reported. |
| 10592 | 12716748 | We studied the role of NF-kappaB activation in pancreatic islet cell death by using a gamma-interferon (IFN-gamma)/TNF-alpha synergism model we had previously reported. |
| 10593 | 12716748 | We studied the role of NF-kappaB activation in pancreatic islet cell death by using a gamma-interferon (IFN-gamma)/TNF-alpha synergism model we had previously reported. |
| 10594 | 12716748 | We studied the role of NF-kappaB activation in pancreatic islet cell death by using a gamma-interferon (IFN-gamma)/TNF-alpha synergism model we had previously reported. |
| 10595 | 12716748 | The NF-kappaB DNA-binding nuclear complex activated by TNF-alpha contained both the p65 and p50 subunit. |
| 10596 | 12716748 | The NF-kappaB DNA-binding nuclear complex activated by TNF-alpha contained both the p65 and p50 subunit. |
| 10597 | 12716748 | The NF-kappaB DNA-binding nuclear complex activated by TNF-alpha contained both the p65 and p50 subunit. |
| 10598 | 12716748 | The NF-kappaB DNA-binding nuclear complex activated by TNF-alpha contained both the p65 and p50 subunit. |
| 10599 | 12716748 | The NF-kappaB DNA-binding nuclear complex activated by TNF-alpha contained both the p65 and p50 subunit. |
| 10600 | 12716748 | IFN-gamma pretreatment did not affect TNF-alpha-induced NF-kappaB activation. |
| 10601 | 12716748 | IFN-gamma pretreatment did not affect TNF-alpha-induced NF-kappaB activation. |
| 10602 | 12716748 | IFN-gamma pretreatment did not affect TNF-alpha-induced NF-kappaB activation. |
| 10603 | 12716748 | IFN-gamma pretreatment did not affect TNF-alpha-induced NF-kappaB activation. |
| 10604 | 12716748 | IFN-gamma pretreatment did not affect TNF-alpha-induced NF-kappaB activation. |
| 10605 | 12716748 | Specific inhibition of NF-kappaB activation by adenoviral transduction of IkappaB "superrepressor" also sensitized insulinoma cells and primary islet beta-cells to TNF-alpha-induced apoptosis. |
| 10606 | 12716748 | Specific inhibition of NF-kappaB activation by adenoviral transduction of IkappaB "superrepressor" also sensitized insulinoma cells and primary islet beta-cells to TNF-alpha-induced apoptosis. |
| 10607 | 12716748 | Specific inhibition of NF-kappaB activation by adenoviral transduction of IkappaB "superrepressor" also sensitized insulinoma cells and primary islet beta-cells to TNF-alpha-induced apoptosis. |
| 10608 | 12716748 | Specific inhibition of NF-kappaB activation by adenoviral transduction of IkappaB "superrepressor" also sensitized insulinoma cells and primary islet beta-cells to TNF-alpha-induced apoptosis. |
| 10609 | 12716748 | Specific inhibition of NF-kappaB activation by adenoviral transduction of IkappaB "superrepressor" also sensitized insulinoma cells and primary islet beta-cells to TNF-alpha-induced apoptosis. |
| 10610 | 12716741 | Genes in the early region 3 (E3) of the adenovirus genome allow the virus to evade host immune responses by interfering with major histocompatibility (MHC) class I-mediated antigen presentation and tumor necrosis factor-alpha (TNF-alpha)- or Fas-induced apoptosis of infected cells. |
| 10611 | 12716741 | Genes in the early region 3 (E3) of the adenovirus genome allow the virus to evade host immune responses by interfering with major histocompatibility (MHC) class I-mediated antigen presentation and tumor necrosis factor-alpha (TNF-alpha)- or Fas-induced apoptosis of infected cells. |
| 10612 | 12716741 | Strong T1D protection mediated at the beta-cell level characterized DL704/NOD mice lacking the E3 gp19K gene suppressing MHC class I expression but retaining the 10.4K, 14.5K, and 14.7K genes inhibiting Fas- or TNF-alpha-induced apoptosis and TNF-alpha-induced NF-kB activation. |
| 10613 | 12716741 | Strong T1D protection mediated at the beta-cell level characterized DL704/NOD mice lacking the E3 gp19K gene suppressing MHC class I expression but retaining the 10.4K, 14.5K, and 14.7K genes inhibiting Fas- or TNF-alpha-induced apoptosis and TNF-alpha-induced NF-kB activation. |
| 10614 | 12715715 | [TNF-alpha PC-1 gene polymorphisms and pre-diabetes quantitative features in the Polish population]. |
| 10615 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10616 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10617 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10618 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10619 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10620 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10621 | 12714600 | Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases. |
| 10622 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10623 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10624 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10625 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10626 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10627 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10628 | 12714600 | In this study, we analyzed the effects of aspirin (acetylsalicylic acid) on serine phosphorylation of insulin receptor substrate 1 (IRS-1) in cells treated with tumor necrosis factor (TNF)-alpha. |
| 10629 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10630 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10631 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10632 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10633 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10634 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10635 | 12714600 | In 3T3-L1 and Hep G2 cells, phosphorylation of IRS-1 at Ser307 in response to TNF-alpha treatment correlated with phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10636 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10637 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10638 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10639 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10640 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10641 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10642 | 12714600 | Moreover, phosphorylation of IRS-1 at Ser307 in embryo fibroblasts derived from either JNK or IKK knockout mice was reduced when compared with that in the wild-type controls. |
| 10643 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10644 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10645 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10646 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10647 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10648 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10649 | 12714600 | Taken together, these data suggest that serine phosphorylation of IRS-1 in response to TNF-alpha is mediated, in part, by JNK and IKK. |
| 10650 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10651 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10652 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10653 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10654 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10655 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10656 | 12714600 | Interestingly, aspirin treatment inhibited the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha. |
| 10657 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10658 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10659 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10660 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10661 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10662 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10663 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 10664 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10665 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10666 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10667 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10668 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10669 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10670 | 12714600 | Phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha was inhibited by aspirin treatment. |
| 10671 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10672 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10673 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10674 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10675 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10676 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10677 | 12714600 | Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. |
| 10678 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10679 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10680 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10681 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10682 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10683 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10684 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10685 | 12714258 | Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes. |
| 10686 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10687 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10688 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10689 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10690 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10691 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10692 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10693 | 12714258 | The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. |
| 10694 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10695 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10696 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10697 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10698 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10699 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10700 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10701 | 12714258 | Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. |
| 10702 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10703 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10704 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10705 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10706 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10707 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10708 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10709 | 12714258 | TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. |
| 10710 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10711 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10712 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10713 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10714 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10715 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10716 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10717 | 12714258 | TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. |
| 10718 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10719 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10720 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10721 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10722 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10723 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10724 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10725 | 12714258 | TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. |
| 10726 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10727 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10728 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10729 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10730 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10731 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10732 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10733 | 12714258 | In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. |
| 10734 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10735 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10736 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10737 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10738 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10739 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10740 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10741 | 12714258 | Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing. |
| 10742 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 10743 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 10744 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 10745 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 10746 | 12713258 | Serum IL-1, IL-2, TNFalpha and INFgamma levels of patients with type 1 diabetes mellitus and their siblings. |
| 10747 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 10748 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 10749 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 10750 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 10751 | 12713258 | The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. |
| 10752 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 10753 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 10754 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 10755 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 10756 | 12713258 | IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. |
| 10757 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 10758 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 10759 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 10760 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 10761 | 12713258 | IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. |
| 10762 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 10763 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 10764 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 10765 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 10766 | 12713258 | In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus. |
| 10767 | 12706864 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to exert potent cytotoxic activity against many tumor cells but not normal cells. |
| 10768 | 12706864 | We found that most TRAIL-resistant and -partial resistant clones expressed low levels of DR5, whereas most TRAIL-sensitive clones expressed high levels of Death Receptor (DR5). |
| 10769 | 12706864 | However, there were clones with a range of different TRAIL-sensitivities that had similar levels of DR5 expression. |
| 10770 | 12706864 | The expression levels of DR4 and the decoy receptors, DcR1 and DcR2, did not correlate with TRAIL sensitivities. |
| 10771 | 12706864 | We also compared the subgroups in terms of the expression of Fas-associated death domain protein (FADD), the levels of activation of Receptor Interacting Protein (RIP) and caspases, and cleavage of Poly (ADP-Ribose)Polymerase (PARP). |
| 10772 | 12706864 | After treatment with TRAIL, both TRAIL-sensitive and partial resistant clones showed high levels of activation of caspase-3, caspase-8, RIP and PARP. |
| 10773 | 12706864 | Relative basal level and induced level of Phosphoprotein over Expressed in Diabetes/Phosphoprotein Enriched in Astrocytes (PED/PEA-15) after TRAIL treatment were compared in the clones. |
| 10774 | 12706864 | TRAIL did not change the PED/PEA-15 level in the clones. |
| 10775 | 12706864 | In addition, transduction and expression of the dominant negative form of the I-kBalpha gene did not change TRAIL-sensitivities. |
| 10776 | 12706864 | Our results showed that the expression levels of DR5, the activation levels of caspase-8, -3 and RIP were critical factors in determining TRAIL-sensitivities in Jurkat cells. |
| 10777 | 12703882 | On-line production of ultrapure substitution fluid reduces TNF-alpha- and IL-6 release in patients on hemodiafiltration therapy. |
| 10778 | 12703882 | On-line production of ultrapure substitution fluid reduces TNF-alpha- and IL-6 release in patients on hemodiafiltration therapy. |
| 10779 | 12703882 | On-line production of ultrapure substitution fluid reduces TNF-alpha- and IL-6 release in patients on hemodiafiltration therapy. |
| 10780 | 12703882 | On-line production of ultrapure substitution fluid reduces TNF-alpha- and IL-6 release in patients on hemodiafiltration therapy. |
| 10781 | 12703882 | In this study, 8 patients undergoing bag-HDF treatment with lactate buffered solution were investigated before on-line HDF treatment with commercially available whole blood stimulation assays testing for TNF-alpha and IL-6 release. |
| 10782 | 12703882 | In this study, 8 patients undergoing bag-HDF treatment with lactate buffered solution were investigated before on-line HDF treatment with commercially available whole blood stimulation assays testing for TNF-alpha and IL-6 release. |
| 10783 | 12703882 | In this study, 8 patients undergoing bag-HDF treatment with lactate buffered solution were investigated before on-line HDF treatment with commercially available whole blood stimulation assays testing for TNF-alpha and IL-6 release. |
| 10784 | 12703882 | In this study, 8 patients undergoing bag-HDF treatment with lactate buffered solution were investigated before on-line HDF treatment with commercially available whole blood stimulation assays testing for TNF-alpha and IL-6 release. |
| 10785 | 12703882 | Both assays are based on phytohemagglutinine (for TNF) and lipo-polysaccharide stimulation (for IL-6). |
| 10786 | 12703882 | Both assays are based on phytohemagglutinine (for TNF) and lipo-polysaccharide stimulation (for IL-6). |
| 10787 | 12703882 | Both assays are based on phytohemagglutinine (for TNF) and lipo-polysaccharide stimulation (for IL-6). |
| 10788 | 12703882 | Both assays are based on phytohemagglutinine (for TNF) and lipo-polysaccharide stimulation (for IL-6). |
| 10789 | 12703882 | The Wilcoxon test (for paired analysis) was done, revealing a statistically significant lower release of proinflammtory cytokines from patients' blood upon stimulation with PHA or LPS. |
| 10790 | 12703882 | The Wilcoxon test (for paired analysis) was done, revealing a statistically significant lower release of proinflammtory cytokines from patients' blood upon stimulation with PHA or LPS. |
| 10791 | 12703882 | The Wilcoxon test (for paired analysis) was done, revealing a statistically significant lower release of proinflammtory cytokines from patients' blood upon stimulation with PHA or LPS. |
| 10792 | 12703882 | The Wilcoxon test (for paired analysis) was done, revealing a statistically significant lower release of proinflammtory cytokines from patients' blood upon stimulation with PHA or LPS. |
| 10793 | 12703882 | The reduction of IL-6 and TNF concentration and release capacity in whole blood may be attributed to the use of high quality ultrapure substitution fluid and dialysate in on-line treatment instead of lactate buffer bag solution. |
| 10794 | 12703882 | The reduction of IL-6 and TNF concentration and release capacity in whole blood may be attributed to the use of high quality ultrapure substitution fluid and dialysate in on-line treatment instead of lactate buffer bag solution. |
| 10795 | 12703882 | The reduction of IL-6 and TNF concentration and release capacity in whole blood may be attributed to the use of high quality ultrapure substitution fluid and dialysate in on-line treatment instead of lactate buffer bag solution. |
| 10796 | 12703882 | The reduction of IL-6 and TNF concentration and release capacity in whole blood may be attributed to the use of high quality ultrapure substitution fluid and dialysate in on-line treatment instead of lactate buffer bag solution. |
| 10797 | 12697153 | The mRNA levels of IFN-gamma, IL-10, TNF-alpha, TGF-beta, and inducible NO synthase in the small intestine and the Peyer's patches were determined by semi-quantitative RT-PCR. |
| 10798 | 12697153 | The mRNA levels of IFN-gamma, IL-10, TNF-alpha, TGF-beta, and inducible NO synthase in the small intestine and the Peyer's patches were determined by semi-quantitative RT-PCR. |
| 10799 | 12697153 | Mice fed on the cereal-based NTP-2000 diet expressed higher levels of the Th1-type and pro-inflammatory markers IFN-gamma, TNF-alpha, and inducible NO synthase mRNA compared to the Prosobee-fed animals. |
| 10800 | 12697153 | Mice fed on the cereal-based NTP-2000 diet expressed higher levels of the Th1-type and pro-inflammatory markers IFN-gamma, TNF-alpha, and inducible NO synthase mRNA compared to the Prosobee-fed animals. |
| 10801 | 12697153 | The expression of the counterregulatory cytokines IL-10 and TGF-beta was unaffected. |
| 10802 | 12697153 | The expression of the counterregulatory cytokines IL-10 and TGF-beta was unaffected. |
| 10803 | 12693661 | Moreover, RT-PCR revealed significant augmentation of macrophages-associated inflammatory molecules (IL-1beta, IL-6, TNF-alpha, and MCP-1) in islets from a BD donor. |
| 10804 | 12690081 | Systemic inflammation, adipose tissue tumor necrosis factor, and leptin expression. |
| 10805 | 12678860 | Finally, we emphasize the possibilities for adipokine-targeted pharmacology in adiponectin (Acrp30, apM1, AdipoQ, GBP28), angiotensin II, estrogens, nerve growth factor, tumor necrosis factor-alpha, and also adipose mast cells. |
| 10806 | 12670740 | The adipocyte in insulin resistance: key molecules and the impact of the thiazolidinediones. |
| 10807 | 12670740 | The adipocyte in insulin resistance: key molecules and the impact of the thiazolidinediones. |
| 10808 | 12670740 | This article reviews factors released from adipose tissue that could contribute to the development of insulin resistance and beta-cell dysfunction, including tumour necrosis factor alpha (TNF-alpha), free fatty acids (FFAs), adiponectin, resistin and leptin. |
| 10809 | 12670740 | This article reviews factors released from adipose tissue that could contribute to the development of insulin resistance and beta-cell dysfunction, including tumour necrosis factor alpha (TNF-alpha), free fatty acids (FFAs), adiponectin, resistin and leptin. |
| 10810 | 12670740 | It also considers whether agonists of the peroxisome proliferator-activated receptor gamma, which is abundant in adipose tissue, might have an important impact on factors associated with adipocyte metabolism. |
| 10811 | 12670740 | It also considers whether agonists of the peroxisome proliferator-activated receptor gamma, which is abundant in adipose tissue, might have an important impact on factors associated with adipocyte metabolism. |
| 10812 | 12670740 | For example, the thiazolidinediones, a class of oral anti-diabetic agents that reduce insulin resistance and improve beta-cell function, might mediate these effects by regulating adipocyte-derived factors, in particular TNF-alpha and FFAs. |
| 10813 | 12670740 | For example, the thiazolidinediones, a class of oral anti-diabetic agents that reduce insulin resistance and improve beta-cell function, might mediate these effects by regulating adipocyte-derived factors, in particular TNF-alpha and FFAs. |
| 10814 | 12669471 | We have also proposed to remove tumor necrosis factor (TNF)-alpha, together with certain types of IFNs, to treat various ADs and AIDS, also an autoimmune condition. |
| 10815 | 12669471 | We have also proposed to remove tumor necrosis factor (TNF)-alpha, together with certain types of IFNs, to treat various ADs and AIDS, also an autoimmune condition. |
| 10816 | 12669471 | Anti-IFN gamma has been tested in several T-helper cell (Th1) ADs, including rheumatoid arthritis (RA), multiple sclerosis (MS), corneal transplant rejection, uveitis, Type I diabetes, schizophrenia (anti-IFN gamma and anti-TNF alpha), and various autoimmune skin diseases (alopecia areata, psoriasis vulgaris, vitiligo, pemphigus vulgaris and epidermolysis bullosa). |
| 10817 | 12669471 | Anti-IFN gamma has been tested in several T-helper cell (Th1) ADs, including rheumatoid arthritis (RA), multiple sclerosis (MS), corneal transplant rejection, uveitis, Type I diabetes, schizophrenia (anti-IFN gamma and anti-TNF alpha), and various autoimmune skin diseases (alopecia areata, psoriasis vulgaris, vitiligo, pemphigus vulgaris and epidermolysis bullosa). |
| 10818 | 12667626 | AM secretion, especially in cardiovascular tissues, is regulated mainly by mechanical stressors such as shear stress, inflammatory cytokines such as interleukin (IL)-1, tumor necrosis factor (TNF), and lipopolysaccharide (LPS), hormones such as angiotensin (Ang) II and endothelin (ET)-1, and metabolic factors such as hypoxia, ischemia, or hyperglycemia. |
| 10819 | 12666961 | Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored. |
| 10820 | 12657523 | Both the CD4(+) and CD8(+) subsets of T cells are required for the normal development of IDDM in NOD mice. |
| 10821 | 12657523 | We have isolated a GAD(65) reactive, cytotoxic CD8(+) T cell clone R1 that produces large quantities of IFNgamma and accelerates the onset of insulitis. |
| 10822 | 12657523 | This clone proliferates and produces IFNgamma in response to GAD(65) presenting APCs and kills GAD(65) presenting targets. |
| 10823 | 12657523 | Furthermore, it expresses TNFalpha, CD25, CD28, CD44, CD45 and LFA1, but not CD95L This is the first example of a GAD(65)specific CD8(+) T cell clone that accelerates the onset of the insulitis, although it does not appear to accelerate the onset of diabetes. |
| 10824 | 12654703 | Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, diabetes mellitus, hypercholesterolemia, and hyperuricemia revealed that 2 polymorphisms (825C-->T in the G protein beta3 subunit gene and 190G-->A in the CC chemokine receptor 2 gene) were significantly associated with hypertension in men and that one polymorphism (-238G-->A in the tumor necrosis factor alpha gene) was significantly associated with hypertension in women. |
| 10825 | 12653967 | Alleles of the proximal promoter of BAT1, a putative anti-inflammatory gene adjacent to the TNF cluster, reduce transcription on a disease-associated MHC haplotype. |
| 10826 | 12653847 | Anti-cytokine autoantibodies in autoimmunity: preponderance of neutralizing autoantibodies against interferon-alpha, interferon-omega and interleukin-12 in patients with thymoma and/or myasthenia gravis. |
| 10827 | 12653847 | We tested for both binding and neutralizing autoantibodies to a range of human cytokines, including interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, interferon-alpha2 (IFN-alpha2), IFN-omega, IFN-beta, IFN-gamma, tumour necrosis factor alpha (TNF-alpha), transforming growth factor beta-1 (TGF-beta1) and granulocyte-macrophage colony stimulating factor (GM-CSF), in plasmas or sera. |
| 10828 | 12653847 | With two notable exceptions described below, we found only occasional, mostly low-titre, non-neutralizing antibodies, mainly to GM-CSF; also to IL-10 in pemphigoid. |
| 10829 | 12653847 | Strikingly, however, high-titre, mainly IgG, autoantibodies to IFN-alpha2, IFN-omega and IL-12 were common at diagnosis in patients with late-onset myasthenia gravis (LOMG+), thymoma (T) but no MG (TMG-) and especially with both thymoma and MG together (TMG+). |
| 10830 | 12653847 | The antibodies recognized other closely related type I IFN-alpha subtypes, but rarely the distantly related type I IFN-beta, and never (detectably) the unrelated type II IFN-gamma. |
| 10831 | 12653847 | Antibodies to IL-12 showed a similar distribution to those against IFN-alpha2, although prevalences were slightly lower; correlations between individual titres against each were so modest that they appear to be entirely different specificities. |
| 10832 | 12653178 | While increased sympathetic activity is associated with increased levels of cortisol, catecholamines, serotonin, renin, aldosterone, angiotensin and free radicals; increased parasympathetic activity may be associated with greater levels of acetylecholine, dopamine, nitric oxide, endorphins, coenzyme Q10, antioxidants and other protective factors. |
| 10833 | 12653178 | While increased sympathetic activity is associated with increased levels of cortisol, catecholamines, serotonin, renin, aldosterone, angiotensin and free radicals; increased parasympathetic activity may be associated with greater levels of acetylecholine, dopamine, nitric oxide, endorphins, coenzyme Q10, antioxidants and other protective factors. |
| 10834 | 12653178 | We have also found that n-3 fatty acids plus CoQ can decrease TNF-alpha and IL-6 in AMI which are pro-inflammatory agents. |
| 10835 | 12653178 | We have also found that n-3 fatty acids plus CoQ can decrease TNF-alpha and IL-6 in AMI which are pro-inflammatory agents. |
| 10836 | 12653178 | Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. |
| 10837 | 12653178 | Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. |
| 10838 | 12651225 | Therapeutic antibodies directed against tumor necrosis factor alpha (TNF-alpha) for the treatment of rheumatoid arthritis, and against the human EGF receptor-2 (HER2) receptor for the treatment of breast cancer have provided significant clinical benefit for the patients. |
| 10839 | 12650740 | Possible underlying pathomechanisms are discussed with special attention to central nervous control of appetite including the role of leptin and the tumor necrosis factor system. |
| 10840 | 12649327 | Antisense protein tyrosine phosphatase 1B reverses activation of p38 mitogen-activated protein kinase in liver of ob/ob mice. |
| 10841 | 12649327 | Antisense protein tyrosine phosphatase 1B reverses activation of p38 mitogen-activated protein kinase in liver of ob/ob mice. |
| 10842 | 12649327 | Phosphorylation of stress-activated kinase p38, a MAPK family member, was increased in liver of ob/ob diabetic mice relative to lean littermates. |
| 10843 | 12649327 | Phosphorylation of stress-activated kinase p38, a MAPK family member, was increased in liver of ob/ob diabetic mice relative to lean littermates. |
| 10844 | 12649327 | Treatment of ob/ob mice with protein tyrosine phosphatase 1B (PTP1B) antisense oligonucleotides (ASO) reduced phosphorylation of p38 in liver-to below lean littermate levels-and normalized plasma glucose while reducing plasma insulin. |
| 10845 | 12649327 | Treatment of ob/ob mice with protein tyrosine phosphatase 1B (PTP1B) antisense oligonucleotides (ASO) reduced phosphorylation of p38 in liver-to below lean littermate levels-and normalized plasma glucose while reducing plasma insulin. |
| 10846 | 12649327 | Phosphorylation of ERK, but not JNK, was also decreased in ASO-treated mice. |
| 10847 | 12649327 | Phosphorylation of ERK, but not JNK, was also decreased in ASO-treated mice. |
| 10848 | 12649327 | PTP1B ASO decreased TNFalpha protein levels and phosphorylation of the transcription factor cAMP response element binding protein (CREB) in liver, both of which can occur through decreased phosphorylation of p38 and both of which have been implicated in insulin resistance or hyperglycemia. |
| 10849 | 12649327 | PTP1B ASO decreased TNFalpha protein levels and phosphorylation of the transcription factor cAMP response element binding protein (CREB) in liver, both of which can occur through decreased phosphorylation of p38 and both of which have been implicated in insulin resistance or hyperglycemia. |
| 10850 | 12649327 | Decreased p38 phosphorylation was not directly due to decreased phosphorylation of the kinases that normally phosphorylate p38-MKK3 and MKK6. |
| 10851 | 12649327 | Decreased p38 phosphorylation was not directly due to decreased phosphorylation of the kinases that normally phosphorylate p38-MKK3 and MKK6. |
| 10852 | 12649327 | Additionally, p38 phosphorylation was not enhanced in liver upon insulin stimulation of ASO-treated ob/ob mice (despite increased activation of other signaling molecules) corroborating that p38 is not directly affected via the insulin receptor. |
| 10853 | 12649327 | Additionally, p38 phosphorylation was not enhanced in liver upon insulin stimulation of ASO-treated ob/ob mice (despite increased activation of other signaling molecules) corroborating that p38 is not directly affected via the insulin receptor. |
| 10854 | 12649327 | Instead, decreased phosphorylation of p38 may be due to increased expression of MAPK phosphatases, particularly the p38/ERK phosphatase PAC1 (phosphatase of activated cells). |
| 10855 | 12649327 | Instead, decreased phosphorylation of p38 may be due to increased expression of MAPK phosphatases, particularly the p38/ERK phosphatase PAC1 (phosphatase of activated cells). |
| 10856 | 12649327 | This study demonstrates that reduction of PTP1B protein using ASO reduces activation of p38 and its substrates TNFalpha and CREB in liver of diabetic mice, which correlates with decreased hyperglycemia and hyperinsulinemia. |
| 10857 | 12649327 | This study demonstrates that reduction of PTP1B protein using ASO reduces activation of p38 and its substrates TNFalpha and CREB in liver of diabetic mice, which correlates with decreased hyperglycemia and hyperinsulinemia. |
| 10858 | 12642010 | Possible mechanisms whereby protease inhibitors can hinder insulin actions include inhibition of glucose transporter isoform Glut 4, and altered expression of leptin and tumor necrosis factor-a in adipose tissue. |
| 10859 | 12632104 | Like the Fas/Fas-L system, the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) transduces apoptosis in a number of cancers; it is also a clinical candidate for cancer therapy. |
| 10860 | 12632104 | Caspase-3 activity and the expression of four types of TRAIL receptor mRNAs were quantitated in tumor and contiguous non-tumor tissues obtained from 27 patients with HCC (HBV-related in 10; HCV-related in 17). |
| 10861 | 12632104 | The expression of caspase-3 and TRAIL receptors was also examined immunohistochemically. |
| 10862 | 12632104 | A significantly positive correlation was observed between caspase-3 activity and TRAIL-R1, -R2. |
| 10863 | 12632104 | Caspase-3 activity and TRAIL-R1, -R2 expression in tumor tissue were significantly lower than those in non-tumor tissue in HBV-related HCC. |
| 10864 | 12632104 | Some HCV-related HCC cases, however, demonstrated elevated caspase-3 activity and TRAIL-R1, -R2 expression in tumor tissue. |
| 10865 | 12632104 | Both TRAIL-R1 and -R2 showed coefficient correlation with caspase-3 activity, and were strongly associated with apoptosis in human HCC. |
| 10866 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10867 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10868 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10869 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10870 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10871 | 12626032 | The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes. |
| 10872 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10873 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10874 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10875 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10876 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10877 | 12626032 | The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). |
| 10878 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10879 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10880 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10881 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10882 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10883 | 12626032 | Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. |
| 10884 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10885 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10886 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10887 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10888 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10889 | 12626032 | TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. |
| 10890 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10891 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10892 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10893 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10894 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10895 | 12626032 | An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. |
| 10896 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10897 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10898 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10899 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10900 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10901 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 10902 | 12623123 | Tumor necrosis factor alpha-induced apoptosis in astrocytes is prevented by the activation of P2Y6, but not P2Y4 nucleotide receptors. |
| 10903 | 12623123 | Tumor necrosis factor alpha-induced apoptosis in astrocytes is prevented by the activation of P2Y6, but not P2Y4 nucleotide receptors. |
| 10904 | 12623123 | Tumor necrosis factor alpha-induced apoptosis in astrocytes is prevented by the activation of P2Y6, but not P2Y4 nucleotide receptors. |
| 10905 | 12623123 | Tumor necrosis factor alpha-induced apoptosis in astrocytes is prevented by the activation of P2Y6, but not P2Y4 nucleotide receptors. |
| 10906 | 12623123 | The physiological role of the uracil nucleotide-preferring P2Y(6) and P2Y(4) receptors is still unclear, although they are widely distributed in various tissues. |
| 10907 | 12623123 | The physiological role of the uracil nucleotide-preferring P2Y(6) and P2Y(4) receptors is still unclear, although they are widely distributed in various tissues. |
| 10908 | 12623123 | The physiological role of the uracil nucleotide-preferring P2Y(6) and P2Y(4) receptors is still unclear, although they are widely distributed in various tissues. |
| 10909 | 12623123 | The physiological role of the uracil nucleotide-preferring P2Y(6) and P2Y(4) receptors is still unclear, although they are widely distributed in various tissues. |
| 10910 | 12623123 | In an effort to identify their biological functions, we found that activation by UDP of the rat P2Y(6) receptor expressed in 1321N1 human astrocytes significantly reduced cell death induced by tumor necrosis factor alpha (TNF alpha). |
| 10911 | 12623123 | In an effort to identify their biological functions, we found that activation by UDP of the rat P2Y(6) receptor expressed in 1321N1 human astrocytes significantly reduced cell death induced by tumor necrosis factor alpha (TNF alpha). |
| 10912 | 12623123 | In an effort to identify their biological functions, we found that activation by UDP of the rat P2Y(6) receptor expressed in 1321N1 human astrocytes significantly reduced cell death induced by tumor necrosis factor alpha (TNF alpha). |
| 10913 | 12623123 | In an effort to identify their biological functions, we found that activation by UDP of the rat P2Y(6) receptor expressed in 1321N1 human astrocytes significantly reduced cell death induced by tumor necrosis factor alpha (TNF alpha). |
| 10914 | 12623123 | Activation of the human P2Y(4) receptor expressed in 1321N1 cells by UTP did not elicit this protective effect, although both receptors were coupled to phospholipase C. |
| 10915 | 12623123 | Activation of the human P2Y(4) receptor expressed in 1321N1 cells by UTP did not elicit this protective effect, although both receptors were coupled to phospholipase C. |
| 10916 | 12623123 | Activation of the human P2Y(4) receptor expressed in 1321N1 cells by UTP did not elicit this protective effect, although both receptors were coupled to phospholipase C. |
| 10917 | 12623123 | Activation of the human P2Y(4) receptor expressed in 1321N1 cells by UTP did not elicit this protective effect, although both receptors were coupled to phospholipase C. |
| 10918 | 12623123 | The activation of P2Y(6) receptors prevented the activation of both caspase-3 and caspase-8 resulting from TNF alpha exposure. |
| 10919 | 12623123 | The activation of P2Y(6) receptors prevented the activation of both caspase-3 and caspase-8 resulting from TNF alpha exposure. |
| 10920 | 12623123 | The activation of P2Y(6) receptors prevented the activation of both caspase-3 and caspase-8 resulting from TNF alpha exposure. |
| 10921 | 12623123 | The activation of P2Y(6) receptors prevented the activation of both caspase-3 and caspase-8 resulting from TNF alpha exposure. |
| 10922 | 12623123 | Therefore, it is suggested that P2Y(6) receptors interact rapidly with the TNF alpha-related intracellular signals to prevent apoptotic cell death. |
| 10923 | 12623123 | Therefore, it is suggested that P2Y(6) receptors interact rapidly with the TNF alpha-related intracellular signals to prevent apoptotic cell death. |
| 10924 | 12623123 | Therefore, it is suggested that P2Y(6) receptors interact rapidly with the TNF alpha-related intracellular signals to prevent apoptotic cell death. |
| 10925 | 12623123 | Therefore, it is suggested that P2Y(6) receptors interact rapidly with the TNF alpha-related intracellular signals to prevent apoptotic cell death. |
| 10926 | 12622777 | Independent of linkage disequilibrium with class II HLA, TNF haplotype TNFA-307*2 - TNFB+252*2 showed a significant protective effect (OR = 0.031), partly exacerbated by partial linkage to protective class II haplotypes. |
| 10927 | 12612942 | Angiotensin II production upregulates the expression of transforming growth factor-beta1, tumor necrosis factor-alpha, nuclear factor-kappaB, and several adhesion molecules and chemoattractants. |
| 10928 | 12612942 | Treatment with one of several growth factors may ameliorate the progression of kidney disease: insulin-like growth factor-1, hepatocyte growth factor, and bone morphogenetic protein-7. |
| 10929 | 12611905 | Characterization of the long pentraxin PTX3 as a TNFalpha-induced secreted protein of adipose cells. |
| 10930 | 12611905 | Characterization of the long pentraxin PTX3 as a TNFalpha-induced secreted protein of adipose cells. |
| 10931 | 12611905 | Characterization of the long pentraxin PTX3 as a TNFalpha-induced secreted protein of adipose cells. |
| 10932 | 12611905 | Characterization of the long pentraxin PTX3 as a TNFalpha-induced secreted protein of adipose cells. |
| 10933 | 12611905 | PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. |
| 10934 | 12611905 | PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. |
| 10935 | 12611905 | PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. |
| 10936 | 12611905 | PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. |
| 10937 | 12611905 | Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. |
| 10938 | 12611905 | Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. |
| 10939 | 12611905 | Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. |
| 10940 | 12611905 | Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. |
| 10941 | 12611905 | In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor alpha (TNFalpha) in a dose-dependent manner. |
| 10942 | 12611905 | In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor alpha (TNFalpha) in a dose-dependent manner. |
| 10943 | 12611905 | In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor alpha (TNFalpha) in a dose-dependent manner. |
| 10944 | 12611905 | In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor alpha (TNFalpha) in a dose-dependent manner. |
| 10945 | 12611905 | PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNFalpha levels. |
| 10946 | 12611905 | PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNFalpha levels. |
| 10947 | 12611905 | PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNFalpha levels. |
| 10948 | 12611905 | PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNFalpha levels. |
| 10949 | 12611905 | In conclusion, PTX3 appears as a TNFalpha-induced protein that provides a new link between chronic low-level inflammatory state and obesity. |
| 10950 | 12611905 | In conclusion, PTX3 appears as a TNFalpha-induced protein that provides a new link between chronic low-level inflammatory state and obesity. |
| 10951 | 12611905 | In conclusion, PTX3 appears as a TNFalpha-induced protein that provides a new link between chronic low-level inflammatory state and obesity. |
| 10952 | 12611905 | In conclusion, PTX3 appears as a TNFalpha-induced protein that provides a new link between chronic low-level inflammatory state and obesity. |
| 10953 | 12607825 | Evidence for increased inflammation includes increased monocyte superoxide and pro-inflammatory cytokine release (IL-1, IL-6, and TNF-alpha), increased monocyte adhesion to endothelium and increased levels of plasma C-reactive protein, the prototypic marker of inflammation. |
| 10954 | 12607825 | Most importantly, alpha tocopherol therapy, especially at high doses, clearly shows a benefit with regards to LDL oxidation, isoprostanes and a decrease in inflammatory markers such as C-reactive protein, pro-inflammatory cytokines and PAI-1 levels. |
| 10955 | 12606524 | We therefore examined prospectively the effects of the central inflammatory cytokines interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) on the development of type 2 diabetes. |
| 10956 | 12606524 | We therefore examined prospectively the effects of the central inflammatory cytokines interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) on the development of type 2 diabetes. |
| 10957 | 12606524 | IL-6 and TNF-alpha levels were found to be elevated in participants with incident type 2 diabetes, whereas IL-1beta plasma levels did not differ between the groups. |
| 10958 | 12606524 | IL-6 and TNF-alpha levels were found to be elevated in participants with incident type 2 diabetes, whereas IL-1beta plasma levels did not differ between the groups. |
| 10959 | 12606524 | Interestingly, combined analysis of the cytokines revealed a significant interaction between IL-1beta and IL-6. |
| 10960 | 12606524 | Interestingly, combined analysis of the cytokines revealed a significant interaction between IL-1beta and IL-6. |
| 10961 | 12606524 | In the fully adjusted model, participants with detectable levels of IL-1beta and elevated levels of IL-6 had an independently increased risk to develop type 2 diabetes (3.3, 1.7-6.8), whereas individuals with increased concentrations of IL-6 but undetectable levels of IL-1beta had no significantly increased risk, both compared with the low-level reference group. |
| 10962 | 12606524 | In the fully adjusted model, participants with detectable levels of IL-1beta and elevated levels of IL-6 had an independently increased risk to develop type 2 diabetes (3.3, 1.7-6.8), whereas individuals with increased concentrations of IL-6 but undetectable levels of IL-1beta had no significantly increased risk, both compared with the low-level reference group. |
| 10963 | 12606524 | In particular, a combined elevation of IL-1beta and IL-6, rather than the isolated elevation of IL-6 alone, independently increases the risk of type 2 diabetes. |
| 10964 | 12606524 | In particular, a combined elevation of IL-1beta and IL-6, rather than the isolated elevation of IL-6 alone, independently increases the risk of type 2 diabetes. |
| 10965 | 12604246 | Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells. |
| 10966 | 12604246 | Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells. |
| 10967 | 12604246 | Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells. |
| 10968 | 12604246 | Role of aldose reductase in TNF-alpha-induced apoptosis of vascular endothelial cells. |
| 10969 | 12604246 | Stimulation of the VECs with TNF-alpha led to an increase in the DNA-binding activity of the transcription factor, nuclear factor-kappa binding protein (NF-kappaB) and the induction of the adhesion molecule (ICAM)-1. |
| 10970 | 12604246 | Stimulation of the VECs with TNF-alpha led to an increase in the DNA-binding activity of the transcription factor, nuclear factor-kappa binding protein (NF-kappaB) and the induction of the adhesion molecule (ICAM)-1. |
| 10971 | 12604246 | Stimulation of the VECs with TNF-alpha led to an increase in the DNA-binding activity of the transcription factor, nuclear factor-kappa binding protein (NF-kappaB) and the induction of the adhesion molecule (ICAM)-1. |
| 10972 | 12604246 | Stimulation of the VECs with TNF-alpha led to an increase in the DNA-binding activity of the transcription factor, nuclear factor-kappa binding protein (NF-kappaB) and the induction of the adhesion molecule (ICAM)-1. |
| 10973 | 12604246 | Treatment of VECs with the AR inhibitor, tolrestat, prevented the activation of NF-kappaB and diminished ICAM-1 induction stimulated by TNF-alpha. |
| 10974 | 12604246 | Treatment of VECs with the AR inhibitor, tolrestat, prevented the activation of NF-kappaB and diminished ICAM-1 induction stimulated by TNF-alpha. |
| 10975 | 12604246 | Treatment of VECs with the AR inhibitor, tolrestat, prevented the activation of NF-kappaB and diminished ICAM-1 induction stimulated by TNF-alpha. |
| 10976 | 12604246 | Treatment of VECs with the AR inhibitor, tolrestat, prevented the activation of NF-kappaB and diminished ICAM-1 induction stimulated by TNF-alpha. |
| 10977 | 12604246 | These results indicate an obligatory requirement of AR activity in the transduction of intracellular signaling initiated by the ligation of the TNF-alpha receptors leading to the activation of NF-kappaB. |
| 10978 | 12604246 | These results indicate an obligatory requirement of AR activity in the transduction of intracellular signaling initiated by the ligation of the TNF-alpha receptors leading to the activation of NF-kappaB. |
| 10979 | 12604246 | These results indicate an obligatory requirement of AR activity in the transduction of intracellular signaling initiated by the ligation of the TNF-alpha receptors leading to the activation of NF-kappaB. |
| 10980 | 12604246 | These results indicate an obligatory requirement of AR activity in the transduction of intracellular signaling initiated by the ligation of the TNF-alpha receptors leading to the activation of NF-kappaB. |
| 10981 | 12604244 | Chronic hyperglycemia is associated with the activation of aldose reductase (AR), an increase in cytokines such as TNF-alpha and IL-8 and oxidative stress. |
| 10982 | 12604244 | Chronic hyperglycemia is associated with the activation of aldose reductase (AR), an increase in cytokines such as TNF-alpha and IL-8 and oxidative stress. |
| 10983 | 12604244 | Chronic hyperglycemia is associated with the activation of aldose reductase (AR), an increase in cytokines such as TNF-alpha and IL-8 and oxidative stress. |
| 10984 | 12604244 | Stimulation with TNF-alpha led to the activation of the transcription factor NF-kappaB and enhanced VSMC growth. |
| 10985 | 12604244 | Stimulation with TNF-alpha led to the activation of the transcription factor NF-kappaB and enhanced VSMC growth. |
| 10986 | 12604244 | Stimulation with TNF-alpha led to the activation of the transcription factor NF-kappaB and enhanced VSMC growth. |
| 10987 | 12604244 | Inhibition of AR also prevented protein kinase C (PKC) activation by TNF-alpha, but did not affect PKC activation by phorbol esters, indicating that inhibition of AR interrupts mitogenic signaling upstream of PKC. |
| 10988 | 12604244 | Inhibition of AR also prevented protein kinase C (PKC) activation by TNF-alpha, but did not affect PKC activation by phorbol esters, indicating that inhibition of AR interrupts mitogenic signaling upstream of PKC. |
| 10989 | 12604244 | Inhibition of AR also prevented protein kinase C (PKC) activation by TNF-alpha, but did not affect PKC activation by phorbol esters, indicating that inhibition of AR interrupts mitogenic signaling upstream of PKC. |
| 10990 | 12601631 | Beraprost significantly decreased tumor necrosis factor-alpha (TNF-alpha)-induced VCAM-1 expression in human vascular endothelial cells. |
| 10991 | 12594256 | HSP60 strongly stimulated DC for maturation and release of TNF-alpha, IL-12, and IL-1 beta. |
| 10992 | 12594256 | However, HSP60 elicited only a weak IL-10 response in DC suggesting a Th1 bias. |
| 10993 | 12594256 | Again, a Th1 bias was noted in that cocultures of allogeneic T cells and HSP60-treated DC released IFN-gamma but only small amounts of IL-10 and no detectable IL-4. |
| 10994 | 12594256 | Signaling via Toll-like receptor 4 was involved in HSP60-induced cytokine release and maturation because DC of C3H/HeJ mice with a mutant Toll-like receptor 4 showed deficient response to HSP60. |
| 10995 | 12594256 | HSP60 was found to rapidly activate the mitogen-activated protein kinases p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase as well as I kappa B in DC. |
| 10996 | 12593603 | Studies have demonstrated that TNF-alpha suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance. |
| 10997 | 12593603 | Studies have demonstrated that TNF-alpha suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance. |
| 10998 | 12593603 | Studies have demonstrated that TNF-alpha suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance. |
| 10999 | 12593603 | Thus, TNF-alpha, produced from monocytic cells due to inflammatory diseases, may have an additive influence on insulin sensitivity to adipocyte-derived TNF-alpha. |
| 11000 | 12593603 | Thus, TNF-alpha, produced from monocytic cells due to inflammatory diseases, may have an additive influence on insulin sensitivity to adipocyte-derived TNF-alpha. |
| 11001 | 12593603 | Thus, TNF-alpha, produced from monocytic cells due to inflammatory diseases, may have an additive influence on insulin sensitivity to adipocyte-derived TNF-alpha. |
| 11002 | 12593603 | Here, we hypothesized that 1) TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation, and 2) TNF-alpha produced due to periodontal inflammation may be an additional important factor influencing insulin sensitivity in both obese and type 2 diabetic patients. |
| 11003 | 12593603 | Here, we hypothesized that 1) TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation, and 2) TNF-alpha produced due to periodontal inflammation may be an additional important factor influencing insulin sensitivity in both obese and type 2 diabetic patients. |
| 11004 | 12593603 | Here, we hypothesized that 1) TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation, and 2) TNF-alpha produced due to periodontal inflammation may be an additional important factor influencing insulin sensitivity in both obese and type 2 diabetic patients. |
| 11005 | 12581487 | In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta cell function in recent onset patients. |
| 11006 | 12581487 | In a second phase I trial, treatment of rheumatoid arthritis (RA) with ingested IFN-alpha reduced the secretion of interleukin-1 (IL-1), a proinflammatory cytokine. |
| 11007 | 12581487 | In a third phase I trial in MS, there was a significant decrease in peripheral blood mononuclear cell (PBMC) IL-2 and IFN-gamma production after ingesting IFN-alpha. |
| 11008 | 12581487 | In a phase II randomized, placebo-controlled, double-blind trial in MS, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. |
| 11009 | 12581487 | Tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. |
| 11010 | 12581487 | Ingested IFN-alpha was not toxic in any of these clinical trials. |
| 11011 | 12581487 | These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. |
| 11012 | 12577054 | TRAIL, the tumor necrosis factor-related apoptosis-inducing ligand, selectively induces apoptosis of tumor cells, but not most normal cells. |
| 11013 | 12577054 | TRAIL-deficient mice are also hypersensitive to collagen-induced arthritis and streptozotocin-induced diabetes and develop heightened autoimmune responses. |
| 11014 | 12576525 | Role of cyclooxygenases COX-1 and COX-2 in modulating adipogenesis in 3T3-L1 cells. |
| 11015 | 12576525 | Role of cyclooxygenases COX-1 and COX-2 in modulating adipogenesis in 3T3-L1 cells. |
| 11016 | 12576525 | Role of cyclooxygenases COX-1 and COX-2 in modulating adipogenesis in 3T3-L1 cells. |
| 11017 | 12576525 | Two COX isoforms have been identified, COX-1, the constitutive form, and COX-2, the inducible form. |
| 11018 | 12576525 | Two COX isoforms have been identified, COX-1, the constitutive form, and COX-2, the inducible form. |
| 11019 | 12576525 | Two COX isoforms have been identified, COX-1, the constitutive form, and COX-2, the inducible form. |
| 11020 | 12576525 | COX-2 was found to be expressed in undifferentiated 3T3-L1 cells and down-regulated during differentiation, whereas the cellular level of COX-1 remained relatively constant. |
| 11021 | 12576525 | COX-2 was found to be expressed in undifferentiated 3T3-L1 cells and down-regulated during differentiation, whereas the cellular level of COX-1 remained relatively constant. |
| 11022 | 12576525 | COX-2 was found to be expressed in undifferentiated 3T3-L1 cells and down-regulated during differentiation, whereas the cellular level of COX-1 remained relatively constant. |
| 11023 | 12576525 | Tumor necrosis factor-alpha (TNFalpha) significantly up-regulated COX-2 expression ( approximately 2-fold) in differentiating 3T3-L1 cells, whereas similar effect was not observed with COX-1 expression. |
| 11024 | 12576525 | Tumor necrosis factor-alpha (TNFalpha) significantly up-regulated COX-2 expression ( approximately 2-fold) in differentiating 3T3-L1 cells, whereas similar effect was not observed with COX-1 expression. |
| 11025 | 12576525 | Tumor necrosis factor-alpha (TNFalpha) significantly up-regulated COX-2 expression ( approximately 2-fold) in differentiating 3T3-L1 cells, whereas similar effect was not observed with COX-1 expression. |
| 11026 | 12576525 | Abrogating the induced COX-2 activity reversed the TNFalpha-induced inhibition of differentiation by approximately 70%, implying a role for COX-2 in mediating TNFalpha signaling. |
| 11027 | 12576525 | Abrogating the induced COX-2 activity reversed the TNFalpha-induced inhibition of differentiation by approximately 70%, implying a role for COX-2 in mediating TNFalpha signaling. |
| 11028 | 12576525 | Abrogating the induced COX-2 activity reversed the TNFalpha-induced inhibition of differentiation by approximately 70%, implying a role for COX-2 in mediating TNFalpha signaling. |
| 11029 | 12576525 | Hence, both COX isoforms were involved in the negative modulation of adipocyte differentiation. |
| 11030 | 12576525 | Hence, both COX isoforms were involved in the negative modulation of adipocyte differentiation. |
| 11031 | 12576525 | Hence, both COX isoforms were involved in the negative modulation of adipocyte differentiation. |
| 11032 | 12576525 | COX-2 appeared to be the main isoform mediating at least part of the negative effects of TNFalpha. |
| 11033 | 12576525 | COX-2 appeared to be the main isoform mediating at least part of the negative effects of TNFalpha. |
| 11034 | 12576525 | COX-2 appeared to be the main isoform mediating at least part of the negative effects of TNFalpha. |
| 11035 | 12574341 | This hyperactivation was detected for different NF-kappaB complexes and correlated with increased IkappaBalpha degradation. |
| 11036 | 12574341 | Furthermore, increased NF-kappaB activation resulted in an enhanced capacity of NOD vs NOR or BALB/c Mphi to secrete IL-12(p70), TNF-alpha, and IL-1alpha, which was inhibited upon infection with an adenoviral recombinant encoding a modified form of IkappaBalpha. |
| 11037 | 12574341 | In contrast, elevated NF-kappaB activation had no significant effect on the capacity of NOD Mphi to stimulate CD4(+) or CD8(+) T cells in an Ag-specific manner. |
| 11038 | 12570760 | Through A(2B) receptors adenosine seems to cause mast cells degranulation, vasodilation, cardiac fibroblast proliferation, inhibition of Tumor Necrosis Factor (TNF-alpha), increased synthesis of interleukin-6 (IL-6), stimulation of Cl(-) secretion in intestinal epithelia and hepatic glucose production. |
| 11039 | 12569167 | In a trial of an FcR nonbinding humanized anti-CD3 mAb hOKT3gamma1(Ala-Ala) for treatment of patients with type 1 diabetes, we found significant increases in IL-10 and IL-5 in the serum of 63% and 72% of patients, respectively, and TNF-alpha and IL-6 levels that were lower than those previously reported following OKT3 therapy. |
| 11040 | 12569167 | However, the production of IL-10, compared to IFN-gamma on a molar basis, was greater after culture with hOKT3gamma1(Ala-Ala) than with OKT3. |
| 11041 | 12569167 | Flow cytometric studies confirmed that OKT3 induced IFN-gamma and IL-10 production, but hOKT3gamma1(Ala-Ala) induced only detectable IL-10 production in CD45RO(+) cells. |
| 11042 | 12569167 | Moreover, in vivo, we found IL-10(+)CD4(+) T cells after drug treatment. |
| 11043 | 12569167 | These cells were heterogeneous but generally CD45RO(+), CTLA-4(-), and expressed CCR4. |
| 11044 | 12568116 | Transmembrane TNF and IFNgamma induce caspase-independent death of primary mouse pancreatic beta cells. |
| 11045 | 12568116 | Transmembrane TNF and IFNgamma induce caspase-independent death of primary mouse pancreatic beta cells. |
| 11046 | 12568116 | Transmembrane TNF and IFNgamma induce caspase-independent death of primary mouse pancreatic beta cells. |
| 11047 | 12568116 | We have shown that TNF + IFNgamma induce islet cell death in vitro. |
| 11048 | 12568116 | We have shown that TNF + IFNgamma induce islet cell death in vitro. |
| 11049 | 12568116 | We have shown that TNF + IFNgamma induce islet cell death in vitro. |
| 11050 | 12568116 | Either sTNF or tmTNF, together with IFNgamma, induced caspase-dependent cell death of the NIT-1 insulinoma cell line, as measured by DNA fragmentation and a fluorogenic caspase 3 activation assay. |
| 11051 | 12568116 | Either sTNF or tmTNF, together with IFNgamma, induced caspase-dependent cell death of the NIT-1 insulinoma cell line, as measured by DNA fragmentation and a fluorogenic caspase 3 activation assay. |
| 11052 | 12568116 | Either sTNF or tmTNF, together with IFNgamma, induced caspase-dependent cell death of the NIT-1 insulinoma cell line, as measured by DNA fragmentation and a fluorogenic caspase 3 activation assay. |
| 11053 | 12568116 | TNF + IFNgamma did not induce caspase 3 activation in primary mouse islets. |
| 11054 | 12568116 | TNF + IFNgamma did not induce caspase 3 activation in primary mouse islets. |
| 11055 | 12568116 | TNF + IFNgamma did not induce caspase 3 activation in primary mouse islets. |
| 11056 | 12559634 | TNF, TNF receptor type 1, and allograft inflammatory factor-1 gene polymorphisms in Japanese patients with type 1 diabetes. |
| 11057 | 12559634 | TNF, TNF receptor type 1, and allograft inflammatory factor-1 gene polymorphisms in Japanese patients with type 1 diabetes. |
| 11058 | 12559634 | TNF, TNF receptor type 1, and allograft inflammatory factor-1 gene polymorphisms in Japanese patients with type 1 diabetes. |
| 11059 | 12559634 | TNF, TNF receptor type 1, and allograft inflammatory factor-1 gene polymorphisms in Japanese patients with type 1 diabetes. |
| 11060 | 12559634 | TNF, TNF receptor type 1, and allograft inflammatory factor-1 gene polymorphisms in Japanese patients with type 1 diabetes. |
| 11061 | 12559634 | Because it contains many genes related to inflammatory and immune responses, including tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and allograft inflammatory factor 1 (AIF-1) genes, it is unclear which gene within the class III region is responsible for the susceptibility to the disease. |
| 11062 | 12559634 | Because it contains many genes related to inflammatory and immune responses, including tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and allograft inflammatory factor 1 (AIF-1) genes, it is unclear which gene within the class III region is responsible for the susceptibility to the disease. |
| 11063 | 12559634 | Because it contains many genes related to inflammatory and immune responses, including tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and allograft inflammatory factor 1 (AIF-1) genes, it is unclear which gene within the class III region is responsible for the susceptibility to the disease. |
| 11064 | 12559634 | Because it contains many genes related to inflammatory and immune responses, including tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and allograft inflammatory factor 1 (AIF-1) genes, it is unclear which gene within the class III region is responsible for the susceptibility to the disease. |
| 11065 | 12559634 | Because it contains many genes related to inflammatory and immune responses, including tumor necrosis factor (TNF), lymphotoxin-alpha (LT-alpha), and allograft inflammatory factor 1 (AIF-1) genes, it is unclear which gene within the class III region is responsible for the susceptibility to the disease. |
| 11066 | 12559634 | Then, we investigated AIF-1, TNF, and LT-alpha gene polymorphisms in 165 patients with type 1 diabetes, consisting of 90 patients with young-onset type 1 diabetes, 75 patients with adult-onset type 1 diabetes, and 200 control patients. |
| 11067 | 12559634 | Then, we investigated AIF-1, TNF, and LT-alpha gene polymorphisms in 165 patients with type 1 diabetes, consisting of 90 patients with young-onset type 1 diabetes, 75 patients with adult-onset type 1 diabetes, and 200 control patients. |
| 11068 | 12559634 | Then, we investigated AIF-1, TNF, and LT-alpha gene polymorphisms in 165 patients with type 1 diabetes, consisting of 90 patients with young-onset type 1 diabetes, 75 patients with adult-onset type 1 diabetes, and 200 control patients. |
| 11069 | 12559634 | Then, we investigated AIF-1, TNF, and LT-alpha gene polymorphisms in 165 patients with type 1 diabetes, consisting of 90 patients with young-onset type 1 diabetes, 75 patients with adult-onset type 1 diabetes, and 200 control patients. |
| 11070 | 12559634 | Then, we investigated AIF-1, TNF, and LT-alpha gene polymorphisms in 165 patients with type 1 diabetes, consisting of 90 patients with young-onset type 1 diabetes, 75 patients with adult-onset type 1 diabetes, and 200 control patients. |
| 11071 | 12559634 | We also analyzed TNF receptors type 1 (TNFR1) and type 2 (TNFR2) gene polymorphisms, located on chromosome 12p13 and 1p36, respectively. |
| 11072 | 12559634 | We also analyzed TNF receptors type 1 (TNFR1) and type 2 (TNFR2) gene polymorphisms, located on chromosome 12p13 and 1p36, respectively. |
| 11073 | 12559634 | We also analyzed TNF receptors type 1 (TNFR1) and type 2 (TNFR2) gene polymorphisms, located on chromosome 12p13 and 1p36, respectively. |
| 11074 | 12559634 | We also analyzed TNF receptors type 1 (TNFR1) and type 2 (TNFR2) gene polymorphisms, located on chromosome 12p13 and 1p36, respectively. |
| 11075 | 12559634 | We also analyzed TNF receptors type 1 (TNFR1) and type 2 (TNFR2) gene polymorphisms, located on chromosome 12p13 and 1p36, respectively. |
| 11076 | 12559634 | Although there were significant differences between type 1 diabetes patients and controls in the distributions of TNF promoter polymorphisms at position -1031 and -857, and LT-alpha gene NcoI polymorphism, none of them was independently associated with the disease after two-locus analysis with HLA class II alleles. |
| 11077 | 12559634 | Although there were significant differences between type 1 diabetes patients and controls in the distributions of TNF promoter polymorphisms at position -1031 and -857, and LT-alpha gene NcoI polymorphism, none of them was independently associated with the disease after two-locus analysis with HLA class II alleles. |
| 11078 | 12559634 | Although there were significant differences between type 1 diabetes patients and controls in the distributions of TNF promoter polymorphisms at position -1031 and -857, and LT-alpha gene NcoI polymorphism, none of them was independently associated with the disease after two-locus analysis with HLA class II alleles. |
| 11079 | 12559634 | Although there were significant differences between type 1 diabetes patients and controls in the distributions of TNF promoter polymorphisms at position -1031 and -857, and LT-alpha gene NcoI polymorphism, none of them was independently associated with the disease after two-locus analysis with HLA class II alleles. |
| 11080 | 12559634 | Although there were significant differences between type 1 diabetes patients and controls in the distributions of TNF promoter polymorphisms at position -1031 and -857, and LT-alpha gene NcoI polymorphism, none of them was independently associated with the disease after two-locus analysis with HLA class II alleles. |
| 11081 | 12559622 | We found that the myocardium of these patients was infiltrated by CD4(+) and CD8(+) T lymphocytes as well as macrophages. |
| 11082 | 12559622 | Finally, mRNA for interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha was detected in the cardiac specimens, although at a lower level compared with specimens from hearts without signs of viral infections. |
| 11083 | 12554784 | TNFalpha, which activates three different MAPKs [ERK, p38, and jun amino terminal kinase (JNK)], also induces insulin resistance. |
| 11084 | 12554784 | To better understand the respective roles of these three MAPK pathways in insulin signaling and their contribution to insulin resistance, constitutively active MAPK/ERK kinase (MEK)1, MAPK kinase (MKK6), and MKK7 mutants were overexpressed in 3T3-L1 adipocytes using an adenovirus-mediated transfection procedure. |
| 11085 | 12554784 | The MEK1 mutant, which activates ERK, markedly down-regulated expression of the insulin receptor (IR) and its major substrates, IRS-1 and IRS-2, mRNA and protein, and in turn reduced tyrosine phosphorylation of IR as well as IRS-1 and IRS-2 and their associated phosphatidyl inositol 3-kinase (PI3K) activity. |
| 11086 | 12554784 | The MKK6 mutant, which activates p38, moderately inhibited IRS-1 and IRS-2 expressions and IRS-1-associated PI3K activity without exerting a significant effect on the IR. |
| 11087 | 12554784 | Finally, the MKK7 mutant, which activates JNK, reduced tyrosine phosphorylation of IRS-1 and IRS-2 and IRS-associated PI3K activity without affecting expression of the IR, IRS-1, or IRS-2. |
| 11088 | 12554784 | In the context of our earlier report showing down-regulation of glucose transporter 4 by MEK1-ERK and MKK6/3-p38, the present findings suggest that chronic activation of ERK, p38, or JNK can induce insulin resistance by affecting glucose transporter expression and insulin signaling, though via distinctly different mechanisms. |
| 11089 | 12540606 | Accelerated diabetes in rat insulin promoter-tumor necrosis factor-alpha transgenic nonobese diabetic mice lacking major histocompatibility class II molecules. |
| 11090 | 12540606 | Accelerated diabetes in rat insulin promoter-tumor necrosis factor-alpha transgenic nonobese diabetic mice lacking major histocompatibility class II molecules. |
| 11091 | 12540606 | Accelerated diabetes in rat insulin promoter-tumor necrosis factor-alpha transgenic nonobese diabetic mice lacking major histocompatibility class II molecules. |
| 11092 | 12540606 | Surprisingly, although diabetes was evident in the F1 intercross expressing rat insulin promoter (RIP)-TNF, offspring lacking either endogenous or transgenic class II molecules developed accelerated diabetes with high frequency in both sexes. |
| 11093 | 12540606 | Surprisingly, although diabetes was evident in the F1 intercross expressing rat insulin promoter (RIP)-TNF, offspring lacking either endogenous or transgenic class II molecules developed accelerated diabetes with high frequency in both sexes. |
| 11094 | 12540606 | Surprisingly, although diabetes was evident in the F1 intercross expressing rat insulin promoter (RIP)-TNF, offspring lacking either endogenous or transgenic class II molecules developed accelerated diabetes with high frequency in both sexes. |
| 11095 | 12540606 | Thus, neonatal expression of TNF-alpha in an islet-specific manner bypassed the requirement of CD4(+) T-cells and resulted in diabetes that could be mediated by CD8(+) T-cells. |
| 11096 | 12540606 | Thus, neonatal expression of TNF-alpha in an islet-specific manner bypassed the requirement of CD4(+) T-cells and resulted in diabetes that could be mediated by CD8(+) T-cells. |
| 11097 | 12540606 | Thus, neonatal expression of TNF-alpha in an islet-specific manner bypassed the requirement of CD4(+) T-cells and resulted in diabetes that could be mediated by CD8(+) T-cells. |
| 11098 | 12538031 | The reduced insulitis may be due to reduced expression of adhesion molecules since decreased numbers of islet-associated blood vessels expressing CD106 and MAdCAM-1 were detected following Linomide treatment. |
| 11099 | 12538031 | Furthermore, short term Linomide treatment (3 or 7 days), which did not alter the number of infiltrating cells, was found to inhibit the production of TNF-alpha which is known to induce the expression of CD106 and MAdCAM-1. |
| 11100 | 12532159 | Tumor necrosis factor alpha and insulin resistance in obese type 2 diabetic patients. |
| 11101 | 12532159 | Tumor necrosis factor alpha and insulin resistance in obese type 2 diabetic patients. |
| 11102 | 12532159 | Tumor necrosis factor alpha and insulin resistance in obese type 2 diabetic patients. |
| 11103 | 12532159 | The relationship between basal serum tumor necrosis factor alpha (TNFalpha) levels and peripheral tissue (muscle) sensitivity to insulin was examined in 63 subjects with normal glucose tolerance (NGT), 18 subjects with impaired glucose tolerance (IGT), and 123 patients with type 2 diabetes mellitus (T2DM). |
| 11104 | 12532159 | The relationship between basal serum tumor necrosis factor alpha (TNFalpha) levels and peripheral tissue (muscle) sensitivity to insulin was examined in 63 subjects with normal glucose tolerance (NGT), 18 subjects with impaired glucose tolerance (IGT), and 123 patients with type 2 diabetes mellitus (T2DM). |
| 11105 | 12532159 | The relationship between basal serum tumor necrosis factor alpha (TNFalpha) levels and peripheral tissue (muscle) sensitivity to insulin was examined in 63 subjects with normal glucose tolerance (NGT), 18 subjects with impaired glucose tolerance (IGT), and 123 patients with type 2 diabetes mellitus (T2DM). |
| 11106 | 12532159 | These results suggest that: (i) an increase in circulating TNFalpha concentration is associated with peripheral insulin resistance and increased plasma glucose and insulin levels prior to the onset of type 2 diabetes; and (ii) the further deterioration in peripheral insulin resistance in T2DM (compared with NGT and IGT) is unrelated to the increase in serum TNFalpha concentration. |
| 11107 | 12532159 | These results suggest that: (i) an increase in circulating TNFalpha concentration is associated with peripheral insulin resistance and increased plasma glucose and insulin levels prior to the onset of type 2 diabetes; and (ii) the further deterioration in peripheral insulin resistance in T2DM (compared with NGT and IGT) is unrelated to the increase in serum TNFalpha concentration. |
| 11108 | 12532159 | These results suggest that: (i) an increase in circulating TNFalpha concentration is associated with peripheral insulin resistance and increased plasma glucose and insulin levels prior to the onset of type 2 diabetes; and (ii) the further deterioration in peripheral insulin resistance in T2DM (compared with NGT and IGT) is unrelated to the increase in serum TNFalpha concentration. |
| 11109 | 12526284 | Tumour necrosis factor-alpha (TNF-alpha) is considered to be involved in the insulin resistance of type 2 diabetes mellitus. |
| 11110 | 12526284 | Tumour necrosis factor-alpha (TNF-alpha) is considered to be involved in the insulin resistance of type 2 diabetes mellitus. |
| 11111 | 12526284 | Tumour necrosis factor-alpha (TNF-alpha) is considered to be involved in the insulin resistance of type 2 diabetes mellitus. |
| 11112 | 12526284 | We studied serum TNF-alpha levels in 30 healthy non-diabetic offspring of type 2 diabetic parents (group A), and the relationship between TNF-alpha levels and variables associated with insulin resistance and diabetes. |
| 11113 | 12526284 | We studied serum TNF-alpha levels in 30 healthy non-diabetic offspring of type 2 diabetic parents (group A), and the relationship between TNF-alpha levels and variables associated with insulin resistance and diabetes. |
| 11114 | 12526284 | We studied serum TNF-alpha levels in 30 healthy non-diabetic offspring of type 2 diabetic parents (group A), and the relationship between TNF-alpha levels and variables associated with insulin resistance and diabetes. |
| 11115 | 12526284 | We conclude that serum TNF-alpha concentration is significantly elevated in non-diabetic offspring of type 2 diabetics and this may predict later impairment of insulin action in these individuals. |
| 11116 | 12526284 | We conclude that serum TNF-alpha concentration is significantly elevated in non-diabetic offspring of type 2 diabetics and this may predict later impairment of insulin action in these individuals. |
| 11117 | 12526284 | We conclude that serum TNF-alpha concentration is significantly elevated in non-diabetic offspring of type 2 diabetics and this may predict later impairment of insulin action in these individuals. |
| 11118 | 12517724 | Effects of tumor necrosis factor-alpha and interleukin-6 in elderly populations. |
| 11119 | 12517724 | Effects of tumor necrosis factor-alpha and interleukin-6 in elderly populations. |
| 11120 | 12517724 | Effects of tumor necrosis factor-alpha and interleukin-6 in elderly populations. |
| 11121 | 12517724 | Effects of tumor necrosis factor-alpha and interleukin-6 in elderly populations. |
| 11122 | 12517724 | Effects of tumor necrosis factor-alpha and interleukin-6 in elderly populations. |
| 11123 | 12517724 | Aging is associated with low-grade increases in circulating levels of TNF-alpha and IL-6. |
| 11124 | 12517724 | Aging is associated with low-grade increases in circulating levels of TNF-alpha and IL-6. |
| 11125 | 12517724 | Aging is associated with low-grade increases in circulating levels of TNF-alpha and IL-6. |
| 11126 | 12517724 | Aging is associated with low-grade increases in circulating levels of TNF-alpha and IL-6. |
| 11127 | 12517724 | Aging is associated with low-grade increases in circulating levels of TNF-alpha and IL-6. |
| 11128 | 12517724 | Several classical risk factors are indeed controlled by TNF-alpha and IL-6. |
| 11129 | 12517724 | Several classical risk factors are indeed controlled by TNF-alpha and IL-6. |
| 11130 | 12517724 | Several classical risk factors are indeed controlled by TNF-alpha and IL-6. |
| 11131 | 12517724 | Several classical risk factors are indeed controlled by TNF-alpha and IL-6. |
| 11132 | 12517724 | Several classical risk factors are indeed controlled by TNF-alpha and IL-6. |
| 11133 | 12517724 | TNF-alpha induces insulin resistance and endothelial dysfunction, IL-6 promotes procoagulant changes and both cytokines cause dyslipidaemia. |
| 11134 | 12517724 | TNF-alpha induces insulin resistance and endothelial dysfunction, IL-6 promotes procoagulant changes and both cytokines cause dyslipidaemia. |
| 11135 | 12517724 | TNF-alpha induces insulin resistance and endothelial dysfunction, IL-6 promotes procoagulant changes and both cytokines cause dyslipidaemia. |
| 11136 | 12517724 | TNF-alpha induces insulin resistance and endothelial dysfunction, IL-6 promotes procoagulant changes and both cytokines cause dyslipidaemia. |
| 11137 | 12517724 | TNF-alpha induces insulin resistance and endothelial dysfunction, IL-6 promotes procoagulant changes and both cytokines cause dyslipidaemia. |
| 11138 | 12517724 | TNF-alpha and IL-6 are also differently and independently of each other associated with mortality in elderly populations, indicating points of distinction in the biological effects of the two cytokines. |
| 11139 | 12517724 | TNF-alpha and IL-6 are also differently and independently of each other associated with mortality in elderly populations, indicating points of distinction in the biological effects of the two cytokines. |
| 11140 | 12517724 | TNF-alpha and IL-6 are also differently and independently of each other associated with mortality in elderly populations, indicating points of distinction in the biological effects of the two cytokines. |
| 11141 | 12517724 | TNF-alpha and IL-6 are also differently and independently of each other associated with mortality in elderly populations, indicating points of distinction in the biological effects of the two cytokines. |
| 11142 | 12517724 | TNF-alpha and IL-6 are also differently and independently of each other associated with mortality in elderly populations, indicating points of distinction in the biological effects of the two cytokines. |
| 11143 | 12516196 | Experiments in mice demonstrate that insulin resistance and NAFLD result from a chronic inflammatory state that is characterized by increased levels of TNF alpha. |
| 11144 | 12516196 | Experiments in mice demonstrate that insulin resistance and NAFLD result from a chronic inflammatory state that is characterized by increased levels of TNF alpha. |
| 11145 | 12516196 | Preliminary work in animal and human studies suggests that diverse strategies that inhibit production of TNF alpha and improve insulin resistance also ameliorate NAFLD. |
| 11146 | 12516196 | Preliminary work in animal and human studies suggests that diverse strategies that inhibit production of TNF alpha and improve insulin resistance also ameliorate NAFLD. |
| 11147 | 12512738 | A series of experiments showed that alterations in the glucose concentrations of the growth medium (5.5-13.5 mmol/L) did not change the cellular content of either VCAM-1 or E-selectin before and after TNF-alpha treatment. |
| 11148 | 12508950 | As reviewed in this paper, the mechanisms explaining this impact of fat distribution is not clearly established, although evidence suggests that free-fatty acids, leptin, TNF-alpha, PPAR-gamma, and F are directly or indirectly involved in this process. |
| 11149 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11150 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11151 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11152 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11153 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11154 | 12504894 | Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. |
| 11155 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11156 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11157 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11158 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11159 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11160 | 12504894 | Circulating levels of inflammatory cytokines such as IL-6 and tumor necrosis factor alpha (TNFalpha) are increased in both type 1 and type 2 diabetes. |
| 11161 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11162 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11163 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11164 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11165 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11166 | 12504894 | TNFalpha plays an important role in the pathogenesis of insulin resistance in type 2 diabetes. |
| 11167 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11168 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11169 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11170 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11171 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11172 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 11173 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11174 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11175 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11176 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11177 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11178 | 12504894 | MGO-BSA stimulated the simultaneous activation of p44/42 and p38 mitogen-activated protein kinase. |
| 11179 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11180 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11181 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11182 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11183 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11184 | 12504894 | PD98059, a selective MEK inhibitor, inhibited MGO-BSA-induced TNFalpha release as well as ERK phosphorylation. |
| 11185 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11186 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11187 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11188 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11189 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11190 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 11191 | 12504805 | To study the effects of high glucose on cytokine-induced NGF expression, rat mesangial cells were treated with the cytokines interleukin-1beta and tumor necrosis factor alpha under normal (1.0 g/L) and high (4.5 g/L) glucose concentrations. |
| 11192 | 12504805 | The specific protein kinase C inhibitors Ro31-8220 and CGP41251 suppressed cytokine-induced NGF expression. |
| 11193 | 12504805 | Moreover, blocking the oxidative activation of the protein kinase C pathway by N-acetylcysteine inhibited glucose effects on NGF synthesis. |
| 11194 | 12504805 | Neutralizing antibodies against transforming growth factor-beta inhibited cytokine-induced NGF expression under normal glucose concentrations but not under high glucose conditions. |
| 11195 | 12502498 | Proinflammatory cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) initiate a variety of signal cascades in pancreatic beta-cells that affect the expression level of genes involved in both the destruction and the protection of the beta-cell. |
| 11196 | 12502498 | Proinflammatory cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) initiate a variety of signal cascades in pancreatic beta-cells that affect the expression level of genes involved in both the destruction and the protection of the beta-cell. |
| 11197 | 12502498 | The aim of this study was to characterize the cytokine-mediated activation of NF-kappaB and the subsequent expression of iNOS protein in insulin-producing RINm5F cells with an improved antioxidant defense status by overexpression of the cytoprotective enzymes catalase (Cat), glutathione peroxidase (Gpx), and the cytoplasmic Cu/Zn superoxide dismutase (Cu/ZnSOD). |
| 11198 | 12502498 | The aim of this study was to characterize the cytokine-mediated activation of NF-kappaB and the subsequent expression of iNOS protein in insulin-producing RINm5F cells with an improved antioxidant defense status by overexpression of the cytoprotective enzymes catalase (Cat), glutathione peroxidase (Gpx), and the cytoplasmic Cu/Zn superoxide dismutase (Cu/ZnSOD). |
| 11199 | 12502498 | Cytokine-induced (IL-1beta or cytokine mix consisting of IL-1beta + TNF-alpha + IFN-gamma) activation of NF-kappaB in RINm5F cells was reduced by >80% through overexpression of MnSOD. |
| 11200 | 12502498 | Cytokine-induced (IL-1beta or cytokine mix consisting of IL-1beta + TNF-alpha + IFN-gamma) activation of NF-kappaB in RINm5F cells was reduced by >80% through overexpression of MnSOD. |
| 11201 | 12502498 | The activity of the iNOS promoter remained at basal levels in cytokine-stimulated MnSOD sense cells. |
| 11202 | 12502498 | The activity of the iNOS promoter remained at basal levels in cytokine-stimulated MnSOD sense cells. |
| 11203 | 12502498 | In contrast, the suppression of MnSOD gene expression in cytokine-stimulated MnSOD antisense cells resulted in a threefold higher activation of NF-kappaB and a twofold higher activation of the iNOS promoter as compared with control cells. |
| 11204 | 12502498 | In contrast, the suppression of MnSOD gene expression in cytokine-stimulated MnSOD antisense cells resulted in a threefold higher activation of NF-kappaB and a twofold higher activation of the iNOS promoter as compared with control cells. |
| 11205 | 12502498 | The iNOS protein expression was significantly reduced after a 6- and 8-h cytokine incubation of MnSOD sense cells. |
| 11206 | 12502498 | The iNOS protein expression was significantly reduced after a 6- and 8-h cytokine incubation of MnSOD sense cells. |
| 11207 | 12502498 | The low activity level of MnSOD in RINm5F MnSOD antisense cells increased the iNOS protein expression in particular during the early phase of cytokine-mediated toxicity. |
| 11208 | 12502498 | The low activity level of MnSOD in RINm5F MnSOD antisense cells increased the iNOS protein expression in particular during the early phase of cytokine-mediated toxicity. |
| 11209 | 12502498 | Cat, Gpx, and the cytoplasmic Cu/ZnSOD did not affect the activation of NF-kappaB and the iNOS promoter. |
| 11210 | 12502498 | Cat, Gpx, and the cytoplasmic Cu/ZnSOD did not affect the activation of NF-kappaB and the iNOS promoter. |
| 11211 | 12502498 | In conclusion, the overexpression of MnSOD, which inactivates specifically mitochondrially derived oxygen free radicals, significantly reduced the activation of NF-kappaB in insulin-producing cells. |
| 11212 | 12502498 | In conclusion, the overexpression of MnSOD, which inactivates specifically mitochondrially derived oxygen free radicals, significantly reduced the activation of NF-kappaB in insulin-producing cells. |
| 11213 | 12502498 | Overexpression of MnSOD may thus be beneficial for beta-cell survival through suppression of oxygen free radical formation, prevention of NF-kappaB activation, and iNOS expression. |
| 11214 | 12502498 | Overexpression of MnSOD may thus be beneficial for beta-cell survival through suppression of oxygen free radical formation, prevention of NF-kappaB activation, and iNOS expression. |
| 11215 | 12490536 | Aldose reductase mediates cytotoxic signals of hyperglycemia and TNF-alpha in human lens epithelial cells. |
| 11216 | 12490536 | Aldose reductase mediates cytotoxic signals of hyperglycemia and TNF-alpha in human lens epithelial cells. |
| 11217 | 12490536 | Aldose reductase mediates cytotoxic signals of hyperglycemia and TNF-alpha in human lens epithelial cells. |
| 11218 | 12490536 | Herein we report that inhibition of the polyol pathway enzyme aldose reductase (AR) by two structurally unrelated inhibitors--sorbinil and tolrestat--prevents, in the human lens epithelial cell line B-3, the apoptosis and activation of caspase-3 caused by exposure to high glucose levels or TNF-alpha. |
| 11219 | 12490536 | Herein we report that inhibition of the polyol pathway enzyme aldose reductase (AR) by two structurally unrelated inhibitors--sorbinil and tolrestat--prevents, in the human lens epithelial cell line B-3, the apoptosis and activation of caspase-3 caused by exposure to high glucose levels or TNF-alpha. |
| 11220 | 12490536 | Herein we report that inhibition of the polyol pathway enzyme aldose reductase (AR) by two structurally unrelated inhibitors--sorbinil and tolrestat--prevents, in the human lens epithelial cell line B-3, the apoptosis and activation of caspase-3 caused by exposure to high glucose levels or TNF-alpha. |
| 11221 | 12490536 | Inhibition of AR attenuated TNF-alpha and hyperglycemia-induced activation of protein kinase C (PKC), phosphorylation of the inhibitory subunit of nuclear factor-kappaB (NF-kappaB), and stimulation of NF-kappaB, but it did not prevent the activation of NF-kappaB and PKC by phorbol ester. |
| 11222 | 12490536 | Inhibition of AR attenuated TNF-alpha and hyperglycemia-induced activation of protein kinase C (PKC), phosphorylation of the inhibitory subunit of nuclear factor-kappaB (NF-kappaB), and stimulation of NF-kappaB, but it did not prevent the activation of NF-kappaB and PKC by phorbol ester. |
| 11223 | 12490536 | Inhibition of AR attenuated TNF-alpha and hyperglycemia-induced activation of protein kinase C (PKC), phosphorylation of the inhibitory subunit of nuclear factor-kappaB (NF-kappaB), and stimulation of NF-kappaB, but it did not prevent the activation of NF-kappaB and PKC by phorbol ester. |
| 11224 | 12490536 | Inhibition of AR also attenuated the increase in p38 mitogen-activated protein kinase and c-Jun N-terminal kinase phosphorylation. |
| 11225 | 12490536 | Inhibition of AR also attenuated the increase in p38 mitogen-activated protein kinase and c-Jun N-terminal kinase phosphorylation. |
| 11226 | 12490536 | Inhibition of AR also attenuated the increase in p38 mitogen-activated protein kinase and c-Jun N-terminal kinase phosphorylation. |
| 11227 | 12486879 | We review how metzincins, working through unique mechanisms, influence the extracellular milieu of several important cytokines and growth factors including transforming growth factor-beta (TGF-beta), TNF-alpha, IGFs and HB-epidermal growth factor (EGF). |
| 11228 | 12486207 | In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta-cell function in recent onset patients. |
| 11229 | 12486207 | In a second phase I trial, treatment of rheumatoid arthritis with ingested IFN-alpha reduced the secretion of interleukin (IL)-1, a pro-inflammatory cytokine. |
| 11230 | 12486207 | In a third phase I trial in multiple sclerosis, there was a significant decrease in peripheral blood mononuclear cell IL-2 and IFN-gamma production after ingesting IFN-alpha. |
| 11231 | 12486207 | In a phase II randomized, placebo-controlled, double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. |
| 11232 | 12486207 | Tumor necrosis factor-alpha and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. |
| 11233 | 12486207 | Ingested IFN-alpha was not toxic in any of these clinical trials. |
| 11234 | 12486207 | These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. |
| 11235 | 12477294 | Local secretion of large amounts of TNF-alpha and IL-1 due to activation of immunocompetent cells characterises the pathophysiology of RA. |
| 11236 | 12475794 | Tumor necrosis factor-alpha (TNF-alpha), a known inducer of NF-kappaB signaling, activated this construct by 3.4-fold (P < 0.01). |
| 11237 | 12475794 | Tumor necrosis factor-alpha (TNF-alpha), a known inducer of NF-kappaB signaling, activated this construct by 3.4-fold (P < 0.01). |
| 11238 | 12475794 | Tumor necrosis factor-alpha (TNF-alpha), a known inducer of NF-kappaB signaling, activated this construct by 3.4-fold (P < 0.01). |
| 11239 | 12475794 | TNF-alpha treatment and depolarization activation of NF-kappaB differed significantly in that TNF-alpha activation was not blocked by PD98059. |
| 11240 | 12475794 | TNF-alpha treatment and depolarization activation of NF-kappaB differed significantly in that TNF-alpha activation was not blocked by PD98059. |
| 11241 | 12475794 | TNF-alpha treatment and depolarization activation of NF-kappaB differed significantly in that TNF-alpha activation was not blocked by PD98059. |
| 11242 | 12475794 | These findings demonstrate that depolarization/Ca(2+) influx, as well as TNF-alpha treatment, can activate NF-kappaB-dependent transcription in pancreatic beta-cells, but by different signaling pathways. |
| 11243 | 12475794 | These findings demonstrate that depolarization/Ca(2+) influx, as well as TNF-alpha treatment, can activate NF-kappaB-dependent transcription in pancreatic beta-cells, but by different signaling pathways. |
| 11244 | 12475794 | These findings demonstrate that depolarization/Ca(2+) influx, as well as TNF-alpha treatment, can activate NF-kappaB-dependent transcription in pancreatic beta-cells, but by different signaling pathways. |
| 11245 | 12453902 | We investigated whether polymorphisms in tumor necrosis factor (TNF)-alpha(G-308A), beta3 adrenoreceptor (ADRB3)(G+250C), and peroxisome proliferator-activated receptor (PPAR)-gamma2(Pro12Ala), key molecules of the adipose tissue, might affect the IR associated with reduced fetal growth. |
| 11246 | 12453902 | We investigated whether polymorphisms in tumor necrosis factor (TNF)-alpha(G-308A), beta3 adrenoreceptor (ADRB3)(G+250C), and peroxisome proliferator-activated receptor (PPAR)-gamma2(Pro12Ala), key molecules of the adipose tissue, might affect the IR associated with reduced fetal growth. |
| 11247 | 12453902 | In the SGA group, fasting insulin-to-glucose ratios were significantly higher in the TNF/-308A (P = 0.03), the PPAR/Ala12 (P = 0.01), and the ADRB3/+250G (P = 0.02) carriers than in the noncarriers. |
| 11248 | 12453902 | In the SGA group, fasting insulin-to-glucose ratios were significantly higher in the TNF/-308A (P = 0.03), the PPAR/Ala12 (P = 0.01), and the ADRB3/+250G (P = 0.02) carriers than in the noncarriers. |
| 11249 | 12453888 | Both isoproterenol (ISO) and tumor necrosis factor (TNF)-alpha stimulated the rate of lipolysis in HSL-/- MEF adipocytes, although to a lesser extent than in wild-type cells, and these lipolytic activities were inhibited by H-89, a cAMP-dependent protein kinase inhibitor, and troglitazone, respectively. |
| 11250 | 12453888 | Both isoproterenol (ISO) and tumor necrosis factor (TNF)-alpha stimulated the rate of lipolysis in HSL-/- MEF adipocytes, although to a lesser extent than in wild-type cells, and these lipolytic activities were inhibited by H-89, a cAMP-dependent protein kinase inhibitor, and troglitazone, respectively. |
| 11251 | 12453888 | Thus, the responses of the residual lipolytic activity to lipolytic hormones and TNF-alpha were well conserved in the absence of HSL. |
| 11252 | 12453888 | Thus, the responses of the residual lipolytic activity to lipolytic hormones and TNF-alpha were well conserved in the absence of HSL. |
| 11253 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 11254 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 11255 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 11256 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 11257 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 11258 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 11259 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 11260 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 11261 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 11262 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 11263 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 11264 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 11265 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 11266 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 11267 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 11268 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 11269 | 12446608 | We investigated some of the mechanisms triggering the apoptotic machinery in rat insulinoma RINm5F cells and human islets treated with IL-1beta plus interferon-gamma plus TNFalpha and assessed the effects of 1,25-(OH)2D3 in these processes. |
| 11270 | 12444887 | Resistin - a mediator of obesity-associated insulin resistance or an innocent bystander? |
| 11271 | 12444887 | Although a seminal proposal by Steppan et al. suggested resistin to be a hormone that links obesity to diabetes, several studies have subsequently been published supporting the concept that insulin resistance and obesity are actually associated with a decreased resistin expression. |
| 11272 | 12444887 | Resistin expression is regulated by a variety of agents and hormones, including thiazolidinediones, insulin, tumor necrosis factor alpha and growth hormone. |
| 11273 | 12444887 | Experiments in humans have shown no differences in resistin expression between normal, insulin-resistant or type 2 diabetic samples. |
| 11274 | 12444887 | However, some recent genetic studies have demonstrated an association between resistin and insulin resistance and obesity. |
| 11275 | 12439784 | IL-4-Ig was found to downregulate LPS-induced IFN-gamma and TNF-alpha production. |
| 11276 | 12439784 | Expression was downregulated for both Th1-specific cytokine IFN-gamma and the Th2-specific cytokine IL-10. |
| 11277 | 12439784 | Interestingly, infiltration increased in the islets of IL-4-Ig-treated animals, and therefore did not correlate with the decreased IFN-gamma expression. |
| 11278 | 12436346 | Decreased expression of adiponectin is correlated with insulin resistance. |
| 11279 | 12436346 | It has been suggested that several agents, such as tumor necrosis factor alpha, could mediate their effects on insulin metabolism through modulating adiponectin secretion from adipocytes. |
| 11280 | 12431986 | Globular adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis. |
| 11281 | 12431986 | The adipocyte-derived hormone adiponectin has been shown to play important roles in the regulation of energy homeostasis and insulin sensitivity. |
| 11282 | 12431986 | In this study, we analyzed globular domain adiponectin (gAd) transgenic (Tg) mice crossed with leptin-deficient ob/ob or apoE-deficient mice. |
| 11283 | 12431986 | Interestingly, despite an unexpected similar body weight, gAd Tg ob/ob mice showed amelioration of insulin resistance and beta-cell degranulation as well as diabetes, indicating that globular adiponectin and leptin appeared to have both distinct and overlapping functions. |
| 11284 | 12431986 | Amelioration of diabetes and insulin resistance was associated with increased expression of molecules involved in fatty acid oxidation such as acyl-CoA oxidase, and molecules involved in energy dissipation such as uncoupling proteins 2 and 3 and increased fatty acid oxidation in skeletal muscle of gAd Tg ob/ob mice. |
| 11285 | 12431986 | Moreover, despite similar plasma glucose and lipid levels on an apoE-deficient background, gAd Tg apoE-deficient mice showed amelioration of atherosclerosis, which was associated with decreased expression of class A scavenger receptor and tumor necrosis factor alpha. |
| 11286 | 12431757 | Free fatty acids, resistin, and tumor necrosis factor (TNF)-alpha potentially worsen the insulin resistance. beta-Cell dysfunction resulting from glucose toxicity and lipotoxicity is potentially reversible with restoration of metabolic control. |
| 11287 | 12429856 | After 6 weeks, peripheral blood mononuclear cell tumor necrosis factor-alpha rose by 86.3% (P = 0.006) and declined by 20% (P, not significant) on H- or L-AGE diet, respectively; C-reactive protein increased by 35% on H-AGE and decreased by 20% on L-AGE (P = 0.014), and vascular adhesion molecule-1 declined by 20% on L-AGE (P < 0.01) and increased by 4% on H-AGE. |
| 11288 | 12426635 | Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice. |
| 11289 | 12426635 | Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice. |
| 11290 | 12426635 | Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice. |
| 11291 | 12426635 | Kinetics of TNF-alpha and IFN-gamma mRNA expression in islets and spleen of NOD mice. |
| 11292 | 12426635 | Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. |
| 11293 | 12426635 | Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. |
| 11294 | 12426635 | Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. |
| 11295 | 12426635 | Cytokines produced by islet-infiltrating mononuclear cells may be directly cytotoxic and can be involved in islet destruction coordinated by CD4+ and CD8+ cells. |
| 11296 | 12426635 | We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. |
| 11297 | 12426635 | We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. |
| 11298 | 12426635 | We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. |
| 11299 | 12426635 | We utilized a semiquantitative RT-PCR assay to analyze in vitro the mRNA expression of TNF-alpha and IFN-gamma cytokine genes in isolated islets (N = 100) and spleen cells (5 x 10(5) cells) from female NOD mice during the development of diabetes and from female CBA-j mice as a related control strain that does not develop diabetes. |
| 11300 | 12426635 | An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 +/- 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. |
| 11301 | 12426635 | An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 +/- 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. |
| 11302 | 12426635 | An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 +/- 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. |
| 11303 | 12426635 | An increase in IFN-gamma expression in islets was observed for females aged 28 weeks (149 +/- 29 arbitrary units (AU), P<0.05, Student t-test) with advanced destructive insulitis when compared with CBA-j mice, while TNF-alpha was expressed in both NOD and CBA-j female islets at the same level at all ages studied. |
| 11304 | 12426635 | The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with beta cell destruction and overt diabetes. |
| 11305 | 12426635 | The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with beta cell destruction and overt diabetes. |
| 11306 | 12426635 | The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with beta cell destruction and overt diabetes. |
| 11307 | 12426635 | The data suggest that IFN-gamma and TNF-alpha expression in pancreatic islets of female NOD mice is associated with beta cell destruction and overt diabetes. |
| 11308 | 12410850 | Comparative effects of ACE inhibition and angiotensin II receptor blockade in the prevention of renal damage. |
| 11309 | 12410850 | In particular, members of the nuclear factor-kappaB family of transcription factors are activated, which in turn fuels at least two autocrine reinforcing loops that amplify Ang II and tumor necrosis factor-alpha formation. |
| 11310 | 12410803 | In this study, peripheral blood monocytes were differentiated to macrophages with macrophage-colony stimulating factor (M-CSF) to determine lipopolysaccharide (LPS)-stimulated tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12 and prostaglandin E-2 (PGE-2) secretion from hetero- or homozygous HLA DQB1*0201 and *0302 type 1 diabetes mellitus patients, first-degree relatives and homozygous HLA DQB1*0602 healthy controls. |
| 11311 | 12410803 | In this study, peripheral blood monocytes were differentiated to macrophages with macrophage-colony stimulating factor (M-CSF) to determine lipopolysaccharide (LPS)-stimulated tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12 and prostaglandin E-2 (PGE-2) secretion from hetero- or homozygous HLA DQB1*0201 and *0302 type 1 diabetes mellitus patients, first-degree relatives and homozygous HLA DQB1*0602 healthy controls. |
| 11312 | 12410803 | LPS-stimulated secretion of TNF-alpha, IL-1beta and IL-6 was immediate and markedly higher in the HLA-DQB1*0201/*0302 type 1 diabetes patients compared with all other groups including HLA-matched healthy first-degree relatives. |
| 11313 | 12410803 | LPS-stimulated secretion of TNF-alpha, IL-1beta and IL-6 was immediate and markedly higher in the HLA-DQB1*0201/*0302 type 1 diabetes patients compared with all other groups including HLA-matched healthy first-degree relatives. |
| 11314 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11315 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11316 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11317 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11318 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11319 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11320 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11321 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11322 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11323 | 12409308 | Salicylic acid reverses phorbol 12-myristate-13-acetate (PMA)- and tumor necrosis factor alpha (TNFalpha)-induced insulin receptor substrate 1 (IRS1) serine 307 phosphorylation and insulin resistance in human embryonic kidney 293 (HEK293) cells. |
| 11324 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11325 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11326 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11327 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11328 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11329 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11330 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11331 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11332 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11333 | 12409308 | Although it has been suggested that salicylates sensitize insulin action by inhibiting IkappaB kinase beta (IKKbeta), the detailed mechanisms remain unclear. |
| 11334 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11335 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11336 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11337 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11338 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11339 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11340 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11341 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11342 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11343 | 12409308 | Protein kinase C isoforms and tumor necrosis factor alpha (TNFalpha) signaling pathways are well described mediators of insulin resistance; they are implicated in the activation of IKKbeta and the subsequent inhibition of proximal insulin signaling via insulin receptor substrate 1 (IRS1) and Akt. |
| 11344 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11345 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11346 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11347 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11348 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11349 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11350 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11351 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11352 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11353 | 12409308 | This study investigated the effect of salicylic acid on phorbol 12-myristate 13-acetate (PMA)- and TNFalpha-induced insulin resistance in a human embryonic kidney 293 (HEK293) cell line stably expressing recombinant human IRS1. |
| 11354 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11355 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11356 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11357 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11358 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11359 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11360 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11361 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11362 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11363 | 12409308 | The results showed that both PMA and TNFalpha inhibited insulin-induced Akt phosphorylation and promoted IRS1 phosphorylation on Ser-307. |
| 11364 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11365 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11366 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11367 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11368 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11369 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11370 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11371 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11372 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11373 | 12409308 | Salicylic acid pretreatment completely reversed the effects of PMA and TNFalpha on both Akt and IRS1. |
| 11374 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11375 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11376 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11377 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11378 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11379 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11380 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11381 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11382 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11383 | 12409308 | Whereas PMA activated protein kinase C isoforms and IKKbeta, TNFalpha activated neither. |
| 11384 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11385 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11386 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11387 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11388 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11389 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11390 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11391 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11392 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11393 | 12409308 | On the other hand, both PMA and TNFalpha activated the c-Jun N-terminal kinase (JNK), which has been reported to directly phosphorylate IRS1 Ser-307. |
| 11394 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11395 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11396 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11397 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11398 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11399 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11400 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11401 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11402 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11403 | 12409308 | SP600125, a JNK inhibitor, prevented PMA and TNFalpha-induced IRS1 Ser-307 phosphorylation. |
| 11404 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11405 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11406 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11407 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11408 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11409 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11410 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11411 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11412 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11413 | 12409308 | Finally, salicylic acid inhibited JNK activation induced by both PMA and TNFalpha. |
| 11414 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11415 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11416 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11417 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11418 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11419 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11420 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11421 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11422 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11423 | 12409308 | Taken together, these observations suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via an IKKbeta-independent mechanism(s), potentially involving the inhibition of JNK activation. |
| 11424 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11425 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11426 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11427 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11428 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11429 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11430 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11431 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11432 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11433 | 12409308 | The role of JNK in salicylic acid-mediated insulin sensitization, however, requires further validation because the JNK inhibitor SP600125 appears to have other nonspecific activity in addition to inhibiting JNK activity. |
| 11434 | 12403851 | Peroxisome proliferator-activated receptor gamma (PPAR-gamma) plays a key role in adipocyte differentiation and insulin sensitivity. |
| 11435 | 12403851 | Here, we report on the identification of a new synthetic PPARgamma antagonist, the phosphonophosphate SR-202, which inhibits both TZD-stimulated recruitment of the coactivator steroid receptor coactivator-1 and TZD-induced transcriptional activity of the receptor. |
| 11436 | 12403851 | In vivo, decreasing PPARgamma activity, either by treatment with SR-202 or by invalidation of one allele of the PPARgamma gene, leads to a reduction of both high fat diet-induced adipocyte hypertrophy and insulin resistance. |
| 11437 | 12403851 | These effects are accompanied by a smaller size of the adipocytes and a reduction of TNFalpha and leptin secretion. |
| 11438 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11439 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11440 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11441 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11442 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11443 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11444 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11445 | 12401708 | Profiling gene transcription in vivo reveals adipose tissue as an immediate target of tumor necrosis factor-alpha: implications for insulin resistance. |
| 11446 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11447 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11448 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11449 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11450 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11451 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11452 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11453 | 12401708 | Despite extensive studies implicating tumor necrosis factor (TNF)-alpha as a contributing cause of insulin resistance, the mechanism(s) by which TNF-alpha alters energy metabolism in vivo and the tissue specificity of TNF-alpha action are unclear. |
| 11454 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11455 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11456 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11457 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11458 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11459 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11460 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11461 | 12401708 | A 1-day TNF-alpha treatment decreased overall insulin sensitivity and caused a 70% increase (P = 0.005) in plasma levels of free fatty acids (FFAs) and a 46% decrease (P = 0.01) in ACRP30. |
| 11462 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11463 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11464 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11465 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11466 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11467 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11468 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11469 | 12401708 | A 4-day TNF-alpha infusion caused insulin resistance and significant elevation of plasma levels of FFAs and triglycerides and reduction of ACRP30. |
| 11470 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11471 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11472 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11473 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11474 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11475 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11476 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11477 | 12401708 | As revealed by oligonucleotide microarrays, TNF-alpha evoked major and rapid changes in adipocyte gene expression, favoring FFA release and cytokine production, and fewer changes in liver gene expression, but favoring FFA and cholesterol synthesis and VLDL production. |
| 11478 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11479 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11480 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11481 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11482 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11483 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11484 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11485 | 12401708 | We demonstrate that TNF-alpha antagonizes the actions of insulin, at least in part, through regulation of adipocyte gene expression including reduction in ACRP30 mRNA and induction of lipolysis resulting in increased plasma FFAs. |
| 11486 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11487 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11488 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11489 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11490 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11491 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11492 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11493 | 12401708 | TNF-alpha later alters systemic energy homeostasis that closely resembles the insulin resistance phenotype. |
| 11494 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11495 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11496 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11497 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11498 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11499 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11500 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11501 | 12401708 | Our data suggest that blockade of TNF-alpha action in adipose tissue may prevent TNF-alpha-induced insulin resistance in vivo. |
| 11502 | 12398773 | Conversely, insulin suppresses production of tumor necrosis factor-alpha and free radicals, enhances endothelial nitric oxide generation, and improves myocardial function. |
| 11503 | 12397577 | The diversity of these secretory factors include enzymes (lipoprotein lipase (LPL) and adipsin), growth factors [vascular endothelial growth factor (VEGF)], cytokines (tumor necrosis factor-alpha, interleukin 6) and several other hormones involved in fatty acid and glucose metabolism (leptin, Acrp30, resistin and acylation stimulation protein). |
| 11504 | 12397577 | In this article, we will review the current knowledge of the trafficking and secretion processes that take place in adipocytes, focusing our attention on two of the best characterized adipokine molecules (leptin and adiponectin) and on one of the most intensively studied regulated membrane proteins, the GLUT4 glucose transporter. |
| 11505 | 12388406 | Administration of a soluble TNF antagonist (TNFR:Fc) to diabetic rats reduces urinary TNF excretion and prevents Na retention and renal hypertrophy. |
| 11506 | 12384822 | Adiponectin expression and/or secretion is increased by insulin like growth factor-1 and ionomycin, and decreased by tumor necrosis factor-alpha, glucocorticoids, beta-adrenergic agonists and cAMP. |
| 11507 | 12384822 | Moreover, adiponectin expression and secretion are increased by activators of peroxisome proliferator-activated receptor (PPAR)-gamma. |
| 11508 | 12384822 | Besides inhibiting inflammatory pathways, recombinant adiponectin increases insulin sensitivity and improves glucose tolerance in various animal models. |
| 11509 | 12384822 | In humans, plasma adiponectin concentrations exceed those of any other hormone by a thousand times; they decrease with obesity and are positively associated with whole-body insulin sensitivity. |
| 11510 | 12384822 | Therefore, low adiponectin may contribute to the decrease in whole-body insulin sensitivity that accompanies obesity. |
| 11511 | 12384822 | Furthermore, there is increasing evidence that genetic variants in the adiponectin gene itself and/or in genes encoding adiponectin-regulatory proteins--such as PPAR-gamma--may be associated with hypoadiponectinemia, insulin resistance and type 2 diabetes. |
| 11512 | 12384822 | This suggests that adiponectin may reflect PPAR-gamma activity in vivo. |
| 11513 | 12371151 | They may also be regulated by endocrine factors like insulin and insulin-like growth factor I (IGF-I) and cytokines such as interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha). |
| 11514 | 12366785 | HLA-DRB1 and MHC class 1 chain-related A haplotypes in Basque families with celiac disease. |
| 11515 | 12366785 | Recent publications have pointed to the possibility that a second, independent susceptibility locus could be located in the same genomic region, and a triplet repeat polymorphism in exon 5 of the gene MHC class I chain-related protein A (MICA; located between TNFA and HLA-B) has been associated with several autoimmune disorders, including type 1 diabetes mellitus (DM1) and Addison's disease. |
| 11516 | 12366785 | On the other hand, a single amino acid change in exon 3 of MICA (M129V) has been shown to strongly reduce MICA binding to NKG2D, an activating natural killer receptor expressed also on T cells, and this could have significant effects on autoimmune reactions. |
| 11517 | 12366785 | In this study, we have analyzed the contribution of these polymorphisms to CD in 37 Basque families, and have constructed MICA-HLA-DRB1 haplotypes to determine whether MICA has an effect independent from the HLA class II conferred risk. |
| 11518 | 12366785 | In view of our results, both HLA-DRB1 and MICA are associated with CD, but stratification analysis did not show any independent contribution of the MICA polymorphisms analyzed to CD risk. |
| 11519 | 12366785 | Besides, MICA allele A4 (also A5.1 was associated with risk for CD and other diseases) is in strong linkage disequilibrium with HLA-DRB1*0301. |
| 11520 | 12364459 | Serum corticosteroid-binding globulin concentration and insulin resistance syndrome: a population study. |
| 11521 | 12364459 | Corticosteroid-binding globulin (CBG), the main plasma protein transport for cortisol, has been shown to be negatively regulated by insulin and IL-6, at least in vitro, suggesting that insulin resistance and inflammation may both contribute to decreasing CBG levels. |
| 11522 | 12364459 | In the present study we measured CBG concentrations in a human healthy population and investigated the relationships of CBG with anthropometric and biochemical markers for inflammation and/or insulin resistance. |
| 11523 | 12364459 | In both sexes serum CBG levels were correlated negatively with age (r = -0.12; P = 0.04), body mass index (r = -0.31; P < 0.0001), waist to hip ratio (WHR; r = -0.39; P < 0.0001), systolic (r = -0.15; P < 0.01) and diastolic (r = -0.15; P = 0.01) blood pressures, and HOMA, an index of insulin resistance (r = -0.12; P = 0.04). |
| 11524 | 12364459 | In addition, the CBG concentration was negatively associated with serum IL-6 concentrations (r = -0.23; P = 0.017) and with the soluble fraction of TNFalpha receptors, soluble TNF receptor 1 (sTNFR1; r = -0.35; P < 0.0001), and sTNFR2 (r = -0.56; P < 0.0001) in women. |
| 11525 | 12364459 | A stepwise regression analysis using CBG as an independent variable showed that sex (P < 0.00001), body mass index (P = 0.0002), and HOMA (P = 0.0005), but not systolic blood pressure, diastolic blood pressure, IL-6, sTNFR1, or sTNFR2, constituted significant independent factors that explained 21% of the CBG variance (14%, 2%, and 5%, respectively). |
| 11526 | 12364459 | These findings support the hypothesis that the CBG level is an interesting indicator for both insulin resistance and low grade inflammation. |
| 11527 | 12364459 | Whether the decrease in CBG levels is genetic by nature or directly associated to increased insulin and/or IL-6 merits further investigation. |
| 11528 | 12364459 | Nevertheless, because CBG has been shown to be expressed by the adipose tissue, decreased CBG could create locally increased cortisol disposal, with no change in circulating cortisol, and facilitate fat accumulation, insulin resistance, and type 2 diabetes. |
| 11529 | 12361776 | We present data showing alterations in tumor necrosis factor-alpha production, insulin secretion, and amino acid metabolism in pancreatic islets of Langerhans cultured in a ground-based cell culture bioreactor that mimics some of the effects of microgravity. |
| 11530 | 12352144 | We studied the effects of TZDs (peroxisome proliferator-activated receptor-gamma [PPARgamma] agonists) and a PPARalpha agonist on HIV replication and TNFalpha production in peripheral blood mononuclear cells (PBMCs) acutely infected with HIV-1, in a chronically infected monoblastoid cell line (U1) and in alveolar macrophages (AMs) from HIV-infected subjects and uninfected controls. |
| 11531 | 12352144 | We studied the effects of TZDs (peroxisome proliferator-activated receptor-gamma [PPARgamma] agonists) and a PPARalpha agonist on HIV replication and TNFalpha production in peripheral blood mononuclear cells (PBMCs) acutely infected with HIV-1, in a chronically infected monoblastoid cell line (U1) and in alveolar macrophages (AMs) from HIV-infected subjects and uninfected controls. |
| 11532 | 12352144 | Rosiglitazone, ciglitazone, troglitazone, and PgJ (PPARgamma agonists) as well as fenofibrate (PPARalpha agonist) inhibited HIV replication in both PBMCs and U1 cells. |
| 11533 | 12352144 | Rosiglitazone, ciglitazone, troglitazone, and PgJ (PPARgamma agonists) as well as fenofibrate (PPARalpha agonist) inhibited HIV replication in both PBMCs and U1 cells. |
| 11534 | 12352144 | Modulation of these pathways using PPAR agonists may improve the metabolic alterations during HAART in conjunction with desirable decreases in HIV replication and TNFalpha production. |
| 11535 | 12352144 | Modulation of these pathways using PPAR agonists may improve the metabolic alterations during HAART in conjunction with desirable decreases in HIV replication and TNFalpha production. |
| 11536 | 12351658 | One mechanism mediating insulin resistance may involve the phosphorylation of serine residues in insulin receptor substrate-1 (IRS-1), leading to impairment in the ability of IRS-1 to activate downstream phosphatidylinositol 3-kinase-dependent pathways. |
| 11537 | 12351658 | One mechanism mediating insulin resistance may involve the phosphorylation of serine residues in insulin receptor substrate-1 (IRS-1), leading to impairment in the ability of IRS-1 to activate downstream phosphatidylinositol 3-kinase-dependent pathways. |
| 11538 | 12351658 | Insulin-resistant states and serine phosphorylation of IRS-1 are associated with the activation of the inhibitor kappaB kinase (IKK) complex. |
| 11539 | 12351658 | Insulin-resistant states and serine phosphorylation of IRS-1 are associated with the activation of the inhibitor kappaB kinase (IKK) complex. |
| 11540 | 12351658 | In this study, using phosphospecific antibodies against rat IRS-1 phosphorylated at Ser(307) (equivalent to Ser(312) in human IRS-1), we observed serine phosphorylation of IRS-1 in response to TNF-alpha or calyculin A treatment that paralleled surrogate markers for IKK activation. |
| 11541 | 12351658 | In this study, using phosphospecific antibodies against rat IRS-1 phosphorylated at Ser(307) (equivalent to Ser(312) in human IRS-1), we observed serine phosphorylation of IRS-1 in response to TNF-alpha or calyculin A treatment that paralleled surrogate markers for IKK activation. |
| 11542 | 12351658 | The phosphorylation of human IRS-1 at Ser(312) in response to tumor necrosis factor-alpha was significantly reduced in cells pretreated with the IKK inhibitor 15 deoxy-prostaglandin J(2) as well as in cells derived from IKK knock-out mice. |
| 11543 | 12351658 | The phosphorylation of human IRS-1 at Ser(312) in response to tumor necrosis factor-alpha was significantly reduced in cells pretreated with the IKK inhibitor 15 deoxy-prostaglandin J(2) as well as in cells derived from IKK knock-out mice. |
| 11544 | 12351658 | Taken together, our data suggest that IRS-1 is a novel direct substrate for IKK and that phosphorylation of IRS-1 at Ser(312) (and other sites) by IKK may contribute to the insulin resistance mediated by activation of inflammatory pathways. |
| 11545 | 12351658 | Taken together, our data suggest that IRS-1 is a novel direct substrate for IKK and that phosphorylation of IRS-1 at Ser(312) (and other sites) by IKK may contribute to the insulin resistance mediated by activation of inflammatory pathways. |
| 11546 | 12351485 | Increased plasma-soluble tumor necrosis factor-alpha receptor 2 level in lean nondiabetic offspring of type 2 diabetic subjects. |
| 11547 | 12351435 | The insulin-sensitizing effects of thiazolidinediones are thought to be mediated through peroxisome proliferator-activated receptor-gamma, a nuclear receptor that is highly abundant in adipose tissue. |
| 11548 | 12351435 | It has been reported that adipocytes secrete a variety of proteins, including tumor necrosis factor-alpha, resistin, plasminogen activator inhibitor-1, and adiponectin. |
| 11549 | 12351435 | Adiponectin is a fat cell-secreted protein that has been reported to increase fat oxidation and improve insulin sensitivity. |
| 11550 | 12351435 | Adiponectin levels correlated with R(d) (r = 0.46, P = 0.016) and HDL cholesterol levels (r = 0.59, P < 0.001) and negatively correlated with fasting insulin (r = -0.39, P = 0.042) and plasma triglyceride (r = -0.61, P < 0.001). |
| 11551 | 12351435 | Insulin also appears to suppress adiponectin levels. |
| 11552 | 12351435 | These findings suggest that adiponectin can be regulated by obesity, diabetes, TZDs, and insulin, and it may play a physiologic role in enhancing insulin sensitivity. |
| 11553 | 12351432 | However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). |
| 11554 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11555 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11556 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11557 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11558 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11559 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11560 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 11561 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11562 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11563 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11564 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11565 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11566 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11567 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 11568 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11569 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11570 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11571 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11572 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11573 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11574 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 11575 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11576 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11577 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11578 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11579 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11580 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11581 | 12351429 | Coincubation with TNF-alpha and MEK inhibitors caused perilipin to migrate as a single 65-kDa band. |
| 11582 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11583 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11584 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11585 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11586 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11587 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11588 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 11589 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11590 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11591 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11592 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11593 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11594 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11595 | 12351429 | Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and the electrophoretic shift of perilipin, suggesting a role for PKA in TNF-alpha-induced lipolysis. |
| 11596 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11597 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11598 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11599 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11600 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11601 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11602 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 11603 | 12239591 | In the present study, we evaluated whether stimulation of human PTEC by LPS is modulated through the soluble or the membrane form of the LPS receptor CD14. |
| 11604 | 12239591 | In the presence of sCD14 and LPS binding protein (LBP), PTEC were 10 to 100-fold more sensitive to LPS activation, resulting in cytokine production (IL-6, IL-8 and TNF-alpha) and NO release. |
| 11605 | 12239095 | Effect of proinflammatory cytokines on gene expression of the diabetes-associated autoantigen IA-2 in INS-1 cells. |
| 11606 | 12239095 | Effect of proinflammatory cytokines on gene expression of the diabetes-associated autoantigen IA-2 in INS-1 cells. |
| 11607 | 12239095 | Effect of proinflammatory cytokines on gene expression of the diabetes-associated autoantigen IA-2 in INS-1 cells. |
| 11608 | 12239095 | Inhibition of insulin expression has been described, but their effects on other major target autoantigens, such as the tyrosine phosphatase-like protein IA-2, is not known. |
| 11609 | 12239095 | Inhibition of insulin expression has been described, but their effects on other major target autoantigens, such as the tyrosine phosphatase-like protein IA-2, is not known. |
| 11610 | 12239095 | Inhibition of insulin expression has been described, but their effects on other major target autoantigens, such as the tyrosine phosphatase-like protein IA-2, is not known. |
| 11611 | 12239095 | In the present study, we established sensitive real-time RT-PCR to measure IA-2, insulin, and inducible nitric oxide (NO) synthase (iNOS) mRNA expression. |
| 11612 | 12239095 | In the present study, we established sensitive real-time RT-PCR to measure IA-2, insulin, and inducible nitric oxide (NO) synthase (iNOS) mRNA expression. |
| 11613 | 12239095 | In the present study, we established sensitive real-time RT-PCR to measure IA-2, insulin, and inducible nitric oxide (NO) synthase (iNOS) mRNA expression. |
| 11614 | 12239095 | Rat insulinoma INS-1 cells were stimulated with IL-1beta, TNF-alpha, interferon (IFN)-gamma, and IL-2 as well as with two combinations of these cytokines (C1: IL-1beta + TNF-alpha + IFN-gamma; C2: TNF-alpha + IFN-gamma). |
| 11615 | 12239095 | Rat insulinoma INS-1 cells were stimulated with IL-1beta, TNF-alpha, interferon (IFN)-gamma, and IL-2 as well as with two combinations of these cytokines (C1: IL-1beta + TNF-alpha + IFN-gamma; C2: TNF-alpha + IFN-gamma). |
| 11616 | 12239095 | Rat insulinoma INS-1 cells were stimulated with IL-1beta, TNF-alpha, interferon (IFN)-gamma, and IL-2 as well as with two combinations of these cytokines (C1: IL-1beta + TNF-alpha + IFN-gamma; C2: TNF-alpha + IFN-gamma). |
| 11617 | 12239095 | Treatment with IL-1beta, TNF-alpha, or IFN-gamma alone caused a significant down-regulation of IA-2 and insulin mRNA levels in a time and dose-dependent manner, whereas IL-2 had no effect. |
| 11618 | 12239095 | Treatment with IL-1beta, TNF-alpha, or IFN-gamma alone caused a significant down-regulation of IA-2 and insulin mRNA levels in a time and dose-dependent manner, whereas IL-2 had no effect. |
| 11619 | 12239095 | Treatment with IL-1beta, TNF-alpha, or IFN-gamma alone caused a significant down-regulation of IA-2 and insulin mRNA levels in a time and dose-dependent manner, whereas IL-2 had no effect. |
| 11620 | 12239095 | The hypothesis that the formation of NO is involved in IA-2 regulation was confirmed by the finding that the coincubation of C1 with 4 mM L-N(G)-monomethyL-L-arginine, an inhibitor of the iNOS, partly reversed the down-regulation of IA-2. |
| 11621 | 12239095 | The hypothesis that the formation of NO is involved in IA-2 regulation was confirmed by the finding that the coincubation of C1 with 4 mM L-N(G)-monomethyL-L-arginine, an inhibitor of the iNOS, partly reversed the down-regulation of IA-2. |
| 11622 | 12239095 | The hypothesis that the formation of NO is involved in IA-2 regulation was confirmed by the finding that the coincubation of C1 with 4 mM L-N(G)-monomethyL-L-arginine, an inhibitor of the iNOS, partly reversed the down-regulation of IA-2. |
| 11623 | 12239095 | In conclusion, we have demonstrated for the first time that IL-1beta, TNF-alpha, and IFN-gamma exert a strong inhibitory effect on expression of the diabetes autoantigen IA-2. |
| 11624 | 12239095 | In conclusion, we have demonstrated for the first time that IL-1beta, TNF-alpha, and IFN-gamma exert a strong inhibitory effect on expression of the diabetes autoantigen IA-2. |
| 11625 | 12239095 | In conclusion, we have demonstrated for the first time that IL-1beta, TNF-alpha, and IFN-gamma exert a strong inhibitory effect on expression of the diabetes autoantigen IA-2. |
| 11626 | 12235730 | Adipocytes secrete numerous substances that contribute to peripheral insulin resistance, including adiponectin, resistin, TNF-alpha and interleukin 6. |
| 11627 | 12235730 | The new class of thiazolidinediones (glitazones), binding to the peroxisome proliferator activated receptor (PPAR-gamma) lowers the levels of resistin and increases adiponectin, resulting in an improvement of glucose homeostasis. |
| 11628 | 12231076 | Inflammatory mediators, including plasma interleukin 6, tumor necrosis factor alpha, and tumor necrosis factor R are elevated in these individuals. |
| 11629 | 12231073 | In addition, recently identified adipocyte-specific chemical messengers, the adipocytokines, such as tumor necrosis factor-alpha, adiponectin, and resistin, appear to modulate the underlying insulin resistance. |
| 11630 | 12231073 | The thiazolidinediones are potent peroxisome proliferator-activated receptor-gamma agonists and directly improve insulin resistance and glycemic control in patients with type 2 diabetes. |
| 11631 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 11632 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 11633 | 12221281 | Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice. |
| 11634 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 11635 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 11636 | 12221281 | CD4+CD25+ T cells have been implicated as mediators of self-tolerance. |
| 11637 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 11638 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 11639 | 12221281 | We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred. |
| 11640 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 11641 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 11642 | 12221281 | These data suggest that alterations in the number and function of CD4+CD25+ T cells may be one mechanism by which TNF and anti-TNF modulate type I diabetes mellitus in NOD mice. |
| 11643 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11644 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11645 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11646 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11647 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11648 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11649 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11650 | 12200753 | Evidence that tumor necrosis factor-alpha-induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats. |
| 11651 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11652 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11653 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11654 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11655 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11656 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11657 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11658 | 12200753 | Administration of tumor necrosis factor-alpha (TNF-alpha) acutely increases leptin gene expression and circulating leptin concentrations in rodents and humans. |
| 11659 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11660 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11661 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11662 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11663 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11664 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11665 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11666 | 12200753 | Since TNF-alpha also induces hyperinsulinemia, and because insulin is a potent stimulator of leptin production, we hypothesized that elevated plasma insulin mediates TNF-alpha-induced increases of circulating leptin. |
| 11667 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11668 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11669 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11670 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11671 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11672 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11673 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11674 | 12200753 | STZ-diabetic and nondiabetic rats were injected with TNF-alpha or vehicle; plasma leptin, insulin, and glucose concentrations were measured during an initial 12-hour postinjection period of fasting and after a subsequent 12-hour period of refeeding. |
| 11675 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11676 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11677 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11678 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11679 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11680 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11681 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11682 | 12200753 | In nondiabetic rats, TNF-alpha increased plasma insulin (P =.016) and prevented the fasting-induced decrease of circulating leptin (P =.004) over the initial 12 hours compared with vehicle. |
| 11683 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11684 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11685 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11686 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11687 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11688 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11689 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11690 | 12200753 | In contrast, TNF-alpha did not affect leptin concentrations in STZ-diabetic animals with clamped plasma insulin levels or their food intake during the refeeding period. |
| 11691 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11692 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11693 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11694 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11695 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11696 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11697 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11698 | 12200753 | These results suggest that TNF-alpha-induced hyperinsulinemia likely mediates the stimulatory effect of TNF-alpha on circulating leptin in vivo. |
| 11699 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11700 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11701 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11702 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11703 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11704 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11705 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11706 | 12200753 | Elevated leptin levels may in turn contribute to the effect of TNF-alpha to decrease food intake. |
| 11707 | 12186840 | CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer. |
| 11708 | 12186840 | These mice have GAD65-specific CD4(+) T cells, as shown by staining with an I-A(g7)(p286) tetramer reagent. |
| 11709 | 12186840 | Lymphocytes from these TCR transgenic mice proliferate and make interferon gamma, interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and IL-10 when stimulated in vitro with GAD65 peptide 286-300, yet these TCR transgenic animals do not spontaneously develop diabetes, and insulitis is virtually undetectable. |
| 11710 | 12186840 | Furthermore, in vitro activated CD4 T cells from GAD 286 TCR transgenic mice express higher levels of CTL-associated antigen (CTLA)-4 than nontransgenic littermates. |
| 11711 | 12186840 | CD4(+) T cells, or p286-tetramer(+)CD4(+) Tcells, from GAD65 286-300-specific TCR transgenic mice delay diabetes induced in NOD.scid mice by diabetic NOD spleen cells. |
| 11712 | 12182843 | Supernatants from cultured splenocytes and peritoneal cells taken from Linomide-treated mice contained lower levels of TNFalpha, IL-1 beta, IFN gamma and IL-12 versus higher levels of IL-4, IL-6 and IL-10 in comparison with supernatants from cultures of untreated mice. |
| 11713 | 12173692 | The mechanism of action involves binding to the peroxisome proliferator-activated receptor (PPAR)gamma, a transcription factor that regulates the expression of specific genes especially in fat cells but also in other tissues. |
| 11714 | 12173692 | Thiazolidinediones have been shown to interfere with expression and release of mediators of insulin resistance originating in adipose tissue (e.g. free fatty acids, adipocytokines such as tumor necrosis factor alpha, resistin, adiponectin) in a way that results in net improvement of insulin sensitivity (i.e. in muscle and liver). |
| 11715 | 12160520 | Regulation of the interleukin-1 receptor antagonist in THP-1 cells by ligands of the peroxisome proliferator-activated receptor gamma. |
| 11716 | 12160520 | Regulation of the interleukin-1 receptor antagonist in THP-1 cells by ligands of the peroxisome proliferator-activated receptor gamma. |
| 11717 | 12160520 | Regulation of the interleukin-1 receptor antagonist in THP-1 cells by ligands of the peroxisome proliferator-activated receptor gamma. |
| 11718 | 12160520 | High concentrations of PPARgamma ligands were shown to have anti-inflammatory activities by inhibiting the secretion of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFalpha) by stimulated monocytes. |
| 11719 | 12160520 | High concentrations of PPARgamma ligands were shown to have anti-inflammatory activities by inhibiting the secretion of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFalpha) by stimulated monocytes. |
| 11720 | 12160520 | High concentrations of PPARgamma ligands were shown to have anti-inflammatory activities by inhibiting the secretion of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFalpha) by stimulated monocytes. |
| 11721 | 12160520 | The aim of this study was to determine whether PGJ2 and TZDs would also exert an immunomodulatory action through the up-regulation of anti-inflammatory cytokines such as the IL-1 receptor antagonist (IL-1Ra). |
| 11722 | 12160520 | The aim of this study was to determine whether PGJ2 and TZDs would also exert an immunomodulatory action through the up-regulation of anti-inflammatory cytokines such as the IL-1 receptor antagonist (IL-1Ra). |
| 11723 | 12160520 | The aim of this study was to determine whether PGJ2 and TZDs would also exert an immunomodulatory action through the up-regulation of anti-inflammatory cytokines such as the IL-1 receptor antagonist (IL-1Ra). |
| 11724 | 12160520 | THP-1 monocytic cells were stimulated with PMA, thereby enhancing the secretion of IL-1, IL-6, TNFalpha, IL-1Ra and metalloproteinases. |
| 11725 | 12160520 | THP-1 monocytic cells were stimulated with PMA, thereby enhancing the secretion of IL-1, IL-6, TNFalpha, IL-1Ra and metalloproteinases. |
| 11726 | 12160520 | THP-1 monocytic cells were stimulated with PMA, thereby enhancing the secretion of IL-1, IL-6, TNFalpha, IL-1Ra and metalloproteinases. |
| 11727 | 12160520 | Addition of PGJ2 had an inhibitory effect on IL-1, IL-6 and TNFalpha secretion, while increasing IL-1Ra production. |
| 11728 | 12160520 | Addition of PGJ2 had an inhibitory effect on IL-1, IL-6 and TNFalpha secretion, while increasing IL-1Ra production. |
| 11729 | 12160520 | Addition of PGJ2 had an inhibitory effect on IL-1, IL-6 and TNFalpha secretion, while increasing IL-1Ra production. |
| 11730 | 12160520 | In contrast, the bona fide PPARgamma ligands (TZDs; rosiglitazone, pioglitazone and troglitazone) barely inhibited proinflammatory cytokines, but strongly enhanced the production of IL-1Ra from PMA-stimulated THP-1 cells. |
| 11731 | 12160520 | In contrast, the bona fide PPARgamma ligands (TZDs; rosiglitazone, pioglitazone and troglitazone) barely inhibited proinflammatory cytokines, but strongly enhanced the production of IL-1Ra from PMA-stimulated THP-1 cells. |
| 11732 | 12160520 | In contrast, the bona fide PPARgamma ligands (TZDs; rosiglitazone, pioglitazone and troglitazone) barely inhibited proinflammatory cytokines, but strongly enhanced the production of IL-1Ra from PMA-stimulated THP-1 cells. |
| 11733 | 12160520 | Unstimulated cells did not respond to TZDs in terms of IL-1Ra production, suggesting that in order to be effective, PPAR ligands depend on PMA signalling. |
| 11734 | 12160520 | Unstimulated cells did not respond to TZDs in terms of IL-1Ra production, suggesting that in order to be effective, PPAR ligands depend on PMA signalling. |
| 11735 | 12160520 | Unstimulated cells did not respond to TZDs in terms of IL-1Ra production, suggesting that in order to be effective, PPAR ligands depend on PMA signalling. |
| 11736 | 12145160 | Peripheral blood mononuclear cells (PBMCs) of 25 patients with newly diagnosed type 1 diabetes, 10 patients with longstanding type 1 diabetes, and 35 healthy control subjects were examined for expression of the chemokine receptors CXCR4 (naive T-cells), CCR5 and CXCR3 (Th1 associated), and CCR3 and CCR4 (Th2 associated) on CD3+ lymphocytes. |
| 11737 | 12145160 | Peripheral blood mononuclear cells (PBMCs) of 25 patients with newly diagnosed type 1 diabetes, 10 patients with longstanding type 1 diabetes, and 35 healthy control subjects were examined for expression of the chemokine receptors CXCR4 (naive T-cells), CCR5 and CXCR3 (Th1 associated), and CCR3 and CCR4 (Th2 associated) on CD3+ lymphocytes. |
| 11738 | 12145160 | Furthermore, we analyzed chemokine serum levels (monocyte chemoattractant protein [MCP]-1, macrophage inflammatory protein [MIP]-1alpha, MIP-1beta, and RANTES [regulated on activation, normal T-cell expressed and secreted]) and phytohemagglutinin (PHA)-stimulated cytokine secretion of Th1- (gamma-interferon [IFN-gamma] and tumor necrosis factor-alpha [TNF-alpha]) and Th2 (interleukin [IL]-4 and -10)-associated cytokines by PBMC. |
| 11739 | 12145160 | Furthermore, we analyzed chemokine serum levels (monocyte chemoattractant protein [MCP]-1, macrophage inflammatory protein [MIP]-1alpha, MIP-1beta, and RANTES [regulated on activation, normal T-cell expressed and secreted]) and phytohemagglutinin (PHA)-stimulated cytokine secretion of Th1- (gamma-interferon [IFN-gamma] and tumor necrosis factor-alpha [TNF-alpha]) and Th2 (interleukin [IL]-4 and -10)-associated cytokines by PBMC. |
| 11740 | 12145160 | The PBMCs of patients with newly diagnosed but not with longstanding type 1 diabetes showed reduced expression of the Th1-associated chemokine receptors CCR5 (P < 0.001 vs. control subjects) and CXCR3 (P < 0.002 vs. control subjects). |
| 11741 | 12145160 | The PBMCs of patients with newly diagnosed but not with longstanding type 1 diabetes showed reduced expression of the Th1-associated chemokine receptors CCR5 (P < 0.001 vs. control subjects) and CXCR3 (P < 0.002 vs. control subjects). |
| 11742 | 12145160 | This reduction correlated with reduced IFN-gamma and TNF-alpha production of PBMCs after PHA stimulation and reversed 6-12 months after diagnosis to normal levels. |
| 11743 | 12145160 | This reduction correlated with reduced IFN-gamma and TNF-alpha production of PBMCs after PHA stimulation and reversed 6-12 months after diagnosis to normal levels. |
| 11744 | 12145160 | CCR4 cells were reduced in both newly diagnosed and longstanding type 1 diabetic patients, which correlated to reduced PHA-stimulated IL-4 production. |
| 11745 | 12145160 | CCR4 cells were reduced in both newly diagnosed and longstanding type 1 diabetic patients, which correlated to reduced PHA-stimulated IL-4 production. |
| 11746 | 12145160 | MIP-1alpha and MIP-1beta levels were considerably elevated in a subgroup of patients with newly diagnosed diabetes. |
| 11747 | 12145160 | MIP-1alpha and MIP-1beta levels were considerably elevated in a subgroup of patients with newly diagnosed diabetes. |
| 11748 | 12145147 | Insulin-induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 was completely blocked, with unaltered expression of IRS-1. |
| 11749 | 12145147 | Insulin-induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 was completely blocked, with unaltered expression of IRS-1. |
| 11750 | 12145147 | Troglitazone increased insulin action on IRS-1 phosphorylation, in both the absence and presence of co-culture. |
| 11751 | 12145147 | Troglitazone increased insulin action on IRS-1 phosphorylation, in both the absence and presence of co-culture. |
| 11752 | 12145147 | Insulin-regulated activation of Akt kinase in the myocytes was significantly reduced after co-culture, with troglitazone restoring insulin action. |
| 11753 | 12145147 | Insulin-regulated activation of Akt kinase in the myocytes was significantly reduced after co-culture, with troglitazone restoring insulin action. |
| 11754 | 12145147 | Addition of tumor necrosis factor (TNF)-alpha (2.5 nmol/l) to myocytes for 48 h reduced IRS-1 expression and inhibited IRS-1 and Akt phosphorylation comparable to the effect of co-culture. |
| 11755 | 12145147 | Addition of tumor necrosis factor (TNF)-alpha (2.5 nmol/l) to myocytes for 48 h reduced IRS-1 expression and inhibited IRS-1 and Akt phosphorylation comparable to the effect of co-culture. |
| 11756 | 12145147 | In conclusion, the release of fat cell factors induces insulin resistance in human skeletal muscle cells; however, TNF-alpha and resistin appear not to be involved in this process. |
| 11757 | 12145147 | In conclusion, the release of fat cell factors induces insulin resistance in human skeletal muscle cells; however, TNF-alpha and resistin appear not to be involved in this process. |
| 11758 | 12145143 | Peroxisome proliferator-activated receptor (PPAR)-gamma is a transcription factor with a key role in adipocyte differentiation. |
| 11759 | 12145143 | The Ala allele of the common Pro12Ala polymorphism in the isoform PPAR-gamma2 is associated with reduced risk for type 2 diabetes. |
| 11760 | 12145143 | The in vivo effects of the polymorphism are secondary to alterations in adipose tissue, where PPAR-gamma2 is predominantly expressed. |
| 11761 | 12145143 | Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. |
| 11762 | 12145143 | In conclusion, the Pro12Ala polymorphism in PPAR-gamma2 represents the first genetic variant with a broad impact on the risk of common type 2 diabetes. |
| 11763 | 12135329 | To evaluate the relative contribution of hypertension to early atherogenesis, we determined FMD, as well as plasma levels of tissue-type plasminogen activator (t-PA; a sensitive index of endothelial damage) and tumor necrosis factor (TNF)-a and interleukin (IL)-6 (established markers of inflammation) in normotensive and hypertensive patients under treatment. |
| 11764 | 12135329 | To evaluate the relative contribution of hypertension to early atherogenesis, we determined FMD, as well as plasma levels of tissue-type plasminogen activator (t-PA; a sensitive index of endothelial damage) and tumor necrosis factor (TNF)-a and interleukin (IL)-6 (established markers of inflammation) in normotensive and hypertensive patients under treatment. |
| 11765 | 12135329 | Plasma t-PA, TNF-alpha, and IL-6 levels were increased in hypertensives despite good blood pressure control. |
| 11766 | 12135329 | Plasma t-PA, TNF-alpha, and IL-6 levels were increased in hypertensives despite good blood pressure control. |
| 11767 | 12127570 | Five mitochondrial uncoupling proteins exist in the human gemone: UCP2, expressed ubiquitously; UCP1, exclusively in brown adipose tissue (BAT); UCP3, predominantly in muscle; UCP4 and BMCP (UCP5), in brain. |
| 11768 | 12127570 | UCP2 (UCP3) roles were inferred from transcriptional up-regulation mediated by FAs via peroxisome proliferator-activated receptors, cytokines, leptin signalling via hypothalamic pathway, and by thyroide and beta2 adrenergic stimulation. |
| 11769 | 12127570 | UCP2 (UCP3) may contribute to body weight regulation, although obesity was not induced in knockout (KO) mice. |
| 11770 | 12127570 | Up-regulated UCP2 transcription by pyrogenic cytokines (tumour necrosis factor alpha (TNFalpha)) suggested a role in fever. |
| 11771 | 12123627 | However, the interaction of the former with a receptor triggers the synthesis of cytokines particularly interleukin 1- beta(IL-1 beta) and tumour necrosis factor- alpha(TNFalpha ). |
| 11772 | 12123627 | However, the interaction of the former with a receptor triggers the synthesis of cytokines particularly interleukin 1- beta(IL-1 beta) and tumour necrosis factor- alpha(TNFalpha ). |
| 11773 | 12123627 | However, the interaction of the former with a receptor triggers the synthesis of cytokines particularly interleukin 1- beta(IL-1 beta) and tumour necrosis factor- alpha(TNFalpha ). |
| 11774 | 12123627 | At the end of the study, plasma glucose, fructosamine, total cholesterol (TC), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), the susceptibility of LDL to copper-catalysed oxidation, catalase activity, NO, IL-1 beta, TNF alpha were measured. |
| 11775 | 12123627 | At the end of the study, plasma glucose, fructosamine, total cholesterol (TC), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), the susceptibility of LDL to copper-catalysed oxidation, catalase activity, NO, IL-1 beta, TNF alpha were measured. |
| 11776 | 12123627 | At the end of the study, plasma glucose, fructosamine, total cholesterol (TC), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), the susceptibility of LDL to copper-catalysed oxidation, catalase activity, NO, IL-1 beta, TNF alpha were measured. |
| 11777 | 12123627 | Finally, it increased the synthesis and release of cytokine (IL-1beta and TNF alpha). |
| 11778 | 12123627 | Finally, it increased the synthesis and release of cytokine (IL-1beta and TNF alpha). |
| 11779 | 12123627 | Finally, it increased the synthesis and release of cytokine (IL-1beta and TNF alpha). |
| 11780 | 12119995 | There is now a preponderance of evidence that adipose tissue is a source of growth factors such as IGF-I, IGF binding proteins, TNF alpha, angiotensin II, and MCSF that are capable of stimulating proliferation. |
| 11781 | 12118901 | To address that question, we studied the inheritance patterns for polymorphisms in several cytokine genes (IL-2, IL-6, IL-10, TNF-alpha, TGF-beta, and IFN-gamma) within an ethnically diverse study population comprised of 216 Whites, 58 Blacks, 25 Hispanics, and 31 Asians. |
| 11782 | 12118901 | Blacks, Hispanics and Asians demonstrated marked differences in the inheritance of IL-6 alleles and IL-10 genotypes that result in high expression when compared with Whites. |
| 11783 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 11784 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 11785 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 11786 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 11787 | 12110133 | Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity. |
| 11788 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 11789 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 11790 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 11791 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 11792 | 12110133 | In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. |
| 11793 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 11794 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 11795 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 11796 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 11797 | 12110133 | The paradoxical effects of neonatal TNF-alpha administration in NOD mice in increasing incidence of and hastening onset of type 1 diabetes, while neonatal anti-TNF administration completely prevents all signs of islet cell autoimmunity, are due partly to the low levels of CD4+CD25+ T cells in NOD mice. |
| 11798 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 11799 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 11800 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 11801 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 11802 | 12110133 | In contrast, neonatal administration of anti-TNF-alpha results in a dramatic increase in the levels of CD4+CD25+ regulatory T cells, to levels beyond those seen in wild-type untreated NOD mice. |
| 11803 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 11804 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 11805 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 11806 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 11807 | 12110133 | TNF-alpha and LTalpha/beta thus have pleomorphic regulatory effects on the development and expression of autoimmunity. |
| 11808 | 12107724 | Impaired glucose tolerance is associated with increased serum concentrations of interleukin 6 and co-regulated acute-phase proteins but not TNF-alpha or its receptors. |
| 11809 | 12093872 | Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis. |
| 11810 | 12093872 | Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis. |
| 11811 | 12093872 | Tumor necrosis factor (TNF)-alpha was also required, although seemingly less critically than IL-1, because a proportion of TNF-alpha-deficient mice developed robust disease. |
| 11812 | 12093872 | Tumor necrosis factor (TNF)-alpha was also required, although seemingly less critically than IL-1, because a proportion of TNF-alpha-deficient mice developed robust disease. |
| 11813 | 12086962 | Fourth, the effect of AA on TNF-alpha secretion was inhibited by specific inhibitors of protein kinase A (H89), p38-mitogen-activated protein kinase (SB203580), and nuclear transcription factor (NF)kappaB (NFkappaB-SN50). |
| 11814 | 12086956 | Pericytes exposed to high glucose showed increased expression of Bax and of tumor necrosis factor-alpha, which were prevented by the NF-kappaB inhibitors and mimicked by transfection with the p65 subunit of NF-kappaB, and failed to increase the levels of the NF-kappaB-dependent inhibitors of apoptosis. |
| 11815 | 12086956 | Colocalization of activated NF-kappaB and Bax overexpression was observed in the retinal pericytes of diabetic donors. |
| 11816 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11817 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11818 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11819 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11820 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11821 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11822 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11823 | 12086951 | TNF-alpha is a predictor of insulin resistance in human pregnancy. |
| 11824 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11825 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11826 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11827 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11828 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11829 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11830 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11831 | 12086951 | The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. |
| 11832 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11833 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11834 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11835 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11836 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11837 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11838 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11839 | 12086951 | Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. |
| 11840 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11841 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11842 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11843 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11844 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11845 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11846 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11847 | 12086951 | TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). |
| 11848 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11849 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11850 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11851 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11852 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11853 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11854 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11855 | 12086951 | During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). |
| 11856 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11857 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11858 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11859 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11860 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11861 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11862 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11863 | 12086951 | Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). |
| 11864 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11865 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11866 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11867 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11868 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11869 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11870 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11871 | 12086951 | Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). |
| 11872 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11873 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11874 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11875 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11876 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11877 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11878 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11879 | 12086951 | These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy. |
| 11880 | 12086930 | In mature adipose tissue, subcutaneous adipocytes have higher leptin secretion, similar tumor necrosis factor (TNF)-alpha secretion, and lower catecholamine-stimulated lipolysis as compared with omental adipocytes. |
| 11881 | 12086930 | In mature adipose tissue, subcutaneous adipocytes have higher leptin secretion, similar tumor necrosis factor (TNF)-alpha secretion, and lower catecholamine-stimulated lipolysis as compared with omental adipocytes. |
| 11882 | 12086930 | In mature adipose tissue, subcutaneous adipocytes have higher leptin secretion, similar tumor necrosis factor (TNF)-alpha secretion, and lower catecholamine-stimulated lipolysis as compared with omental adipocytes. |
| 11883 | 12086930 | In this study, lipolysis and leptin and TNF-alpha secretion were compared between human omental and subcutaneous preadipocytes. |
| 11884 | 12086930 | In this study, lipolysis and leptin and TNF-alpha secretion were compared between human omental and subcutaneous preadipocytes. |
| 11885 | 12086930 | In this study, lipolysis and leptin and TNF-alpha secretion were compared between human omental and subcutaneous preadipocytes. |
| 11886 | 12086930 | In the presence of rosiglitazone, leptin secretion remained about three times higher and norepinephrine-induced lipolysis about six times lower in subcutaneous as compared with omental preadipocytes (P < 0.05), whereas TNF-alpha secretion and basal lipolysis were similar in preadipocytes from the two regions. |
| 11887 | 12086930 | In the presence of rosiglitazone, leptin secretion remained about three times higher and norepinephrine-induced lipolysis about six times lower in subcutaneous as compared with omental preadipocytes (P < 0.05), whereas TNF-alpha secretion and basal lipolysis were similar in preadipocytes from the two regions. |
| 11888 | 12086930 | In the presence of rosiglitazone, leptin secretion remained about three times higher and norepinephrine-induced lipolysis about six times lower in subcutaneous as compared with omental preadipocytes (P < 0.05), whereas TNF-alpha secretion and basal lipolysis were similar in preadipocytes from the two regions. |
| 11889 | 12086930 | Thus, regional differences in adipocyte leptin secretion as well as in norepinephrine-induced lipolysis are marked and present during different stages of preadipocyte differentiation and seem to be determined by intrinsic (i.e., primary) factors. |
| 11890 | 12086930 | Thus, regional differences in adipocyte leptin secretion as well as in norepinephrine-induced lipolysis are marked and present during different stages of preadipocyte differentiation and seem to be determined by intrinsic (i.e., primary) factors. |
| 11891 | 12086930 | Thus, regional differences in adipocyte leptin secretion as well as in norepinephrine-induced lipolysis are marked and present during different stages of preadipocyte differentiation and seem to be determined by intrinsic (i.e., primary) factors. |
| 11892 | 12067295 | An increase in mRNA levels for TNF and Tnfrsf1 in the bile ducts of Tnfsf5-/-(CD40 ligand or CD154 knockout) mice developing cholangitis following infection by Cryptosporidium parvum (CP) is accompanied by staining for TNFalpha in areas of inflammation. |
| 11893 | 12067295 | An increase in mRNA levels for TNF and Tnfrsf1 in the bile ducts of Tnfsf5-/-(CD40 ligand or CD154 knockout) mice developing cholangitis following infection by Cryptosporidium parvum (CP) is accompanied by staining for TNFalpha in areas of inflammation. |
| 11894 | 12067295 | An increase in mRNA levels for TNF and Tnfrsf1 in the bile ducts of Tnfsf5-/-(CD40 ligand or CD154 knockout) mice developing cholangitis following infection by Cryptosporidium parvum (CP) is accompanied by staining for TNFalpha in areas of inflammation. |
| 11895 | 12067295 | To determine whether TNF contributed to the bile duct damage seen in chronically-infected animals, we bred B6 mice with disrupted genes for Tnfrsf1a, Tnfrsf1b and Tnfsf5. |
| 11896 | 12067295 | To determine whether TNF contributed to the bile duct damage seen in chronically-infected animals, we bred B6 mice with disrupted genes for Tnfrsf1a, Tnfrsf1b and Tnfsf5. |
| 11897 | 12067295 | To determine whether TNF contributed to the bile duct damage seen in chronically-infected animals, we bred B6 mice with disrupted genes for Tnfrsf1a, Tnfrsf1b and Tnfsf5. |
| 11898 | 12067295 | Mice with disruptions of Tnfsf5, and either Tnfrsf1a or Tnfrsf1b, developed bile duct sclerosis similar to that seen in CD40 and Tnfsf5 knockouts. |
| 11899 | 12067295 | Mice with disruptions of Tnfsf5, and either Tnfrsf1a or Tnfrsf1b, developed bile duct sclerosis similar to that seen in CD40 and Tnfsf5 knockouts. |
| 11900 | 12067295 | Mice with disruptions of Tnfsf5, and either Tnfrsf1a or Tnfrsf1b, developed bile duct sclerosis similar to that seen in CD40 and Tnfsf5 knockouts. |
| 11901 | 12067295 | Our data indicate that signalling through either TNF receptor is sufficient for the bile duct damage that follows chronic CP infection in mice, with disruption of the Tnfsf5 molecule. |
| 11902 | 12067295 | Our data indicate that signalling through either TNF receptor is sufficient for the bile duct damage that follows chronic CP infection in mice, with disruption of the Tnfsf5 molecule. |
| 11903 | 12067295 | Our data indicate that signalling through either TNF receptor is sufficient for the bile duct damage that follows chronic CP infection in mice, with disruption of the Tnfsf5 molecule. |
| 11904 | 12065204 | Here, we studied the effect of pentoxifylline, a potent anti-inflammatory agent, on diabetes development in both BB rat models of insulin-dependent diabetes mellitus and investigated whether these effects were related to differential modulation of tumour necrosis factor (TNF)-alpha and interleukin-10. |
| 11905 | 12065204 | Here, we studied the effect of pentoxifylline, a potent anti-inflammatory agent, on diabetes development in both BB rat models of insulin-dependent diabetes mellitus and investigated whether these effects were related to differential modulation of tumour necrosis factor (TNF)-alpha and interleukin-10. |
| 11906 | 12065204 | Here, we studied the effect of pentoxifylline, a potent anti-inflammatory agent, on diabetes development in both BB rat models of insulin-dependent diabetes mellitus and investigated whether these effects were related to differential modulation of tumour necrosis factor (TNF)-alpha and interleukin-10. |
| 11907 | 12065204 | In both BB rat models, in vivo pentoxifylline treatment potently suppressed TNF-alpha, but only moderately affected interleukin-10 production in vitro. |
| 11908 | 12065204 | In both BB rat models, in vivo pentoxifylline treatment potently suppressed TNF-alpha, but only moderately affected interleukin-10 production in vitro. |
| 11909 | 12065204 | In both BB rat models, in vivo pentoxifylline treatment potently suppressed TNF-alpha, but only moderately affected interleukin-10 production in vitro. |
| 11910 | 12065204 | The observed pentoxifylline-induced increase of the interleukin-10/TNF-alpha ratio might be a mechanism for protection or delay of the diabetes development. |
| 11911 | 12065204 | The observed pentoxifylline-induced increase of the interleukin-10/TNF-alpha ratio might be a mechanism for protection or delay of the diabetes development. |
| 11912 | 12065204 | The observed pentoxifylline-induced increase of the interleukin-10/TNF-alpha ratio might be a mechanism for protection or delay of the diabetes development. |
| 11913 | 12058258 | In addition to the promoter polymorphism, TNFa and TNFc microsatellite genotypes were determined but these polymorphisms were not associated with morbidity or mortality. |
| 11914 | 12054123 | Effect of cytokines on production of insulin-like growth factor binding proteins (IGFBPs) from human fibroblasts in culture. |
| 11915 | 12054123 | Effect of cytokines on production of insulin-like growth factor binding proteins (IGFBPs) from human fibroblasts in culture. |
| 11916 | 12054123 | Effect of cytokines on production of insulin-like growth factor binding proteins (IGFBPs) from human fibroblasts in culture. |
| 11917 | 12054123 | Effect of cytokines on production of insulin-like growth factor binding proteins (IGFBPs) from human fibroblasts in culture. |
| 11918 | 12054123 | Bioactivity of Insulin-like growth factors (IGEs) are positively or negatively regulated by IGF binding proteins (IGFBPs). |
| 11919 | 12054123 | Bioactivity of Insulin-like growth factors (IGEs) are positively or negatively regulated by IGF binding proteins (IGFBPs). |
| 11920 | 12054123 | Bioactivity of Insulin-like growth factors (IGEs) are positively or negatively regulated by IGF binding proteins (IGFBPs). |
| 11921 | 12054123 | Bioactivity of Insulin-like growth factors (IGEs) are positively or negatively regulated by IGF binding proteins (IGFBPs). |
| 11922 | 12054123 | Both IL-1beta and TNF-alpha inhibited IGFBP-3 (42/38 KDa species) production in a concentration dependent manner judged by Western ligand blot. |
| 11923 | 12054123 | Both IL-1beta and TNF-alpha inhibited IGFBP-3 (42/38 KDa species) production in a concentration dependent manner judged by Western ligand blot. |
| 11924 | 12054123 | Both IL-1beta and TNF-alpha inhibited IGFBP-3 (42/38 KDa species) production in a concentration dependent manner judged by Western ligand blot. |
| 11925 | 12054123 | Both IL-1beta and TNF-alpha inhibited IGFBP-3 (42/38 KDa species) production in a concentration dependent manner judged by Western ligand blot. |
| 11926 | 12054123 | Moreover, the treatment with IL-1beta and TNF-alpha resulted in appearance of smaller mol weight (26 KDa) immunoreactive IGFBP-3 fragment(s) which lacked the ability to bind 125I-IGFs, indicating that these cytokines degrade IGFBP-3 via activation of proteases. |
| 11927 | 12054123 | Moreover, the treatment with IL-1beta and TNF-alpha resulted in appearance of smaller mol weight (26 KDa) immunoreactive IGFBP-3 fragment(s) which lacked the ability to bind 125I-IGFs, indicating that these cytokines degrade IGFBP-3 via activation of proteases. |
| 11928 | 12054123 | Moreover, the treatment with IL-1beta and TNF-alpha resulted in appearance of smaller mol weight (26 KDa) immunoreactive IGFBP-3 fragment(s) which lacked the ability to bind 125I-IGFs, indicating that these cytokines degrade IGFBP-3 via activation of proteases. |
| 11929 | 12054123 | Moreover, the treatment with IL-1beta and TNF-alpha resulted in appearance of smaller mol weight (26 KDa) immunoreactive IGFBP-3 fragment(s) which lacked the ability to bind 125I-IGFs, indicating that these cytokines degrade IGFBP-3 via activation of proteases. |
| 11930 | 12054123 | Both IL-1beta and TNF-alpha decreased production of IGFBP-4, whereas they increased that of IGFBP-6, IL-6 had little effect on production of IGFBPs. |
| 11931 | 12054123 | Both IL-1beta and TNF-alpha decreased production of IGFBP-4, whereas they increased that of IGFBP-6, IL-6 had little effect on production of IGFBPs. |
| 11932 | 12054123 | Both IL-1beta and TNF-alpha decreased production of IGFBP-4, whereas they increased that of IGFBP-6, IL-6 had little effect on production of IGFBPs. |
| 11933 | 12054123 | Both IL-1beta and TNF-alpha decreased production of IGFBP-4, whereas they increased that of IGFBP-6, IL-6 had little effect on production of IGFBPs. |
| 11934 | 12054123 | The present data demonstrate that cytokines, especially IL-1beta and TNF-alpha are potent regulators of IGFBPs production and degradation. |
| 11935 | 12054123 | The present data demonstrate that cytokines, especially IL-1beta and TNF-alpha are potent regulators of IGFBPs production and degradation. |
| 11936 | 12054123 | The present data demonstrate that cytokines, especially IL-1beta and TNF-alpha are potent regulators of IGFBPs production and degradation. |
| 11937 | 12054123 | The present data demonstrate that cytokines, especially IL-1beta and TNF-alpha are potent regulators of IGFBPs production and degradation. |
| 11938 | 12050371 | A comparison of intrahepatic cytokine levels in Ch1552 and Ch1605 showed greater and earlier gamma interferon (IFN-gamma) and tumor necrosis factor alpha responses in the previously infected animal, responses that were 30-fold greater than baseline responses at week 4 p.i. for IFN-gamma in Ch1552 compared to 12-fold in Ch1605 at week 10 p.i. |
| 11939 | 12040173 | The interaction of TNF with TNF receptor-1 (TNF-R1) activates several signal transduction pathways. |
| 11940 | 12032749 | TNFalpha expression of subcutaneous adipose tissue in obese and morbid obese females: relationship to adipocyte LPL activity and leptin synthesis. |
| 11941 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11942 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11943 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11944 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11945 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11946 | 12032139 | Suppressor of cytokine signaling-1 regulates the sensitivity of pancreatic beta cells to tumor necrosis factor. |
| 11947 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11948 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11949 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11950 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11951 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11952 | 12032139 | By studying the effects of SOCS-1 deficiency, we investigated whether SOCS-1 is involved in preventing cytokine-induced death of pancreatic islet cells, a potential mechanism of insulin deficiency in autoimmune diabetes. |
| 11953 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11954 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11955 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11956 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11957 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11958 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 11959 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11960 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11961 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11962 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11963 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11964 | 12032139 | Interleukin-1 + IFNgamma induced the same level of cell death in SOCS-1-/- and wild-type islets, suggesting that the sensitivity of islets to IFNgamma or interleukin-1-mediated cytotoxicity is not affected by SOCS-1 deficiency. |
| 11965 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11966 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11967 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11968 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11969 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11970 | 12032139 | Additionally, SOCS-1-/- beta cells were responsive to lower concentrations of TNF measured by class I major histocompatibility complex up-regulation. |
| 11971 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11972 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11973 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11974 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11975 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11976 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 11977 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11978 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11979 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11980 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11981 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11982 | 12032139 | A further analysis revealed that SOCS-1 deficiency results in augmented TNF signaling via the p38 mitogen-activated protein kinase pathway but not NFkappaB or c-Jun N-terminal kinase pathways. |
| 11983 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11984 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11985 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11986 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11987 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11988 | 12032139 | Increased p38 signaling may be responsible for the increased iNOS expression in SOCS-1-/- islets. |
| 11989 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11990 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11991 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11992 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11993 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11994 | 12032139 | Therefore, these findings provide evidence that physiological levels of SOCS-1 negatively regulate TNF signaling. |
| 11995 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 11996 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 11997 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 11998 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 11999 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12000 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12001 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12002 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12003 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12004 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12005 | 12031982 | Differential effects of tumor necrosis factor-alpha on protein kinase C isoforms alpha and delta mediate inhibition of insulin receptor signaling. |
| 12006 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12007 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12008 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12009 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12010 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12011 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12012 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12013 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12014 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12015 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12016 | 12031982 | Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that interferes with insulin signaling, but the molecular mechanisms of this effect are unclear. |
| 12017 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12018 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12019 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12020 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12021 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12022 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12023 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12024 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12025 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12026 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12027 | 12031982 | Because certain protein kinase C (PKC) isoforms are activated by insulin, we examined the role of PKC in TNF-alpha inhibition of insulin signaling in primary cultures of mouse skeletal muscle. |
| 12028 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12029 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12030 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12031 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12032 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12033 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12034 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12035 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12036 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12037 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12038 | 12031982 | TNF-alpha, given 5 min before insulin, inhibited insulin-induced tyrosine phosphorylation of insulin receptor (IR), IR substrate (IRS)-1, insulin-induced association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase (PI3-K), and insulin-induced glucose uptake. |
| 12039 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12040 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12041 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12042 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12043 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12044 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12045 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12046 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12047 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12048 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12049 | 12031982 | Insulin and TNF-alpha each caused tyrosine phosphorylation and activation of PKCs delta and alpha, but when TNF-alpha preceded insulin, the effects were less than that produced by each substance alone. |
| 12050 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12051 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12052 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12053 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12054 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12055 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12056 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12057 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12058 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12059 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12060 | 12031982 | Insulin induced PKCdelta specifically to coprecipitate with IR, an effect blocked by TNF-alpha. |
| 12061 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12062 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12063 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12064 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12065 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12066 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12067 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12068 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12069 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12070 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12071 | 12031982 | Both PKCalpha and -delta are constitutively associated with IRS-1. |
| 12072 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12073 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12074 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12075 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12076 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12077 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12078 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12079 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12080 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12081 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12082 | 12031982 | Whereas insulin decreased coprecipitation of IRS-1 with PKCalpha, it increased coprecipitation of IRS-1 with PKCdelta. |
| 12083 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12084 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12085 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12086 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12087 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12088 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12089 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12090 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12091 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12092 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12093 | 12031982 | TNF-alpha blocked the effects of insulin on association of both PKCs with IRS-1. |
| 12094 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12095 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12096 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12097 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12098 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12099 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12100 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12101 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12102 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12103 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12104 | 12031982 | To further investigate the involvement of PKCs in inhibitory actions of TNF-alpha on insulin signaling, we overexpressed specific PKC isoforms in mature myotubes. |
| 12105 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12106 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12107 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12108 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12109 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12110 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12111 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12112 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12113 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12114 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12115 | 12031982 | PKCalpha overexpression inhibited basal and insulin-induced IR autophosphorylation, whereas PKCdelta overexpression increased IR autophosphorylation and abrogated the inhibitory effect of TNF-alpha on IR autophosphorylation and signaling to PI3-K. |
| 12116 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12117 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12118 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12119 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12120 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12121 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12122 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12123 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12124 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12125 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12126 | 12031982 | Blockade of PKCalpha antagonized the inhibitory effects of TNF-alpha on both insulin-induced IR tyrosine phosphorylation and IR signaling to PI3-K. |
| 12127 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12128 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12129 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12130 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12131 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12132 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12133 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12134 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12135 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12136 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12137 | 12031982 | We suggest that the effects of TNF-alpha on IR tyrosine phosphorylation are mediated via alteration of insulin-induced activation and association of PKCdelta and -alpha with upstream signaling molecules. |
| 12138 | 12031976 | There was no apparent deficiency in the level of the major TNF-alpha converting enzyme in adipose tissue to account for the excess amount of mTNF-alpha produced in obesity. |
| 12139 | 12031968 | cFLIP protein prevents tumor necrosis factor-alpha-mediated induction of caspase-8-dependent apoptosis in insulin-secreting betaTc-Tet cells. |
| 12140 | 12031968 | cFLIP protein prevents tumor necrosis factor-alpha-mediated induction of caspase-8-dependent apoptosis in insulin-secreting betaTc-Tet cells. |
| 12141 | 12031968 | cFLIP protein prevents tumor necrosis factor-alpha-mediated induction of caspase-8-dependent apoptosis in insulin-secreting betaTc-Tet cells. |
| 12142 | 12031968 | cFLIP protein prevents tumor necrosis factor-alpha-mediated induction of caspase-8-dependent apoptosis in insulin-secreting betaTc-Tet cells. |
| 12143 | 12031968 | cFLIP protein prevents tumor necrosis factor-alpha-mediated induction of caspase-8-dependent apoptosis in insulin-secreting betaTc-Tet cells. |
| 12144 | 12031968 | The exact role played by interferon-gamma, tumor necrosis factor (TNF)-alpha, and interleukin-1beta in this pathogenic process is still only partially understood. |
| 12145 | 12031968 | The exact role played by interferon-gamma, tumor necrosis factor (TNF)-alpha, and interleukin-1beta in this pathogenic process is still only partially understood. |
| 12146 | 12031968 | The exact role played by interferon-gamma, tumor necrosis factor (TNF)-alpha, and interleukin-1beta in this pathogenic process is still only partially understood. |
| 12147 | 12031968 | The exact role played by interferon-gamma, tumor necrosis factor (TNF)-alpha, and interleukin-1beta in this pathogenic process is still only partially understood. |
| 12148 | 12031968 | The exact role played by interferon-gamma, tumor necrosis factor (TNF)-alpha, and interleukin-1beta in this pathogenic process is still only partially understood. |
| 12149 | 12031968 | We previously reported that it was susceptible to apoptosis induced by TNF-alpha, in combination with interleukin-1beta and interferon-gamma. |
| 12150 | 12031968 | We previously reported that it was susceptible to apoptosis induced by TNF-alpha, in combination with interleukin-1beta and interferon-gamma. |
| 12151 | 12031968 | We previously reported that it was susceptible to apoptosis induced by TNF-alpha, in combination with interleukin-1beta and interferon-gamma. |
| 12152 | 12031968 | We previously reported that it was susceptible to apoptosis induced by TNF-alpha, in combination with interleukin-1beta and interferon-gamma. |
| 12153 | 12031968 | We previously reported that it was susceptible to apoptosis induced by TNF-alpha, in combination with interleukin-1beta and interferon-gamma. |
| 12154 | 12031968 | We show that in betaTc-Tet cells, overexpression of cFLIP, the cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, completely abolished cytokine-dependent activation of caspase-8 and protected the cells against apoptosis. |
| 12155 | 12031968 | We show that in betaTc-Tet cells, overexpression of cFLIP, the cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, completely abolished cytokine-dependent activation of caspase-8 and protected the cells against apoptosis. |
| 12156 | 12031968 | We show that in betaTc-Tet cells, overexpression of cFLIP, the cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, completely abolished cytokine-dependent activation of caspase-8 and protected the cells against apoptosis. |
| 12157 | 12031968 | We show that in betaTc-Tet cells, overexpression of cFLIP, the cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, completely abolished cytokine-dependent activation of caspase-8 and protected the cells against apoptosis. |
| 12158 | 12031968 | We show that in betaTc-Tet cells, overexpression of cFLIP, the cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, completely abolished cytokine-dependent activation of caspase-8 and protected the cells against apoptosis. |
| 12159 | 12031968 | Furthermore, cFLIP overexpression increased the basal and interleukin-1beta-mediated transcriptional activity of nuclear factor (NF)-kappaB, whereas it did not change cytokine-induced inducible nitric oxide synthase gene transcription and nitric oxide secretion. |
| 12160 | 12031968 | Furthermore, cFLIP overexpression increased the basal and interleukin-1beta-mediated transcriptional activity of nuclear factor (NF)-kappaB, whereas it did not change cytokine-induced inducible nitric oxide synthase gene transcription and nitric oxide secretion. |
| 12161 | 12031968 | Furthermore, cFLIP overexpression increased the basal and interleukin-1beta-mediated transcriptional activity of nuclear factor (NF)-kappaB, whereas it did not change cytokine-induced inducible nitric oxide synthase gene transcription and nitric oxide secretion. |
| 12162 | 12031968 | Furthermore, cFLIP overexpression increased the basal and interleukin-1beta-mediated transcriptional activity of nuclear factor (NF)-kappaB, whereas it did not change cytokine-induced inducible nitric oxide synthase gene transcription and nitric oxide secretion. |
| 12163 | 12031968 | Furthermore, cFLIP overexpression increased the basal and interleukin-1beta-mediated transcriptional activity of nuclear factor (NF)-kappaB, whereas it did not change cytokine-induced inducible nitric oxide synthase gene transcription and nitric oxide secretion. |
| 12164 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 12165 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 12166 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 12167 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 12168 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 12169 | 12031968 | Together, our data demonstrate that overexpression of cFLIP protects mouse beta-cells against TNF-alpha-induced caspase-8 activation and apoptosis and is correlated with enhanced NF-kappaB transcriptional activity, suggesting that cFLIP may have an impact on the outcome of death receptor-triggered responses by directing the intracellular signals from beta-cell death to beta-cell survival. |
| 12170 | 12031968 | Together, our data demonstrate that overexpression of cFLIP protects mouse beta-cells against TNF-alpha-induced caspase-8 activation and apoptosis and is correlated with enhanced NF-kappaB transcriptional activity, suggesting that cFLIP may have an impact on the outcome of death receptor-triggered responses by directing the intracellular signals from beta-cell death to beta-cell survival. |
| 12171 | 12031968 | Together, our data demonstrate that overexpression of cFLIP protects mouse beta-cells against TNF-alpha-induced caspase-8 activation and apoptosis and is correlated with enhanced NF-kappaB transcriptional activity, suggesting that cFLIP may have an impact on the outcome of death receptor-triggered responses by directing the intracellular signals from beta-cell death to beta-cell survival. |
| 12172 | 12031968 | Together, our data demonstrate that overexpression of cFLIP protects mouse beta-cells against TNF-alpha-induced caspase-8 activation and apoptosis and is correlated with enhanced NF-kappaB transcriptional activity, suggesting that cFLIP may have an impact on the outcome of death receptor-triggered responses by directing the intracellular signals from beta-cell death to beta-cell survival. |
| 12173 | 12031968 | Together, our data demonstrate that overexpression of cFLIP protects mouse beta-cells against TNF-alpha-induced caspase-8 activation and apoptosis and is correlated with enhanced NF-kappaB transcriptional activity, suggesting that cFLIP may have an impact on the outcome of death receptor-triggered responses by directing the intracellular signals from beta-cell death to beta-cell survival. |
| 12174 | 12031960 | In the present study, we investigated how the expression of resistin is affected by glucose and by mediators known to affect insulin sensitivity, including insulin, dexamethasone, tumor necrosis factor-alpha (TNF-alpha), epinephrine, and somatropin. |
| 12175 | 12031960 | In the present study, we investigated how the expression of resistin is affected by glucose and by mediators known to affect insulin sensitivity, including insulin, dexamethasone, tumor necrosis factor-alpha (TNF-alpha), epinephrine, and somatropin. |
| 12176 | 12031960 | In contrast, treatment with troglitazone, a thiazolidinedione antihyperglycemic agent, or TNF-alpha suppressed resistin expression by approximately 80%. |
| 12177 | 12031960 | In contrast, treatment with troglitazone, a thiazolidinedione antihyperglycemic agent, or TNF-alpha suppressed resistin expression by approximately 80%. |
| 12178 | 12031960 | Furthermore, they suggest that these factors affect insulin sensitivity and fat tissue mass in part by altering the expression and eventual secretion of resistin from adipose cells. |
| 12179 | 12031960 | Furthermore, they suggest that these factors affect insulin sensitivity and fat tissue mass in part by altering the expression and eventual secretion of resistin from adipose cells. |
| 12180 | 12028372 | Pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha) have deleterious effects on both glucose homeostasis and beta-cell function, and can disrupt insulin signalling pathways in both pancreatic beta cells and liver and adipose tissue. |
| 12181 | 12021199 | Lisofylline (LSF), an anti-inflammatory agent, has been shown to protect pancreatic islets from IL-1 beta-induced inhibitory effects on insulin release. |
| 12182 | 12021199 | To examine the direct effects of LSF on beta-cells, insulin-secreting INS-1 cells were exposed to a combination of recombinant IL-1 beta, TNF alpha, and IFN gamma with or without LSF for 18 h. |
| 12183 | 12021142 | Tumor necrosis factor-alpha allele 2 shows an association with insulin-dependent diabetes mellitus in Latvians. |
| 12184 | 12021142 | Tumor necrosis factor-alpha allele 2 shows an association with insulin-dependent diabetes mellitus in Latvians. |
| 12185 | 12021142 | Tumor necrosis factor-alpha allele 2 shows an association with insulin-dependent diabetes mellitus in Latvians. |
| 12186 | 12021142 | Tumor necrosis factor-alpha allele 2 shows an association with insulin-dependent diabetes mellitus in Latvians. |
| 12187 | 12021142 | Tumor necrosis factor-alpha allele 2 shows an association with insulin-dependent diabetes mellitus in Latvians. |
| 12188 | 12021142 | Insulin-dependent diabetes mellitus (IDDM) is one of the most common chronic diseases. |
| 12189 | 12021142 | Insulin-dependent diabetes mellitus (IDDM) is one of the most common chronic diseases. |
| 12190 | 12021142 | Insulin-dependent diabetes mellitus (IDDM) is one of the most common chronic diseases. |
| 12191 | 12021142 | Insulin-dependent diabetes mellitus (IDDM) is one of the most common chronic diseases. |
| 12192 | 12021142 | Insulin-dependent diabetes mellitus (IDDM) is one of the most common chronic diseases. |
| 12193 | 12021142 | Genes contributing the most for development of IDDM are located on chromosome 6p21.3 in the region called the major histocompatibility complex (MHC). |
| 12194 | 12021142 | Genes contributing the most for development of IDDM are located on chromosome 6p21.3 in the region called the major histocompatibility complex (MHC). |
| 12195 | 12021142 | Genes contributing the most for development of IDDM are located on chromosome 6p21.3 in the region called the major histocompatibility complex (MHC). |
| 12196 | 12021142 | Genes contributing the most for development of IDDM are located on chromosome 6p21.3 in the region called the major histocompatibility complex (MHC). |
| 12197 | 12021142 | Genes contributing the most for development of IDDM are located on chromosome 6p21.3 in the region called the major histocompatibility complex (MHC). |
| 12198 | 12021142 | HLA-DQ8/DR4 and DQ2/DR3 have shown positive association with IDDM, while DQ6 has negative association with IDDM in most Caucasian populations. |
| 12199 | 12021142 | HLA-DQ8/DR4 and DQ2/DR3 have shown positive association with IDDM, while DQ6 has negative association with IDDM in most Caucasian populations. |
| 12200 | 12021142 | HLA-DQ8/DR4 and DQ2/DR3 have shown positive association with IDDM, while DQ6 has negative association with IDDM in most Caucasian populations. |
| 12201 | 12021142 | HLA-DQ8/DR4 and DQ2/DR3 have shown positive association with IDDM, while DQ6 has negative association with IDDM in most Caucasian populations. |
| 12202 | 12021142 | HLA-DQ8/DR4 and DQ2/DR3 have shown positive association with IDDM, while DQ6 has negative association with IDDM in most Caucasian populations. |
| 12203 | 12021142 | The location of the tumor necrosis factor alpha (TNF-alpha) gene in the MHC suggests the role of TNF in the etiology of IDDM as an autoimmune disease. |
| 12204 | 12021142 | The location of the tumor necrosis factor alpha (TNF-alpha) gene in the MHC suggests the role of TNF in the etiology of IDDM as an autoimmune disease. |
| 12205 | 12021142 | The location of the tumor necrosis factor alpha (TNF-alpha) gene in the MHC suggests the role of TNF in the etiology of IDDM as an autoimmune disease. |
| 12206 | 12021142 | The location of the tumor necrosis factor alpha (TNF-alpha) gene in the MHC suggests the role of TNF in the etiology of IDDM as an autoimmune disease. |
| 12207 | 12021142 | The location of the tumor necrosis factor alpha (TNF-alpha) gene in the MHC suggests the role of TNF in the etiology of IDDM as an autoimmune disease. |
| 12208 | 12021142 | Ninety-two Latvian IDDM patients corresponding to WHO diagnostic criteria and 107 unrelated age- and sex-matched healthy controls were analyzed for the frequency of TNF-alpha alleles to test the hypothesis that TNF-alpha is associated with IDDM. |
| 12209 | 12021142 | Ninety-two Latvian IDDM patients corresponding to WHO diagnostic criteria and 107 unrelated age- and sex-matched healthy controls were analyzed for the frequency of TNF-alpha alleles to test the hypothesis that TNF-alpha is associated with IDDM. |
| 12210 | 12021142 | Ninety-two Latvian IDDM patients corresponding to WHO diagnostic criteria and 107 unrelated age- and sex-matched healthy controls were analyzed for the frequency of TNF-alpha alleles to test the hypothesis that TNF-alpha is associated with IDDM. |
| 12211 | 12021142 | Ninety-two Latvian IDDM patients corresponding to WHO diagnostic criteria and 107 unrelated age- and sex-matched healthy controls were analyzed for the frequency of TNF-alpha alleles to test the hypothesis that TNF-alpha is associated with IDDM. |
| 12212 | 12021142 | Ninety-two Latvian IDDM patients corresponding to WHO diagnostic criteria and 107 unrelated age- and sex-matched healthy controls were analyzed for the frequency of TNF-alpha alleles to test the hypothesis that TNF-alpha is associated with IDDM. |
| 12213 | 12021142 | We found that TNF-alpha microsatellite allele 2 is associated with IDDM, 29/92 (32%), versus 14/107 (13%) in healthy controls. |
| 12214 | 12021142 | We found that TNF-alpha microsatellite allele 2 is associated with IDDM, 29/92 (32%), versus 14/107 (13%) in healthy controls. |
| 12215 | 12021142 | We found that TNF-alpha microsatellite allele 2 is associated with IDDM, 29/92 (32%), versus 14/107 (13%) in healthy controls. |
| 12216 | 12021142 | We found that TNF-alpha microsatellite allele 2 is associated with IDDM, 29/92 (32%), versus 14/107 (13%) in healthy controls. |
| 12217 | 12021142 | We found that TNF-alpha microsatellite allele 2 is associated with IDDM, 29/92 (32%), versus 14/107 (13%) in healthy controls. |
| 12218 | 12021142 | The test of the strongest association of the MICA A5 allele and TNF-alpha allele 2 with IDDM showed that both are independently associated with the disease. |
| 12219 | 12021142 | The test of the strongest association of the MICA A5 allele and TNF-alpha allele 2 with IDDM showed that both are independently associated with the disease. |
| 12220 | 12021142 | The test of the strongest association of the MICA A5 allele and TNF-alpha allele 2 with IDDM showed that both are independently associated with the disease. |
| 12221 | 12021142 | The test of the strongest association of the MICA A5 allele and TNF-alpha allele 2 with IDDM showed that both are independently associated with the disease. |
| 12222 | 12021142 | The test of the strongest association of the MICA A5 allele and TNF-alpha allele 2 with IDDM showed that both are independently associated with the disease. |
| 12223 | 12021108 | Cytokine secretion (TNF-alpha, IFN-gamma, IL-2, IL-4, IL-5, and IL-10) was measured in the supernatants of the cultures stimulated with 21 overlapping preproinsulin peptides as well as proinsulin and insulin. |
| 12224 | 12021108 | In Ab+ individuals our results reveal higher IL-4 levels in CD45RO+ memory cells and higher IL-5 levels in CD45RA+ naive/resting cells, while higher IL-2 production was found in PBMCs. |
| 12225 | 12021108 | In contrast, in PBMCs of T1D patients higher IFN-gamma and IL-10 secretion was found. |
| 12226 | 12021107 | The role of Fas ligand in beta cell destruction in autoimmune diabetes of NOD mice. |
| 12227 | 12021107 | Fas ligand (FasL), a type 2 membrane protein belonging to the TNF family, plays an important role in the induction of cell death. |
| 12228 | 12021107 | Ligation of Fas receptors by FasL results in apoptosis of the Fas-expressing cell. |
| 12229 | 12021107 | To address this issue it is important to know whether beta cells express Fas and/or FasL and, if so, whether induction of these molecules leads to beta cell death. |
| 12230 | 12021107 | In fact, both Fas and FasL have been demonstrated to be expressed by beta cells in response to cytokine stimulation, although there remains an argument in the literature as to whether beta cells truly express FasL. |
| 12231 | 12021099 | Apoptosis of autoreactive CD8 lymphocytes as a potential mechanism for the abrogation of type 1 diabetes by islet-specific TNF-alpha expression at a time when the autoimmune process is already ongoing. |
| 12232 | 12021099 | Apoptosis of autoreactive CD8 lymphocytes as a potential mechanism for the abrogation of type 1 diabetes by islet-specific TNF-alpha expression at a time when the autoimmune process is already ongoing. |
| 12233 | 12021099 | Here we provide a model of how experienced autoaggressive CD8 lymphocytes are dying by apoptosis as a result of beta cell-specific TNF-alpha expression at a time when the autoimmune process is already ongoing. |
| 12234 | 12021099 | Here we provide a model of how experienced autoaggressive CD8 lymphocytes are dying by apoptosis as a result of beta cell-specific TNF-alpha expression at a time when the autoimmune process is already ongoing. |
| 12235 | 12009572 | Our data are compatible with the notion that interferon-gamma (IFN-gamma)/tumor necrosis factor (TNF)/nitric oxide (NO)-induced apoptosis of beta-cells in experimental diabetes is attenuated by PTX. |
| 12236 | 12006640 | Association of the TNF-alpha -308 G/A promoter polymorphism with insulin resistance in obesity. |
| 12237 | 12006357 | Parallel in vitro studies on human whole blood were undertaken to determine whether there was a direct effect of glucose, insulin, and leptin on proinflammatory cytokine production. |
| 12238 | 12006357 | Parallel in vitro studies on human whole blood were undertaken to determine whether there was a direct effect of glucose, insulin, and leptin on proinflammatory cytokine production. |
| 12239 | 12006357 | Infusion of glucose and insulin significantly amplified and/or prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and counterregulatory hormone responses to LPS, whereas the effects on fever, plasma norepinephrine concentrations, and oxygen consumption were unaffected. |
| 12240 | 12006357 | Infusion of glucose and insulin significantly amplified and/or prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and counterregulatory hormone responses to LPS, whereas the effects on fever, plasma norepinephrine concentrations, and oxygen consumption were unaffected. |
| 12241 | 12006357 | In vitro studies showed no modulation of LPS-stimulated IL-6 or TNF-alpha production by glucose, insulin, or leptin at physiologically relevant concentrations. |
| 12242 | 12006357 | In vitro studies showed no modulation of LPS-stimulated IL-6 or TNF-alpha production by glucose, insulin, or leptin at physiologically relevant concentrations. |
| 12243 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 12244 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 12245 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 12246 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 12247 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 12248 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 12249 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 12250 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 12251 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 12252 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 12253 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 12254 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 12255 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 12256 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 12257 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 12258 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 12259 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 12260 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 12261 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 12262 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 12263 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 12264 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 12265 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 12266 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 12267 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 12268 | 11994455 | In GM-CSF/IL-4-supplemented bone marrow cultures, DC developed in significantly greater numbers from NOD than from NOR, BALB/c, and BL/6 mice. |
| 12269 | 11994455 | Likewise, DC developed in greater numbers from sorted (lineage(-)IL-7Ralpha(-)SCA-1(-)c-kit(+)) NOD myeloid progenitors in either GM-CSF/IL-4 or GM-CSF/stem cell factor (SCF)/TNF-alpha. [(3)H]TdR incorporation indicated that the increased generation of NOD DC was due to higher levels of myeloid progenitor proliferation. |
| 12270 | 11994455 | Consistent with these findings, NOD and NOR mice had increased numbers of DC in blood and thymus and NOD had an increased proportion of the putative myeloid DC (CD11c(+)CD11b(+)) subset within spleen. |
| 12271 | 11994345 | Adipose tissue IL-6 content correlates with resistance to insulin activation of glucose uptake both in vivo and in vitro. |
| 12272 | 11994345 | A significant correlation between circulating IL-6 level and insulin sensitivity has recently been found in humans. |
| 12273 | 11994345 | Because adipose tissue could be a significant source of IL-6, we analyzed the relationship between the levels of adipose tissue IL-6 and insulin action in vivo, during a hyperinsulinemic normoglycemic clamp, and in vitro by measuring glucose transport in adipocytes from 12 obese subjects with (n = 7) or without (n = 5) diabetes. |
| 12274 | 11994345 | We observed an inverse correlation between adipose tissue IL-6 content and maximal insulin-responsiveness measured in vivo (P < 0.02) and in vitro (P < 0.02). |
| 12275 | 11994345 | Conversely, there was no significant correlation between these two later parameters and adipose tissue leptin or tumor necrosis factor-alpha protein contents. |
| 12276 | 11994345 | In conclusion, increased IL-6 production by sc adipose cells might participate to the insulin-resistant state observed in human obesity. |
| 12277 | 11988817 | Comparison of serum NO, TNF-alpha, IL-1beta, sIL-2R, IL-6 and IL-8 levels with grades of retinopathy in patients with diabetes mellitus. |
| 12278 | 11985903 | This receptor is transcriptionally upregulated by tumor necrosis factor-alpha, angiotensin II, shear stress and ox-LDL itself. |
| 12279 | 11978647 | Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. |
| 12280 | 11978647 | In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 +/- 0.0 [mean +/- SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 +/- 0.13; 100 nmol/l insulin, 1.68 +/- 0.19; P < 0.001). |
| 12281 | 11978647 | In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 +/- 0.05; P < 0.05), while no significant reduction was observed at other doses. |
| 12282 | 11978647 | Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 +/- 0.07; P < 0.01) and LPL (control 1.00 +/- 0.0; 1,000 nmol/l insulin, 2.66 +/- 0.27; P < 0.01) protein expression. |
| 12283 | 11978647 | Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). |
| 12284 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 12285 | 11978647 | In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. |
| 12286 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12287 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12288 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12289 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12290 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12291 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12292 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12293 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12294 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12295 | 11978627 | Tumor necrosis factor-alpha suppresses adipocyte-specific genes and activates expression of preadipocyte genes in 3T3-L1 adipocytes: nuclear factor-kappaB activation by TNF-alpha is obligatory. |
| 12296 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12297 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12298 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12299 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12300 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12301 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12302 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12303 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12304 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12305 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 12306 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12307 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12308 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12309 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12310 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12311 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12312 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12313 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12314 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12315 | 11978627 | TNF-alpha-induced genes include transcription factors implicated in preadipocyte gene expression or NF-kappaB activation, cytokines and cytokine-induced proteins, growth factors, enzymes, and signaling molecules. |
| 12316 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12317 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12318 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12319 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12320 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12321 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12322 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12323 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12324 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12325 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 12326 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12327 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12328 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12329 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12330 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12331 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12332 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12333 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12334 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12335 | 11978627 | Correspondingly, 24-h exposure of 3T3-L1 adipocytes to TNF-alpha resulted in reduced protein levels of GLUT4 and several insulin signaling proteins, including the insulin receptor, insulin receptor substrate 1 (IRS-1), and protein kinase B (AKT). |
| 12336 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12337 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12338 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12339 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12340 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12341 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12342 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12343 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12344 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12345 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 12346 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12347 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12348 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12349 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12350 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12351 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12352 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12353 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12354 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12355 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 12356 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12357 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12358 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12359 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12360 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12361 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12362 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12363 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12364 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12365 | 11978627 | Moreover, extensive cell death occurred in IkappaBalpha-DN-expressing adipocytes after 2 h of TNF-alpha treatment. |
| 12366 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12367 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12368 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12369 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12370 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12371 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12372 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12373 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12374 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12375 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 12376 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12377 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12378 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12379 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12380 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12381 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12382 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12383 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12384 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12385 | 11978627 | Further, NF-kappaB is an obligatory mediator of most of these TNF-alpha responses. |
| 12386 | 11976344 | Tumor necrosis factor-related apoptosis-inducing ligand-induced death-inducing signaling complex and its modulation by c-FLIP and PED/PEA-15 in glioma cells. |
| 12387 | 11976344 | Tumor necrosis factor-related apoptosis-inducing ligand-induced death-inducing signaling complex and its modulation by c-FLIP and PED/PEA-15 in glioma cells. |
| 12388 | 11976344 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can trigger apoptosis in some tumor cells but not other tumor cells. |
| 12389 | 11976344 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can trigger apoptosis in some tumor cells but not other tumor cells. |
| 12390 | 11976344 | Caspase-8 and caspase-10 were recruited to the DISC, where they were proteolytically activated to initiate apoptosis in TRAIL-sensitive glioma cells. |
| 12391 | 11976344 | Caspase-8 and caspase-10 were recruited to the DISC, where they were proteolytically activated to initiate apoptosis in TRAIL-sensitive glioma cells. |
| 12392 | 11976344 | Caspase-8 and caspase-10 were also recruited to the DISC in TRAIL-resistant cells, but their further activation was inhibited by two antiapoptotic proteins termed cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15kDa (PED/PEA-15). |
| 12393 | 11976344 | Caspase-8 and caspase-10 were also recruited to the DISC in TRAIL-resistant cells, but their further activation was inhibited by two antiapoptotic proteins termed cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15kDa (PED/PEA-15). |
| 12394 | 11976344 | Of the three isoforms of PED/PEA-15 proteins, only the doubly phosphorylated form was expressed and recruited to the DISC in TRAIL-resistant cells, indicating that the phosphorylation status of PED/PEA-15 determines its recruitment in the cells. |
| 12395 | 11976344 | Of the three isoforms of PED/PEA-15 proteins, only the doubly phosphorylated form was expressed and recruited to the DISC in TRAIL-resistant cells, indicating that the phosphorylation status of PED/PEA-15 determines its recruitment in the cells. |
| 12396 | 11970897 | Here we show that, during 3T3 L1 adipocyte differentiation, expression of fatty acid transport proteins (FATPs) 1 and 4 is induced. |
| 12397 | 11970897 | Using subcellular membrane fractionation and immunofluorescence microscopy, we demonstrate that, in adipocytes, insulin induces plasma membrane translocation of FATPs from an intracellular perinuclear compartment to the plasma membrane. |
| 12398 | 11970897 | In contrast, treatment with TNF-alpha inhibited basal and insulin-induced LCFA uptake and reduced FATP1 and -4 levels. |
| 12399 | 11949882 | The body weight, daily food intake, plasma levels of fat, insulin, leptin and the wet weight of visceral fat were not influenced, but the levels of blood hemoglobin Alc and plasma tumor necrosis factor a were decreased by pioglitazone. |
| 12400 | 11928538 | The study of the actions of tumour necrosing factor alpha (TNF-alpha) and interleukin-6 (IL-6), classically implicated in inflammatory processes and in fighting infection, has revealed numerous metabolic effects. |
| 12401 | 11928538 | The study of the actions of tumour necrosing factor alpha (TNF-alpha) and interleukin-6 (IL-6), classically implicated in inflammatory processes and in fighting infection, has revealed numerous metabolic effects. |
| 12402 | 11928538 | Some gene polymorphisms of TNF-alpha and IL-6 (associated with a different TNF-alpha or IL-6 transcription rate) and the plasma concentrations of the soluble TNF-alpha receptor are found to be simultaneously associated with resistance to insulin, the proportion of body fat and with the mortality linked with different chronic infections. |
| 12403 | 11928538 | Some gene polymorphisms of TNF-alpha and IL-6 (associated with a different TNF-alpha or IL-6 transcription rate) and the plasma concentrations of the soluble TNF-alpha receptor are found to be simultaneously associated with resistance to insulin, the proportion of body fat and with the mortality linked with different chronic infections. |
| 12404 | 11921433 | TZDs exert their antidiabetic effects through a mechanism that involves activation of the gamma isoform of the peroxisome proliferator-activated receptor (PPAR gamma), a nuclear receptor. |
| 12405 | 11921433 | TZD-induced activation of PPAR gamma alters the transcription of several genes involved in glucose and lipid metabolism and energy balance, including those that code for lipoprotein lipase, fatty acid transporter protein, adipocyte fatty acid binding protein, fatty acyl-CoA synthase, malic enzyme, glucokinase and the GLUT4 glucose transporter. |
| 12406 | 11921433 | However, PPAR gamma is predominantly expressed in adipose tissue. |
| 12407 | 11921433 | Potential signalling factors include free fatty acids (FFA) (well-known mediators of insulin resistance linked to obesity) or adipocyte-derived tumour necrosis factor-alpha (TNF-alpha), which is overexpressed in obesity and insulin resistance. |
| 12408 | 11916923 | Human obesity and type 2 diabetes are associated with alterations in SREBP1 isoform expression that are reproduced ex vivo by tumor necrosis factor-alpha. |
| 12409 | 11916923 | Human obesity and type 2 diabetes are associated with alterations in SREBP1 isoform expression that are reproduced ex vivo by tumor necrosis factor-alpha. |
| 12410 | 11916923 | Exposure of isolated human adipocytes to insulin enhanced SREBP1 gene expression and promoted its proteolytic cleavage to the active form. |
| 12411 | 11916923 | Exposure of isolated human adipocytes to insulin enhanced SREBP1 gene expression and promoted its proteolytic cleavage to the active form. |
| 12412 | 11916923 | Exposure of isolated human adipocytes to tumor necrosis factor-alpha (TNF-alpha) produced a marked and specific decrease in the mRNA encoding the SREBP1c isoform and completely blocked the insulin-induced cleavage of SREBP1 protein. |
| 12413 | 11916923 | Exposure of isolated human adipocytes to tumor necrosis factor-alpha (TNF-alpha) produced a marked and specific decrease in the mRNA encoding the SREBP1c isoform and completely blocked the insulin-induced cleavage of SREBP1 protein. |
| 12414 | 11914744 | IFN gamma/TNF alpha synergism in MHC class II induction: effect of nicotinamide on MHC class II expression but not on islet-cell apoptosis. |
| 12415 | 11912559 | Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. |
| 12416 | 11912559 | Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. |
| 12417 | 11912559 | Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. |
| 12418 | 11912559 | Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. |
| 12419 | 11912559 | Tumor necrosis factor-alpha inhibits insulin-induced increase in endothelial nitric oxide synthase and reduces insulin receptor content and phosphorylation in human aortic endothelial cells. |
| 12420 | 11912559 | We have recently demonstrated that insulin also inhibits the expression of intracellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), 2 major proinflammatory mediators, by human aortic endothelial cells (HAEC) and the proinflammatory mediator, nuclear factor (NF-kappa B), in the nucleus in parallel with an increase in endothelial nitric oxide synthase (e-NOS) expression. |
| 12421 | 11912559 | We have recently demonstrated that insulin also inhibits the expression of intracellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), 2 major proinflammatory mediators, by human aortic endothelial cells (HAEC) and the proinflammatory mediator, nuclear factor (NF-kappa B), in the nucleus in parallel with an increase in endothelial nitric oxide synthase (e-NOS) expression. |
| 12422 | 11912559 | We have recently demonstrated that insulin also inhibits the expression of intracellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), 2 major proinflammatory mediators, by human aortic endothelial cells (HAEC) and the proinflammatory mediator, nuclear factor (NF-kappa B), in the nucleus in parallel with an increase in endothelial nitric oxide synthase (e-NOS) expression. |
| 12423 | 11912559 | We have recently demonstrated that insulin also inhibits the expression of intracellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), 2 major proinflammatory mediators, by human aortic endothelial cells (HAEC) and the proinflammatory mediator, nuclear factor (NF-kappa B), in the nucleus in parallel with an increase in endothelial nitric oxide synthase (e-NOS) expression. |
| 12424 | 11912559 | We have recently demonstrated that insulin also inhibits the expression of intracellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), 2 major proinflammatory mediators, by human aortic endothelial cells (HAEC) and the proinflammatory mediator, nuclear factor (NF-kappa B), in the nucleus in parallel with an increase in endothelial nitric oxide synthase (e-NOS) expression. |
| 12425 | 11912559 | The inhibition of ICAM-1 by insulin is NO dependent. |
| 12426 | 11912559 | The inhibition of ICAM-1 by insulin is NO dependent. |
| 12427 | 11912559 | The inhibition of ICAM-1 by insulin is NO dependent. |
| 12428 | 11912559 | The inhibition of ICAM-1 by insulin is NO dependent. |
| 12429 | 11912559 | The inhibition of ICAM-1 by insulin is NO dependent. |
| 12430 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 12431 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 12432 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 12433 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 12434 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 12435 | 11912559 | TNF-alpha also inhibited tyrosine autophosphorylation of the IR in HAEC induced by insulin and reduced IR beta-subunit protein expression in HAEC. |
| 12436 | 11912559 | TNF-alpha also inhibited tyrosine autophosphorylation of the IR in HAEC induced by insulin and reduced IR beta-subunit protein expression in HAEC. |
| 12437 | 11912559 | TNF-alpha also inhibited tyrosine autophosphorylation of the IR in HAEC induced by insulin and reduced IR beta-subunit protein expression in HAEC. |
| 12438 | 11912559 | TNF-alpha also inhibited tyrosine autophosphorylation of the IR in HAEC induced by insulin and reduced IR beta-subunit protein expression in HAEC. |
| 12439 | 11912559 | TNF-alpha also inhibited tyrosine autophosphorylation of the IR in HAEC induced by insulin and reduced IR beta-subunit protein expression in HAEC. |
| 12440 | 11912559 | These effects of insulin and TNF-alpha were independent of cell proliferation, as cell counts did not change with insulin or TNF-alpha. |
| 12441 | 11912559 | These effects of insulin and TNF-alpha were independent of cell proliferation, as cell counts did not change with insulin or TNF-alpha. |
| 12442 | 11912559 | These effects of insulin and TNF-alpha were independent of cell proliferation, as cell counts did not change with insulin or TNF-alpha. |
| 12443 | 11912559 | These effects of insulin and TNF-alpha were independent of cell proliferation, as cell counts did not change with insulin or TNF-alpha. |
| 12444 | 11912559 | These effects of insulin and TNF-alpha were independent of cell proliferation, as cell counts did not change with insulin or TNF-alpha. |
| 12445 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 12446 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 12447 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 12448 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 12449 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 12450 | 11891022 | Relationship of the tumor necrosis factor-alpha -308 A/G promoter polymorphism with insulin sensitivity and abdominal fat distribution in Japanese patients with type 2 diabetes mellitus. |
| 12451 | 11891022 | Relationship of the tumor necrosis factor-alpha -308 A/G promoter polymorphism with insulin sensitivity and abdominal fat distribution in Japanese patients with type 2 diabetes mellitus. |
| 12452 | 11891022 | Relationship of the tumor necrosis factor-alpha -308 A/G promoter polymorphism with insulin sensitivity and abdominal fat distribution in Japanese patients with type 2 diabetes mellitus. |
| 12453 | 11891022 | Relationship of the tumor necrosis factor-alpha -308 A/G promoter polymorphism with insulin sensitivity and abdominal fat distribution in Japanese patients with type 2 diabetes mellitus. |
| 12454 | 11891022 | We investigated the relationship of the A/G variant of the tumor necrosis factor-alpha (TNF-alpha) gene promoter at position -308 with insulin resistance and abdominal fat distribution in type 2 diabetic patients in the Japanese population. |
| 12455 | 11891022 | We investigated the relationship of the A/G variant of the tumor necrosis factor-alpha (TNF-alpha) gene promoter at position -308 with insulin resistance and abdominal fat distribution in type 2 diabetic patients in the Japanese population. |
| 12456 | 11891022 | We investigated the relationship of the A/G variant of the tumor necrosis factor-alpha (TNF-alpha) gene promoter at position -308 with insulin resistance and abdominal fat distribution in type 2 diabetic patients in the Japanese population. |
| 12457 | 11891022 | We investigated the relationship of the A/G variant of the tumor necrosis factor-alpha (TNF-alpha) gene promoter at position -308 with insulin resistance and abdominal fat distribution in type 2 diabetic patients in the Japanese population. |
| 12458 | 11891022 | Glucose infusion rate (GIR), an index of insulin sensitivity, was not significantly different between diabetic patients with and without TNF-alpha polymorphism (40.4 +/- 4.1 vs. 45.0 +/- 1.8 micromol/kg per min). |
| 12459 | 11891022 | Glucose infusion rate (GIR), an index of insulin sensitivity, was not significantly different between diabetic patients with and without TNF-alpha polymorphism (40.4 +/- 4.1 vs. 45.0 +/- 1.8 micromol/kg per min). |
| 12460 | 11891022 | Glucose infusion rate (GIR), an index of insulin sensitivity, was not significantly different between diabetic patients with and without TNF-alpha polymorphism (40.4 +/- 4.1 vs. 45.0 +/- 1.8 micromol/kg per min). |
| 12461 | 11891022 | Glucose infusion rate (GIR), an index of insulin sensitivity, was not significantly different between diabetic patients with and without TNF-alpha polymorphism (40.4 +/- 4.1 vs. 45.0 +/- 1.8 micromol/kg per min). |
| 12462 | 11891022 | These results suggest that A/G heterozygotes of the TNF-alpha gene promoter at position -308 play no major role in the pathogenesis of insulin resistance or abdominal fat distribution in Japanese type 2 diabetic patients. |
| 12463 | 11891022 | These results suggest that A/G heterozygotes of the TNF-alpha gene promoter at position -308 play no major role in the pathogenesis of insulin resistance or abdominal fat distribution in Japanese type 2 diabetic patients. |
| 12464 | 11891022 | These results suggest that A/G heterozygotes of the TNF-alpha gene promoter at position -308 play no major role in the pathogenesis of insulin resistance or abdominal fat distribution in Japanese type 2 diabetic patients. |
| 12465 | 11891022 | These results suggest that A/G heterozygotes of the TNF-alpha gene promoter at position -308 play no major role in the pathogenesis of insulin resistance or abdominal fat distribution in Japanese type 2 diabetic patients. |
| 12466 | 11891016 | Tumor necrosis factor system in insulin resistance in gestational diabetes. |
| 12467 | 11888838 | Plasma soluble tumor necrosis factor alpha receptors and leptin levels in normal-weight and obese women: effect of adiposity and diabetes. |
| 12468 | 11887456 | Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. |
| 12469 | 11887456 | Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. |
| 12470 | 11887456 | Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. |
| 12471 | 11887456 | Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. |
| 12472 | 11887456 | Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. |
| 12473 | 11887456 | Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. |
| 12474 | 11887456 | In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. |
| 12475 | 11887456 | In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. |
| 12476 | 11887456 | In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. |
| 12477 | 11887455 | Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. |
| 12478 | 11882611 | Effect of TNF-alpha--converting enzyme inhibitor on insulin resistance in fructose-fed rats. |
| 12479 | 11882611 | Effect of TNF-alpha--converting enzyme inhibitor on insulin resistance in fructose-fed rats. |
| 12480 | 11882611 | Effect of TNF-alpha--converting enzyme inhibitor on insulin resistance in fructose-fed rats. |
| 12481 | 11882611 | Effect of TNF-alpha--converting enzyme inhibitor on insulin resistance in fructose-fed rats. |
| 12482 | 11882611 | It is well known that tumor necrosis factor (TNF)-alpha is one of the factors linked to obesity-induced insulin resistance; however, there have been no reports on the role of TNF-alpha in insulin resistance in nonobese insulin-resistant hypertensives. |
| 12483 | 11882611 | It is well known that tumor necrosis factor (TNF)-alpha is one of the factors linked to obesity-induced insulin resistance; however, there have been no reports on the role of TNF-alpha in insulin resistance in nonobese insulin-resistant hypertensives. |
| 12484 | 11882611 | It is well known that tumor necrosis factor (TNF)-alpha is one of the factors linked to obesity-induced insulin resistance; however, there have been no reports on the role of TNF-alpha in insulin resistance in nonobese insulin-resistant hypertensives. |
| 12485 | 11882611 | It is well known that tumor necrosis factor (TNF)-alpha is one of the factors linked to obesity-induced insulin resistance; however, there have been no reports on the role of TNF-alpha in insulin resistance in nonobese insulin-resistant hypertensives. |
| 12486 | 11882611 | We tested the hypothesis that TNF-alpha affects insulin resistance in nonobese insulin-resistant hypertensive fructose-fed rats (FFR) and that a TNF-alpha--converting enzyme (TACE) inhibitor that blocks TNF-alpha secretion improves insulin resistance in FFR. |
| 12487 | 11882611 | We tested the hypothesis that TNF-alpha affects insulin resistance in nonobese insulin-resistant hypertensive fructose-fed rats (FFR) and that a TNF-alpha--converting enzyme (TACE) inhibitor that blocks TNF-alpha secretion improves insulin resistance in FFR. |
| 12488 | 11882611 | We tested the hypothesis that TNF-alpha affects insulin resistance in nonobese insulin-resistant hypertensive fructose-fed rats (FFR) and that a TNF-alpha--converting enzyme (TACE) inhibitor that blocks TNF-alpha secretion improves insulin resistance in FFR. |
| 12489 | 11882611 | We tested the hypothesis that TNF-alpha affects insulin resistance in nonobese insulin-resistant hypertensive fructose-fed rats (FFR) and that a TNF-alpha--converting enzyme (TACE) inhibitor that blocks TNF-alpha secretion improves insulin resistance in FFR. |
| 12490 | 11882611 | Insulin sensitivity (M-value) was reduced in FFR compared with that in the control rats (16.7 +/- 1.1 mg/kg per min and 10.3 +/- 0.6 mg/kg per min in the control rats and FFR, respectively, P<0.001), and the TACE inhibitor improved insulin sensitivity to the level of the control rats (14.3 +/- 1.2 mg/kg per min in FFR+TACE-I, P<0.01). |
| 12491 | 11882611 | Insulin sensitivity (M-value) was reduced in FFR compared with that in the control rats (16.7 +/- 1.1 mg/kg per min and 10.3 +/- 0.6 mg/kg per min in the control rats and FFR, respectively, P<0.001), and the TACE inhibitor improved insulin sensitivity to the level of the control rats (14.3 +/- 1.2 mg/kg per min in FFR+TACE-I, P<0.01). |
| 12492 | 11882611 | Insulin sensitivity (M-value) was reduced in FFR compared with that in the control rats (16.7 +/- 1.1 mg/kg per min and 10.3 +/- 0.6 mg/kg per min in the control rats and FFR, respectively, P<0.001), and the TACE inhibitor improved insulin sensitivity to the level of the control rats (14.3 +/- 1.2 mg/kg per min in FFR+TACE-I, P<0.01). |
| 12493 | 11882611 | Insulin sensitivity (M-value) was reduced in FFR compared with that in the control rats (16.7 +/- 1.1 mg/kg per min and 10.3 +/- 0.6 mg/kg per min in the control rats and FFR, respectively, P<0.001), and the TACE inhibitor improved insulin sensitivity to the level of the control rats (14.3 +/- 1.2 mg/kg per min in FFR+TACE-I, P<0.01). |
| 12494 | 11882611 | These data indicate that TNF-alpha plays a major role in insulin resistance in nonobese insulin-resistant models and also suggest that TACE would be a good target for controlling insulin resistance not only in obese models but also in nonobese insulin-resistant models. |
| 12495 | 11882611 | These data indicate that TNF-alpha plays a major role in insulin resistance in nonobese insulin-resistant models and also suggest that TACE would be a good target for controlling insulin resistance not only in obese models but also in nonobese insulin-resistant models. |
| 12496 | 11882611 | These data indicate that TNF-alpha plays a major role in insulin resistance in nonobese insulin-resistant models and also suggest that TACE would be a good target for controlling insulin resistance not only in obese models but also in nonobese insulin-resistant models. |
| 12497 | 11882611 | These data indicate that TNF-alpha plays a major role in insulin resistance in nonobese insulin-resistant models and also suggest that TACE would be a good target for controlling insulin resistance not only in obese models but also in nonobese insulin-resistant models. |
| 12498 | 11882518 | Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus. |
| 12499 | 11882518 | Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus. |
| 12500 | 11882518 | Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus. |
| 12501 | 11882518 | Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus. |
| 12502 | 11882518 | Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus. |
| 12503 | 11882518 | Tumor necrosis factor-alpha (TNF-alpha) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. |
| 12504 | 11882518 | Tumor necrosis factor-alpha (TNF-alpha) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. |
| 12505 | 11882518 | Tumor necrosis factor-alpha (TNF-alpha) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. |
| 12506 | 11882518 | Tumor necrosis factor-alpha (TNF-alpha) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. |
| 12507 | 11882518 | Tumor necrosis factor-alpha (TNF-alpha) is increasingly recognized as a key component in the development of insulin resistance and increased blood pressure. |
| 12508 | 11882518 | The TNF-alpha receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. |
| 12509 | 11882518 | The TNF-alpha receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. |
| 12510 | 11882518 | The TNF-alpha receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. |
| 12511 | 11882518 | The TNF-alpha receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. |
| 12512 | 11882518 | The TNF-alpha receptor 1 (TNFR1) density in peripheral blood monocytes was similar in DM-2 patients and in nondiabetic subjects. |
| 12513 | 11882518 | After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity (r = 0.54, P = 0.03). |
| 12514 | 11882518 | After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity (r = 0.54, P = 0.03). |
| 12515 | 11882518 | After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity (r = 0.54, P = 0.03). |
| 12516 | 11882518 | After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity (r = 0.54, P = 0.03). |
| 12517 | 11882518 | After phorbol 12-myristate 13-acetate, TNFR1 shedding was significantly decreased in DM-2 compared with control subjects, and it was directly associated with insulin sensitivity (r = 0.54, P = 0.03). |
| 12518 | 11882518 | Conversely, TNF-alpha receptor 2 shedding was negatively associated with insulin sensitivity (r = -0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. |
| 12519 | 11882518 | Conversely, TNF-alpha receptor 2 shedding was negatively associated with insulin sensitivity (r = -0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. |
| 12520 | 11882518 | Conversely, TNF-alpha receptor 2 shedding was negatively associated with insulin sensitivity (r = -0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. |
| 12521 | 11882518 | Conversely, TNF-alpha receptor 2 shedding was negatively associated with insulin sensitivity (r = -0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. |
| 12522 | 11882518 | Conversely, TNF-alpha receptor 2 shedding was negatively associated with insulin sensitivity (r = -0.54, P = 0.03), whereas shedding of L-selectin showed no significant association. |
| 12523 | 11882518 | Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in DM-2. |
| 12524 | 11882518 | Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in DM-2. |
| 12525 | 11882518 | Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in DM-2. |
| 12526 | 11882518 | Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in DM-2. |
| 12527 | 11882518 | Our findings suggest that insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in DM-2. |
| 12528 | 11872660 | C(2)-ceramide influences the expression and insulin-mediated regulation of cyclic nucleotide phosphodiesterase 3B and lipolysis in 3T3-L1 adipocytes. |
| 12529 | 11872660 | C(2)-ceramide influences the expression and insulin-mediated regulation of cyclic nucleotide phosphodiesterase 3B and lipolysis in 3T3-L1 adipocytes. |
| 12530 | 11872660 | Cyclic nucleotide phosphodiesterase (PDE) 3B plays an important role in the antilipolytic action of insulin and, thereby, the release of fatty acids from adipocytes. |
| 12531 | 11872660 | Cyclic nucleotide phosphodiesterase (PDE) 3B plays an important role in the antilipolytic action of insulin and, thereby, the release of fatty acids from adipocytes. |
| 12532 | 11872660 | The lipolytic action of tumor necrosis factor (TNF)-alpha is thought to be one of the mechanisms by which TNF-alpha induces insulin resistance. |
| 12533 | 11872660 | The lipolytic action of tumor necrosis factor (TNF)-alpha is thought to be one of the mechanisms by which TNF-alpha induces insulin resistance. |
| 12534 | 11872660 | Ceramide is the suggested second messenger of TNF-alpha action, and in this study, we used 3T3-L1 adipocytes to investigate the effects of C(2)-ceramide (a short-chain ceramide analog) on the expression and regulation of PDE3B and lipolysis. |
| 12535 | 11872660 | Ceramide is the suggested second messenger of TNF-alpha action, and in this study, we used 3T3-L1 adipocytes to investigate the effects of C(2)-ceramide (a short-chain ceramide analog) on the expression and regulation of PDE3B and lipolysis. |
| 12536 | 11872660 | In addition to downregulation of PDE3B, the antilipolytic action of insulin was decreased by ceramide treatment. |
| 12537 | 11872660 | In addition to downregulation of PDE3B, the antilipolytic action of insulin was decreased by ceramide treatment. |
| 12538 | 11872660 | These results, together with data from other studies on PDE3B and lipolysis in diabetic humans and animals, suggest a novel pathway by which ceramide induces insulin resistance. |
| 12539 | 11872660 | These results, together with data from other studies on PDE3B and lipolysis in diabetic humans and animals, suggest a novel pathway by which ceramide induces insulin resistance. |
| 12540 | 11869680 | Pancreatic lymph node-derived CD4(+)CD25(+) Treg cells: highly potent regulators of diabetes that require TRANCE-RANK signals. |
| 12541 | 11869680 | Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. |
| 12542 | 11869680 | PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. |
| 12543 | 11869680 | Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes. |
| 12544 | 11867679 | Lead-pretreated cells released up to tenfold increased amounts of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-12, and prostaglandin E(2) (PGE(2)) but less IL-10 compared with controls. |
| 12545 | 11867679 | Lead-pretreated cells released up to tenfold increased amounts of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-12, and prostaglandin E(2) (PGE(2)) but less IL-10 compared with controls. |
| 12546 | 11867679 | Inhibition of protein kinase C or of protein synthesis during the priming phase blocked the lead-induced increase of TNF-alpha and IL-6 release. |
| 12547 | 11867679 | Inhibition of protein kinase C or of protein synthesis during the priming phase blocked the lead-induced increase of TNF-alpha and IL-6 release. |
| 12548 | 11861793 | The pancreatic levels of the Th1 cytokines interleukin (IL)-12, IL-1, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were increased in both MLDS-induced and spontaneous NOD diabetes, an effect prevented by nicotine treatment. |
| 12549 | 11861793 | Nicotine treatment increased the pancreatic levels of the Th2 cytokines IL-4 and IL-10. |
| 12550 | 11857053 | A family-based study was carried out in 67 Bangladeshi families, consisting of a proband with FCPD and both parents, to determine whether an association exists between FCPD susceptibility and either the major histocompatiblity complex (MHC) or insulin gene (INS) loci. |
| 12551 | 11857053 | HLA-DQB1 typing was done using allele-specific primers, and INS was typed using the restriction enzyme HphI. |
| 12552 | 11857053 | Three microsatellites (TNFa, TNFc and TNFd), from within and flanking the TNF-LT locus, were used for MHC Class IV typing and a PCR-RFLP assay was used to define the -308G/A TNF promoter polymorphism. |
| 12553 | 11857053 | This study confirms an association between FCPD and the MHC using a family-based study design and the stringent ETDT analysis; a novel protective association was found with HLA-DQB1*0202 in Bangladeshi FCPD subjects. |
| 12554 | 11823504 | We have analyzed the effects of CTB on macrophages in vitro and have found that preincubation with CTB (10 microg/ml) suppresses the proinflammatory reaction to LPS challenge, as demonstrated by suppressed production of TNF-alpha, IL-6, IL-12(p70), and NO (p < 0.01) in cells of macrophage lines. |
| 12555 | 11823504 | We have analyzed the effects of CTB on macrophages in vitro and have found that preincubation with CTB (10 microg/ml) suppresses the proinflammatory reaction to LPS challenge, as demonstrated by suppressed production of TNF-alpha, IL-6, IL-12(p70), and NO (p < 0.01) in cells of macrophage lines. |
| 12556 | 11823504 | We have analyzed the effects of CTB on macrophages in vitro and have found that preincubation with CTB (10 microg/ml) suppresses the proinflammatory reaction to LPS challenge, as demonstrated by suppressed production of TNF-alpha, IL-6, IL-12(p70), and NO (p < 0.01) in cells of macrophage lines. |
| 12557 | 11823504 | Pre-exposure to CTB also suppresses LPS-induced TNF-alpha and IL-12(p70) formation in human PBMC. |
| 12558 | 11823504 | Pre-exposure to CTB also suppresses LPS-induced TNF-alpha and IL-12(p70) formation in human PBMC. |
| 12559 | 11823504 | Pre-exposure to CTB also suppresses LPS-induced TNF-alpha and IL-12(p70) formation in human PBMC. |
| 12560 | 11823504 | The suppression of TNF-alpha and IL-6 production could be counteracted by the addition of Abs to IL-10 and TGF-beta. |
| 12561 | 11823504 | The suppression of TNF-alpha and IL-6 production could be counteracted by the addition of Abs to IL-10 and TGF-beta. |
| 12562 | 11823504 | The suppression of TNF-alpha and IL-6 production could be counteracted by the addition of Abs to IL-10 and TGF-beta. |
| 12563 | 11822971 | Clinical markers of inflammation, including C-reactive protein, modified low-density lipoprotein, homocysteine, tumor necrosis factor, and thermogenicity, have been identified as emerging risk factors that may add prognostic information in patient management. |
| 12564 | 11821258 | Intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes. |
| 12565 | 11821258 | Intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes. |
| 12566 | 11821258 | Following one week of diabetes, neutrophil CD11a, CD11b, and CD18 expression was increased significantly, as were retinal ICAM-1 levels. |
| 12567 | 11821258 | Following one week of diabetes, neutrophil CD11a, CD11b, and CD18 expression was increased significantly, as were retinal ICAM-1 levels. |
| 12568 | 11821258 | Animals were treated with aspirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept). |
| 12569 | 11821258 | Animals were treated with aspirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept). |
| 12570 | 11821258 | High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not. |
| 12571 | 11821258 | High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not. |
| 12572 | 11821258 | Taken together, these data identify COX-2 and TNF-alpha as operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease. |
| 12573 | 11821258 | Taken together, these data identify COX-2 and TNF-alpha as operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease. |
| 12574 | 11817710 | Leptin, insulin and TNF-alpha in weight loss. |
| 12575 | 11817710 | Leptin, insulin and TNF-alpha in weight loss. |
| 12576 | 11817710 | Leptin, insulin and TNF-alpha in weight loss. |
| 12577 | 11817710 | In a subgroup of 14 patients (8 S+6 N-S), serial assessments of serum leptin, insulin and tumor necrosis factor-alpha (TNF-alpha) were performed. |
| 12578 | 11817710 | In a subgroup of 14 patients (8 S+6 N-S), serial assessments of serum leptin, insulin and tumor necrosis factor-alpha (TNF-alpha) were performed. |
| 12579 | 11817710 | In a subgroup of 14 patients (8 S+6 N-S), serial assessments of serum leptin, insulin and tumor necrosis factor-alpha (TNF-alpha) were performed. |
| 12580 | 11817710 | Serum insulin levels decreased with weight loss similar in magnitude to that noted for leptin; however, the insulin changes occurred more rapidly. |
| 12581 | 11817710 | Serum insulin levels decreased with weight loss similar in magnitude to that noted for leptin; however, the insulin changes occurred more rapidly. |
| 12582 | 11817710 | Serum insulin levels decreased with weight loss similar in magnitude to that noted for leptin; however, the insulin changes occurred more rapidly. |
| 12583 | 11817710 | In summary, serum leptin, insulin and TNF-alpha all decreased during a rapid weight loss program but at differing rates and variability, precluding their usefulness as markers of week-to-week weight loss compliance. |
| 12584 | 11817710 | In summary, serum leptin, insulin and TNF-alpha all decreased during a rapid weight loss program but at differing rates and variability, precluding their usefulness as markers of week-to-week weight loss compliance. |
| 12585 | 11817710 | In summary, serum leptin, insulin and TNF-alpha all decreased during a rapid weight loss program but at differing rates and variability, precluding their usefulness as markers of week-to-week weight loss compliance. |
| 12586 | 11813268 | After 72 h exposure of human pancreatic islets to a cytotoxic cytokine combination of interleukin 1 beta (50 U/ml), tumor necrosis factor alpha (1,000 U/ml), and interferon gamma (1,000 U/ml), an increase of cell death vs. control islets was demonstrated by TUNEL and cell death detection ELISA method. |
| 12587 | 11813268 | This effect was correlated with a marked decrease of Bcl-2 mRNA expression (without any major change of Bax mRNA) and a marked increase of inducible nitric oxide synthase mRNA. |
| 12588 | 11812741 | We found that the SOD mimic significantly inhibited antigen-presenting cell-dependent T-cell proliferation and IFN-gamma production in vitro. |
| 12589 | 11812741 | In addition, pretreatment of lipopolysaccharide (LPS)-stimulated peritoneal macrophages with SOD mimic inhibited the LPS-dependent increase in TNF-alpha as well as the NADPH oxidase-dependent release of superoxide. |
| 12590 | 11808322 | Chronic administration of beta 3-adrenergic receptor agonists into obese rodents reduce the size of adipocytes by the breakdown of triglyceride and ameliorate insulin resistance associated with the normalization of the expression of adipocytokines, such as leptin and tumor necrosis factor-alpha. |
| 12591 | 11807829 | Obesity modulates the expression of haptoglobin in the white adipose tissue via TNFalpha. |
| 12592 | 11807829 | Obesity modulates the expression of haptoglobin in the white adipose tissue via TNFalpha. |
| 12593 | 11807829 | Obesity modulates the expression of haptoglobin in the white adipose tissue via TNFalpha. |
| 12594 | 11807829 | Obesity modulates the expression of haptoglobin in the white adipose tissue via TNFalpha. |
| 12595 | 11807829 | Two important examples are tumor necrosis factor alpha (TNFalpha) and leptin, both of which are upregulated in adipose tissue in obesity. |
| 12596 | 11807829 | Two important examples are tumor necrosis factor alpha (TNFalpha) and leptin, both of which are upregulated in adipose tissue in obesity. |
| 12597 | 11807829 | Two important examples are tumor necrosis factor alpha (TNFalpha) and leptin, both of which are upregulated in adipose tissue in obesity. |
| 12598 | 11807829 | Two important examples are tumor necrosis factor alpha (TNFalpha) and leptin, both of which are upregulated in adipose tissue in obesity. |
| 12599 | 11807829 | To identify the potential signals for an increase in Hp expression in obesity, we examined leptin and TNFalpha in vivo. |
| 12600 | 11807829 | To identify the potential signals for an increase in Hp expression in obesity, we examined leptin and TNFalpha in vivo. |
| 12601 | 11807829 | To identify the potential signals for an increase in Hp expression in obesity, we examined leptin and TNFalpha in vivo. |
| 12602 | 11807829 | To identify the potential signals for an increase in Hp expression in obesity, we examined leptin and TNFalpha in vivo. |
| 12603 | 11807829 | These results demonstrate that haptoglobin expression in WAT is increased in obesity in rodents and TNFalpha is an important signal for this regulation. |
| 12604 | 11807829 | These results demonstrate that haptoglobin expression in WAT is increased in obesity in rodents and TNFalpha is an important signal for this regulation. |
| 12605 | 11807829 | These results demonstrate that haptoglobin expression in WAT is increased in obesity in rodents and TNFalpha is an important signal for this regulation. |
| 12606 | 11807829 | These results demonstrate that haptoglobin expression in WAT is increased in obesity in rodents and TNFalpha is an important signal for this regulation. |
| 12607 | 11799073 | In the present study, we show that glycated serum albumin (GSA) induces a parallel activation of the redox-responsive transcription factors (nuclear factor kappaB) and AP-1 and increases activity of mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase (ERK), and p38 MAPK in vascular smooth muscle cells (VSMCs). |
| 12608 | 11799073 | GSA increased expression of early response genes, c-fos and c-jun, and inflammatory genes, monocyte chemoattractant peptide (MCP-1), and interleukin (IL)-6. |
| 12609 | 11799073 | These effects were comparable to bacterial lipopolysaccharide, tumor necrosis factor-alphaa, (TNF-alphaa), IL-1alphab, angiotensin II, epidermal growth factor, and the phorbol ester PMA. |
| 12610 | 11799073 | One of signaling pathways by which GSA activates VSMCs appears to be via nuclear factor kappaB activation, leading to induction of MCP-1 and IL-6 gene expression, comparable to the effects of lipopolysaccharide, TNF-alphaa, and IL-1alphab. |
| 12611 | 11799073 | These effects are comparable to the effects of angiotensin II, epidermal growth factor, and PMA. |
| 12612 | 11799073 | Incubation of VSMCs with the antioxidant N-acetylcysteine suppressed GSA-elicited mRNA induction of MCP-1 and IL-6. |
| 12613 | 11799073 | Inhibition of p38 MAPK but not ERK caused attenuation of MCP-1 and IL-6 mRNA induction. |
| 12614 | 11796489 | We show here that although insulin increased kappaB-dependent reporter gene expression and augmented nuclear translocation of the p65/RelA subunit of NFkappaB and its DNA binding, it was able to induce a time-dependent accumulation of phosphorylated and ubiquitinated IkappaBalpha without its proteolytic degradation. |
| 12615 | 11796489 | Immunofluorescence studies revealed the presence of a large pool of phosphorylated IkappaBalpha in the nucleus of unstimulated and insulin-treated cells. |
| 12616 | 11796489 | IkappaB kinase alpha and beta, central players in the phosphorylation of IkappaBalpha, were rapidly induced following exposure to TNFalpha but not insulin. |
| 12617 | 11796489 | Furthermore, insulin-stimulated IkappaBalpha phosphorylation did not depend on activation of the Ras/ERK cascade. |
| 12618 | 11796489 | Expression of a dominant-negative mutant of Akt1 or class I PI3K inhibited the insulin stimulation of PI3K/Akt1 signaling without affecting phosphorylation of IkappaBalpha. |
| 12619 | 11796489 | Interestingly, the PI3K inhibitors wortmannin and LY294002 blocked insulin-stimulated class I PI3K-dependent events at much lower doses than that required to inhibit phosphorylation of IkappaBalpha. |
| 12620 | 11796489 | These data demonstrate that insulin regulates IkappaBalpha function through a distinct low-affinity wortmannin-sensitive pathway. |
| 12621 | 11793013 | Data obtained on non-obese diabetic (NOD) mice suggest that macrophages and CD4+ T-cells are the main cellular effectors, whereas CD8+ T-cells are more important initiators of the immune process leading to beta-cell death. |
| 12622 | 11793013 | Data obtained on non-obese diabetic (NOD) mice suggest that macrophages and CD4+ T-cells are the main cellular effectors, whereas CD8+ T-cells are more important initiators of the immune process leading to beta-cell death. |
| 12623 | 11793013 | Perforin could be the effector molecule utilized by CD8+ T-cell initiation, whereas CD4+ mediated beta-cell destruction is mostly dependent on Fas/FasL and the cytokines IFNgamma and TNF-alpha. |
| 12624 | 11793013 | Perforin could be the effector molecule utilized by CD8+ T-cell initiation, whereas CD4+ mediated beta-cell destruction is mostly dependent on Fas/FasL and the cytokines IFNgamma and TNF-alpha. |
| 12625 | 11793013 | The macrophage cytokine IL-1beta in combination with IFN-gamma and TNF-alpha, plays an important role for beta-cell dysfunction and death. |
| 12626 | 11793013 | The macrophage cytokine IL-1beta in combination with IFN-gamma and TNF-alpha, plays an important role for beta-cell dysfunction and death. |
| 12627 | 11793013 | Signal transduction by these cytokines involves: (i) binding to specific receptors, (ii) signal transduction by cytosolic kinases (especially the so-called mitogen- and stress-activated protein kinases) and/or phosphatases, (iii) mobilization of diverse transcription factors - with nuclear factor kappaB (NF-kappaB), AP-1 and STAT-1 probably playing key roles for beta-cell apoptosis; (iv) up-regulation or down-regulation of gene transcription. |
| 12628 | 11793013 | Signal transduction by these cytokines involves: (i) binding to specific receptors, (ii) signal transduction by cytosolic kinases (especially the so-called mitogen- and stress-activated protein kinases) and/or phosphatases, (iii) mobilization of diverse transcription factors - with nuclear factor kappaB (NF-kappaB), AP-1 and STAT-1 probably playing key roles for beta-cell apoptosis; (iv) up-regulation or down-regulation of gene transcription. |
| 12629 | 11784851 | Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the Ste20p homologue GCK and the adapter protein TRAF2. |
| 12630 | 11784851 | Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the Ste20p homologue GCK and the adapter protein TRAF2. |
| 12631 | 11784851 | Recombinant forms of MAP3K MEK kinase 1 (MEKK1) interact in vivo and in vitro with the STE20 protein homologue germinal center kinase (GCK), and both GCK and MEKK1 associate in vivo with the adapter protein tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2). |
| 12632 | 11784851 | Recombinant forms of MAP3K MEK kinase 1 (MEKK1) interact in vivo and in vitro with the STE20 protein homologue germinal center kinase (GCK), and both GCK and MEKK1 associate in vivo with the adapter protein tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2). |
| 12633 | 11784851 | These interactions may couple TNF receptors to the SAPK/JNK family of MAPKs; however, a molecular mechanism by which these proteins might collaborate to recruit the SAPKs/JNKs has remained elusive. |
| 12634 | 11784851 | These interactions may couple TNF receptors to the SAPK/JNK family of MAPKs; however, a molecular mechanism by which these proteins might collaborate to recruit the SAPKs/JNKs has remained elusive. |
| 12635 | 11784851 | Here we show that endogenous GCK and MEKK1 associate in vivo. |
| 12636 | 11784851 | Here we show that endogenous GCK and MEKK1 associate in vivo. |
| 12637 | 11784851 | In addition, we have developed an in vitro assay system with which we demonstrate that purified, active GCK and TRAF2 activate MEKK1. |
| 12638 | 11784851 | In addition, we have developed an in vitro assay system with which we demonstrate that purified, active GCK and TRAF2 activate MEKK1. |
| 12639 | 11784851 | The RING domain of TRAF2 is necessary for optimal in vitro activation of MEKK1, but the kinase domain of GCK is not. |
| 12640 | 11784851 | The RING domain of TRAF2 is necessary for optimal in vitro activation of MEKK1, but the kinase domain of GCK is not. |
| 12641 | 11784851 | Forced oligomerization also activates MEKK1, and GCK elicits enhanced oligomerization of coexpressed MEKK1 in vivo. |
| 12642 | 11784851 | Forced oligomerization also activates MEKK1, and GCK elicits enhanced oligomerization of coexpressed MEKK1 in vivo. |
| 12643 | 11782876 | Elevated soluble intercellular adhesion molecule-1 levels in obesity: relationship to insulin resistance and tumor necrosis factor-alpha system activity. |
| 12644 | 11782876 | Elevated soluble intercellular adhesion molecule-1 levels in obesity: relationship to insulin resistance and tumor necrosis factor-alpha system activity. |
| 12645 | 11782876 | Elevated soluble intercellular adhesion molecule-1 levels in obesity: relationship to insulin resistance and tumor necrosis factor-alpha system activity. |
| 12646 | 11782876 | Therefore, the aim of the present study was to assess plasma soluble ICAM-1 (sICAM-1) levels in obese subjects with normal glucose tolerance and to evaluate whether those levels may be related to insulin resistance and tumor necrosis factor-alpha (TNFalpha) system activity. |
| 12647 | 11782876 | Therefore, the aim of the present study was to assess plasma soluble ICAM-1 (sICAM-1) levels in obese subjects with normal glucose tolerance and to evaluate whether those levels may be related to insulin resistance and tumor necrosis factor-alpha (TNFalpha) system activity. |
| 12648 | 11782876 | Therefore, the aim of the present study was to assess plasma soluble ICAM-1 (sICAM-1) levels in obese subjects with normal glucose tolerance and to evaluate whether those levels may be related to insulin resistance and tumor necrosis factor-alpha (TNFalpha) system activity. |
| 12649 | 11782876 | Obese subjects were markedly more hyperinsulinemic and insulin resistant and had higher plasma soluble TNF receptor 2 (sTNFR2) and sICAM-1 levels. sICAM-1 was related positively to body mass index (BMI), waist-to-hip ratio (WHR), percent of body fat, glycated hemoglobin (HbA(1c)), plasma insulin and triglycerides (TG), TNFalpha, and sTNFR2 and negatively to insulin sensitivity. |
| 12650 | 11782876 | Obese subjects were markedly more hyperinsulinemic and insulin resistant and had higher plasma soluble TNF receptor 2 (sTNFR2) and sICAM-1 levels. sICAM-1 was related positively to body mass index (BMI), waist-to-hip ratio (WHR), percent of body fat, glycated hemoglobin (HbA(1c)), plasma insulin and triglycerides (TG), TNFalpha, and sTNFR2 and negatively to insulin sensitivity. |
| 12651 | 11782876 | Obese subjects were markedly more hyperinsulinemic and insulin resistant and had higher plasma soluble TNF receptor 2 (sTNFR2) and sICAM-1 levels. sICAM-1 was related positively to body mass index (BMI), waist-to-hip ratio (WHR), percent of body fat, glycated hemoglobin (HbA(1c)), plasma insulin and triglycerides (TG), TNFalpha, and sTNFR2 and negatively to insulin sensitivity. |
| 12652 | 11782874 | The stimulation of tumor necrosis factor and inhibition of glucose transport and lipoprotein lipase in adipose cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin. |
| 12653 | 11782874 | The stimulation of tumor necrosis factor and inhibition of glucose transport and lipoprotein lipase in adipose cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin. |
| 12654 | 11782874 | The stimulation of tumor necrosis factor and inhibition of glucose transport and lipoprotein lipase in adipose cells by 2,3,7,8-tetrachlorodibenzo-p-dioxin. |
| 12655 | 11782874 | In addition to the stimulation of TNF, TCDD affected glucose transport and lipoprotein lipase (LPL) activity. |
| 12656 | 11782874 | In addition to the stimulation of TNF, TCDD affected glucose transport and lipoprotein lipase (LPL) activity. |
| 12657 | 11782874 | In addition to the stimulation of TNF, TCDD affected glucose transport and lipoprotein lipase (LPL) activity. |
| 12658 | 11782874 | Thus, the addition of TCDD to adipocyte cultures resulted in an increase in TNF secretion and a decrease in glucose transport and LPL activity. |
| 12659 | 11782874 | Thus, the addition of TCDD to adipocyte cultures resulted in an increase in TNF secretion and a decrease in glucose transport and LPL activity. |
| 12660 | 11782874 | Thus, the addition of TCDD to adipocyte cultures resulted in an increase in TNF secretion and a decrease in glucose transport and LPL activity. |
| 12661 | 11756326 | Previous studies using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) have demonstrated that islet xenograft rejection in mice is dominated by Th2-associated cytokines, i.e., interleukin (IL)-4 and IL-10. |
| 12662 | 11756326 | By day 1, mRNA expression levels of IL-1 beta, IL-2, IL-12p40, interferon-gamma, and tumor necrosis factor-alpha were already induced in the lymph nodes. |
| 12663 | 11756323 | Expression of MCP-1 was increased by primary inflammatory cytokines (interleukin-1 beta, tumor necrosis factor-alpha) and lipopolysaccharide at both the mRNA and protein levels but not by glucose. |
| 12664 | 11756323 | However, MCP-1 did not modulate insulin secretion. |
| 12665 | 11756323 | In fact, low MCP-1 secretion resulted as the most relevant factor for long-lasting insulin independence. |
| 12666 | 11751962 | We have recently demonstrated that dendritic cells (DC) prepared from nonobese diabetic (NOD) mice, a spontaneous model for insulin-dependent diabetes mellitus, exhibit elevated levels of NF-kappaB activation upon stimulation. |
| 12667 | 11751962 | The T cell stimulatory capacity of NOD DC was suppressed by gene transfer of a modified form of IkappaBalpha, indicating a direct role for NF-kappaB in this process. |
| 12668 | 11751962 | Furthermore, neutralization of IL-12(p70) to block autocrine-mediated activation of DC also significantly reduced the capacity of NOD DC to stimulate T cells. |
| 12669 | 11751962 | Finally, DC from nonobese diabetes-resistant mice, a strain genotypically similar to NOD yet disease resistant, resembled BALB/c and not NOD DC in terms of the level of NF-kappaB activation, secretion of IL-12(p70) and TNF-alpha, and the capacity to stimulate T cells. |
| 12670 | 11751962 | Therefore, elevated NF-kappaB activation and enhanced APC function are specific for the NOD genotype and correlate with the progression of insulin-dependent diabetes mellitus. |
| 12671 | 11750858 | Resistin and obesity-associated insulin resistance. |
| 12672 | 11750858 | These include leptin, tumor necrosis factor alpha, Acrp30/adiponectin/adipoQ and interleukin 6, the potential roles of which are briefly reviewed here. |
| 12673 | 11750858 | Thus, resistin is a potential link between TZDs, obesity and insulin resistance in the mouse. |
| 12674 | 11748258 | To analyze the function of the Th1-promoting cytokine IL-12 in vivo, we generated transgenic (tg) mice (RIP-IL12 mice) whose pancreatic beta cells constitutively express bioactive IL-12 or one of its components, p35 or p40. |
| 12675 | 11748258 | Expression of bioactive IL-12 primarily upregulated transcript levels of IFN-inducible protein-10 (IP-10), RANTES, IFN-gamma, and TNF-alpha in the pancreas. |
| 12676 | 11748258 | However, when RIP-IL12 x RIP-LCMV tg mice were infected with LCMV, antigen-specific anti-self/viral T cells were induced, which led to an acceleration in the kinetics and severity of insulin-dependent diabetes mellitus (IDDM). |
| 12677 | 11744348 | Overweight and obese children and adults have elevated serum levels of C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and leptin, which are known markers of inflammation and closely associated with cardiovascular risk factors and cardiovascular and non-cardiovascular causes of death. |
| 12678 | 11744348 | The complex interaction between several neurotransmitters such as dopamine, serotonin, neuropeptide Y, leptin, acetylcholine, melanin-concentrating hormone, ghrelin, nitric oxide, and cytokines and insulin and insulin receptors in the brain ultimately determines and regulates food intake. |
| 12679 | 11744348 | Acetylcholine and insulin inhibit the production of proinflammatory cytokines and provide a negative feedback loop for postprandial inhibition of food intake, in part, by regulating leptin action. |
| 12680 | 11742842 | The relationship of leptin gene expression to adipocyte volume was investigated in lean 10-wk-old male C57BL/6J mice. mRNA levels for leptin, insulin receptor, glucocorticoid receptor, and tumor necrosis factor (TNF)-alpha in inguinal, epididymal, and retroperitoneal adipose tissues were quantified and related to adipocyte volume. |
| 12681 | 11742842 | The relationship of leptin gene expression to adipocyte volume was investigated in lean 10-wk-old male C57BL/6J mice. mRNA levels for leptin, insulin receptor, glucocorticoid receptor, and tumor necrosis factor (TNF)-alpha in inguinal, epididymal, and retroperitoneal adipose tissues were quantified and related to adipocyte volume. |
| 12682 | 11742842 | Leptin mRNA levels were highly correlated with adipocyte volume within each fat depot. |
| 12683 | 11742842 | Leptin mRNA levels were highly correlated with adipocyte volume within each fat depot. |
| 12684 | 11742842 | Multiple regression analysis of pooled data from the three depots showed that leptin mRNA levels were strongly correlated with adipocyte volumes (beta = 0.84, P < 0.001) and, to a smaller degree, with glucocorticoid receptor mRNA levels (beta = 0.36, P < 0.001). |
| 12685 | 11742842 | Multiple regression analysis of pooled data from the three depots showed that leptin mRNA levels were strongly correlated with adipocyte volumes (beta = 0.84, P < 0.001) and, to a smaller degree, with glucocorticoid receptor mRNA levels (beta = 0.36, P < 0.001). |
| 12686 | 11742842 | Rates of leptin secretion in vitro were strongly correlated with leptin mRNA levels (r = 0.89, P < 0.001). mRNA levels for TNF-alpha, insulin receptor, and glucocorticoid receptor showed no significant correlation with adipocyte volume. |
| 12687 | 11742842 | Rates of leptin secretion in vitro were strongly correlated with leptin mRNA levels (r = 0.89, P < 0.001). mRNA levels for TNF-alpha, insulin receptor, and glucocorticoid receptor showed no significant correlation with adipocyte volume. |
| 12688 | 11742842 | The strong correlation between leptin gene expression and adipocyte volume supports leptin's physiological role as a humoral signal of fat mass. |
| 12689 | 11742842 | The strong correlation between leptin gene expression and adipocyte volume supports leptin's physiological role as a humoral signal of fat mass. |
| 12690 | 11727511 | Administration of cDNA encoding soluble IFN-gamma receptor (IFN-gamma R)/IgG-Fc fusion proteins, soluble TNF-alpha receptors, or IL-1 receptor antagonist (IL-1ra), protects against either lupus, various forms of arthritis, autoimmune diabetes, or other autoimmune diseases. |
| 12691 | 11723054 | Interleukin-1beta stimulation of c-Jun NH(2)-terminal kinase activity in insulin-secreting cells: evidence for cytoplasmic restriction. |
| 12692 | 11723054 | Interleukin-1beta stimulation of c-Jun NH(2)-terminal kinase activity in insulin-secreting cells: evidence for cytoplasmic restriction. |
| 12693 | 11723054 | It is well established that cytokines such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and gamma-interferon (IFN-gamma) inhibit beta-cell function and are cytotoxic to human and rodent pancreatic islets in vitro. |
| 12694 | 11723054 | It is well established that cytokines such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and gamma-interferon (IFN-gamma) inhibit beta-cell function and are cytotoxic to human and rodent pancreatic islets in vitro. |
| 12695 | 11723054 | In this report, we have examined IL-1beta stimulation of c-Jun NH(2)-terminal kinase (JNK) activity in insulin-secreting clonal cell lines. |
| 12696 | 11723054 | In this report, we have examined IL-1beta stimulation of c-Jun NH(2)-terminal kinase (JNK) activity in insulin-secreting clonal cell lines. |
| 12697 | 11723054 | We demonstrate that IL-1beta transiently activates 46- and 54-kDa isoforms of JNK in cultured RINm5F beta-cells. |
| 12698 | 11723054 | We demonstrate that IL-1beta transiently activates 46- and 54-kDa isoforms of JNK in cultured RINm5F beta-cells. |
| 12699 | 11723054 | Furthermore, IL-1beta stimulation of JNK activity is specific, because TNF-alpha and IFN-gamma were without effect. |
| 12700 | 11723054 | Furthermore, IL-1beta stimulation of JNK activity is specific, because TNF-alpha and IFN-gamma were without effect. |
| 12701 | 11723054 | JNK-interacting protein (JIP) associates with endogenous as well as overexpressed JNK, suggesting that JIP may serve to regulate JNK activity. |
| 12702 | 11723054 | JNK-interacting protein (JIP) associates with endogenous as well as overexpressed JNK, suggesting that JIP may serve to regulate JNK activity. |
| 12703 | 11723054 | Together, these data indicate that IL-1beta-stimulated JNK activity may be distinctly targeted to cytoplasmic and/or membrane compartments in clonal insulin-producing cells, and that JIP may serve to localize JNK activity to specific substrates. |
| 12704 | 11723054 | Together, these data indicate that IL-1beta-stimulated JNK activity may be distinctly targeted to cytoplasmic and/or membrane compartments in clonal insulin-producing cells, and that JIP may serve to localize JNK activity to specific substrates. |
| 12705 | 11717249 | Two such genes encoding the LMP2 and LMP7 proteasome subunits are located in this high-risk MHC genomic region. |
| 12706 | 11717249 | The spontaneous defective LMP2 expression in NOD mice, which is gender biased toward female cohorts, is restricted to select lymphoid and myeloid cells and is developmentally controlled with lowered LMP2 protein and heightened tumor necrosis factor-alpha-induced apoptosis. |
| 12707 | 11715473 | [The mechanism of tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance by variation in promoter region of TNF-alpha gene]. |
| 12708 | 11714198 | IL-1 and TNF-alpha release by cultured islets was markedly decreased for op/op islets compared with control islets (IL-1: 0 vs. 4.2 pg/ml, p = 0.07; TNF-alpha: 67 vs. 311 pg/ml, p = 0.002). |
| 12709 | 11712861 | One of the mechanisms by which beta-cells are killed in type I diabetes is by the release of the cytokines interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) by immune cells. |
| 12710 | 11712415 | [The molecular mechanisms by which PPAR gamma/RXR inhibitors improve insulin resistance]. |
| 12711 | 11712415 | Potent activation of PPAR gamma by thiazolidinediones(TZD) increases TG content of WAT, thereby decreasing TG content of liver/muscle, leading to amelioration of insulin resistance at the expense of obesity. |
| 12712 | 11712415 | Moderate reduction of PPAR gamma activity by PPAR gamma/RXR inhibitors decreases TG content of WAT/muscle/liver due to increased leptin and increase in fatty-acid combustion and decrease in lipogenesis, thereby ameliorating HF diet-induced obesity and insulin resistance. |
| 12713 | 11712415 | Moreover, PPAR gamma/RXR inhibitors decrease lipogenesis in WAT, while TZD stimulate adipocyte differentiation and apoptosis, thereby both preventing adipocyte hypertrophy, which is associated with alleviation of insulin resistance presumably due to decreases in FFA, and TNF alpha, and upregulation of adiponectin. |
| 12714 | 11712415 | We conclude that although by different mechanisms, both PPAR gamma/RXR inhibitors and PPAR gamma agonist improve insulin resistance, which is associated with decreased TG content of muscle/liver and prevention of adipocyte hypertrophy. |
| 12715 | 11712406 | This effect seems to be due to the inhibitory action of pioglitazone on TNF-alpha production, which is one of the factors responsible for insulin resistance. |
| 12716 | 11712406 | This effect seems to be due to the inhibitory action of pioglitazone on TNF-alpha production, which is one of the factors responsible for insulin resistance. |
| 12717 | 11712406 | Pioglitazone is a potent agonist for the peroxisome proliferator activated receptor(PPAR)-gamma, that is related to differentiation of adipocytes, and the relationship between TNF-alpha production and PPAR-gamma has been reported. |
| 12718 | 11712406 | Pioglitazone is a potent agonist for the peroxisome proliferator activated receptor(PPAR)-gamma, that is related to differentiation of adipocytes, and the relationship between TNF-alpha production and PPAR-gamma has been reported. |
| 12719 | 11712406 | Therefore, the agonistic activity of pioglitazone on PPAR-gamma may be involved in the mechanism for reducing insulin resistance. |
| 12720 | 11712406 | Therefore, the agonistic activity of pioglitazone on PPAR-gamma may be involved in the mechanism for reducing insulin resistance. |
| 12721 | 11712406 | Recently, it was demonstrated that pioglitazone is also an agonist of PPAR-alpha, which plays a central role in lipid metabolism through enhancing the synthesis of apo AI, apo AII and reverse cholesterol transporters, such as fatty acid transporter molecules, and SR-B1 and ABCA1 reverse cholesterol transport receptors. |
| 12722 | 11712406 | Recently, it was demonstrated that pioglitazone is also an agonist of PPAR-alpha, which plays a central role in lipid metabolism through enhancing the synthesis of apo AI, apo AII and reverse cholesterol transporters, such as fatty acid transporter molecules, and SR-B1 and ABCA1 reverse cholesterol transport receptors. |
| 12723 | 11712393 | Current concept is that, when PPAR-gamma is activated by these drugs, the number of small adipocytes is increased to replace large adipocytes, thereby decreasing the release of TNF-alpha and FFA from adipose tissue. |
| 12724 | 11712393 | However, there seems to be a complex relationship between the activity of PPAR-gamma and insulin sensitivity. |
| 12725 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12726 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12727 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12728 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12729 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12730 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 12731 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12732 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12733 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12734 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12735 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12736 | 11707432 | We also demonstrated that TNF-alpha simultaneously produced insulin resistance by uncoupling insulin receptor activity toward insulin receptor substrate-1 (IRS-1) and suppressing insulin-sensitive glucose transport. |
| 12737 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12738 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12739 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12740 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12741 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12742 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 12743 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12744 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12745 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12746 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12747 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12748 | 11707432 | Moreover, when the adipocytes were incubated with exogenous GM3, suppression of tyrosine phosphorylation of insulin receptor and IRS-1 and glucose uptake in response to insulin stimulation was observed, demonstrating that GM3 itself is able to mimic the effects of TNF on insulin signaling. |
| 12749 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12750 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12751 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12752 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12753 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12754 | 11707432 | We used the obese Zucker fa/fa rat and ob/ob mouse, which are known to overproduce TNF-alpha mRNA in adipose tissues, as typical models of insulin resistance. |
| 12755 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12756 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12757 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12758 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12759 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12760 | 11707432 | Taken together, the increased synthesis of cellular GM3 by TNF may participate in the pathological conditions of insulin resistance in type 2 diabetes. |
| 12761 | 11698039 | The induction and increased expression of B(1) receptor occur following tissue injury or after treatment with bacterial endotoxins or cytokines such as interleukin-1 beta and tumor necrosis factor-alpha. |
| 12762 | 11698039 | New information is provided regarding the role of sensory mechanisms subserving spinal hyperalgesia and intrapleural neutrophil migration that occur upon B(1) receptor activation in streptozotocin-treated rats, a model of insulin-dependent diabetes mellitus in which the B(1) receptor seems to be rapidly overexpressed. |
| 12763 | 11689013 | Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. |
| 12764 | 11689013 | Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. |
| 12765 | 11689013 | Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. |
| 12766 | 11689013 | Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. |
| 12767 | 11689013 | Tumor necrosis factor alpha is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes. |
| 12768 | 11689013 | Resistin has recently been implicated as an adipocytokine leading to insulin resistance and, therefore, potentially linking obesity and diabetes. |
| 12769 | 11689013 | Resistin has recently been implicated as an adipocytokine leading to insulin resistance and, therefore, potentially linking obesity and diabetes. |
| 12770 | 11689013 | Resistin has recently been implicated as an adipocytokine leading to insulin resistance and, therefore, potentially linking obesity and diabetes. |
| 12771 | 11689013 | Resistin has recently been implicated as an adipocytokine leading to insulin resistance and, therefore, potentially linking obesity and diabetes. |
| 12772 | 11689013 | Resistin has recently been implicated as an adipocytokine leading to insulin resistance and, therefore, potentially linking obesity and diabetes. |
| 12773 | 11689013 | To further characterize the regulation of this fat-secreted protein by insulin sensitivity-modulating hormones, 3T3-L1 adipocytes were treated with tumor necrosis factor (TNF) alpha, angiotensin (AT) 2, as well as growth hormone (GH), and resistin gene expression and protein secretion were determined by quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. |
| 12774 | 11689013 | To further characterize the regulation of this fat-secreted protein by insulin sensitivity-modulating hormones, 3T3-L1 adipocytes were treated with tumor necrosis factor (TNF) alpha, angiotensin (AT) 2, as well as growth hormone (GH), and resistin gene expression and protein secretion were determined by quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. |
| 12775 | 11689013 | To further characterize the regulation of this fat-secreted protein by insulin sensitivity-modulating hormones, 3T3-L1 adipocytes were treated with tumor necrosis factor (TNF) alpha, angiotensin (AT) 2, as well as growth hormone (GH), and resistin gene expression and protein secretion were determined by quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. |
| 12776 | 11689013 | To further characterize the regulation of this fat-secreted protein by insulin sensitivity-modulating hormones, 3T3-L1 adipocytes were treated with tumor necrosis factor (TNF) alpha, angiotensin (AT) 2, as well as growth hormone (GH), and resistin gene expression and protein secretion were determined by quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. |
| 12777 | 11689013 | To further characterize the regulation of this fat-secreted protein by insulin sensitivity-modulating hormones, 3T3-L1 adipocytes were treated with tumor necrosis factor (TNF) alpha, angiotensin (AT) 2, as well as growth hormone (GH), and resistin gene expression and protein secretion were determined by quantitative real-time reverse transcription-polymerase chain reaction and Western blotting. |
| 12778 | 11689013 | Interestingly, both, resistin mRNA expression and protein secretion, were inhibited by 70-90% after TNFalpha-treatment whereas AT2 and GH did not have any effect. |
| 12779 | 11689013 | Interestingly, both, resistin mRNA expression and protein secretion, were inhibited by 70-90% after TNFalpha-treatment whereas AT2 and GH did not have any effect. |
| 12780 | 11689013 | Interestingly, both, resistin mRNA expression and protein secretion, were inhibited by 70-90% after TNFalpha-treatment whereas AT2 and GH did not have any effect. |
| 12781 | 11689013 | Interestingly, both, resistin mRNA expression and protein secretion, were inhibited by 70-90% after TNFalpha-treatment whereas AT2 and GH did not have any effect. |
| 12782 | 11689013 | Interestingly, both, resistin mRNA expression and protein secretion, were inhibited by 70-90% after TNFalpha-treatment whereas AT2 and GH did not have any effect. |
| 12783 | 11689013 | Pharmacological inhibition of protein kinase A (PKA), p44/42, and p38 mitogen-activated protein (MAP) kinase did not reverse the inhibitory effect of TNFalpha suggesting that neither of these signaling molecules is involved in suppression of resistin gene expression by TNFalpha. |
| 12784 | 11689013 | Pharmacological inhibition of protein kinase A (PKA), p44/42, and p38 mitogen-activated protein (MAP) kinase did not reverse the inhibitory effect of TNFalpha suggesting that neither of these signaling molecules is involved in suppression of resistin gene expression by TNFalpha. |
| 12785 | 11689013 | Pharmacological inhibition of protein kinase A (PKA), p44/42, and p38 mitogen-activated protein (MAP) kinase did not reverse the inhibitory effect of TNFalpha suggesting that neither of these signaling molecules is involved in suppression of resistin gene expression by TNFalpha. |
| 12786 | 11689013 | Pharmacological inhibition of protein kinase A (PKA), p44/42, and p38 mitogen-activated protein (MAP) kinase did not reverse the inhibitory effect of TNFalpha suggesting that neither of these signaling molecules is involved in suppression of resistin gene expression by TNFalpha. |
| 12787 | 11689013 | Pharmacological inhibition of protein kinase A (PKA), p44/42, and p38 mitogen-activated protein (MAP) kinase did not reverse the inhibitory effect of TNFalpha suggesting that neither of these signaling molecules is involved in suppression of resistin gene expression by TNFalpha. |
| 12788 | 11689013 | Furthermore, suppression of resistin mRNA levels could be completely reversed to control levels by withdrawal of TNFalpha for 24 h. |
| 12789 | 11689013 | Furthermore, suppression of resistin mRNA levels could be completely reversed to control levels by withdrawal of TNFalpha for 24 h. |
| 12790 | 11689013 | Furthermore, suppression of resistin mRNA levels could be completely reversed to control levels by withdrawal of TNFalpha for 24 h. |
| 12791 | 11689013 | Furthermore, suppression of resistin mRNA levels could be completely reversed to control levels by withdrawal of TNFalpha for 24 h. |
| 12792 | 11689013 | Furthermore, suppression of resistin mRNA levels could be completely reversed to control levels by withdrawal of TNFalpha for 24 h. |
| 12793 | 11689013 | Taken together, these results suggest that TNFalpha is a pivotal negative regulator of resistin gene expression. |
| 12794 | 11689013 | Taken together, these results suggest that TNFalpha is a pivotal negative regulator of resistin gene expression. |
| 12795 | 11689013 | Taken together, these results suggest that TNFalpha is a pivotal negative regulator of resistin gene expression. |
| 12796 | 11689013 | Taken together, these results suggest that TNFalpha is a pivotal negative regulator of resistin gene expression. |
| 12797 | 11689013 | Taken together, these results suggest that TNFalpha is a pivotal negative regulator of resistin gene expression. |
| 12798 | 11679435 | Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12799 | 11679435 | Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12800 | 11679435 | Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12801 | 11679435 | Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12802 | 11679435 | Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12803 | 11679435 | Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. |
| 12804 | 11679435 | Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. |
| 12805 | 11679435 | Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. |
| 12806 | 11679435 | Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. |
| 12807 | 11679435 | Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. |
| 12808 | 11679435 | A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. |
| 12809 | 11679435 | A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. |
| 12810 | 11679435 | A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. |
| 12811 | 11679435 | A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. |
| 12812 | 11679435 | A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4. |
| 12813 | 11679435 | Analysis of the phosphatidylinositol (PI) 3-kinase signaling pathway indicated that C2-ceramide precluded insulin stimulation of Akt kinase activity, but not of PI-3 kinase or protein kinase C-zeta activity. |
| 12814 | 11679435 | Analysis of the phosphatidylinositol (PI) 3-kinase signaling pathway indicated that C2-ceramide precluded insulin stimulation of Akt kinase activity, but not of PI-3 kinase or protein kinase C-zeta activity. |
| 12815 | 11679435 | Analysis of the phosphatidylinositol (PI) 3-kinase signaling pathway indicated that C2-ceramide precluded insulin stimulation of Akt kinase activity, but not of PI-3 kinase or protein kinase C-zeta activity. |
| 12816 | 11679435 | Analysis of the phosphatidylinositol (PI) 3-kinase signaling pathway indicated that C2-ceramide precluded insulin stimulation of Akt kinase activity, but not of PI-3 kinase or protein kinase C-zeta activity. |
| 12817 | 11679435 | Analysis of the phosphatidylinositol (PI) 3-kinase signaling pathway indicated that C2-ceramide precluded insulin stimulation of Akt kinase activity, but not of PI-3 kinase or protein kinase C-zeta activity. |
| 12818 | 11679435 | C2-ceramide completely abolished insulin-stimulated Akt/protein kinase B phosphorylation on regulatory residues Thr 308 and Ser 473, as did TNF-alpha, and inhibited insulin-induced mobility shift in Akt1 and Akt2 separated in PAGE. |
| 12819 | 11679435 | C2-ceramide completely abolished insulin-stimulated Akt/protein kinase B phosphorylation on regulatory residues Thr 308 and Ser 473, as did TNF-alpha, and inhibited insulin-induced mobility shift in Akt1 and Akt2 separated in PAGE. |
| 12820 | 11679435 | C2-ceramide completely abolished insulin-stimulated Akt/protein kinase B phosphorylation on regulatory residues Thr 308 and Ser 473, as did TNF-alpha, and inhibited insulin-induced mobility shift in Akt1 and Akt2 separated in PAGE. |
| 12821 | 11679435 | C2-ceramide completely abolished insulin-stimulated Akt/protein kinase B phosphorylation on regulatory residues Thr 308 and Ser 473, as did TNF-alpha, and inhibited insulin-induced mobility shift in Akt1 and Akt2 separated in PAGE. |
| 12822 | 11679435 | C2-ceramide completely abolished insulin-stimulated Akt/protein kinase B phosphorylation on regulatory residues Thr 308 and Ser 473, as did TNF-alpha, and inhibited insulin-induced mobility shift in Akt1 and Akt2 separated in PAGE. |
| 12823 | 11679435 | Moreover, C2-ceramide seemed to activate a protein phosphatase (PP) involved in dephosphorylating Akt because 1) PP2A activity was increased in C2-ceramide- and TNF-alpha-treated cells, 2) treatment with okadaic acid concomitantly with C2-ceramide completely restored Akt phosphorylation by insulin, and 3) transient transfection of a constitutively active form of Akt did not restore Akt activity. |
| 12824 | 11679435 | Moreover, C2-ceramide seemed to activate a protein phosphatase (PP) involved in dephosphorylating Akt because 1) PP2A activity was increased in C2-ceramide- and TNF-alpha-treated cells, 2) treatment with okadaic acid concomitantly with C2-ceramide completely restored Akt phosphorylation by insulin, and 3) transient transfection of a constitutively active form of Akt did not restore Akt activity. |
| 12825 | 11679435 | Moreover, C2-ceramide seemed to activate a protein phosphatase (PP) involved in dephosphorylating Akt because 1) PP2A activity was increased in C2-ceramide- and TNF-alpha-treated cells, 2) treatment with okadaic acid concomitantly with C2-ceramide completely restored Akt phosphorylation by insulin, and 3) transient transfection of a constitutively active form of Akt did not restore Akt activity. |
| 12826 | 11679435 | Moreover, C2-ceramide seemed to activate a protein phosphatase (PP) involved in dephosphorylating Akt because 1) PP2A activity was increased in C2-ceramide- and TNF-alpha-treated cells, 2) treatment with okadaic acid concomitantly with C2-ceramide completely restored Akt phosphorylation by insulin, and 3) transient transfection of a constitutively active form of Akt did not restore Akt activity. |
| 12827 | 11679435 | Moreover, C2-ceramide seemed to activate a protein phosphatase (PP) involved in dephosphorylating Akt because 1) PP2A activity was increased in C2-ceramide- and TNF-alpha-treated cells, 2) treatment with okadaic acid concomitantly with C2-ceramide completely restored Akt phosphorylation by insulin, and 3) transient transfection of a constitutively active form of Akt did not restore Akt activity. |
| 12828 | 11679435 | Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12829 | 11679435 | Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12830 | 11679435 | Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12831 | 11679435 | Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12832 | 11679435 | Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state. |
| 12833 | 11669476 | Pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), produced from adipose tissues in obese subjects, is known to play a predominant role in inducing insulin resistance. |
| 12834 | 11669476 | Pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), produced from adipose tissues in obese subjects, is known to play a predominant role in inducing insulin resistance. |
| 12835 | 11669476 | Therefore, it can be hypothesized that anti-infectious periodontal treatment may improve metabolic control of diabetes via improved insulin sensitivity by reducing peripheral TNF-alpha concentration. |
| 12836 | 11669476 | Therefore, it can be hypothesized that anti-infectious periodontal treatment may improve metabolic control of diabetes via improved insulin sensitivity by reducing peripheral TNF-alpha concentration. |
| 12837 | 11641367 | Total muscle content of the proposed IR inhibitors cytokine tumor necrosis factor-alpha and membrane glycoprotein PC-1 was not significantly changed in HFS animals at either 2 or 8 wk. |
| 12838 | 11595659 | We undertook this study 1) to reexplore insulin sensitivity in patients with IGT and 2) to evaluate potential mechanisms of insulin resistance in CF, including GLUT-4 translocation, elevation of serum cytokines, and free fatty acid (FFA) levels. |
| 12839 | 11595659 | A muscle biopsy was obtained at maximal insulin stimulation for measure of GLUT-4 translocation with sucrose gradients. |
| 12840 | 11595659 | Mechanisms include elevation of TNF-alpha and impaired translocation of GLUT-4. |
| 12841 | 11594239 | Pioglitazone improves glycaemic control in people with Type 2 diabetes by improving insulin sensitivity through its action at PPAR gamma 1 and PPAR gamma 2, and affects lipid metabolism through action at PPAR alpha. |
| 12842 | 11594239 | The results of these interactions include increases in glucose transporters 1 and 4, lowered free fatty acids, enhanced insulin signalling, reduced tumour necrosis factor alpha (TNF alpha) and remodelling of adipose tissue. |
| 12843 | 11593036 | Suppressor of cytokine signaling 3 (SOCS-3) protects beta -cells against interleukin-1beta - and interferon-gamma -mediated toxicity. |
| 12844 | 11593036 | Suppressor of cytokine signaling 3 (SOCS-3) protects beta -cells against interleukin-1beta - and interferon-gamma -mediated toxicity. |
| 12845 | 11593036 | Suppressor of cytokine signaling 3 (SOCS-3) is a negative feedback regulator of IFN-gamma signaling, shown up-regulated in mouse bone marrow cells by the proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and IFN-gamma. |
| 12846 | 11593036 | Suppressor of cytokine signaling 3 (SOCS-3) is a negative feedback regulator of IFN-gamma signaling, shown up-regulated in mouse bone marrow cells by the proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and IFN-gamma. |
| 12847 | 11593036 | IL-1beta and IFN-gamma alone, or potentiated by TNF-alpha, are cytotoxic to the insulin producing pancreatic beta-cells and beta-cell lines in vitro and suggested to contribute to the specific beta-cell destruction in Type-1 diabetes mellitus (T1DM). |
| 12848 | 11593036 | IL-1beta and IFN-gamma alone, or potentiated by TNF-alpha, are cytotoxic to the insulin producing pancreatic beta-cells and beta-cell lines in vitro and suggested to contribute to the specific beta-cell destruction in Type-1 diabetes mellitus (T1DM). |
| 12849 | 11593036 | Using a doxycycline-inducible SOCS-3 expression system in the rat beta-cell line INS-1, we demonstrate that the toxic effect of both IL-1beta or IFN-gamma at concentrations that reduced the viability by 50% over 3 days, was fully preventable when SOCS-3 expression was turned on in the cells. |
| 12850 | 11593036 | Using a doxycycline-inducible SOCS-3 expression system in the rat beta-cell line INS-1, we demonstrate that the toxic effect of both IL-1beta or IFN-gamma at concentrations that reduced the viability by 50% over 3 days, was fully preventable when SOCS-3 expression was turned on in the cells. |
| 12851 | 11593036 | Whereas SOCS-3-mediated inhibition of IFN-gamma signaling is described in other cell systems, SOCS-3 mediated inhibition of IL-1beta signaling has not previously been described. |
| 12852 | 11593036 | Whereas SOCS-3-mediated inhibition of IFN-gamma signaling is described in other cell systems, SOCS-3 mediated inhibition of IL-1beta signaling has not previously been described. |
| 12853 | 11593036 | In addition we show that SOCS-3 prevention of IL-1beta-induced toxicity is accompanied by inhibited transcription of the inducible nitric oxide synthase (iNOS) by 80%, resulting in 60% decreased formation of the toxic nitric oxide (NO). |
| 12854 | 11593036 | In addition we show that SOCS-3 prevention of IL-1beta-induced toxicity is accompanied by inhibited transcription of the inducible nitric oxide synthase (iNOS) by 80%, resulting in 60% decreased formation of the toxic nitric oxide (NO). |
| 12855 | 11593036 | Analysis of isolated native rat islets exposed to IL-1beta revealed a naturally occurring but delayed up-regulated SOCS-3 transcription. |
| 12856 | 11593036 | Analysis of isolated native rat islets exposed to IL-1beta revealed a naturally occurring but delayed up-regulated SOCS-3 transcription. |
| 12857 | 11587538 | Inhibition of ceramide production reverses TNF-induced insulin resistance. |
| 12858 | 11587538 | Inhibition of ceramide production reverses TNF-induced insulin resistance. |
| 12859 | 11587538 | Inhibition of ceramide production reverses TNF-induced insulin resistance. |
| 12860 | 11587538 | Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes. |
| 12861 | 11587538 | Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes. |
| 12862 | 11587538 | Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes. |
| 12863 | 11587538 | Neither exogenous short-chain ceramide analogs nor pharmacologic increases in endogenous caveolar pools of ceramide inhibited insulin-induced tyrosine phosphorylation of the IR and IRS-1. |
| 12864 | 11587538 | Neither exogenous short-chain ceramide analogs nor pharmacologic increases in endogenous caveolar pools of ceramide inhibited insulin-induced tyrosine phosphorylation of the IR and IRS-1. |
| 12865 | 11587538 | Neither exogenous short-chain ceramide analogs nor pharmacologic increases in endogenous caveolar pools of ceramide inhibited insulin-induced tyrosine phosphorylation of the IR and IRS-1. |
| 12866 | 11587538 | These results suggest that TNF-independent increases in caveolar pools of ceramide are not sufficient to inhibit insulin signaling but that in conjunction with other TNF-dependent signals, caveolar pools of ceramide are a critical component for insulin resistance by TNF. |
| 12867 | 11587538 | These results suggest that TNF-independent increases in caveolar pools of ceramide are not sufficient to inhibit insulin signaling but that in conjunction with other TNF-dependent signals, caveolar pools of ceramide are a critical component for insulin resistance by TNF. |
| 12868 | 11587538 | These results suggest that TNF-independent increases in caveolar pools of ceramide are not sufficient to inhibit insulin signaling but that in conjunction with other TNF-dependent signals, caveolar pools of ceramide are a critical component for insulin resistance by TNF. |
| 12869 | 11584100 | Increased life span was partially associated with decreased body weight, blunting renal proinflammatory cytokine (interferon-gamma, interleukins-10 and -12 and tumor necrosis factor-alpha) levels and lower nuclear factor-kappaB (NF-kappaB). |
| 12870 | 11584100 | Reductions in NF-kappaB were preceded by enhanced superoxide dismutase, catalase and glutathione peroxidase activities. |
| 12871 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 12872 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 12873 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |
| 12874 | 11574415 | Both TLK16998 and Merck L7 improved IR autophosphorylation in cells with diminished IR signaling due to either treatment with tumor necrosis factor-alpha or overexpression of membrane glycoprotein PC-1. |
| 12875 | 11571673 | Here we evaluated the effect of nitric oxide synthase (NOS) inhibitors on the bone particle resorbing activity and TNF-alpha release of cultured peripheral blood monocytes (PBM) obtained from 10 premenopausal (PreM) and 10 postmenopausal (PostM) women. |
| 12876 | 11571673 | Here we evaluated the effect of nitric oxide synthase (NOS) inhibitors on the bone particle resorbing activity and TNF-alpha release of cultured peripheral blood monocytes (PBM) obtained from 10 premenopausal (PreM) and 10 postmenopausal (PostM) women. |
| 12877 | 11571673 | Based on these findings and on the evidence that estrogen stimulates NOS, we suggest that estrogen withdrawal may reduce the inhibitory effect of NO on TNF-alpha release. |
| 12878 | 11571673 | Based on these findings and on the evidence that estrogen stimulates NOS, we suggest that estrogen withdrawal may reduce the inhibitory effect of NO on TNF-alpha release. |
| 12879 | 11564813 | To establish a model of continuous endothelial activation and to elucidate the role of endothelial derived TNF in vivo, we generated transgenic mice expressing a noncleavable transmembrane form of TNF under the control of the endothelial-specific tie2 promoter. |
| 12880 | 11564813 | To establish a model of continuous endothelial activation and to elucidate the role of endothelial derived TNF in vivo, we generated transgenic mice expressing a noncleavable transmembrane form of TNF under the control of the endothelial-specific tie2 promoter. |
| 12881 | 11564813 | To establish a model of continuous endothelial activation and to elucidate the role of endothelial derived TNF in vivo, we generated transgenic mice expressing a noncleavable transmembrane form of TNF under the control of the endothelial-specific tie2 promoter. |
| 12882 | 11564813 | Adult tie2-transmembrane TNF-transgenic mice developed chronic inflammatory pathology in kidney and liver, characterized by perivascular infiltration of mononuclear cells into these organs. |
| 12883 | 11564813 | Adult tie2-transmembrane TNF-transgenic mice developed chronic inflammatory pathology in kidney and liver, characterized by perivascular infiltration of mononuclear cells into these organs. |
| 12884 | 11564813 | Adult tie2-transmembrane TNF-transgenic mice developed chronic inflammatory pathology in kidney and liver, characterized by perivascular infiltration of mononuclear cells into these organs. |
| 12885 | 11564813 | Along with the infiltrate, an up-regulation of the adhesion molecules ICAM-1 and VCAM-1, but not E-selectin, in the endothelium was observed. |
| 12886 | 11564813 | Along with the infiltrate, an up-regulation of the adhesion molecules ICAM-1 and VCAM-1, but not E-selectin, in the endothelium was observed. |
| 12887 | 11564813 | Along with the infiltrate, an up-regulation of the adhesion molecules ICAM-1 and VCAM-1, but not E-selectin, in the endothelium was observed. |
| 12888 | 11564813 | Although the blood levels of soluble TNF and IFN-gamma were increased in transgenic animals after challenge with Con A, no damage of hepatocytes could be detected, as assessed by the lack of increase in plasma transaminase activities and the absence of TUNEL staining in the liver. |
| 12889 | 11564813 | Although the blood levels of soluble TNF and IFN-gamma were increased in transgenic animals after challenge with Con A, no damage of hepatocytes could be detected, as assessed by the lack of increase in plasma transaminase activities and the absence of TUNEL staining in the liver. |
| 12890 | 11564813 | Although the blood levels of soluble TNF and IFN-gamma were increased in transgenic animals after challenge with Con A, no damage of hepatocytes could be detected, as assessed by the lack of increase in plasma transaminase activities and the absence of TUNEL staining in the liver. |
| 12891 | 11544177 | Increased spontaneous apoptosis is also observed in the thymi of Akt1(-/-) mice, and Akt1(-/-) thymocytes are more sensitive to apoptosis induced by gamma-irradiation and dexamethasone. |
| 12892 | 11544177 | Finally, Akt1(-/-) mouse embryo fibroblasts (MEFs) are more susceptible to apoptosis induced by TNF, anti-Fas, UV irradiation, and serum withdrawal. |
| 12893 | 11533853 | This holds true for the tumor necrosis factor(TNF)-system, the interleukin(IL)-2-system, IL-6, and granulocyte colony-stimulating factor (G-CSF). |
| 12894 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12895 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12896 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12897 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12898 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12899 | 11523631 | Mechanisms involved in tumor necrosis factor-alpha induction of insulin resistance and its reversal by thiazolidinedione(s). |
| 12900 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12901 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12902 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12903 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12904 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12905 | 11523631 | In past experiments, we used both labeled glucose uptake, lipogenesis, and stimulation of calmodulin gene expression to quantify the ability of the antidiabetic drugs (pioglitazone and metformin) to reverse tumor necrosis factor-alpha (TNF-alpha)-induced IR in these insulin-treated cells. |
| 12906 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12907 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12908 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12909 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12910 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12911 | 11523631 | In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents. |
| 12912 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12913 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12914 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12915 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12916 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12917 | 11523631 | C2 Cer, like TNF-alpha, inhibited insulin action. |
| 12918 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12919 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12920 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12921 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12922 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12923 | 11523631 | Our data demonstrate a powerful effect of TRG in reducing IR and restoring insulin sensitivity in TNF-alpha-treated H-411E cells. |
| 12924 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12925 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12926 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12927 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12928 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12929 | 11523631 | These data support the efficacy of using thiazolidinediones (TRG) in human type 2 diabetes, and support the use of this cell culture model to further study the effects of thiazolidinediones on TNF-alpha-induced insulin resistance. |
| 12930 | 11522676 | Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. |
| 12931 | 11522676 | Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. |
| 12932 | 11522676 | A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. |
| 12933 | 11522676 | A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. |
| 12934 | 11522676 | The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. |
| 12935 | 11522676 | The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. |
| 12936 | 11522676 | On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. |
| 12937 | 11522676 | On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. |
| 12938 | 11522676 | TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter. |
| 12939 | 11522676 | TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter. |
| 12940 | 11522500 | We measured concentrations of interleukin-6, 8 (IL-6, 8) and tumor necrosis factor (TNF)-alpha by enzyme-linked immunosorbent assay (ELISA) in vitreous and serum from 47 patients with proliferative diabetic retinopathy and 21 patients with vitreous noninflammatory retinopathies. |
| 12941 | 11522500 | In sera, concentrations of IL-6 and IL-8 were not different between proliferative and noninflammatory retinopathy. |
| 12942 | 11521435 | Ten cytokines (alpha-IFN, gamma-IFN, GM-CSF, TGF-beta 1, Il-1, Il-4, Il-6, Il-6sR, TNF alpha) were measured in the serum, lacrimal fluid, and vitreous and subretinal fluid collected during operations. |
| 12943 | 11521435 | Ten cytokines (alpha-IFN, gamma-IFN, GM-CSF, TGF-beta 1, Il-1, Il-4, Il-6, Il-6sR, TNF alpha) were measured in the serum, lacrimal fluid, and vitreous and subretinal fluid collected during operations. |
| 12944 | 11521435 | The data indicate that excessive or insufficient local and/or systemic production of at least seven cytokines (TNF alpha, gamma-IFN, Il-6, Il-pR, alpha-IFN, Il-8, and RGF-beta 1) can affect the retinal involvement in the pathological process and development of proliferative retinopathy in patients with insulin-dependent diabetes mellitus. |
| 12945 | 11521435 | The data indicate that excessive or insufficient local and/or systemic production of at least seven cytokines (TNF alpha, gamma-IFN, Il-6, Il-pR, alpha-IFN, Il-8, and RGF-beta 1) can affect the retinal involvement in the pathological process and development of proliferative retinopathy in patients with insulin-dependent diabetes mellitus. |
| 12946 | 11520059 | Rosiglitazone treatment decreased adiponectin and resistin mRNA levels by 57 and 72%, respectively (P < 0.001), with no effect on the level of TNFalpha or RELMalpha transcripts. |
| 12947 | 11520059 | Rosiglitazone treatment decreased adiponectin and resistin mRNA levels by 57 and 72%, respectively (P < 0.001), with no effect on the level of TNFalpha or RELMalpha transcripts. |
| 12948 | 11520059 | Our results indicate that although a reduction in adiponectin and resistin mRNA levels in WAT by rosiglitazone treatment of diabetic mice may contribute to the antidiabetic effects, an alteration in TNFalpha, adiponectin, resistin, or RELMalpha mRNA expression is not absolutely required for the regulation of blood glucose concentration in the db/db mouse. |
| 12949 | 11520059 | Our results indicate that although a reduction in adiponectin and resistin mRNA levels in WAT by rosiglitazone treatment of diabetic mice may contribute to the antidiabetic effects, an alteration in TNFalpha, adiponectin, resistin, or RELMalpha mRNA expression is not absolutely required for the regulation of blood glucose concentration in the db/db mouse. |
| 12950 | 11517007 | Changes in tumor necrosis factor-alpha system and insulin sensitivity during an exercise training program in obese women with normal and impaired glucose tolerance. |
| 12951 | 11502070 | TNF and TNFR biology in health and disease. |
| 12952 | 11502070 | TNF and TNFR biology in health and disease. |
| 12953 | 11502070 | There has been a gradual realisation of the value of TNF/TNFR ratios as predictors of disease outcome, and the discovery of functional regulatory polymorphisms of the TNF gene and mutations of TNFRSF1A (TNFR1 receptor) have led to conceptual breakthroughs in our understanding of the genetic control of inflammation. |
| 12954 | 11502070 | There has been a gradual realisation of the value of TNF/TNFR ratios as predictors of disease outcome, and the discovery of functional regulatory polymorphisms of the TNF gene and mutations of TNFRSF1A (TNFR1 receptor) have led to conceptual breakthroughs in our understanding of the genetic control of inflammation. |
| 12955 | 11496827 | However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). |
| 12956 | 11485910 | In parallel with accelerated wound closure at later times, blockade of RAGE suppressed levels of cytokines; tumor necrosis factor-alpha; interleukin-6; and matrix metalloproteinases-2, -3, and -9. |
| 12957 | 11485910 | In addition, generation of thick, well-vascularized granulation tissue was enhanced, in parallel with increased levels of platelet-derived growth factor-B and vascular endothelial growth factor. |
| 12958 | 11473092 | Plasma total homocysteine levels are associated with von Willebrand factor, soluble intercellular adhesion molecule-1, and soluble tumor necrosis factor-alpha receptors in young type 1 diabetic patients without clinical evidence of macrovascular complications. |
| 12959 | 11473052 | The molecular mechanisms by which peroxisome proliferator-activated receptor (PPAR) activation by fibrates reduces fat deposition and improves insulin sensitivity are not completely understood. |
| 12960 | 11473052 | These changes were accompanied by an increase in the transcript levels of the uncoupling protein-2 (UCP-2; 1.5-fold induction; P < 0.05) and UCP-3 (3.7-fold induction; P < 0.001), mitochondrial proteins that reduce ATP yield and may facilitate the oxidation of fatty acids. |
| 12961 | 11473052 | Moreover, bezafibrate reduced the mRNA expression of several adipocyte markers, including PPARgamma (30% reduction; P = 0.05), tumor necrosis factor-alpha (33% reduction; P < 0.05), and the ob gene (26% reduction). |
| 12962 | 11473052 | The reduction of the adipocyte markers caused by bezafibrate was accompanied by an increase in the mRNA levels of the preadipocyte marker Pref-1 (1.6-fold induction; P < 0.01). |
| 12963 | 11473052 | Similarly, fatty acid translocase (2.6-fold induction; P = 0.002) and Pref-1 (5.6-fold induction) mRNA levels increased, although differences in the latter were not significant because of huge individual variations. |
| 12964 | 11473028 | We observed that transduction of the anti-apoptotic proteins Bcl-X(L) and PEA-15 fused to TAT/PTD prevented apoptosis induced by tumor necrosis factor-alpha in a pancreatic beta-cell line, indicating that TAT/PTD anti-apoptotic proteins retained their biological activity. |
| 12965 | 11473028 | Finally, we demonstrated that TAT-fusion proteins did not affect the insulin secretion capability of islets, as determined by glucose static incubation and by reversion of hyperglycemia in diabetic immunodeficient mice. |
| 12966 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 12967 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 12968 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 12969 | 11472752 | Plasma leptin and tumor necrosis factor-alpha (TNF-alpha), two adipocyte products, are also proposed to be associated with the development of CVD risk. |
| 12970 | 11472752 | Plasma leptin and tumor necrosis factor-alpha (TNF-alpha), two adipocyte products, are also proposed to be associated with the development of CVD risk. |
| 12971 | 11472752 | Plasma leptin and tumor necrosis factor-alpha (TNF-alpha), two adipocyte products, are also proposed to be associated with the development of CVD risk. |
| 12972 | 11472752 | The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. |
| 12973 | 11472752 | The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. |
| 12974 | 11472752 | The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. |
| 12975 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 12976 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 12977 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 12978 | 11472752 | Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m(2)) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). |
| 12979 | 11472752 | Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m(2)) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). |
| 12980 | 11472752 | Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m(2)) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). |
| 12981 | 11472752 | In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. |
| 12982 | 11472752 | In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. |
| 12983 | 11472752 | In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. |
| 12984 | 11472752 | The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. |
| 12985 | 11472752 | The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. |
| 12986 | 11472752 | The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. |
| 12987 | 11472752 | These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. |
| 12988 | 11472752 | These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. |
| 12989 | 11472752 | These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. |
| 12990 | 11469400 | Whereas the biological function of apM1 is presently unknown, the tissue specific expression, structural similarities to TNFalpha, and the dysregulated expression observed in obese Type 2 diabetic patients suggest that this factor may play a role in the pathogenesis of insulin resistance and Type 2 diabetes. |
| 12991 | 11467344 | A specific proteasome defect has been identified in NOD mouse in select lymphocytic and monocytic lineages that results from down-regulation of expression of the proteasome subunit LMP2, which is encoded by a gene in the MHC genomic region. |
| 12992 | 11467344 | This defect prevents the proteolytic processing required for the production and activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which plays important roles in immune and inflammatory responses, as well as increases the susceptibility of the affected cells to apoptosis induced by tumor necrosis factor-alpha (TNF-alpha). |
| 12993 | 11465949 | Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. |
| 12994 | 11465949 | Both CD4 and CD8 T cells have been shown to be independently capable of beta cell destruction. |
| 12995 | 11465949 | It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. |
| 12996 | 11465949 | It has previously been shown that the absence of TNF-alpha receptor 1 (p55) on the islets protected islets from CD4 T-cell-mediated destruction as long as the T cells did not have access to wild-type islets in vivo. |
| 12997 | 11465949 | In this study, we demonstrate that islet TNF-alpha receptor 1 (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. |
| 12998 | 11465949 | In this study, we demonstrate that islet TNF-alpha receptor 1 (p55) influences the expression of LIGHT (TNFSF-14), a TNF family member with both cytolytic and costimulatory properties, on BDC2.5 T cells and the expression of its receptor HVEM (TNFRSF-14) by islets, indicating a role for LIGHT-HVEM interactions in autoimmune diabetes. |
| 12999 | 11463859 | This unique RXR ligand triggers cellular RXR:PPARgamma-dependent pathways including adipocyte differentiation and inhibition of TNFalpha-mediated hypophosphorylation of the insulin receptor, but does not activate key farnesoid X receptor and liver X receptor target genes. |
| 13000 | 11459814 | Calbindin-D(28k) expression resulted in increased cell survival in the presence of the cytotoxic combination of the cytokines IL-1beta (30 U/ml), TNFalpha (10(3) U/ml), and interferon gamma (10(3) U/ml). |
| 13001 | 11458880 | This review article summarizes our major findings concerning the synthesis of TNF-alpha and IL-1beta in the uterus of diabetic rats, and in cultures of rodent uterine cells upon their exposure to high concentrations of glucose. |
| 13002 | 11454665 | Activation of poly(ADP-ribose) synthetase (PARS, also termed polyADP-ribose polymerase or PARP) has been proposed as a major mechanism contributing to beta-cell destruction in type I diabetes. |
| 13003 | 11454665 | In vitro the cytokine combination; interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma inhibited glucose-stimulated insulin secretion from isolated rat islets of Langerhans and decreased RIN-5F cell viability. |
| 13004 | 11454665 | The present study provides evidence for in vivo PARS activation contributing to beta-cell damage and death in the MLDS model of diabetes, and indicates a role for PARS activation in cytokine-mediated depression of insulin secretion and cell viability in vitro. |
| 13005 | 11453240 | The effect of antimicrobial periodontal treatment on circulating tumor necrosis factor-alpha and glycated hemoglobin level in patients with type 2 diabetes. |
| 13006 | 11443501 | TNFalpha and leptin inhibit basal and glucose-stimulated insulin secretion and gene transcription in the HIT-T15 pancreatic cells. |
| 13007 | 11437493 | In addition, GED significantly inhibited nitric oxide and nitrotyrosine formation and decreased destruction of beta-cells in NOD mouse islets incubated in vitro with the combination of proinflammatory cytokines interleukin 1-beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). |
| 13008 | 11437491 | The respective implication in this phenomenon of the various apoptotic pathways driven by Fas, perforin, or tumor necrosis factor is still ill- defined. |
| 13009 | 11437491 | To block the in vivo Fas-Fas ligand (Fas L) interaction we administered a biologically active recombinant fusion protein coupling mouse Fas to the Fc portion of human IgG1 (FAS-Fc). |
| 13010 | 11437072 | The TNF response was partly inhibited with antibodies against CD14, which is a well-known receptor for lipopolysaccharide (LPS). |
| 13011 | 11437072 | This indicates that PLL and LPS bind to different sites on monocytes, but because they both are inhibited by a p38 MAP kinase inhibitor, they seem to have a common element in the signal transducing pathway. |
| 13012 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13013 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13014 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13015 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13016 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13017 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13018 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13019 | 11416024 | Leptin and tumor necrosis factor-alpha induce the tyrosine phosphorylation of signal transducer and activator of transcription proteins in the hypothalamus of normal rats in vivo. |
| 13020 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13021 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13022 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13023 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13024 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13025 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13026 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13027 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 13028 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13029 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13030 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13031 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13032 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13033 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13034 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13035 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 13036 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13037 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13038 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13039 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13040 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13041 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13042 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13043 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 13044 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13045 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13046 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13047 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13048 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13049 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13050 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13051 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 13052 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13053 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13054 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13055 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13056 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13057 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13058 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13059 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 13060 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13061 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13062 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13063 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13064 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13065 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13066 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13067 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 13068 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13069 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13070 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13071 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13072 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13073 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13074 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13075 | 11416024 | We therefore suggest that TNFalpha may represent a modulator of leptin action in the hypothalamus. |
| 13076 | 11409655 | The results suggest that the Chinese medicine JTKL improves insulin resistance and modulates TNF-alpha in the soleus and EDL muscles in hypertensive and insulin-resistant fructose-fed rats. |
| 13077 | 11409298 | Stimulatory and synergistic effects of luteinising hormone and insulin like growth factor 1 on the secretion of vascular endothelial growth factor and progesterone of cultured bovine granulosa cells. |
| 13078 | 11409298 | The aim of the study was to test under in vitro conditions the stimulation of VEGF and progesterone (P) secretion of bovine granulosa cells by LH, IGF1 (insulin like growth factor) or by factors known to be produced by luteinised granulosa cells or in the early CL. |
| 13079 | 11409298 | LH and IGF1 stimulated dose dependently and significantly P and VEGF when tested alone. |
| 13080 | 11409298 | In contrast, VEGF was stimulated only additively with 0.1 ng/ml of LH plus 5 or 10 ng IGF1. |
| 13081 | 11409298 | Endothelin, oxytocin, progesterone, atrial natiuretic peptide, angiotensin II, prostaglandin F2 alpha alpha, prostaglandin E2, cortisol, fibroblast growth factor 1 and 2 and growth hormone showed no effect neither on P nor on VEGF. |
| 13082 | 11409298 | Tumour necrosis factor alpha (TNF alpha) stimulated (P < 0.05) VEGF with 10 or 100 ng/ml but not P. |
| 13083 | 11411343 | These effects seem to be due to the inhibitory action of pioglitazone on TNF-alpha production, which is one of the factors responsible for insulin resistance. |
| 13084 | 11411343 | These effects seem to be due to the inhibitory action of pioglitazone on TNF-alpha production, which is one of the factors responsible for insulin resistance. |
| 13085 | 11411343 | Pioglitazone is a potent agonist for the peroxisome proliferator-activated receptor, (PPAR)-gamma, that is related to differentiation of adipocytes, and the relationship between TNF-alpha production and PPAR-gamma has been reported. |
| 13086 | 11411343 | Pioglitazone is a potent agonist for the peroxisome proliferator-activated receptor, (PPAR)-gamma, that is related to differentiation of adipocytes, and the relationship between TNF-alpha production and PPAR-gamma has been reported. |
| 13087 | 11411343 | Therefore, the agonistic activity of pioglitazone on PPAR-gamma may be involved in the mechanism of reduction of insulin resistance. |
| 13088 | 11411343 | Therefore, the agonistic activity of pioglitazone on PPAR-gamma may be involved in the mechanism of reduction of insulin resistance. |
| 13089 | 11410238 | Tumor necrosis factor-alpha (TNF-alpha) is a key component of obesity-diabetes link, we therefore examined the attenuating effect of VO(opt)(2) on impaired insulin signal transduction induced by TNF-alpha. |
| 13090 | 11410238 | Tumor necrosis factor-alpha (TNF-alpha) is a key component of obesity-diabetes link, we therefore examined the attenuating effect of VO(opt)(2) on impaired insulin signal transduction induced by TNF-alpha. |
| 13091 | 11410238 | Tumor necrosis factor-alpha (TNF-alpha) is a key component of obesity-diabetes link, we therefore examined the attenuating effect of VO(opt)(2) on impaired insulin signal transduction induced by TNF-alpha. |
| 13092 | 11410238 | Tumor necrosis factor-alpha (TNF-alpha) is a key component of obesity-diabetes link, we therefore examined the attenuating effect of VO(opt)(2) on impaired insulin signal transduction induced by TNF-alpha. |
| 13093 | 11410238 | Incubation of 3T3-L1, mouse adipocytes, with TNF-alpha reduced the phosphorylation of insulin receptor substrate-1 (IRS-1), whereas VO(opt)(2) treatment resulted in an enhancement of IRS-1 phosphorylation, irrespective of the presence or absence of TNF-alpha. |
| 13094 | 11410238 | Incubation of 3T3-L1, mouse adipocytes, with TNF-alpha reduced the phosphorylation of insulin receptor substrate-1 (IRS-1), whereas VO(opt)(2) treatment resulted in an enhancement of IRS-1 phosphorylation, irrespective of the presence or absence of TNF-alpha. |
| 13095 | 11410238 | Incubation of 3T3-L1, mouse adipocytes, with TNF-alpha reduced the phosphorylation of insulin receptor substrate-1 (IRS-1), whereas VO(opt)(2) treatment resulted in an enhancement of IRS-1 phosphorylation, irrespective of the presence or absence of TNF-alpha. |
| 13096 | 11410238 | Incubation of 3T3-L1, mouse adipocytes, with TNF-alpha reduced the phosphorylation of insulin receptor substrate-1 (IRS-1), whereas VO(opt)(2) treatment resulted in an enhancement of IRS-1 phosphorylation, irrespective of the presence or absence of TNF-alpha. |
| 13097 | 11410238 | Overall, the present study demonstrates that VO(opt)(2) exerts an anti-diabetic effect in ob/ob mice by ameliorating impaired glucose tolerance, and furthermore, attenuates the TNF-alpha-induced decrease in IRS-1 phosphorylation in adipocytes. |
| 13098 | 11410238 | Overall, the present study demonstrates that VO(opt)(2) exerts an anti-diabetic effect in ob/ob mice by ameliorating impaired glucose tolerance, and furthermore, attenuates the TNF-alpha-induced decrease in IRS-1 phosphorylation in adipocytes. |
| 13099 | 11410238 | Overall, the present study demonstrates that VO(opt)(2) exerts an anti-diabetic effect in ob/ob mice by ameliorating impaired glucose tolerance, and furthermore, attenuates the TNF-alpha-induced decrease in IRS-1 phosphorylation in adipocytes. |
| 13100 | 11410238 | Overall, the present study demonstrates that VO(opt)(2) exerts an anti-diabetic effect in ob/ob mice by ameliorating impaired glucose tolerance, and furthermore, attenuates the TNF-alpha-induced decrease in IRS-1 phosphorylation in adipocytes. |
| 13101 | 11410238 | These results suggest that the anti-diabetic action of VO(opt)(2) is derived from an attenuation of a TNF-alpha induced impaired insulin signal transduction via inhibition of protein tyrosine phosphatase, providing a potential clinical utility for VO(opt)(2) in the treatment of NIDDM. |
| 13102 | 11410238 | These results suggest that the anti-diabetic action of VO(opt)(2) is derived from an attenuation of a TNF-alpha induced impaired insulin signal transduction via inhibition of protein tyrosine phosphatase, providing a potential clinical utility for VO(opt)(2) in the treatment of NIDDM. |
| 13103 | 11410238 | These results suggest that the anti-diabetic action of VO(opt)(2) is derived from an attenuation of a TNF-alpha induced impaired insulin signal transduction via inhibition of protein tyrosine phosphatase, providing a potential clinical utility for VO(opt)(2) in the treatment of NIDDM. |
| 13104 | 11410238 | These results suggest that the anti-diabetic action of VO(opt)(2) is derived from an attenuation of a TNF-alpha induced impaired insulin signal transduction via inhibition of protein tyrosine phosphatase, providing a potential clinical utility for VO(opt)(2) in the treatment of NIDDM. |
| 13105 | 11404500 | Temporary reversal by topotecan of marked insulin resistance in a patient with myelodysplastic syndrome: case report and possible mechanism for tumor necrosis factor alpha (TNF-alpha)-induced insulin resistance. |
| 13106 | 11404500 | Temporary reversal by topotecan of marked insulin resistance in a patient with myelodysplastic syndrome: case report and possible mechanism for tumor necrosis factor alpha (TNF-alpha)-induced insulin resistance. |
| 13107 | 11404500 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor. |
| 13108 | 11404500 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor. |
| 13109 | 11390446 | In a transgenic model (rat insulin promoter-lymphocytic choriomeningitis virus) of virally induced diabetes, TNF-alpha enhanced disease incidence when induced through an islet-specific tetracycline-dependent promoter system early during pathogenesis. |
| 13110 | 11390446 | In a transgenic model (rat insulin promoter-lymphocytic choriomeningitis virus) of virally induced diabetes, TNF-alpha enhanced disease incidence when induced through an islet-specific tetracycline-dependent promoter system early during pathogenesis. |
| 13111 | 11390446 | In contrast, TNF-alpha expression abrogated the autoimmune process when induced late, which was associated with a reduction of autoreactive CD8 lymphocytes in islets and their lytic activities. |
| 13112 | 11390446 | In contrast, TNF-alpha expression abrogated the autoimmune process when induced late, which was associated with a reduction of autoreactive CD8 lymphocytes in islets and their lytic activities. |
| 13113 | 11377135 | I suggest that insulin suppresses the secretion and antagonizes the harmful effects of tumor necrosis factor-alpha, macrophage migration-inhibitory factor, and superoxide anion. |
| 13114 | 11377135 | I suggest that insulin suppresses the secretion and antagonizes the harmful effects of tumor necrosis factor-alpha, macrophage migration-inhibitory factor, and superoxide anion. |
| 13115 | 11377135 | Therefore, the glucose-insulin-potassium regimen might be beneficial in acute myocardial infarction and useful in the management of patients with septicemia, septic shock, and other inflammatory diseases in which tumor necrosis factor-alpha and macrophage migration-inhibitory factor have important roles. |
| 13116 | 11377135 | Therefore, the glucose-insulin-potassium regimen might be beneficial in acute myocardial infarction and useful in the management of patients with septicemia, septic shock, and other inflammatory diseases in which tumor necrosis factor-alpha and macrophage migration-inhibitory factor have important roles. |
| 13117 | 11375353 | Requirement for p38 and p44/p42 mitogen-activated protein kinases in RAGE-mediated nuclear factor-kappaB transcriptional activation and cytokine secretion. |
| 13118 | 11375353 | CML-modified albumin produced rapid transient activation of tyrosine phosphorylation, extracellular signal-regulated kinase 1 and 2, and p38 mitogen-activated protein kinase (MAPK), but not c-Jun NH(2)-terminal kinase. |
| 13119 | 11375353 | RAGE-mediated NF-kappaB activation was suppressed by the selective p38 MAPK inhibitor SB203580 and by coexpression of a kinase-dead p38 dominant-negative mutant. |
| 13120 | 11375353 | Activation of NF-kappaB by CML-modified albumin increased secretion of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, and monocyte chemoattractant protein-1) severalfold, and inhibition of p38 MAPK blocked these increases. |
| 13121 | 11375353 | These results indicate that p38 MAPK activation mediates RAGE-induced NF-kappaB-dependent secretion of proinflammatory cytokines and suggest that accelerated inflammation may be a consequence of cellular activation induced by this receptor. |
| 13122 | 11357882 | MLDSTZ-induced insulitis and increases in IFN-gamma, TNFalpha and IL-12 mRNA expression were all reduced on Day 11 by co-administration of delta9-THC. |
| 13123 | 11350075 | In this study, the relationship between GH effect on insulin sensitivity and adipocyte differentiation in vivo was investigated. |
| 13124 | 11350075 | Insulin treatment increased PPARgamma and GLUT4 expression in adipose tissue of WT mice but had no effect in TG mice. |
| 13125 | 11350075 | Content of transcription factors, PPARgamma and C/EBPalpha and beta, was higher in adipose tissue of WT mice, and for C/EBPalpha and PPARgamma, the difference occurred primarily in 24-, compared to 12-week-old, mice. |
| 13126 | 11350075 | Expression of preadipocyte factor-1 was higher in adipose tissue of TG mice, and expression of TNF-alpha and leptin was reduced in adipose tissue of 24-week-old TG mice. |
| 13127 | 11342558 | SOCS-1 protein prevents Janus Kinase/STAT-dependent inhibition of beta cell insulin gene transcription and secretion in response to interferon-gamma. |
| 13128 | 11342558 | Interferon (IFN)-gamma, tumor necrosis factor-alpha and interleukin (IL)-1 beta play important, although not completely defined, roles in these mechanisms. |
| 13129 | 11342558 | Here, using the highly differentiated beta Tc-Tet insulin-secreting cell line, we showed that IFN-gamma dose- and time-dependently suppressed insulin synthesis and glucose-stimulated secretion. |
| 13130 | 11342558 | As described previously IFN-gamma, in combination with IL-1 beta, also induces inducible NO synthase expression and apoptosis (Dupraz, P., Cottet, S., Hamburger, F., Dolci, W., Felley-Bosco, E., and Thorens, B. (2000) J. |
| 13131 | 11342558 | To assess the role of the Janus kinase/signal transducer and activator of transcription (STAT) pathway in IFN-gamma intracellular signaling, we stably overexpressed SOCS-1 (suppressor of cytokine signaling-1) in the beta cell line. |
| 13132 | 11342558 | We demonstrated that SOCS-1 suppressed cytokine-induced STAT-1 phosphorylation and increased cellular accumulation. |
| 13133 | 11342558 | This was accompanied by a suppression of the effect of IFN-gamma on: (i) reduction in insulin promoter-luciferase reporter gene transcription, (ii) decrease in insulin mRNA and peptide content, and (iii) suppression of glucose-stimulated insulin secretion. |
| 13134 | 11342558 | Furthermore, SOCS-1 also suppressed the cellular effects that require the combined presence of IL-1 beta and IFN-gamma: induction of nitric oxide production and apoptosis. |
| 13135 | 11342558 | Together our data demonstrate that IFN-gamma is responsible for the cytokine-induced defect in insulin gene expression and secretion and that this effect can be completely blocked by constitutive inhibition of the Janus kinase/STAT pathway. |
| 13136 | 11342531 | Cytokines, such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, and hormones, such as growth hormone, are known to cause insulin resistance, but the mechanisms by which they inhibit the cellular response to insulin have not been elucidated. |
| 13137 | 11342531 | SOCS proteins are therefore attractive candidates as mediators of cytokine-induced insulin resistance. |
| 13138 | 11342531 | We have found that SOCS-1 and SOCS-6 interact with the IR when expressed in human hepatoma cells (HepG2) or in rat hepatoma cells overexpressing the human IR. |
| 13139 | 11342531 | In SOCS-1-expressing cells, insulin treatment increases the extent of interaction with the IR, whereas in SOCS-6-expressing cells the association with the IR appears to require insulin treatment. |
| 13140 | 11342531 | SOCS-1 and SOCS-6 do not inhibit insulin-dependent IR autophosphorylation, but both proteins inhibit insulin-dependent activation of ERK1/2 and protein kinase B in vivo and IR-directed phosphorylation of IRS-1 in vitro. |
| 13141 | 11342531 | These results suggest that SOCS proteins may be inhibitors of IR signaling and could mediate cytokine-induced insulin resistance and contribute to the pathogenesis of type II diabetes. |
| 13142 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13143 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13144 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13145 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13146 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13147 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13148 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13149 | 11334414 | Effects of tumor necrosis factor-alpha on insulin action in cultured human muscle cells. |
| 13150 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13151 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13152 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13153 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13154 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13155 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13156 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13157 | 11334414 | Reported discrepancies in the effects of tumor necrosis factor (TNF)-alpha in modulating insulin sensitivity of cultured cells may relate both to cell types studied and to the time course of exposure to the cytokine. |
| 13158 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13159 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13160 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13161 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13162 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13163 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13164 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13165 | 11334414 | The presence of TNF (5 ng/ml) during the process of differentiation of myoblasts into mature myotubes diminished the response of glycogen synthesis to acute insulin stimulation. |
| 13166 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13167 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13168 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13169 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13170 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13171 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13172 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13173 | 11334414 | Under the same conditions of TNF exposure, there was no effect on the response to acute insulin stimulation of the fractional activity of GS. |
| 13174 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13175 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13176 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13177 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13178 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13179 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13180 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13181 | 11334414 | Similarly, there was no effect on the insulin stimulation of protein kinase B (PKB) and inhibition of glycogen synthase kinase 3 (GSK-3). |
| 13182 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13183 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13184 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13185 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13186 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13187 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13188 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13189 | 11334414 | Acute insulin stimulation brought about a 4.08 +/- 0.44-fold stimulation of activity of PKB in the absence of TNF, with 4.81 +/- 0.70-fold stimulation in cells exposed to TNF. |
| 13190 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13191 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13192 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13193 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13194 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13195 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13196 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13197 | 11334414 | GSK-3 activity decreased to 74.0 +/- 5.8% of basal after insulin stimulation without TNF and 78.3 +/- 5.0% after TNF exposure. |
| 13198 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13199 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13200 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13201 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13202 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13203 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13204 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13205 | 11334414 | However, differentiation of myocytes, as defined by an increase in the acetylcholine receptor, myogenin, and mature creatine kinase isoform expression, was impaired in TNF-treated cells. |
| 13206 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13207 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13208 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13209 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13210 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13211 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13212 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13213 | 11334414 | These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. |
| 13214 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13215 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13216 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13217 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13218 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13219 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13220 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13221 | 11334412 | Pioglitazone ameliorates tumor necrosis factor-alpha-induced insulin resistance by a mechanism independent of adipogenic activity of peroxisome proliferator--activated receptor-gamma. |
| 13222 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13223 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13224 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13225 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13226 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13227 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13228 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13229 | 11334412 | Tumor necrosis factor (TNF)-alpha is one of the candidate mediators of insulin resistance associated with obesity, a major risk factor for the development of type 2 diabetes. |
| 13230 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13231 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13232 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13233 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13234 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13235 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13236 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13237 | 11334412 | The insulin resistance induced by TNF-alpha is antagonized by thiazolidinediones (TZDs), a new class of insulin-sensitizing drugs. |
| 13238 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13239 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13240 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13241 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13242 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13243 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13244 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13245 | 11334412 | The aim of the current study was to dissect the mechanism whereby pioglitazone, one of the TZDs, ameliorates TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes. |
| 13246 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13247 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13248 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13249 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13250 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13251 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13252 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13253 | 11334412 | Pioglitazone restored insulin-stimulated 2-deoxyglucose (DOG) uptake, which was reduced by TNF-alpha, with concomitant restorations in tyrosine phosphorylation and protein levels of insulin receptor (IR) and insulin receptor substrate (IRS)-1, as well as association of the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase with IRS-1 and PI 3-kinase activity. |
| 13254 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13255 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13256 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13257 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13258 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13259 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13260 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13261 | 11334412 | Adenovirus-mediated gene transfer of either wild-type human peroxisome proliferator-activated receptor (PPAR)-gamma2 or a mutant carrying a replacement at the consensus mitogen-activated protein kinase phosphorylation site (hPPAR-gamma2-S112A) promoted adipogenesis of 3T3-L1 fibroblasts and restored TNF-alpha-induced decrease of triglyceride in adipocytes as effectively as pioglitazone. |
| 13262 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13263 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13264 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13265 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13266 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13267 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13268 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13269 | 11334412 | Overexpression of the PPAR-gamma proteins in TNF-alpha-treated adipocytes restored protein levels of IR/IRS-1, but did not improve insulin-stimulated tyrosine phosphorylation of IR/IRS-1 or insulin-stimulated 2-DOG uptake. |
| 13270 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13271 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13272 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13273 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13274 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13275 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13276 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13277 | 11334412 | These results indicate that the ability of pioglitazone to restore insulin-stimulated tyrosine phosphorylation of IR/IRS-1, which is necessary for amelioration of TNF-alpha-induced insulin resistance, may be independent of the adipogenic activity of PPAR-gamma that regulates protein levels of IR/IRS-1. |
| 13278 | 11334407 | In addition to inhibiting matrix metalloproteinase-2 and matrix metalloproteinase-9 activity, recent studies suggest that tissue inhibitor of metalloproteinase (TIMP)-1 may inhibit apoptosis in various cell lines. |
| 13279 | 11334407 | To address this question in pancreatic islets and beta-cells, we treated rat pancreatic islets and INS-1 cells with a high-dose combination of the cytokines interleukin (IL)-1beta, tumor necrosis factor-alpha, and interferon-gamma with or without the addition of TIMP-1 and TIMP-2 protein. |
| 13280 | 11334407 | Next, we transfected the mouse TIMP-1 gene into INS-1 cells and performed Western immunoblotting to demonstrate expression of TIMP-1 protein. |
| 13281 | 11334407 | We also evaluated the effect of TIMP-1 on IL-1beta-induced inhibition of glucose-stimulated insulin secretion (GSIS) in freshly isolated rat pancreatic islets. |
| 13282 | 11334407 | Finally, we evaluated the effect of TIMP-1 on inducible nitric oxide synthase (iNOS) gene expression and nuclear factor (NF)-kappaB activity in INS-1 cells stimulated with high-dose cytokines. |
| 13283 | 11334407 | TIMP-1 but not TIMP-2 prevented cytokine-induced apoptosis and cytokine-mediated inhibition of GSIS in rat islets and beta-cells. |
| 13284 | 11334407 | TIMP-1 mediated these effects by inhibiting cytokine activation of NF-kappaB, but it did not affect nitric oxide production or iNOS gene expression. |
| 13285 | 11327370 | The metalloprotease TACE (tumor necrosis factor-alpha converting enzyme) is the likely enzyme responsible for cleavage, but the structural requirements for TACE recognition or catalysis, and hence the precise cleavage point in the GHR, are unknown. |
| 13286 | 11323020 | NO is produced through L-arginine pathway by three different isoforms of nitric oxide synthase (NOS), an inducible form that can be activated by cytokines such as tumor necrosis factor alpha (TNFalpha). |
| 13287 | 11323020 | NO is produced through L-arginine pathway by three different isoforms of nitric oxide synthase (NOS), an inducible form that can be activated by cytokines such as tumor necrosis factor alpha (TNFalpha). |
| 13288 | 11323020 | NO is produced through L-arginine pathway by three different isoforms of nitric oxide synthase (NOS), an inducible form that can be activated by cytokines such as tumor necrosis factor alpha (TNFalpha). |
| 13289 | 11323020 | We evaluated NO plasmatic levels, endothelial damage markers such as von Willebrand factor (vWF), platelet activation, soluble P-selectin (sP-Sel), TNFalpha levels, insulinaemia (I), glycosylated haemoglobin (HbA1c), glycaemia and blood pressure in 32 hypertensive diabetic type II patients (Group A), 37 hypertensive patients (Group B) and 35 healthy subjects (Group C) matched in sex, age, body mass index and dietary habits. |
| 13290 | 11323020 | We evaluated NO plasmatic levels, endothelial damage markers such as von Willebrand factor (vWF), platelet activation, soluble P-selectin (sP-Sel), TNFalpha levels, insulinaemia (I), glycosylated haemoglobin (HbA1c), glycaemia and blood pressure in 32 hypertensive diabetic type II patients (Group A), 37 hypertensive patients (Group B) and 35 healthy subjects (Group C) matched in sex, age, body mass index and dietary habits. |
| 13291 | 11323020 | We evaluated NO plasmatic levels, endothelial damage markers such as von Willebrand factor (vWF), platelet activation, soluble P-selectin (sP-Sel), TNFalpha levels, insulinaemia (I), glycosylated haemoglobin (HbA1c), glycaemia and blood pressure in 32 hypertensive diabetic type II patients (Group A), 37 hypertensive patients (Group B) and 35 healthy subjects (Group C) matched in sex, age, body mass index and dietary habits. |
| 13292 | 11323020 | These parameters described a prothrombotic state associated with an insulin resistance state, an increased vWF release, raised sP-Sel and TNFalpha levels and, maybe, low NO bioavailability, which could lead to a higher risk of development of thrombotic events in hypertensive diabetic patients (Group A) than in the hypertensive patients in Group B. |
| 13293 | 11323020 | These parameters described a prothrombotic state associated with an insulin resistance state, an increased vWF release, raised sP-Sel and TNFalpha levels and, maybe, low NO bioavailability, which could lead to a higher risk of development of thrombotic events in hypertensive diabetic patients (Group A) than in the hypertensive patients in Group B. |
| 13294 | 11323020 | These parameters described a prothrombotic state associated with an insulin resistance state, an increased vWF release, raised sP-Sel and TNFalpha levels and, maybe, low NO bioavailability, which could lead to a higher risk of development of thrombotic events in hypertensive diabetic patients (Group A) than in the hypertensive patients in Group B. |
| 13295 | 11317656 | The Src kinases, particularly hck, play an important part in the activation of macrophages and the subsequent production of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and nitric oxide (NO), leading to the destruction of beta cells which results in the development of diabetes. |
| 13296 | 11317656 | The infection of DR-BB rats with KRV results in the disruption of the finely tuned immune balance of Th1-like CD45RC+CD4+ and Th2-like CD45RC-CD4+ T cells, leading to the selective activation of beta-cell-cytotoxic effector T cells. |
| 13297 | 11312119 | IL-18 is a potent proinflammatory cytokine able to induce IFNgamma, GM-CSF, TNFalpha and IL-1 in immunocompetent cells, to activate killing by lymphocytes, and to up-regulate the expression of certain chemokine receptors. |
| 13298 | 11312119 | Moreover, IL-18 also induces IL-13 and/or IL-4 production by NK cells, mast cells and basophils. |
| 13299 | 11311966 | Relationship between serum tumor necrosis factor-alpha and insulin resistance in obese men with Type 2 diabetes mellitus. |
| 13300 | 11311966 | Relationship between serum tumor necrosis factor-alpha and insulin resistance in obese men with Type 2 diabetes mellitus. |
| 13301 | 11311966 | Relationship between serum tumor necrosis factor-alpha and insulin resistance in obese men with Type 2 diabetes mellitus. |
| 13302 | 11311966 | Relationship between serum tumor necrosis factor-alpha and insulin resistance in obese men with Type 2 diabetes mellitus. |
| 13303 | 11311966 | We analyzed serum concentrations of tumor necrosis factor-alpha (TNF-alpha) for their role in insulin resistance in 12 obese men with untreated Type 2 diabetes mellitus and in 6 age-and BMI-matched obese controls. |
| 13304 | 11311966 | We analyzed serum concentrations of tumor necrosis factor-alpha (TNF-alpha) for their role in insulin resistance in 12 obese men with untreated Type 2 diabetes mellitus and in 6 age-and BMI-matched obese controls. |
| 13305 | 11311966 | We analyzed serum concentrations of tumor necrosis factor-alpha (TNF-alpha) for their role in insulin resistance in 12 obese men with untreated Type 2 diabetes mellitus and in 6 age-and BMI-matched obese controls. |
| 13306 | 11311966 | We analyzed serum concentrations of tumor necrosis factor-alpha (TNF-alpha) for their role in insulin resistance in 12 obese men with untreated Type 2 diabetes mellitus and in 6 age-and BMI-matched obese controls. |
| 13307 | 11311966 | Serum levels of TNF-alpha were higher in patients with insulin resistance (4.19+/-0.96 pg/ml) than in patients without insulin resistance (2.52+/-1.64 pg/ml) and in controls (2.03+/-1.21 pg/ml). |
| 13308 | 11311966 | Serum levels of TNF-alpha were higher in patients with insulin resistance (4.19+/-0.96 pg/ml) than in patients without insulin resistance (2.52+/-1.64 pg/ml) and in controls (2.03+/-1.21 pg/ml). |
| 13309 | 11311966 | Serum levels of TNF-alpha were higher in patients with insulin resistance (4.19+/-0.96 pg/ml) than in patients without insulin resistance (2.52+/-1.64 pg/ml) and in controls (2.03+/-1.21 pg/ml). |
| 13310 | 11311966 | Serum levels of TNF-alpha were higher in patients with insulin resistance (4.19+/-0.96 pg/ml) than in patients without insulin resistance (2.52+/-1.64 pg/ml) and in controls (2.03+/-1.21 pg/ml). |
| 13311 | 11311966 | These data suggest that high levels of serum TNF-alpha in patients with insulin resistance are related to high levels of fasting insulin and HOMA-R. |
| 13312 | 11311966 | These data suggest that high levels of serum TNF-alpha in patients with insulin resistance are related to high levels of fasting insulin and HOMA-R. |
| 13313 | 11311966 | These data suggest that high levels of serum TNF-alpha in patients with insulin resistance are related to high levels of fasting insulin and HOMA-R. |
| 13314 | 11311966 | These data suggest that high levels of serum TNF-alpha in patients with insulin resistance are related to high levels of fasting insulin and HOMA-R. |
| 13315 | 11303144 | Aging is associated with increased inflammatory activity reflected by increased circulating levels of TNF-alpha, IL-6, cytokine antagonists and acute phase proteins in vivo. |
| 13316 | 11301286 | Tumor necrosis factor (TNF)-converting enzyme (TACE) and other ADAM proteases (those that contain a disintegrin and a metalloprotease domain) have emerged as potential therapeutic targets in the areas of arthritis, cancer, diabetes and HIV cachexia. |
| 13317 | 11301286 | Tumor necrosis factor (TNF)-converting enzyme (TACE) and other ADAM proteases (those that contain a disintegrin and a metalloprotease domain) have emerged as potential therapeutic targets in the areas of arthritis, cancer, diabetes and HIV cachexia. |
| 13318 | 11301286 | TACE is the first ADAM protease to process the known physiological substrate and inflammatory cytokine, membrane-bound precursor-TNF-alpha, to its mature soluble form. |
| 13319 | 11301286 | TACE is the first ADAM protease to process the known physiological substrate and inflammatory cytokine, membrane-bound precursor-TNF-alpha, to its mature soluble form. |
| 13320 | 11301286 | Subsequently, TACE was shown to be required for several different processing events such as tumor growth factor-alpha (TGF-alpha) precursor and amyloid precursor protein (APP) cleavage. |
| 13321 | 11301286 | Subsequently, TACE was shown to be required for several different processing events such as tumor growth factor-alpha (TGF-alpha) precursor and amyloid precursor protein (APP) cleavage. |
| 13322 | 11298122 | NOD DC, in contrast to CBA DC, have very low levels of intracellular I-A molecules and cell surface expression of MHC class II, CD80, CD86 and CD40 but normal beta 2-microglobulin expression. |
| 13323 | 11298122 | Incubation with the strong inflammatory stimulus of LPS and IFN-gamma does not increase class II MHC, CD80 or CD86, but upregulates the level of CD40. |
| 13324 | 11298122 | However all the DC irrespective of origin were able to produce TNF-alpha, IL-6, low levels of IL-12(p70) and NO in response to LPS plus IFN-gamma. |
| 13325 | 11298122 | A gene or genes specific to the NOD strain, but outside the MHC region, therefore must regulate the differentiation of DC in response to GM-CSF. |
| 13326 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13327 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13328 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13329 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13330 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13331 | 11287357 | Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. |
| 13332 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13333 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13334 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13335 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13336 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13337 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 13338 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13339 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13340 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13341 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13342 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13343 | 11287357 | We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. |
| 13344 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13345 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13346 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13347 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13348 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13349 | 11287357 | In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. |
| 13350 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13351 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13352 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13353 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13354 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13355 | 11287357 | By use of this approach, subjects with low S(I) demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level (P < 0.05) compared with matched subjects with a high S(I). |
| 13356 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13357 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13358 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13359 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13360 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13361 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 13362 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 13363 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 13364 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 13365 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 13366 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 13367 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 13368 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 13369 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 13370 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 13371 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 13372 | 11259402 | Uncoupling protein 3 transcription is regulated by peroxisome proliferator-activated receptor (alpha) in the adult rodent heart. |
| 13373 | 11259402 | We investigated in the adult rodent heart 1) whether changes in workload, substrate supply, or cytokine (TNF-alpha) administration affect UCP-2 and UCP-3 expression, and 2) whether peroxisome proliferator-activated receptor alpha (PPARalpha) regulates the expression of either UCP-2 or UCP-3. |
| 13374 | 11259402 | UCP-2, UCP-3, and PPARalpha expression were reduced when cardiac workload was either increased (pressure overload by aortic constriction) or decreased (mechanical unloading by heterotopic transplantation). |
| 13375 | 11259402 | Reduced dietary fatty acid availability resulted in decreased expression of both cardiac UCP-2 and UCP-3. |
| 13376 | 11259402 | However, when fatty acid (the natural ligand for PPARalpha) supply was increased (high-fat feeding, fasting, and STZ-induced diabetes), cardiac UCP-3 but not UCP-2 expression increased. |
| 13377 | 11259402 | The level of cardiac UCP-3 but not UCP-2 expression was severely reduced (20-fold) in PPARalpha-/- mice compared to wild-type mice. |
| 13378 | 11259402 | These results suggest that in the adult rodent heart, UCP-3 expression is regulated by PPARalpha. |
| 13379 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13380 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13381 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13382 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13383 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13384 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13385 | 11254704 | IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. |
| 13386 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13387 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13388 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13389 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13390 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13391 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13392 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 13393 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13394 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13395 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13396 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13397 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13398 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13399 | 11254704 | Here, we identified IFN-gamma/TNF-alpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. |
| 13400 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13401 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13402 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13403 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13404 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13405 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13406 | 11254704 | A combination of IFN-gamma and TNF-alpha, but neither cytokine alone, induced classical caspase-dependent apoptosis in insulinoma and pancreatic islet cells. |
| 13407 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13408 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13409 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13410 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13411 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13412 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13413 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 13414 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13415 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13416 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13417 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13418 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13419 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13420 | 11254704 | IRF-1 played a central role in IFN-gamma/TNF-alpha-induced cytotoxicity because inhibition of IRF-1 induction by antisense oligonucleotides blocked IFN-gamma/TNF-alpha-induced cytotoxicity, and transfection of IRF-1 rendered insulinoma cells susceptible to TNF-alpha-induced cytotoxicity. |
| 13421 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13422 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13423 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13424 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13425 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13426 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13427 | 11254704 | STAT1 and IRF-1 were expressed in pancreatic islets of diabetic NOD mice and colocalized with apoptotic cells. |
| 13428 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13429 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13430 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13431 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13432 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13433 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13434 | 11254704 | Taken together, our results indicate that IFN-gamma/TNF-alpha synergism is responsible for autoimmune diabetes in vivo as well as beta cell apoptosis in vitro and suggest a novel signal transduction in IFN-gamma/TNF-alpha synergism that may have relevance in other autoimmune diseases and synergistic anti-tumor effects of the two cytokines. |
| 13435 | 11250945 | Insulin deprivation leads to deficiency of Sp1 transcription factor in H-411E hepatoma cells and in streptozotocin-induced diabetic ketoacidosis in the rat. |
| 13436 | 11250945 | Members of the family of Sp transcription factors include Sp1, Sp3, and Sp4 and are important regulators of eukaryotic gene expression. |
| 13437 | 11250945 | To test whether other members of the Sp family are direct targets of insulin action, we compared the levels of Sp1 and Sp3 proteins from nuclear extracts obtained from both insulin-treated and untreated rat hepatoma (H-411E) cells. |
| 13438 | 11250945 | We demonstrated by Western blot analysis that levels of Sp1 and Sp3 proteins were increased more than 2-fold in the insulin-treated group. |
| 13439 | 11250945 | Additionally, the up-regulation of both Sp1 and Sp3 transcription factors by insulin was antagonized by tumor necrosis factor-alpha, a known inhibitor of insulin action. |
| 13440 | 11250945 | Immunohistochemical analysis demonstrated that H-411E cells treated with insulin (10,000 microU/ml) had a marked increase in demonstrable Sp1 in the nucleus compared with cells incubated in insulin-free medium. |
| 13441 | 11250945 | We demonstrated in rat liver tissue by both Western blot and immunohistochemical staining with anti-Sp1 antibody that 1) livers of fully diabetic streptozotocin rats have low levels of Sp1 transcription factor; and 2) insulin treatment of the diabetic rat rapidly reversed this process by markedly stimulating accumulation of Sp1 in rat liver. |
| 13442 | 11250945 | Studies of the signal transduction mechanisms involved in insulin's effect on Sp1 demonstrate a facilitating role for phosphoinositol 3-kinase and an inhibitory role for cyclic nucleotides. |
| 13443 | 11250945 | In summary, insulin stimulates Sp1 protein, a transcription factor that is shown to regulate calmodulin gene expression and most likely other, as yet untested, genes. |
| 13444 | 11250657 | Human pancreatic islets, isolated from heart-beating donors, were treated with a combination of three cytokines, IL-1beta+tumor necrosis factor alpha+interferon gamma, in the presence or absence of vitamin D, and compared with with untreated control cells. |
| 13445 | 11250657 | Oxidative stress was estimated by heat shock protein 70 (hsp70) expression, cell manganese superoxide dismutase (MnSOD) activity and nitrite release, a reflexion of nitric oxide (NO) synthesis. |
| 13446 | 11250657 | MHC expression significantly increased six- to sevenfold as well as NO and IL-6 release (two- to threefold enhancement). |
| 13447 | 11250657 | MnSOD activity was not significantly induced and hsp70 expression was not affected by the combination of cytokines. |
| 13448 | 11250657 | The addition of 1,25 D(3) significantly reduced nitrite release, IL-6 production and MHC class I expression which then became not significantly different from controls. |
| 13449 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 13450 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 13451 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 13452 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 13453 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 13454 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 13455 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 13456 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 13457 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 13458 | 11246473 | Several studies have indicated that additional genes in the major histocompatibility complex (MHC) region, other than the class II genes HLA-DQB1 and -DRB1 (the IDDM1 locus), may contribute to susceptibility and resistance to type 1 diabetes. |
| 13459 | 11246473 | The homozygous parent test has been proposed as a method for detection of additional risk factors conditional on HLA-DQB1 and -DRB1. |
| 13460 | 11246473 | The Conditional ETDT was then applied to the HLA TNF (tumour necrosis factor) region and microsatellite marker D6S273 region, both of which have been reported to contribute to IDDM1 independent of the HLA-DQB1-DRB1 genes. |
| 13461 | 11238525 | We measured intranuclear NFkappaB, total cellular NFkappaB, inhibitor kappaB (IkappaB)alpha, reactive oxygen species (ROS) generation, and p47(phox) subunit (a key component protein of nicotinamide adenine dinucleotide phosphate oxidase) in MNC. |
| 13462 | 11238525 | We measured intranuclear NFkappaB, total cellular NFkappaB, inhibitor kappaB (IkappaB)alpha, reactive oxygen species (ROS) generation, and p47(phox) subunit (a key component protein of nicotinamide adenine dinucleotide phosphate oxidase) in MNC. |
| 13463 | 11238525 | We measured intranuclear NFkappaB, total cellular NFkappaB, inhibitor kappaB (IkappaB)alpha, reactive oxygen species (ROS) generation, and p47(phox) subunit (a key component protein of nicotinamide adenine dinucleotide phosphate oxidase) in MNC. |
| 13464 | 11238525 | Plasma tumor necrosis factor (TNF)-alpha, soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor type 1 (PAI-1), C-reactive protein (CRP), and interleukin (IL)-10 (antiinflammatory cytokine) concentrations were also measured as mediators of inflammatory activity that are regulated by the proinflammatory transcription factor NFkappaB. |
| 13465 | 11238525 | Plasma tumor necrosis factor (TNF)-alpha, soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor type 1 (PAI-1), C-reactive protein (CRP), and interleukin (IL)-10 (antiinflammatory cytokine) concentrations were also measured as mediators of inflammatory activity that are regulated by the proinflammatory transcription factor NFkappaB. |
| 13466 | 11238525 | Plasma tumor necrosis factor (TNF)-alpha, soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor type 1 (PAI-1), C-reactive protein (CRP), and interleukin (IL)-10 (antiinflammatory cytokine) concentrations were also measured as mediators of inflammatory activity that are regulated by the proinflammatory transcription factor NFkappaB. |
| 13467 | 11238525 | MNC were separated; and the levels of intranuclear NFkappaB, total cellular NFkappaB, IkappaBalpha, and p47 (phox) subunit and ROS generation were determined. |
| 13468 | 11238525 | MNC were separated; and the levels of intranuclear NFkappaB, total cellular NFkappaB, IkappaBalpha, and p47 (phox) subunit and ROS generation were determined. |
| 13469 | 11238525 | MNC were separated; and the levels of intranuclear NFkappaB, total cellular NFkappaB, IkappaBalpha, and p47 (phox) subunit and ROS generation were determined. |
| 13470 | 11238525 | Plasma was used to measure insulin glucose, TNFalpha, sICAM, MCP-1, PAI-1, CRP, and IL-10. |
| 13471 | 11238525 | Plasma was used to measure insulin glucose, TNFalpha, sICAM, MCP-1, PAI-1, CRP, and IL-10. |
| 13472 | 11238525 | Plasma was used to measure insulin glucose, TNFalpha, sICAM, MCP-1, PAI-1, CRP, and IL-10. |
| 13473 | 11238525 | There was a fall in intranuclear NFkappaB, total cellular NFkappaB, and p47 (phox) subunit, with an increase in cellular IkappaBalpha at week 2, which persisted until week 4. |
| 13474 | 11238525 | There was a fall in intranuclear NFkappaB, total cellular NFkappaB, and p47 (phox) subunit, with an increase in cellular IkappaBalpha at week 2, which persisted until week 4. |
| 13475 | 11238525 | There was a fall in intranuclear NFkappaB, total cellular NFkappaB, and p47 (phox) subunit, with an increase in cellular IkappaBalpha at week 2, which persisted until week 4. |
| 13476 | 11238525 | Plasma TNF-alpha, sICAM-1, MCP-1, and PAI-1 concentrations fell significantly at week 4. |
| 13477 | 11238525 | Plasma TNF-alpha, sICAM-1, MCP-1, and PAI-1 concentrations fell significantly at week 4. |
| 13478 | 11238525 | Plasma TNF-alpha, sICAM-1, MCP-1, and PAI-1 concentrations fell significantly at week 4. |
| 13479 | 11238525 | Plasma IL-10 concentration increased significantly, whereas plasma CRP concentrations decreased. |
| 13480 | 11238525 | Plasma IL-10 concentration increased significantly, whereas plasma CRP concentrations decreased. |
| 13481 | 11238525 | Plasma IL-10 concentration increased significantly, whereas plasma CRP concentrations decreased. |
| 13482 | 11230277 | Emerging evidence suggests that insulin resistance, which has been linked to essential hypertension, may play a role in PIH. |
| 13483 | 11230277 | Furthermore, metabolic abnormalities linked to the insulin resistance syndrome are also observed in women with PIH to a greater degree than in normotensive pregnant women: These include glucose intolerance, hyperinsulinemia, hyperlipidemia, and high levels of plasminogen activator inhibitor-1, leptin, and tumor necrosis factor-alpha. |
| 13484 | 11230277 | These observations suggest the possibility that insulin resistance may be involved in the pathogenesis of PIH and that approaches that improve insulin sensitivity might have benefit in the prevention or treatment of this syndrome, although this requires further study. |
| 13485 | 11221847 | Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated apotosis in human malignant glioma cells. |
| 13486 | 11221847 | Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated apotosis in human malignant glioma cells. |
| 13487 | 11221847 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) preferentially triggers apoptosis in tumor cells versus normal cells, thus providing a therapeutic potential. |
| 13488 | 11221847 | Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) preferentially triggers apoptosis in tumor cells versus normal cells, thus providing a therapeutic potential. |
| 13489 | 11221847 | TRAIL-induced cell death was characterized by activation of caspase-8 and -3, poly(ADP-ribose) polymerase cleavage, and DNA fragmentation. |
| 13490 | 11221847 | TRAIL-induced cell death was characterized by activation of caspase-8 and -3, poly(ADP-ribose) polymerase cleavage, and DNA fragmentation. |
| 13491 | 11221847 | Decoy receptor (DcR1 and DcR2) expression was limited in the glioma cell lines and did not correlate with TRAIL sensitivity. |
| 13492 | 11221847 | Decoy receptor (DcR1 and DcR2) expression was limited in the glioma cell lines and did not correlate with TRAIL sensitivity. |
| 13493 | 11221847 | Both sensitive and resistant cell lines expressed TRAIL death receptor (DR5), adapter protein Fas-associated death domain (FADD), and caspase-8; but resistant cell lines expressed 2-fold higher levels of the apoptosis inhibitor phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15 kDa (PED/PEA-15). |
| 13494 | 11221847 | Both sensitive and resistant cell lines expressed TRAIL death receptor (DR5), adapter protein Fas-associated death domain (FADD), and caspase-8; but resistant cell lines expressed 2-fold higher levels of the apoptosis inhibitor phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15 kDa (PED/PEA-15). |
| 13495 | 11221847 | In contrast, cellular FADD-like IL-1beta-converting enzyme-like inhibitory protein (cFLIP) expression was similar in sensitive and resistant cells. |
| 13496 | 11221847 | In contrast, cellular FADD-like IL-1beta-converting enzyme-like inhibitory protein (cFLIP) expression was similar in sensitive and resistant cells. |
| 13497 | 11221847 | Inhibition of protein kinase C (PKC) activity restored TRAIL sensitivity in resistant cells, suggesting that PED/ PEA-15 function might be dependent on PKC-mediated phosphorylation. |
| 13498 | 11221847 | Inhibition of protein kinase C (PKC) activity restored TRAIL sensitivity in resistant cells, suggesting that PED/ PEA-15 function might be dependent on PKC-mediated phosphorylation. |
| 13499 | 11221847 | This caspase-8-induced apoptotic cascade is regulated by intracellular PED/PEA-15, but not by cFLIP or decoy receptors. |
| 13500 | 11221847 | This caspase-8-induced apoptotic cascade is regulated by intracellular PED/PEA-15, but not by cFLIP or decoy receptors. |
| 13501 | 11221996 | Ex vivo analysis of the islets of Langerhans performed in early disease development revealed that PTX downregulates production of proinflammatory cytokines IFN-gamma and TNF, as well as inducible nitric oxide synthase (iNOS) expression and NO production. |
| 13502 | 11221996 | In addition, PTX treatment suppressed splenocyte autoreactivity, as well as the frequency of cells expressing IL-2R and MHC class II antigens. |
| 13503 | 11221996 | There was no evidence of any changes in proportion of ICAM-1 and LFA-1 expressing splenocytes in comparison to control MLD-SZ-treated animals. |
| 13504 | 11213887 | Plasma levels of tumor necrosis factor-alpha, angiotensin II, growth hormone, and IGF-I are not elevated in insulin-resistant obese individuals with impaired glucose tolerance. |
| 13505 | 11212327 | In recent years, a number of cross-talk systems have been identified which feed into the insulin signalling cascade at the level of insulin receptor substrate (IRS) tyrosine phosphorylation, e.g., receptor and non-receptor tyrosine kinases and G-protein-coupled receptors. |
| 13506 | 11212327 | At the molecular level, a number of negative modulator and feedback systems somehow interacting with the beta-subunit (catecholamine-, phorbolester-, or tumor necrosis factor-alpha-induced serine/threonine phosphorylation, carboxy-terminal trimming by a thiol-dependent protease, association of inhibitory/regulatory proteins such as RAD, PC1, PED, alpha2-HS-glycoprotein) have been identified as candidate mechanisms for the impairment of insulin receptor function by elevations in the activity and/or amount of the corresponding modification enzymes/inhibitors. |
| 13507 | 11212327 | Both decreased responsiveness and sensitivity of the insulin receptor beta-subunit for insulin-induced tyrosine autophosphorylation have been demonstrated in several cellular and animal models of metabolic insulin resistance as well as in the adipose tissue and skeletal muscle of diabetic patients and obese Pima Indians compared to non-obese subjects. |
| 13508 | 11208454 | I suggest that glucose-insulin can suppress the secretion and antagonize the harmful effects of tumor necrosis factor alpha (TNF alpha) and macrophage migration inhibitory factor (MIF). |
| 13509 | 11208454 | I suggest that glucose-insulin can suppress the secretion and antagonize the harmful effects of tumor necrosis factor alpha (TNF alpha) and macrophage migration inhibitory factor (MIF). |
| 13510 | 11208454 | If this is true, it suggests that GIK regimen may be useful in septicemia and septic shock, and other inflammatory conditions such as ulcerative colitis, Crohn's disease, rheumatoid arthritis, systemic lupus erythematosus and cancer, conditions in which TNF alpha and MIF appear to play a major role. |
| 13511 | 11208454 | If this is true, it suggests that GIK regimen may be useful in septicemia and septic shock, and other inflammatory conditions such as ulcerative colitis, Crohn's disease, rheumatoid arthritis, systemic lupus erythematosus and cancer, conditions in which TNF alpha and MIF appear to play a major role. |
| 13512 | 11180921 | Tumor necrosis factor-alpha (TNF alpha), interleukin 1beta (IL-1beta), platelet-derived growth factor BB (PDGF-BB) and transforming growth factor-beta1 (TGF-beta1) in cytoplasm were quantified by enzyme-linked immunosorbent assays (ELISA). |
| 13513 | 11180921 | Alkaline phosphatase (ALP) activity was standardized by the DNA content of the cells. |
| 13514 | 11160694 | Soluble mediators such as interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus. |
| 13515 | 11160694 | Soluble mediators such as interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus. |
| 13516 | 11160694 | Soluble mediators such as interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) produced from activated macrophages play an important role in the destruction of pancreatic beta cells in mice infected with a low dose of the D variant of encephalomyocarditis (EMC-D) virus. |
| 13517 | 11160694 | We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus. |
| 13518 | 11160694 | We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus. |
| 13519 | 11160694 | We examined the activation of p59/p56(Hck), p55(Fgr), and p56/p53(Lyn) in macrophages from DBA/2 mice infected with the virus. |
| 13520 | 11160694 | We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not. |
| 13521 | 11160694 | We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not. |
| 13522 | 11160694 | We found that p59/p56(Hck) showed a marked increase in both autophosphorylation and kinase activity at 48 h after infection, whereas p55(Fgr) and p56/p53(Lyn) did not. |
| 13523 | 11160694 | The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav. |
| 13524 | 11160694 | The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav. |
| 13525 | 11160694 | The p59/p56(Hck) activity was closely correlated with the tyrosine phosphorylation level of Vav. |
| 13526 | 11160694 | Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice. |
| 13527 | 11160694 | Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice. |
| 13528 | 11160694 | Treatment of EMC-D virus-infected mice with the Src kinase inhibitor, PP2, resulted in the inhibition of p59/p56(Hck) activity and almost complete inhibition of the production of TNF-alpha and iNOS in macrophages and the subsequent prevention of diabetes in mice. |
| 13529 | 11160694 | On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus. |
| 13530 | 11160694 | On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus. |
| 13531 | 11160694 | On the basis of these observations, we conclude that the Src kinase, p59/p56(Hck), plays an important role in the activation of macrophages and the subsequent production of TNF-alpha and nitric oxide, leading to the destruction of pancreatic beta cells, which results in the development of diabetes in mice infected with a low dose of EMC-D virus. |
| 13532 | 11160134 | Insulin/IGF-1 and TNF-alpha stimulate phosphorylation of IRS-1 at inhibitory Ser307 via distinct pathways. |
| 13533 | 11160134 | Insulin/IGF-1 and TNF-alpha stimulate phosphorylation of IRS-1 at inhibitory Ser307 via distinct pathways. |
| 13534 | 11160134 | Insulin/IGF-1 and TNF-alpha stimulate phosphorylation of IRS-1 at inhibitory Ser307 via distinct pathways. |
| 13535 | 11160134 | Serine/threonine phosphorylation of IRS-1 might inhibit insulin signaling, but the relevant phosphorylation sites are difficult to identify in cultured cells and to validate in isolated tissues. |
| 13536 | 11160134 | Serine/threonine phosphorylation of IRS-1 might inhibit insulin signaling, but the relevant phosphorylation sites are difficult to identify in cultured cells and to validate in isolated tissues. |
| 13537 | 11160134 | Serine/threonine phosphorylation of IRS-1 might inhibit insulin signaling, but the relevant phosphorylation sites are difficult to identify in cultured cells and to validate in isolated tissues. |
| 13538 | 11160134 | Recently, we discovered that recombinant NH2-terminal Jun kinase phosphorylates IRS-1 at Ser307, which inhibits insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 13539 | 11160134 | Recently, we discovered that recombinant NH2-terminal Jun kinase phosphorylates IRS-1 at Ser307, which inhibits insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 13540 | 11160134 | Recently, we discovered that recombinant NH2-terminal Jun kinase phosphorylates IRS-1 at Ser307, which inhibits insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 13541 | 11160134 | This antibody revealed that TNF-alpha, IGF-1, or insulin stimulated phosphorylation of IRS-1 at Ser307 in 3T3-L1 preadipocytes and adipocytes. |
| 13542 | 11160134 | This antibody revealed that TNF-alpha, IGF-1, or insulin stimulated phosphorylation of IRS-1 at Ser307 in 3T3-L1 preadipocytes and adipocytes. |
| 13543 | 11160134 | This antibody revealed that TNF-alpha, IGF-1, or insulin stimulated phosphorylation of IRS-1 at Ser307 in 3T3-L1 preadipocytes and adipocytes. |
| 13544 | 11160134 | Insulin injected into mice or rats also stimulated phosphorylation of Ser307 on IRS-1 immunoprecipitated from muscle; moreover, Ser307 was phosphorylated in human muscle during the hyperinsulinemic euglycemic clamp. |
| 13545 | 11160134 | Insulin injected into mice or rats also stimulated phosphorylation of Ser307 on IRS-1 immunoprecipitated from muscle; moreover, Ser307 was phosphorylated in human muscle during the hyperinsulinemic euglycemic clamp. |
| 13546 | 11160134 | Insulin injected into mice or rats also stimulated phosphorylation of Ser307 on IRS-1 immunoprecipitated from muscle; moreover, Ser307 was phosphorylated in human muscle during the hyperinsulinemic euglycemic clamp. |
| 13547 | 11160134 | Experiments in 3T3-L1 preadipocytes and adipocytes revealed that insulin-stimulated phosphorylation of Ser307 was inhibited by LY294002 or wortmannin, whereas TNF-alpha-stimulated phosphorylation was inhibited by PD98059. |
| 13548 | 11160134 | Experiments in 3T3-L1 preadipocytes and adipocytes revealed that insulin-stimulated phosphorylation of Ser307 was inhibited by LY294002 or wortmannin, whereas TNF-alpha-stimulated phosphorylation was inhibited by PD98059. |
| 13549 | 11160134 | Experiments in 3T3-L1 preadipocytes and adipocytes revealed that insulin-stimulated phosphorylation of Ser307 was inhibited by LY294002 or wortmannin, whereas TNF-alpha-stimulated phosphorylation was inhibited by PD98059. |
| 13550 | 11160134 | Thus, distinct kinase pathways might converge at Ser307 to mediate feedback or heterologous inhibition of IRS-1 signaling to counterregulate the insulin response. |
| 13551 | 11160134 | Thus, distinct kinase pathways might converge at Ser307 to mediate feedback or heterologous inhibition of IRS-1 signaling to counterregulate the insulin response. |
| 13552 | 11160134 | Thus, distinct kinase pathways might converge at Ser307 to mediate feedback or heterologous inhibition of IRS-1 signaling to counterregulate the insulin response. |
| 13553 | 11147775 | AJ-9677 reduced the total weight of white adipose tissues by reducing the size of the adipocytes, an effect associated with the normalization of tumor necrosis factor-alpha (TNF-alpha) and leptin expression levels. |
| 13554 | 11147775 | AJ-9677 reduced the total weight of white adipose tissues by reducing the size of the adipocytes, an effect associated with the normalization of tumor necrosis factor-alpha (TNF-alpha) and leptin expression levels. |
| 13555 | 11147775 | The generation of small adipocytes, presumably mediated by increased expression of UCP-1 in addition to increased lipolysis in response to AJ-9677, was associated with decreased TNF-alpha and free fatty acid production and may be the mechanism of amelioration of insulin resistance in KK-Ay/Ta diabetic obese mice. |
| 13556 | 11147775 | The generation of small adipocytes, presumably mediated by increased expression of UCP-1 in addition to increased lipolysis in response to AJ-9677, was associated with decreased TNF-alpha and free fatty acid production and may be the mechanism of amelioration of insulin resistance in KK-Ay/Ta diabetic obese mice. |
| 13557 | 11145126 | Tumor necrosis factor alpha gene G-308A polymorphism, insulin resistance, and fasting plasma glucose in young, older, and diabetic Japanese men. |
| 13558 | 11145126 | Tumor necrosis factor alpha gene G-308A polymorphism, insulin resistance, and fasting plasma glucose in young, older, and diabetic Japanese men. |
| 13559 | 11145126 | Tumor necrosis factor alpha gene G-308A polymorphism, insulin resistance, and fasting plasma glucose in young, older, and diabetic Japanese men. |
| 13560 | 11145126 | Tumor necrosis factor alpha gene G-308A polymorphism, insulin resistance, and fasting plasma glucose in young, older, and diabetic Japanese men. |
| 13561 | 11145126 | A recent study of Caucasians suggested that the TNF-alpha gene promoter region polymorphism at position -308 influences insulin resistance and percent body fat and increases serum leptin levels, although conflicting data are also reported. |
| 13562 | 11145126 | A recent study of Caucasians suggested that the TNF-alpha gene promoter region polymorphism at position -308 influences insulin resistance and percent body fat and increases serum leptin levels, although conflicting data are also reported. |
| 13563 | 11145126 | A recent study of Caucasians suggested that the TNF-alpha gene promoter region polymorphism at position -308 influences insulin resistance and percent body fat and increases serum leptin levels, although conflicting data are also reported. |
| 13564 | 11145126 | A recent study of Caucasians suggested that the TNF-alpha gene promoter region polymorphism at position -308 influences insulin resistance and percent body fat and increases serum leptin levels, although conflicting data are also reported. |
| 13565 | 11145126 | The BMI, blood pressure, and fasting plasma glucose (FPG), serum lipids, uric acid, insulin, and leptin concentrations were measured. |
| 13566 | 11145126 | The BMI, blood pressure, and fasting plasma glucose (FPG), serum lipids, uric acid, insulin, and leptin concentrations were measured. |
| 13567 | 11145126 | The BMI, blood pressure, and fasting plasma glucose (FPG), serum lipids, uric acid, insulin, and leptin concentrations were measured. |
| 13568 | 11145126 | The BMI, blood pressure, and fasting plasma glucose (FPG), serum lipids, uric acid, insulin, and leptin concentrations were measured. |
| 13569 | 11145126 | Plasma triglycerides and the insulin resistance index tended to be higher and high-density lipoprotein (HDL) cholesterol tended to be lower in the TNF2 group (P = .06, .20, and .07, respectively), although these differences were not statistically significant. |
| 13570 | 11145126 | Plasma triglycerides and the insulin resistance index tended to be higher and high-density lipoprotein (HDL) cholesterol tended to be lower in the TNF2 group (P = .06, .20, and .07, respectively), although these differences were not statistically significant. |
| 13571 | 11145126 | Plasma triglycerides and the insulin resistance index tended to be higher and high-density lipoprotein (HDL) cholesterol tended to be lower in the TNF2 group (P = .06, .20, and .07, respectively), although these differences were not statistically significant. |
| 13572 | 11145126 | Plasma triglycerides and the insulin resistance index tended to be higher and high-density lipoprotein (HDL) cholesterol tended to be lower in the TNF2 group (P = .06, .20, and .07, respectively), although these differences were not statistically significant. |
| 13573 | 11145126 | In conclusion, no major difference was associated with TNF1 and TNF2 polymorphisms in terms of obesity, blood pressure, lipids, or glucose in young, older, or diabetic Japanese men, although FPG was significantly higher in older men, possibly through increased insulin resistance. |
| 13574 | 11145126 | In conclusion, no major difference was associated with TNF1 and TNF2 polymorphisms in terms of obesity, blood pressure, lipids, or glucose in young, older, or diabetic Japanese men, although FPG was significantly higher in older men, possibly through increased insulin resistance. |
| 13575 | 11145126 | In conclusion, no major difference was associated with TNF1 and TNF2 polymorphisms in terms of obesity, blood pressure, lipids, or glucose in young, older, or diabetic Japanese men, although FPG was significantly higher in older men, possibly through increased insulin resistance. |
| 13576 | 11145126 | In conclusion, no major difference was associated with TNF1 and TNF2 polymorphisms in terms of obesity, blood pressure, lipids, or glucose in young, older, or diabetic Japanese men, although FPG was significantly higher in older men, possibly through increased insulin resistance. |
| 13577 | 11136257 | Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions, with little investigation of innate susceptibility determinants expressed at the level of target beta cells. |
| 13578 | 11136257 | ALR islets were found to be remarkably resistant to two different combinations of beta-cytotoxic cytokines (IL-1beta, tumor necrosis factor alpha, and IFN-gamma) that destroyed islets from the related NOD and alloxan-susceptible strains. |
| 13579 | 11136257 | The close MHC relatedness between the NOD and ALR strains (H2-Kd and H2-Ag7 identical) allowed us to examine whether ALR islet cells could survive autoimmune destruction by NOD-derived Kd-restricted diabetogenic cytotoxic T lymphocyte clones (AI4 and the insulin-reactive G9C8 clones). |
| 13580 | 11133172 | N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. |
| 13581 | 11133172 | N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. |
| 13582 | 11133172 | Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. |
| 13583 | 11133172 | Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. |
| 13584 | 11126408 | TNFalpha and IFNgamma potentiate IL-1beta induced mitogen activated protein kinase activity in rat pancreatic islets of Langerhans. |
| 13585 | 11126235 | Molecular mechanisms of insulin resistance and the role of the adipocyte. |
| 13586 | 11126235 | Molecular mechanisms of insulin resistance and the role of the adipocyte. |
| 13587 | 11126235 | The role of TNFalpha in insulin resistance and other pathologies associated with obesity, have been examined in several experimental systems including obese mice with homozygous null mutations at the TNFalpha or TNF receptor loci. |
| 13588 | 11126235 | The role of TNFalpha in insulin resistance and other pathologies associated with obesity, have been examined in several experimental systems including obese mice with homozygous null mutations at the TNFalpha or TNF receptor loci. |
| 13589 | 11126235 | Analysis of these animals demonstrated that the genetic absence of TNF signaling in obesity: (i) significantly improves insulin receptor signaling capacity and consequently insulin sensitivity; (ii) prevents brown adipose tissue atrophy and beta3-adrenoreceptor deficiency and improves thermo-adaptive responses, (iii) decreases the elevated PAI-1 and TGFbeta production; and (iv) lowers hyperlipidemia and hyperleptinemia. |
| 13590 | 11126235 | Analysis of these animals demonstrated that the genetic absence of TNF signaling in obesity: (i) significantly improves insulin receptor signaling capacity and consequently insulin sensitivity; (ii) prevents brown adipose tissue atrophy and beta3-adrenoreceptor deficiency and improves thermo-adaptive responses, (iii) decreases the elevated PAI-1 and TGFbeta production; and (iv) lowers hyperlipidemia and hyperleptinemia. |
| 13591 | 11120663 | Altered TNF-alpha, glucose, insulin, and amino acids in islets of Langerhans cultured in a microgravity model system. |
| 13592 | 11120663 | Altered TNF-alpha, glucose, insulin, and amino acids in islets of Langerhans cultured in a microgravity model system. |
| 13593 | 11120663 | The present studies were designed to determine effects of a microgravity model system upon lipopolysaccharide (LPS)-stimulated tumor necrosis factor-alpha (TNF-alpha) activity and indexes of insulin and fuel homeostasis of pancreatic islets of Langerhans. |
| 13594 | 11120663 | The present studies were designed to determine effects of a microgravity model system upon lipopolysaccharide (LPS)-stimulated tumor necrosis factor-alpha (TNF-alpha) activity and indexes of insulin and fuel homeostasis of pancreatic islets of Langerhans. |
| 13595 | 11120352 | They produce antithrombotic and thrombotic factors such as t-PA and PAI-1 and respond to TNFalpha, an important factor correlated with the inflammatory process by modifying growth characteristics by producing cytokines such as GM-CSF by expressing ICAM-1 on the surface and by producing large amounts of nitric oxide and endothelin. |
| 13596 | 11114578 | Indeed, elevated levels of pro-inflammatory cytokines (such as TNF-alpha, IL-1 and IL-6) may cause malnutrition and progressive atherosclerotic cardiovascular disease by several pathogenetic mechanisms, which will be discussed in this review. |
| 13597 | 11095103 | Certain cytokines (interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma) either alone or in combination, are able to activate signal transduction pathways in beta-cells leading to transcription factor activation and de novo gene expression. |
| 13598 | 11095103 | However, other induced proteins SUCH AS heat shock protein 70 and superoxide dismutase may reflect a defense reaction elicited in the beta-cells by the cytokines. |
| 13599 | 11092698 | Dual-label immunohistochemical study of interleukin-4-and interferon-gamma-expressing cells within the pancreas of the NOD mouse during disease acceleration with cyclophosphamide. |
| 13600 | 11092698 | Beta cell destruction has been shown to occur when rodent or human islets are exposed in vitro to inflammatory cytokines, such as interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). |
| 13601 | 11092698 | Other cytokines such as interleukin-4 (IL-4) or interleukin-10 (IL-10), when given to NOD mice, prevent insulin-dependent diabetes mellitus (IDDM). |
| 13602 | 11092698 | In this study, we have employed immunofluorescence histochemistry to study the expression of IFN-gamma and IL-4 in the pancreas of female NOD mice at various time-points (days 0, 4, 7, 11 and at onset of diabetes) following disease acceleration with cyclophosphamide (Cy). |
| 13603 | 11092698 | Our results demonstrate that during Cy-induced diabetes, there is increasing expression of both IL-4 and IFN-gamma in specific immune cells within the inflamed islets in the late prediabetic stage and at onset of diabetes. |
| 13604 | 11092520 | Tumor necrosis factor-beta gene NcoI polymorphism decreases insulin resistance in Japanese men. |
| 13605 | 11092520 | Tumor necrosis factor-beta gene NcoI polymorphism decreases insulin resistance in Japanese men. |
| 13606 | 11092520 | Tumor necrosis factor-beta gene NcoI polymorphism decreases insulin resistance in Japanese men. |
| 13607 | 11092520 | Tumor necrosis factor-beta gene NcoI polymorphism decreases insulin resistance in Japanese men. |
| 13608 | 11092520 | Given that the NcoI polymorphism of the tumor necrosis factor-beta (TNF-beta) gene has been shown to be associated with tumor necrosis factor-alpha (TNF-alpha) secretory capacity, we know that this TNF-beta gene polymorphism may influence insulin resistance. |
| 13609 | 11092520 | Given that the NcoI polymorphism of the tumor necrosis factor-beta (TNF-beta) gene has been shown to be associated with tumor necrosis factor-alpha (TNF-alpha) secretory capacity, we know that this TNF-beta gene polymorphism may influence insulin resistance. |
| 13610 | 11092520 | Given that the NcoI polymorphism of the tumor necrosis factor-beta (TNF-beta) gene has been shown to be associated with tumor necrosis factor-alpha (TNF-alpha) secretory capacity, we know that this TNF-beta gene polymorphism may influence insulin resistance. |
| 13611 | 11092520 | Given that the NcoI polymorphism of the tumor necrosis factor-beta (TNF-beta) gene has been shown to be associated with tumor necrosis factor-alpha (TNF-alpha) secretory capacity, we know that this TNF-beta gene polymorphism may influence insulin resistance. |
| 13612 | 11092520 | In Caucasians, 2 polymorphisms of the TNF-alpha promoter region (positions -308 and -238) have been reported to be associated with insulin resistance. |
| 13613 | 11092520 | In Caucasians, 2 polymorphisms of the TNF-alpha promoter region (positions -308 and -238) have been reported to be associated with insulin resistance. |
| 13614 | 11092520 | In Caucasians, 2 polymorphisms of the TNF-alpha promoter region (positions -308 and -238) have been reported to be associated with insulin resistance. |
| 13615 | 11092520 | In Caucasians, 2 polymorphisms of the TNF-alpha promoter region (positions -308 and -238) have been reported to be associated with insulin resistance. |
| 13616 | 11092520 | Thus, we investigated how genetic variation in the TNF-beta and TNF-alpha genes was associated with insulin resistance in 211 Japanese men. |
| 13617 | 11092520 | Thus, we investigated how genetic variation in the TNF-beta and TNF-alpha genes was associated with insulin resistance in 211 Japanese men. |
| 13618 | 11092520 | Thus, we investigated how genetic variation in the TNF-beta and TNF-alpha genes was associated with insulin resistance in 211 Japanese men. |
| 13619 | 11092520 | Thus, we investigated how genetic variation in the TNF-beta and TNF-alpha genes was associated with insulin resistance in 211 Japanese men. |
| 13620 | 11092520 | The frequency of the TNF-beta gene polymorphism was 0.41, and insulin resistance, estimated by homeostasis model assessment (HOMA), was significantly lower in variant homozygotes versus wild-type allele. |
| 13621 | 11092520 | The frequency of the TNF-beta gene polymorphism was 0.41, and insulin resistance, estimated by homeostasis model assessment (HOMA), was significantly lower in variant homozygotes versus wild-type allele. |
| 13622 | 11092520 | The frequency of the TNF-beta gene polymorphism was 0.41, and insulin resistance, estimated by homeostasis model assessment (HOMA), was significantly lower in variant homozygotes versus wild-type allele. |
| 13623 | 11092520 | The frequency of the TNF-beta gene polymorphism was 0.41, and insulin resistance, estimated by homeostasis model assessment (HOMA), was significantly lower in variant homozygotes versus wild-type allele. |
| 13624 | 11092520 | Our results suggest that the TNF-beta gene polymorphism decreases insulin resistance, and that the -308 and -238 polymorphisms of the TNF-alpha promoter region are not a major contributing factor to insulin resistance in Japanese men. |
| 13625 | 11092520 | Our results suggest that the TNF-beta gene polymorphism decreases insulin resistance, and that the -308 and -238 polymorphisms of the TNF-alpha promoter region are not a major contributing factor to insulin resistance in Japanese men. |
| 13626 | 11092520 | Our results suggest that the TNF-beta gene polymorphism decreases insulin resistance, and that the -308 and -238 polymorphisms of the TNF-alpha promoter region are not a major contributing factor to insulin resistance in Japanese men. |
| 13627 | 11092520 | Our results suggest that the TNF-beta gene polymorphism decreases insulin resistance, and that the -308 and -238 polymorphisms of the TNF-alpha promoter region are not a major contributing factor to insulin resistance in Japanese men. |
| 13628 | 11092307 | Are tumor necrosis factor-alpha receptor 2 levels associated with age? |
| 13629 | 11090238 | On day 14 after SZ, fusidin markedly altered the circulating cytokine profile induced in vivo by ConA, reducing the levels of IFN-gamma, IL-2 and TNF-alpha and augmenting the level of IL-6. |
| 13630 | 11090238 | On day 14 after SZ, fusidin markedly altered the circulating cytokine profile induced in vivo by ConA, reducing the levels of IFN-gamma, IL-2 and TNF-alpha and augmenting the level of IL-6. |
| 13631 | 11090238 | In fact, the disease was prevented by a neutralizing monoclonal antibody (mAb) against IFN-gamma, but not by anti-IL-2 receptor mAb, a soluble form of TNF-receptor type 1 or recombinant human IL-6. |
| 13632 | 11090238 | In fact, the disease was prevented by a neutralizing monoclonal antibody (mAb) against IFN-gamma, but not by anti-IL-2 receptor mAb, a soluble form of TNF-receptor type 1 or recombinant human IL-6. |
| 13633 | 11086099 | Because the TNF type 1 (p55) receptor shares a common signaling pathway with Fas (CD95), NOD and B6 mice were treated with the Fas agonist antibody, Jo-2. |
| 13634 | 11086099 | Because the TNF type 1 (p55) receptor shares a common signaling pathway with Fas (CD95), NOD and B6 mice were treated with the Fas agonist antibody, Jo-2. |
| 13635 | 11086099 | The resistance to LPS- and TNF-alpha-mediated lethality and hepatic injury in D-galactosamine-sensitized NOD mice is apparently due to a post-TNFR binding defect, and independent of signaling pathways shared with Fas. |
| 13636 | 11086099 | The resistance to LPS- and TNF-alpha-mediated lethality and hepatic injury in D-galactosamine-sensitized NOD mice is apparently due to a post-TNFR binding defect, and independent of signaling pathways shared with Fas. |
| 13637 | 11079813 | There were also significant decreases in CD4+ and CD8+ thymocytes and the proliferative response of splenocytes. |
| 13638 | 11079813 | Our results suggest that the number and function of T cells in WF may be reduced, which may be related at least in part to elevated TNF-alpha levels, although the role of the other factors such as glucose, insulin, cholesterol, and triglycerides on T-cell immunity should be further investigated. |
| 13639 | 11078458 | Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. |
| 13640 | 11078458 | Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. |
| 13641 | 11078458 | Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. |
| 13642 | 11078458 | Acute impairment of insulin-mediated capillary recruitment and glucose uptake in rat skeletal muscle in vivo by TNF-alpha. |
| 13643 | 11078458 | Another agent that may have vascular effects is the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), which has been reported to play an important role in the insulin resistance of obesity, type 2 diabetes, and sepsis in both animals and humans. |
| 13644 | 11078458 | Another agent that may have vascular effects is the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), which has been reported to play an important role in the insulin resistance of obesity, type 2 diabetes, and sepsis in both animals and humans. |
| 13645 | 11078458 | Another agent that may have vascular effects is the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), which has been reported to play an important role in the insulin resistance of obesity, type 2 diabetes, and sepsis in both animals and humans. |
| 13646 | 11078458 | Another agent that may have vascular effects is the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), which has been reported to play an important role in the insulin resistance of obesity, type 2 diabetes, and sepsis in both animals and humans. |
| 13647 | 11078458 | Insulin alone caused a significant (P < 0.05) increase in FBF (1.7-fold) and capillary recruitment (2.5-fold), with a significant decrease in VR. |
| 13648 | 11078458 | Insulin alone caused a significant (P < 0.05) increase in FBF (1.7-fold) and capillary recruitment (2.5-fold), with a significant decrease in VR. |
| 13649 | 11078458 | Insulin alone caused a significant (P < 0.05) increase in FBF (1.7-fold) and capillary recruitment (2.5-fold), with a significant decrease in VR. |
| 13650 | 11078458 | Insulin alone caused a significant (P < 0.05) increase in FBF (1.7-fold) and capillary recruitment (2.5-fold), with a significant decrease in VR. |
| 13651 | 11078458 | TNF completely prevented the insulin-mediated changes in FBF, VR, and capillary recruitment and significantly reduced (P < 0.05) the insulin-mediated increase in total hind-leg glucose uptake (by 61%) and muscle 2-DG uptake (by at least 50%). |
| 13652 | 11078458 | TNF completely prevented the insulin-mediated changes in FBF, VR, and capillary recruitment and significantly reduced (P < 0.05) the insulin-mediated increase in total hind-leg glucose uptake (by 61%) and muscle 2-DG uptake (by at least 50%). |
| 13653 | 11078458 | TNF completely prevented the insulin-mediated changes in FBF, VR, and capillary recruitment and significantly reduced (P < 0.05) the insulin-mediated increase in total hind-leg glucose uptake (by 61%) and muscle 2-DG uptake (by at least 50%). |
| 13654 | 11078458 | TNF completely prevented the insulin-mediated changes in FBF, VR, and capillary recruitment and significantly reduced (P < 0.05) the insulin-mediated increase in total hind-leg glucose uptake (by 61%) and muscle 2-DG uptake (by at least 50%). |
| 13655 | 11078458 | It is concluded that acute administration in vivo of TNF completely blocks the hemodynamic actions of insulin on rat skeletal muscle vasculature and blocks approximately half of the glucose uptake by muscle. |
| 13656 | 11078458 | It is concluded that acute administration in vivo of TNF completely blocks the hemodynamic actions of insulin on rat skeletal muscle vasculature and blocks approximately half of the glucose uptake by muscle. |
| 13657 | 11078458 | It is concluded that acute administration in vivo of TNF completely blocks the hemodynamic actions of insulin on rat skeletal muscle vasculature and blocks approximately half of the glucose uptake by muscle. |
| 13658 | 11078458 | It is concluded that acute administration in vivo of TNF completely blocks the hemodynamic actions of insulin on rat skeletal muscle vasculature and blocks approximately half of the glucose uptake by muscle. |
| 13659 | 11069063 | We show that exposure of MODC to IS-PL, but not IS-ODN, induced a dose-dependent strong up-regulation of HLA class II and co-stimulatory molecules (CD80, CD86), similar to that observed after treatment with TNF-alpha. |
| 13660 | 11069063 | We show that exposure of MODC to IS-PL, but not IS-ODN, induced a dose-dependent strong up-regulation of HLA class II and co-stimulatory molecules (CD80, CD86), similar to that observed after treatment with TNF-alpha. |
| 13661 | 11069063 | Functional activity was assessed by the detection of increased secretions of IL-6 and IL-12(p75) following treatment with IS-PL. |
| 13662 | 11069063 | Functional activity was assessed by the detection of increased secretions of IL-6 and IL-12(p75) following treatment with IS-PL. |
| 13663 | 11069063 | T cells stimulated by tetanus toxoid-pulsed, IS-PL-matured MODC were significantly more frequently IFN-gamma positive (25.2+/-2.7%) as compared to TNF-alpha-treated MODC (15.4+/-1.4%), indicating a strong activation of Th1 lymphocytes. |
| 13664 | 11069063 | T cells stimulated by tetanus toxoid-pulsed, IS-PL-matured MODC were significantly more frequently IFN-gamma positive (25.2+/-2.7%) as compared to TNF-alpha-treated MODC (15.4+/-1.4%), indicating a strong activation of Th1 lymphocytes. |
| 13665 | 11061332 | The proinflammatory cytokines tumor necrosis factor-a (TNF) and interleukin-1b (IL-1) play an important role in the pathogenesis of insulin-dependent diabetes mellitus, while TNF is also involved in promoting insulin resistance. |
| 13666 | 11061332 | The proinflammatory cytokines tumor necrosis factor-a (TNF) and interleukin-1b (IL-1) play an important role in the pathogenesis of insulin-dependent diabetes mellitus, while TNF is also involved in promoting insulin resistance. |
| 13667 | 11061332 | The proinflammatory cytokines tumor necrosis factor-a (TNF) and interleukin-1b (IL-1) play an important role in the pathogenesis of insulin-dependent diabetes mellitus, while TNF is also involved in promoting insulin resistance. |
| 13668 | 11061332 | It has been recently shown that glucose can induce the synthesis of TNF and IL-6 in human monocytes. |
| 13669 | 11061332 | It has been recently shown that glucose can induce the synthesis of TNF and IL-6 in human monocytes. |
| 13670 | 11061332 | It has been recently shown that glucose can induce the synthesis of TNF and IL-6 in human monocytes. |
| 13671 | 11061332 | The aim of the present study was to investigate the effect of glucose on unstimulated and lipopolysaccharide (LPS)-induced TNF and IL-1 production by human peripheral blood mononuclear cells (PBMC). |
| 13672 | 11061332 | The aim of the present study was to investigate the effect of glucose on unstimulated and lipopolysaccharide (LPS)-induced TNF and IL-1 production by human peripheral blood mononuclear cells (PBMC). |
| 13673 | 11061332 | The aim of the present study was to investigate the effect of glucose on unstimulated and lipopolysaccharide (LPS)-induced TNF and IL-1 production by human peripheral blood mononuclear cells (PBMC). |
| 13674 | 11046041 | In the large granular lymphoma line YT, CD30 signals down-regulate the expression of cytotoxic effector molecules, Fas ligand, perforin, granzyme B, and abrogate cytotoxicity. c-myc, a regulator of proliferation and an upstream regulator of Fas ligand expression, is completely suppressed by CD30. |
| 13675 | 11046041 | The up-regulation of Fas, death receptor 3, and TNF-related apoptosis-inducing ligand by CD30 indicates an increase in susceptibility to apoptotic signals whereas up-regulation of TNFR-associated factor 1 and cellular inhibitor of apoptosis 2 protect cells from certain types of apoptosis. |
| 13676 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13677 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13678 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13679 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13680 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13681 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13682 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13683 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13684 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13685 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13686 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13687 | 11043572 | Tumor necrosis factor alpha-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes. |
| 13688 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13689 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13690 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13691 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13692 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13693 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13694 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13695 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13696 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13697 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13698 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13699 | 11043572 | Tumor necrosis factor-alpha (TNFalpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. |
| 13700 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13701 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13702 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13703 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13704 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13705 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13706 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13707 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13708 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13709 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13710 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13711 | 11043572 | Previous studies have demonstrated that TNFalpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. |
| 13712 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13713 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13714 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13715 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13716 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13717 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13718 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13719 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13720 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13721 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13722 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13723 | 11043572 | However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNFalpha-stimulated IRS-1 serine phosphorylation. |
| 13724 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13725 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13726 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13727 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13728 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13729 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13730 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13731 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13732 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13733 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13734 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13735 | 11043572 | In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNFalpha. |
| 13736 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13737 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13738 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13739 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13740 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13741 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13742 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13743 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13744 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13745 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13746 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13747 | 11043572 | Additional experiments show that MEK1/2 activity is required for TNFalpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. |
| 13748 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13749 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13750 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13751 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13752 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13753 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13754 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13755 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13756 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13757 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13758 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13759 | 11043572 | We observe that TNFalpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. |
| 13760 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13761 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13762 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13763 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13764 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13765 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13766 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13767 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13768 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13769 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13770 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13771 | 11043572 | Although TNFalpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. |
| 13772 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13773 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13774 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13775 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13776 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13777 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13778 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13779 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13780 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13781 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13782 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13783 | 11043572 | To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. |
| 13784 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13785 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13786 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13787 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13788 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13789 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13790 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13791 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13792 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13793 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13794 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13795 | 11043572 | These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNFalpha-induced p42/44 activity. |
| 13796 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13797 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13798 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13799 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13800 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13801 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13802 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13803 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13804 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13805 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13806 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13807 | 11043572 | Chronic TNFalpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. |
| 13808 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13809 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13810 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13811 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13812 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13813 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13814 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13815 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13816 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13817 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13818 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13819 | 11043572 | We observe that this longer term TNFalpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. |
| 13820 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13821 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13822 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13823 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13824 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13825 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13826 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13827 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13828 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13829 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13830 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13831 | 11043572 | This study suggests that TNFalpha-mediated insulin resistance, but not adipocyte dedifferentiation, is mediated by the MEK1/2-p42/44 MAP kinase pathway. |
| 13832 | 11038062 | Cytokines typically produced in the xenograft environment (e.g., IL-1 and TNF) inhibit insulin biosynthesis and secretion from isolated pancreatic islets, and are associated with the production of nitric oxide (NO). |
| 13833 | 11031068 | Also, changes of the amino acid pattern as well as interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, prostaglandin (PG) E(2)at 6, 12, and 24 h after CLP were investigated. |
| 13834 | 11031068 | Also, changes of the amino acid pattern as well as interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, prostaglandin (PG) E(2)at 6, 12, and 24 h after CLP were investigated. |
| 13835 | 11031068 | Also, changes of the amino acid pattern as well as interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, prostaglandin (PG) E(2)at 6, 12, and 24 h after CLP were investigated. |
| 13836 | 11031068 | Concentrations of IL-1 beta in peritoneal lavage fluid (PLF) at 6 h and TNF-alpha at 6 h as well as at 12 h after CLP in the FOS group were significantly higher than those in the SOS group. |
| 13837 | 11031068 | Concentrations of IL-1 beta in peritoneal lavage fluid (PLF) at 6 h and TNF-alpha at 6 h as well as at 12 h after CLP in the FOS group were significantly higher than those in the SOS group. |
| 13838 | 11031068 | Concentrations of IL-1 beta in peritoneal lavage fluid (PLF) at 6 h and TNF-alpha at 6 h as well as at 12 h after CLP in the FOS group were significantly higher than those in the SOS group. |
| 13839 | 11031068 | These results suggest that differences in IL-1 beta, TNF-alpha, and PGE(2)levels in PLF in the early period of sepsis did not influence the survival rates and plasma amino acid profiles of the FOS and SOS groups. |
| 13840 | 11031068 | These results suggest that differences in IL-1 beta, TNF-alpha, and PGE(2)levels in PLF in the early period of sepsis did not influence the survival rates and plasma amino acid profiles of the FOS and SOS groups. |
| 13841 | 11031068 | These results suggest that differences in IL-1 beta, TNF-alpha, and PGE(2)levels in PLF in the early period of sepsis did not influence the survival rates and plasma amino acid profiles of the FOS and SOS groups. |
| 13842 | 11025557 | A specific proteasome defect has now been identified in NOD mouse lymphocytes that results from down-regulation of expression of the proteasome subunit LMP2, which is encoded by a gene in the MHC genomic region. |
| 13843 | 11025557 | This defect both prevents the proteolytic processing required for the production and activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which plays an important role in immune and inflammatory responses, in addition to increasing the susceptibility of the affected cells to apoptosis induced by tumor necrosis factor-alpha (TNF-alpha). |
| 13844 | 11024034 | Destruction of pancreatic islet beta-cells in type 1 diabetes appears to result from direct contact with infiltrating T-cells and macrophages and exposure to inflammatory cytokines such as interferon (IFN)-gamma, interleukin (IL)-1 beta, and tumor necrosis factor TNF-alpha that such cells produce. |
| 13845 | 11024034 | We recently reported on a method for selection of insulinoma cells that are resistant to the cytotoxic effects of inflammatory cytokines (INS-1(res)), involving their growth in progressively increasing concentrations of IL-1 beta plus IFN-gamma, and selection of surviving cells. |
| 13846 | 11024034 | By focusing on the known components of the IFN-gamma receptor signaling pathway, we have discovered that expression levels of signal transducer and activator of transcription (STAT)-1 alpha are closely correlated with the cytokine-resistant and -sensitive phenotypes. |
| 13847 | 11024034 | That STAT-1 alpha is directly involved in development of cytokine resistance is demonstrated by an increase of viability from 10 +/- 2% in control cells to 50 +/- 6% in cells with adenovirus-mediated overexpression of STAT-1 alpha (p < 0.001) after culture of both cell groups in the presence of 100 units/ml IFN-gamma plus 10 ng/ml IL-1 beta for 48 h. |
| 13848 | 11024034 | The resistance to IL-1 beta plus IFN-gamma in STAT-1 alpha-expressing cells is due in part to interference with IL-1 beta-mediated stimulation of inducible nitric-oxide synthase expression and nitric oxide production. |
| 13849 | 11024034 | Furthermore, overexpression of STAT-1 alpha does not impair robust glucose-stimulated insulin secretion in the INS-1-derived cell line 832/13. |
| 13850 | 11024034 | We conclude that expression of STAT-1 alpha may be a means of protecting insulin-producing cell lines from cytokine damage, which, in conjunction with appropriate cell-impermeant macroencapsulation devices, may allow such cells to be used for insulin replacement in type 1 diabetes. |
| 13851 | 10999832 | Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB1*1502-DQB1*0601 allele and anti-glutamic acid decarboxylase antibodies. |
| 13852 | 10999832 | Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB1*1502-DQB1*0601 allele and anti-glutamic acid decarboxylase antibodies. |
| 13853 | 10999832 | Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB1*1502-DQB1*0601 allele and anti-glutamic acid decarboxylase antibodies. |
| 13854 | 10999832 | This study investigates the influence of TNFalpha on the predisposition to insulin dependency in adult-onset diabetic patients with type 1 diabetes-protective human leukocyte antigen haplotypes. |
| 13855 | 10999832 | This study investigates the influence of TNFalpha on the predisposition to insulin dependency in adult-onset diabetic patients with type 1 diabetes-protective human leukocyte antigen haplotypes. |
| 13856 | 10999832 | This study investigates the influence of TNFalpha on the predisposition to insulin dependency in adult-onset diabetic patients with type 1 diabetes-protective human leukocyte antigen haplotypes. |
| 13857 | 10999832 | These results suggest that TNFalpha is associated with a predisposition to progression to insulin dependency in GADab/DRB1*1502DQB1*0601-positive diabetic patients initially diagnosed with type 2 diabetes and that determination of these patients' TNFalpha genotype may allow for better prediction of their clinical course. |
| 13858 | 10999832 | These results suggest that TNFalpha is associated with a predisposition to progression to insulin dependency in GADab/DRB1*1502DQB1*0601-positive diabetic patients initially diagnosed with type 2 diabetes and that determination of these patients' TNFalpha genotype may allow for better prediction of their clinical course. |
| 13859 | 10999832 | These results suggest that TNFalpha is associated with a predisposition to progression to insulin dependency in GADab/DRB1*1502DQB1*0601-positive diabetic patients initially diagnosed with type 2 diabetes and that determination of these patients' TNFalpha genotype may allow for better prediction of their clinical course. |
| 13860 | 10999830 | To that end, we compared: 1) serum concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), and leptin in eight healthy lean control females and in android obese female without (n = 14) and with (n = 7) type 2 diabetes; and 2) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet (VLCD). |
| 13861 | 10999830 | To that end, we compared: 1) serum concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), and leptin in eight healthy lean control females and in android obese female without (n = 14) and with (n = 7) type 2 diabetes; and 2) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet (VLCD). |
| 13862 | 10999830 | To that end, we compared: 1) serum concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), and leptin in eight healthy lean control females and in android obese female without (n = 14) and with (n = 7) type 2 diabetes; and 2) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet (VLCD). |
| 13863 | 10999830 | To that end, we compared: 1) serum concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), and leptin in eight healthy lean control females and in android obese female without (n = 14) and with (n = 7) type 2 diabetes; and 2) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet (VLCD). |
| 13864 | 10999830 | As compared with lean controls, obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin, IL-6, TNFalpha, and C-reactive protein. |
| 13865 | 10999830 | As compared with lean controls, obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin, IL-6, TNFalpha, and C-reactive protein. |
| 13866 | 10999830 | As compared with lean controls, obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin, IL-6, TNFalpha, and C-reactive protein. |
| 13867 | 10999830 | As compared with lean controls, obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin, IL-6, TNFalpha, and C-reactive protein. |
| 13868 | 10999830 | In the whole group, IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values. |
| 13869 | 10999830 | In the whole group, IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values. |
| 13870 | 10999830 | In the whole group, IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values. |
| 13871 | 10999830 | In the whole group, IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values. |
| 13872 | 10999830 | Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels. |
| 13873 | 10999830 | Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels. |
| 13874 | 10999830 | Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels. |
| 13875 | 10999830 | Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels. |
| 13876 | 10999830 | In contrast, VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum. |
| 13877 | 10999830 | In contrast, VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum. |
| 13878 | 10999830 | In contrast, VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum. |
| 13879 | 10999830 | In contrast, VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum. |
| 13880 | 10999830 | These results suggest that, as for leptin, circulating IL-6 concentrations reflect, at least in part, adipose tissue production. |
| 13881 | 10999830 | These results suggest that, as for leptin, circulating IL-6 concentrations reflect, at least in part, adipose tissue production. |
| 13882 | 10999830 | These results suggest that, as for leptin, circulating IL-6 concentrations reflect, at least in part, adipose tissue production. |
| 13883 | 10999830 | These results suggest that, as for leptin, circulating IL-6 concentrations reflect, at least in part, adipose tissue production. |
| 13884 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13885 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13886 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13887 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13888 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13889 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13890 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13891 | 10995595 | Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. |
| 13892 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13893 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13894 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13895 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13896 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13897 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13898 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13899 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 13900 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13901 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13902 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13903 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13904 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13905 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13906 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13907 | 10995595 | In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. |
| 13908 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13909 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13910 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13911 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13912 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13913 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13914 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13915 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 13916 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13917 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13918 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13919 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13920 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13921 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13922 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13923 | 10995595 | Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). |
| 13924 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13925 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13926 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13927 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13928 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13929 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13930 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13931 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 13932 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13933 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13934 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13935 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13936 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13937 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13938 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13939 | 10995595 | PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. |
| 13940 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13941 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13942 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13943 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13944 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13945 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13946 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13947 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 13948 | 10989952 | The silent PPARgamma exon 6 CAC(His) --> CAT(His) polymorphism does not affect the plasma leptin levels in a collective of first degree relatives of type 2 diabetes patients from South West Germany. |
| 13949 | 10989952 | The peroxisome proliferator activated receptors-gamma (PPARgamma) belong to the superfamily of nuclear transcription factors acting as master genes regulating events in adipocyte differentiation. |
| 13950 | 10989952 | Thus, PPARgamma is a candidate gene for affecting insulin sensitivity and the pathogenesis of insulin resistance. |
| 13951 | 10989952 | PPARs trigger endocrine response of two important adipose tissue-derived signalling factors, leptin and tumor necrosis factor-alpha. |
| 13952 | 10989952 | It generates insulin-like signals for glucose transport and glycogen synthesis via leptin receptors and the PI3-kinase and could, therefore, play a role as a mediator of obesity-related insulin resistance. |
| 13953 | 10989952 | In a recent study, it was proposed that mutations in PPARgamma could play a role in individuals who are at increased risk for developing obesity and type 2 diabetes mellitus by influencing leptin levels. |
| 13954 | 10989952 | We therefore examined the prevalence of the CAC(His) --> CAT(His) mutation in non-diabetic first degree relatives of subjects with type 2 diabetes to determine a possible association of this mutation to leptin levels and insulin sensitivity. 138 probands were characterised by oral glucose tolerance tests, euglycemic-hyperinsulinemic glucose-clamp and by measuring leptin levels. |
| 13955 | 10989952 | When the whole group was analysed for an association of the mutation with plasma leptin concentration and insulin sensitivity, no statistical significance could be demonstrated. |
| 13956 | 10987645 | Genetic contribution of the BAT2 gene microsatellite polymorphism to the age-at-onset of insulin-dependent diabetes mellitus. |
| 13957 | 10987645 | We investigated the frequency of the BAT2 microsatellite alleles (BAT2) in 74 young-onset insulin-dependent diabetes mellitus (IDDM) patients, 51 adult-onset IDDM patients, and 85 normal control subjects, and assessed the associations among these BAT2 alleles, TNFa microsatellite alleles (TNFa), and HLA-DRB1 alleles. |
| 13958 | 10987645 | The BAT2.9 allele was strongly associated with TNFa9 in the young-onset IDDM patients, although no association was found between the BAT2.9 and HLA-DRB1 alleles. |
| 13959 | 10987645 | These results suggest that the BAT2 microsatellite polymorphism is associated with the age-at-onset of IDDM and possibly with the inflammatory process of pancreatic beta-cell destruction during the development of IDDM. |
| 13960 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13961 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13962 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13963 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13964 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13965 | 10983873 | We sought to confirm that circulating concentrations of the cytokine acute-phase mediators IL-6 and tumour necrosis factor alpha [TNFalpha] are elevated in type 2 diabetes, and investigated blood as a source of cytokines in type 2 diabetes. |
| 13966 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13967 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13968 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13969 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13970 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13971 | 10983873 | Plasma IL-6 and TNFalpha were significantly increased in type 2 diabetes compared to normal subjects. |
| 13972 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13973 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13974 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13975 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13976 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13977 | 10983873 | However, basal production of IL-6 and TNFalpha in cultured diabetic blood was markedly depressed in comparison with non-diabetic samples. |
| 13978 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13979 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13980 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13981 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13982 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13983 | 10983873 | IL-6 and TNFalpha production was increased in blood in response to LPS, reaching similar levels in diabetic and non-diabetic subjects, though IL-6 was slightly but significantly higher in controls. |
| 13984 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13985 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13986 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13987 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13988 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13989 | 10983873 | We conclude that circulating levels of IL-6 and TNFalpha are increased in type 2 diabetes but there is downregulation of basal cytokine production in blood cells in type 2 diabetes. |
| 13990 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13991 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13992 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13993 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13994 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13995 | 10983873 | Blood has the capacity to produce cytokines in diabetes which contribute to the augmented acute-phase response, but the main source of the increased plasma IL-6 and TNFalpha concentrations may be from non-circulating cells. |
| 13996 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 13997 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 13998 | 10975477 | Intracellular cytokine staining and flow cytometry were used to investigate whether immunoadsorption (IA) of immunoglobulins alters intracytoplasmic cytokine production in CD4+ and CD8+ T cells from the blood of patients with refractory rheumatoid arthritis (n = 7), membrane proliferative glomerulonephritis (n = 1), and Goodpasture's syndrome (n = 1). |
| 13999 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 14000 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 14001 | 10975477 | Four patients (Group 1) showed severely depressed production of TNF-alpha, IL-2, IFN-gamma, and IL-4 by CD4+ and CD8+ T cells and responded to 3 IA sessions with significant increases in CD4+TNF-alpha+, CD4+IL-2+, and CD8+IL-2+ T cells. |
| 14002 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 14003 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 14004 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 14005 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 14006 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 14007 | 10975477 | Group 2 (n = 5) showed unimpaired intracellular cytokine levels and responded to IA with a heterogeneous pattern of changes in TNF-alpha, IL-2, IFN-gamma, and IL-4 production, but these alterations were smaller than those in Group 1. |
| 14008 | 10969838 | Tumor necrosis factor (TNF)-alpha and uncoupling protein (UCP)-2 mRNA levels increased 12- and 6-fold, respectively, in isolated adipocytes from CLA-fed mice compared with control mice. |
| 14009 | 10969838 | Tumor necrosis factor (TNF)-alpha and uncoupling protein (UCP)-2 mRNA levels increased 12- and 6-fold, respectively, in isolated adipocytes from CLA-fed mice compared with control mice. |
| 14010 | 10969838 | Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. |
| 14011 | 10969838 | Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. |
| 14012 | 10969838 | CLA supplementation decreased blood leptin levels, but continuous leptin infusion reversed hyperinsulinemia, indicating that leptin depletion contributes to the development of insulin resistance. |
| 14013 | 10969838 | CLA supplementation decreased blood leptin levels, but continuous leptin infusion reversed hyperinsulinemia, indicating that leptin depletion contributes to the development of insulin resistance. |
| 14014 | 10969828 | We found that the release of tumor necrosis factor-alpha and interleukin-1beta from lipopolysaccharide plus interferon-gamma-stimulated macrophages and vascular endothelial growth factor from both stimulated and nonstimulated macrophages was significantly reduced in diabetic animals compared with nondiabetic controls. |
| 14015 | 10961356 | Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males. |
| 14016 | 10961356 | Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males. |
| 14017 | 10961356 | Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males. |
| 14018 | 10961356 | Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males. |
| 14019 | 10961356 | Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males. |
| 14020 | 10961356 | Leptin and TNF alpha are thought to influence blood pressure. |
| 14021 | 10961356 | Leptin and TNF alpha are thought to influence blood pressure. |
| 14022 | 10961356 | Leptin and TNF alpha are thought to influence blood pressure. |
| 14023 | 10961356 | Leptin and TNF alpha are thought to influence blood pressure. |
| 14024 | 10961356 | Leptin and TNF alpha are thought to influence blood pressure. |
| 14025 | 10961356 | Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. |
| 14026 | 10961356 | Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. |
| 14027 | 10961356 | Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. |
| 14028 | 10961356 | Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. |
| 14029 | 10961356 | Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. |
| 14030 | 10961356 | In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. |
| 14031 | 10961356 | In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. |
| 14032 | 10961356 | In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. |
| 14033 | 10961356 | In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. |
| 14034 | 10961356 | In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. |
| 14035 | 10961356 | Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. |
| 14036 | 10961356 | Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. |
| 14037 | 10961356 | Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. |
| 14038 | 10961356 | Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. |
| 14039 | 10961356 | Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. |
| 14040 | 10961356 | No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. |
| 14041 | 10961356 | No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. |
| 14042 | 10961356 | No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. |
| 14043 | 10961356 | No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. |
| 14044 | 10961356 | No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. |
| 14045 | 10954020 | Tumor necrosis factor alpha (TNF-alpha) is a multifunctional cytokine constitutively produced by adipose tissue that may mediate insulin resistance. |
| 14046 | 10954020 | Tumor necrosis factor alpha (TNF-alpha) is a multifunctional cytokine constitutively produced by adipose tissue that may mediate insulin resistance. |
| 14047 | 10954020 | Studies in Caucasian subjects have suggested that the G-308A transition in the 5' region of the TNF-alpha gene may be associated with insulin resistance and obesity. |
| 14048 | 10954020 | Studies in Caucasian subjects have suggested that the G-308A transition in the 5' region of the TNF-alpha gene may be associated with insulin resistance and obesity. |
| 14049 | 10953913 | Genes encoding transforming growth factor beta, interleukin-4 (IL-4) and IL-10 are most frequently protective. |
| 14050 | 10953913 | Genes encoding transforming growth factor beta, interleukin-4 (IL-4) and IL-10 are most frequently protective. |
| 14051 | 10953913 | Autoimmune/ inflammatory diseases are associated with excessive production of inflammatory cytokines such as IL-1, IL-12, tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma). |
| 14052 | 10953913 | Autoimmune/ inflammatory diseases are associated with excessive production of inflammatory cytokines such as IL-1, IL-12, tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma). |
| 14053 | 10953913 | Vectors encoding inhibitors of these cytokines, such as IL-1 receptor antagonist, soluble IL-1 receptors, IL-12p40, soluble TNFalpha receptors or IFNgamma-receptor/IgG-Fc fusion proteins are protective in models of either arthritis, Type 1 DM, SLE or EAE. |
| 14054 | 10953913 | Vectors encoding inhibitors of these cytokines, such as IL-1 receptor antagonist, soluble IL-1 receptors, IL-12p40, soluble TNFalpha receptors or IFNgamma-receptor/IgG-Fc fusion proteins are protective in models of either arthritis, Type 1 DM, SLE or EAE. |
| 14055 | 10953027 | Peroxisome proliferator-activated receptor gamma ligands inhibit development of atherosclerosis in LDL receptor-deficient mice. |
| 14056 | 10953027 | The peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that regulates fat-cell development and glucose homeostasis and is the molecular target of a class of insulin-sensitizing agents used for the management of type 2 diabetes mellitus. |
| 14057 | 10953027 | We report here that the PPARgamma-specific agonists rosiglitazone and GW7845 strongly inhibited the development of atherosclerosis in LDL receptor-deficient male mice, despite increased expression of the CD36 scavenger receptor in the arterial wall. |
| 14058 | 10953027 | The antiatherogenic effect in male mice was correlated with improved insulin sensitivity and decreased tissue expression of TNF-alpha and gelatinase B, indicating both systemic and local actions of PPARgamma. |
| 14059 | 10946317 | Islet-specific expression of IL-10 promotes diabetes in nonobese diabetic mice independent of Fas, perforin, TNF receptor-1, and TNF receptor-2 molecules. |
| 14060 | 10946317 | Groups of IL-10-NOD mice, each deficient in either Fas, perforin, or TNFR-1 molecules, readily developed insulitis, and subsequently succumbed to diabetes with an accelerated kinetics and incidence similar to that observed in their wild-type or heterozygous IL-10-NOD littermates. |
| 14061 | 10946317 | These results demonstrate that pancreatic IL-10 promotes diabetes independent of Fas, perforin, TNFR-1, and TNFR-2 molecules. |
| 14062 | 10946317 | Our data suggest that cyclophosphamide- but not IL-10-induced diabetes is Fas dependent. |
| 14063 | 10946317 | Overall, these findings provide evidence that pancreatic expression of IL-10 promotes diabetes independent of the major death pathways and provide impetus for identification of novel death pathways precipitating autoimmune destruction of insulin-producing beta cells. |
| 14064 | 10934453 | There are many other molecules, including Fas ligand and cytokines such as interferon-gamma, interleukin-1 and tumor necrosis factor-alpha, which may lead to beta cell destruction either directly or indirectly via regulation of toxic molecules such as nitric oxide. |
| 14065 | 10913943 | Plasma soluble tumor necrosis factor-alpha receptors circulate in proportion to leptin levels during the menstrual cycle in lean but not in obese women. |
| 14066 | 10909968 | We therefore examined whether overexpression of catalase (Cat), glutathione peroxidase (Gpx), and Cu/Zn superoxide dismutase (SOD) can provide protection for bioengineered RINm5F cells against cytokine-mediated toxicity. |
| 14067 | 10909968 | A 72-h exposure of RINm5F control cells to interleukin-1beta (IL-1beta) alone or a combination of IL-1beta, tumor necrosis factor-alpha, and gamma-interferon resulted in a time- and concentration-dependent decrease of cell viability in the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) cytotoxicity assay. |
| 14068 | 10909968 | Overexpression of Cat, Gpx, and Cu/Zn SOD protected against toxicity of the cytokine mixture but not against that of IL-1beta alone. |
| 14069 | 10909966 | Aberrant macrophage cytokine production is a conserved feature among autoimmune-prone mouse strains: elevated interleukin (IL)-12 and an imbalance in tumor necrosis factor-alpha and IL-10 define a unique cytokine profile in macrophages from young nonobese diabetic mice. |
| 14070 | 10909966 | Aberrant macrophage cytokine production is a conserved feature among autoimmune-prone mouse strains: elevated interleukin (IL)-12 and an imbalance in tumor necrosis factor-alpha and IL-10 define a unique cytokine profile in macrophages from young nonobese diabetic mice. |
| 14071 | 10909966 | Aberrant macrophage cytokine production is a conserved feature among autoimmune-prone mouse strains: elevated interleukin (IL)-12 and an imbalance in tumor necrosis factor-alpha and IL-10 define a unique cytokine profile in macrophages from young nonobese diabetic mice. |
| 14072 | 10909966 | Aberrant macrophage cytokine production is a conserved feature among autoimmune-prone mouse strains: elevated interleukin (IL)-12 and an imbalance in tumor necrosis factor-alpha and IL-10 define a unique cytokine profile in macrophages from young nonobese diabetic mice. |
| 14073 | 10909966 | Aberrant macrophage cytokine production is a conserved feature among autoimmune-prone mouse strains: elevated interleukin (IL)-12 and an imbalance in tumor necrosis factor-alpha and IL-10 define a unique cytokine profile in macrophages from young nonobese diabetic mice. |
| 14074 | 10909966 | Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains but reduced compared with the congenic diabetes-resistant NOR strain. |
| 14075 | 10909966 | Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains but reduced compared with the congenic diabetes-resistant NOR strain. |
| 14076 | 10909966 | Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains but reduced compared with the congenic diabetes-resistant NOR strain. |
| 14077 | 10909966 | Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains but reduced compared with the congenic diabetes-resistant NOR strain. |
| 14078 | 10909966 | Endotoxin-activated peritoneal Mø from young prediseased NOD mice produced interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha levels similar to those of Mø from a panel of control strains but reduced compared with the congenic diabetes-resistant NOR strain. |
| 14079 | 10909966 | IL-6 and IL-10 production were similar in NOD and NOR Mø, indicating that reduction in NOD IL-1 and TNF-alpha expression was selective. |
| 14080 | 10909966 | IL-6 and IL-10 production were similar in NOD and NOR Mø, indicating that reduction in NOD IL-1 and TNF-alpha expression was selective. |
| 14081 | 10909966 | IL-6 and IL-10 production were similar in NOD and NOR Mø, indicating that reduction in NOD IL-1 and TNF-alpha expression was selective. |
| 14082 | 10909966 | IL-6 and IL-10 production were similar in NOD and NOR Mø, indicating that reduction in NOD IL-1 and TNF-alpha expression was selective. |
| 14083 | 10909966 | IL-6 and IL-10 production were similar in NOD and NOR Mø, indicating that reduction in NOD IL-1 and TNF-alpha expression was selective. |
| 14084 | 10909966 | Nevertheless, the ratio of TNF-alpha and IL-10 production, a stringent index of normal Mø function, distinguished NOD from all normal strains. |
| 14085 | 10909966 | Nevertheless, the ratio of TNF-alpha and IL-10 production, a stringent index of normal Mø function, distinguished NOD from all normal strains. |
| 14086 | 10909966 | Nevertheless, the ratio of TNF-alpha and IL-10 production, a stringent index of normal Mø function, distinguished NOD from all normal strains. |
| 14087 | 10909966 | Nevertheless, the ratio of TNF-alpha and IL-10 production, a stringent index of normal Mø function, distinguished NOD from all normal strains. |
| 14088 | 10909966 | Nevertheless, the ratio of TNF-alpha and IL-10 production, a stringent index of normal Mø function, distinguished NOD from all normal strains. |
| 14089 | 10909966 | This response was induced not only by endotoxin but also by bacillus Calmette-Guerin (BCG) and CD40 ligand and was associated with (and likely caused by) the enhanced and prolonged expression of p40 mRNA. |
| 14090 | 10909966 | This response was induced not only by endotoxin but also by bacillus Calmette-Guerin (BCG) and CD40 ligand and was associated with (and likely caused by) the enhanced and prolonged expression of p40 mRNA. |
| 14091 | 10909966 | This response was induced not only by endotoxin but also by bacillus Calmette-Guerin (BCG) and CD40 ligand and was associated with (and likely caused by) the enhanced and prolonged expression of p40 mRNA. |
| 14092 | 10909966 | This response was induced not only by endotoxin but also by bacillus Calmette-Guerin (BCG) and CD40 ligand and was associated with (and likely caused by) the enhanced and prolonged expression of p40 mRNA. |
| 14093 | 10909966 | This response was induced not only by endotoxin but also by bacillus Calmette-Guerin (BCG) and CD40 ligand and was associated with (and likely caused by) the enhanced and prolonged expression of p40 mRNA. |
| 14094 | 10909966 | Accompanied by a unique profile of TNF-alpha and IL-10, the dramatic elevation of IL-12 expression by NOD Mø reflects intrinsic defects of the innate immune system with the potential to initiate and propagate the pathogenic autoreactive T-helper type 1 response characteristic of type 1 diabetes. |
| 14095 | 10909966 | Accompanied by a unique profile of TNF-alpha and IL-10, the dramatic elevation of IL-12 expression by NOD Mø reflects intrinsic defects of the innate immune system with the potential to initiate and propagate the pathogenic autoreactive T-helper type 1 response characteristic of type 1 diabetes. |
| 14096 | 10909966 | Accompanied by a unique profile of TNF-alpha and IL-10, the dramatic elevation of IL-12 expression by NOD Mø reflects intrinsic defects of the innate immune system with the potential to initiate and propagate the pathogenic autoreactive T-helper type 1 response characteristic of type 1 diabetes. |
| 14097 | 10909966 | Accompanied by a unique profile of TNF-alpha and IL-10, the dramatic elevation of IL-12 expression by NOD Mø reflects intrinsic defects of the innate immune system with the potential to initiate and propagate the pathogenic autoreactive T-helper type 1 response characteristic of type 1 diabetes. |
| 14098 | 10909966 | Accompanied by a unique profile of TNF-alpha and IL-10, the dramatic elevation of IL-12 expression by NOD Mø reflects intrinsic defects of the innate immune system with the potential to initiate and propagate the pathogenic autoreactive T-helper type 1 response characteristic of type 1 diabetes. |
| 14099 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14100 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14101 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14102 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14103 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14104 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14105 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14106 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14107 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14108 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14109 | 10905491 | Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase. |
| 14110 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14111 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14112 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14113 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14114 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14115 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14116 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14117 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14118 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14119 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14120 | 10905491 | The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. |
| 14121 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14122 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14123 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14124 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14125 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14126 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14127 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14128 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14129 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14130 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14131 | 10905491 | Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. |
| 14132 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14133 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14134 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14135 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14136 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14137 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14138 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14139 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14140 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14141 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14142 | 10905491 | To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). |
| 14143 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14144 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14145 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14146 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14147 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14148 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14149 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14150 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14151 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14152 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14153 | 10905491 | Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. |
| 14154 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14155 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14156 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14157 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14158 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14159 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14160 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14161 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14162 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14163 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14164 | 10905491 | To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. |
| 14165 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14166 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14167 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14168 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14169 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14170 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14171 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14172 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14173 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14174 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14175 | 10905491 | Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. |
| 14176 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14177 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14178 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14179 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14180 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14181 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14182 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14183 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14184 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14185 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14186 | 10905491 | In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. |
| 14187 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14188 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14189 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14190 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14191 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14192 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14193 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14194 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14195 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14196 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14197 | 10905491 | Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. |
| 14198 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14199 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14200 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14201 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14202 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14203 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14204 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14205 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14206 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14207 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14208 | 10905491 | Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. |
| 14209 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14210 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14211 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14212 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14213 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14214 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14215 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14216 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14217 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14218 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14219 | 10905491 | These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. |
| 14220 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14221 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14222 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14223 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14224 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14225 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14226 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14227 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14228 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14229 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14230 | 10905491 | This probably represents the interface between TNF-alpha and insulin signaling in the liver. |
| 14231 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14232 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14233 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14234 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14235 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14236 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14237 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14238 | 10905474 | Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. |
| 14239 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14240 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14241 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14242 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14243 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14244 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14245 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14246 | 10905474 | Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. |
| 14247 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14248 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14249 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14250 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14251 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14252 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14253 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14254 | 10905474 | However, in vivo data in humans have given conflicting results regarding the relationship between circulating TNF-alpha levels and insulin sensitivity. |
| 14255 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14256 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14257 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14258 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14259 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14260 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14261 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14262 | 10905474 | In the present study, the potential local role of TNF-alpha on insulin action in human subcutaneous adipose tissue was studied in 42 obese women (BMI 39+/-10 kg/m2). |
| 14263 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14264 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14265 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14266 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14267 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14268 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14269 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14270 | 10905474 | We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). |
| 14271 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14272 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14273 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14274 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14275 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14276 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14277 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14278 | 10905474 | As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. |
| 14279 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14280 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14281 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14282 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14283 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14284 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14285 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14286 | 10905474 | Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). |
| 14287 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14288 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14289 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14290 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14291 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14292 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14293 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14294 | 10905474 | In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. |
| 14295 | 10903798 | Interleukin-18 mRNA, but not interleukin-18 receptor mRNA, is constitutively expressed in islet beta-cells and up-regulated by interferon-gamma. |
| 14296 | 10903798 | Interleukin-18 mRNA, but not interleukin-18 receptor mRNA, is constitutively expressed in islet beta-cells and up-regulated by interferon-gamma. |
| 14297 | 10903798 | Interleukin-18 mRNA, but not interleukin-18 receptor mRNA, is constitutively expressed in islet beta-cells and up-regulated by interferon-gamma. |
| 14298 | 10903798 | Since species differences have been shown between human and murine IL-18, the aims of this study were to investigate 1) if species homologous IL-18 alone or following IL-12 pre-exposure affected rat islet function, 2) if IL-18 dose-dependently modulated IL-1 beta or interferon-gamma (IFN-gamma) + tumor necrosis factor-alpha (TNF-alpha) actions on islet function, and 3) if IL-18 and IL-18 receptor (IL-18R) were expressed in rat islet beta-cells. |
| 14299 | 10903798 | Since species differences have been shown between human and murine IL-18, the aims of this study were to investigate 1) if species homologous IL-18 alone or following IL-12 pre-exposure affected rat islet function, 2) if IL-18 dose-dependently modulated IL-1 beta or interferon-gamma (IFN-gamma) + tumor necrosis factor-alpha (TNF-alpha) actions on islet function, and 3) if IL-18 and IL-18 receptor (IL-18R) were expressed in rat islet beta-cells. |
| 14300 | 10903798 | Since species differences have been shown between human and murine IL-18, the aims of this study were to investigate 1) if species homologous IL-18 alone or following IL-12 pre-exposure affected rat islet function, 2) if IL-18 dose-dependently modulated IL-1 beta or interferon-gamma (IFN-gamma) + tumor necrosis factor-alpha (TNF-alpha) actions on islet function, and 3) if IL-18 and IL-18 receptor (IL-18R) were expressed in rat islet beta-cells. |
| 14301 | 10903798 | There were no significant effects of 0.625-10 nM recombinant murine (rm) IL-18 alone on accumulated or glucose-challenged insulin release or NO production after 24 hours. |
| 14302 | 10903798 | There were no significant effects of 0.625-10 nM recombinant murine (rm) IL-18 alone on accumulated or glucose-challenged insulin release or NO production after 24 hours. |
| 14303 | 10903798 | There were no significant effects of 0.625-10 nM recombinant murine (rm) IL-18 alone on accumulated or glucose-challenged insulin release or NO production after 24 hours. |
| 14304 | 10903798 | Fifteen pg/ml of recombinant human (rh) IL-1 beta as well as 200 U/ml recombinant rat (rr) IFN-gamma + 250 U/ml rhTNF-alpha significantly increased islet NO production and inhibited both accumulated and glucose-challenged islet insulin release. |
| 14305 | 10903798 | Fifteen pg/ml of recombinant human (rh) IL-1 beta as well as 200 U/ml recombinant rat (rr) IFN-gamma + 250 U/ml rhTNF-alpha significantly increased islet NO production and inhibited both accumulated and glucose-challenged islet insulin release. |
| 14306 | 10903798 | Fifteen pg/ml of recombinant human (rh) IL-1 beta as well as 200 U/ml recombinant rat (rr) IFN-gamma + 250 U/ml rhTNF-alpha significantly increased islet NO production and inhibited both accumulated and glucose-challenged islet insulin release. |
| 14307 | 10903798 | However, rmIL-18 failed to modulate these effects of IL-1 beta or IFN-gamma + TNF-alpha. |
| 14308 | 10903798 | However, rmIL-18 failed to modulate these effects of IL-1 beta or IFN-gamma + TNF-alpha. |
| 14309 | 10903798 | However, rmIL-18 failed to modulate these effects of IL-1 beta or IFN-gamma + TNF-alpha. |
| 14310 | 10903798 | Although IL-12 induces IL-18R expression in Th1 and B lymphocytes, 24-hours rmIL-12 preincubation neither sensitized islets to effects of 10 nM of rm or rrIL-18 alone nor primed the islets to IL-1 beta actions on insulin release and NO production. |
| 14311 | 10903798 | Although IL-12 induces IL-18R expression in Th1 and B lymphocytes, 24-hours rmIL-12 preincubation neither sensitized islets to effects of 10 nM of rm or rrIL-18 alone nor primed the islets to IL-1 beta actions on insulin release and NO production. |
| 14312 | 10903798 | Although IL-12 induces IL-18R expression in Th1 and B lymphocytes, 24-hours rmIL-12 preincubation neither sensitized islets to effects of 10 nM of rm or rrIL-18 alone nor primed the islets to IL-1 beta actions on insulin release and NO production. |
| 14313 | 10903798 | IL-18R beta mRNA, which was expressed in human peripheral blood mononuclear cells (PBMC), was not expressed in rat insulinoma (RIN) cells or in isolated rat islets, even after exposure to IL-1 beta and/or IFN-gamma + TNF-alpha or IL-12. |
| 14314 | 10903798 | IL-18R beta mRNA, which was expressed in human peripheral blood mononuclear cells (PBMC), was not expressed in rat insulinoma (RIN) cells or in isolated rat islets, even after exposure to IL-1 beta and/or IFN-gamma + TNF-alpha or IL-12. |
| 14315 | 10903798 | IL-18R beta mRNA, which was expressed in human peripheral blood mononuclear cells (PBMC), was not expressed in rat insulinoma (RIN) cells or in isolated rat islets, even after exposure to IL-1 beta and/or IFN-gamma + TNF-alpha or IL-12. |
| 14316 | 10903798 | IL-18 mRNA was constitutively expressed in RIN cells, in FACS-purified rat beta-cells and in intact rat and mouse islets, and was up-regulated by IFN-gamma in an interferon regulatory factor-1- IRF-1) and NO - independent manner. |
| 14317 | 10903798 | IL-18 mRNA was constitutively expressed in RIN cells, in FACS-purified rat beta-cells and in intact rat and mouse islets, and was up-regulated by IFN-gamma in an interferon regulatory factor-1- IRF-1) and NO - independent manner. |
| 14318 | 10903798 | IL-18 mRNA was constitutively expressed in RIN cells, in FACS-purified rat beta-cells and in intact rat and mouse islets, and was up-regulated by IFN-gamma in an interferon regulatory factor-1- IRF-1) and NO - independent manner. |
| 14319 | 10892347 | Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells. |
| 14320 | 10892347 | Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells. |
| 14321 | 10892347 | Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells. |
| 14322 | 10892347 | Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells. |
| 14323 | 10892347 | The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). |
| 14324 | 10892347 | The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). |
| 14325 | 10892347 | The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). |
| 14326 | 10892347 | The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). |
| 14327 | 10892347 | In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated human umbilical vein endothelial cells (HUVECs). |
| 14328 | 10892347 | In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated human umbilical vein endothelial cells (HUVECs). |
| 14329 | 10892347 | In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated human umbilical vein endothelial cells (HUVECs). |
| 14330 | 10892347 | In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated human umbilical vein endothelial cells (HUVECs). |
| 14331 | 10892347 | Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa B. |
| 14332 | 10892347 | Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa B. |
| 14333 | 10892347 | Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa B. |
| 14334 | 10892347 | Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa B. |
| 14335 | 10892347 | Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was dose-dependently reduced by pycnogenol. |
| 14336 | 10892347 | Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was dose-dependently reduced by pycnogenol. |
| 14337 | 10892347 | Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was dose-dependently reduced by pycnogenol. |
| 14338 | 10892347 | Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was dose-dependently reduced by pycnogenol. |
| 14339 | 10892347 | The ability of pycnogenol to inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process. |
| 14340 | 10892347 | The ability of pycnogenol to inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process. |
| 14341 | 10892347 | The ability of pycnogenol to inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process. |
| 14342 | 10892347 | The ability of pycnogenol to inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process. |
| 14343 | 10880890 | TNF-alpha is considered as one of the potential determinants of insulin resistance. |
| 14344 | 10880890 | TNF-alpha is considered as one of the potential determinants of insulin resistance. |
| 14345 | 10880890 | TNF-alpha is considered as one of the potential determinants of insulin resistance. |
| 14346 | 10880890 | TNF-alpha is considered as one of the potential determinants of insulin resistance. |
| 14347 | 10880890 | TNF-alpha is considered as one of the potential determinants of insulin resistance. |
| 14348 | 10880890 | However several data suggest that TNF-alpha expression itself, could be modulated by the degree of adiposity and/or plasma insulin levels. |
| 14349 | 10880890 | However several data suggest that TNF-alpha expression itself, could be modulated by the degree of adiposity and/or plasma insulin levels. |
| 14350 | 10880890 | However several data suggest that TNF-alpha expression itself, could be modulated by the degree of adiposity and/or plasma insulin levels. |
| 14351 | 10880890 | However several data suggest that TNF-alpha expression itself, could be modulated by the degree of adiposity and/or plasma insulin levels. |
| 14352 | 10880890 | However several data suggest that TNF-alpha expression itself, could be modulated by the degree of adiposity and/or plasma insulin levels. |
| 14353 | 10880890 | To clarify the determinants of plasma TNF-alpha levels in type 2 diabetes mellitus, we studied the impact of intensive insulin treatment on plasma TNF-alpha levels in 16 type 2 diabetic subjects with failure to oral antidiabetic medication (HbA1c: 10.8 +/- 1.2 %). |
| 14354 | 10880890 | To clarify the determinants of plasma TNF-alpha levels in type 2 diabetes mellitus, we studied the impact of intensive insulin treatment on plasma TNF-alpha levels in 16 type 2 diabetic subjects with failure to oral antidiabetic medication (HbA1c: 10.8 +/- 1.2 %). |
| 14355 | 10880890 | To clarify the determinants of plasma TNF-alpha levels in type 2 diabetes mellitus, we studied the impact of intensive insulin treatment on plasma TNF-alpha levels in 16 type 2 diabetic subjects with failure to oral antidiabetic medication (HbA1c: 10.8 +/- 1.2 %). |
| 14356 | 10880890 | To clarify the determinants of plasma TNF-alpha levels in type 2 diabetes mellitus, we studied the impact of intensive insulin treatment on plasma TNF-alpha levels in 16 type 2 diabetic subjects with failure to oral antidiabetic medication (HbA1c: 10.8 +/- 1.2 %). |
| 14357 | 10880890 | To clarify the determinants of plasma TNF-alpha levels in type 2 diabetes mellitus, we studied the impact of intensive insulin treatment on plasma TNF-alpha levels in 16 type 2 diabetic subjects with failure to oral antidiabetic medication (HbA1c: 10.8 +/- 1.2 %). |
| 14358 | 10880890 | The plasma TNF-alpha level was neither affected by plasma glucose level variations nor intensive insulin treatment despite a 37 % decrease in daily insulin needs at the end of insulin therapy (total duration: 11.5 +/- 2.0 days). |
| 14359 | 10880890 | The plasma TNF-alpha level was neither affected by plasma glucose level variations nor intensive insulin treatment despite a 37 % decrease in daily insulin needs at the end of insulin therapy (total duration: 11.5 +/- 2.0 days). |
| 14360 | 10880890 | The plasma TNF-alpha level was neither affected by plasma glucose level variations nor intensive insulin treatment despite a 37 % decrease in daily insulin needs at the end of insulin therapy (total duration: 11.5 +/- 2.0 days). |
| 14361 | 10880890 | The plasma TNF-alpha level was neither affected by plasma glucose level variations nor intensive insulin treatment despite a 37 % decrease in daily insulin needs at the end of insulin therapy (total duration: 11.5 +/- 2.0 days). |
| 14362 | 10880890 | The plasma TNF-alpha level was neither affected by plasma glucose level variations nor intensive insulin treatment despite a 37 % decrease in daily insulin needs at the end of insulin therapy (total duration: 11.5 +/- 2.0 days). |
| 14363 | 10880890 | These results show that plasma TNF-alpha levels are essentially dependent on visceral fat amount, thus suggesting that TNF-alpha could be one of the factors mediating insulin resistance and cardiovascular risk in obese type 2 diabetic patients. |
| 14364 | 10880890 | These results show that plasma TNF-alpha levels are essentially dependent on visceral fat amount, thus suggesting that TNF-alpha could be one of the factors mediating insulin resistance and cardiovascular risk in obese type 2 diabetic patients. |
| 14365 | 10880890 | These results show that plasma TNF-alpha levels are essentially dependent on visceral fat amount, thus suggesting that TNF-alpha could be one of the factors mediating insulin resistance and cardiovascular risk in obese type 2 diabetic patients. |
| 14366 | 10880890 | These results show that plasma TNF-alpha levels are essentially dependent on visceral fat amount, thus suggesting that TNF-alpha could be one of the factors mediating insulin resistance and cardiovascular risk in obese type 2 diabetic patients. |
| 14367 | 10880890 | These results show that plasma TNF-alpha levels are essentially dependent on visceral fat amount, thus suggesting that TNF-alpha could be one of the factors mediating insulin resistance and cardiovascular risk in obese type 2 diabetic patients. |
| 14368 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14369 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14370 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14371 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14372 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14373 | 10878750 | Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. |
| 14374 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14375 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14376 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14377 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14378 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14379 | 10878750 | Recently, increased TNF-alpha production has been observed in adipose tissue derived from obese rodents or human subjects and TNF-alpha has been implicated as a causative factor in obesity-associated insulin resistance and the pathogenesis of type 2 diabetes. |
| 14380 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14381 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14382 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14383 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14384 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14385 | 10878750 | Thus, current evidence suggests that administration of exogenous TNF-alpha to animals can induce insulin resistance, whereas neutralization of TNF-alpha can improve insulin sensitivity. |
| 14386 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14387 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14388 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14389 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14390 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14391 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 14392 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14393 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14394 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14395 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14396 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14397 | 10878750 | However, the absence of TNF-alpha action might only partially protect against obesity-induced insulin resistance in mice. |
| 14398 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14399 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14400 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14401 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14402 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14403 | 10878750 | These include the downregulation of genes that are required for normal insulin action, direct effects on insulin signaling, induction of elevated free fatty acids via stimulation of lipolysis, and negative regulation of PPAR gamma, an important insulin-sensitizing nuclear receptor. |
| 14404 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14405 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14406 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14407 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14408 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14409 | 10878750 | Although current evidence suggests that neutralizing TNF-alpha in type 2 diabetic subjects is not sufficient to cause metabolic improvement, it is still probable that TNF-alpha is a contributing factor in common metabolic disturbances such as insulin resistance and dyslipidemia. |
| 14410 | 10875261 | Tumor necrosis factor-alpha (TNF) inhibits fat cell differentiation and may also mediate insulin resistance in adipocytes. |
| 14411 | 10875261 | Tumor necrosis factor-alpha (TNF) inhibits fat cell differentiation and may also mediate insulin resistance in adipocytes. |
| 14412 | 10875261 | Tumor necrosis factor-alpha (TNF) inhibits fat cell differentiation and may also mediate insulin resistance in adipocytes. |
| 14413 | 10875261 | Tumor necrosis factor-alpha (TNF) inhibits fat cell differentiation and may also mediate insulin resistance in adipocytes. |
| 14414 | 10875261 | We therefore studied the effect of receptor-specific TNF muteins on adipose differentiation and insulin-stimulated glucose transport of in vitro differentiated human adipocytes in primary culture. |
| 14415 | 10875261 | We therefore studied the effect of receptor-specific TNF muteins on adipose differentiation and insulin-stimulated glucose transport of in vitro differentiated human adipocytes in primary culture. |
| 14416 | 10875261 | We therefore studied the effect of receptor-specific TNF muteins on adipose differentiation and insulin-stimulated glucose transport of in vitro differentiated human adipocytes in primary culture. |
| 14417 | 10875261 | We therefore studied the effect of receptor-specific TNF muteins on adipose differentiation and insulin-stimulated glucose transport of in vitro differentiated human adipocytes in primary culture. |
| 14418 | 10875261 | Adipocyte precursor cells exposed to the 60-kDa TNF receptor (p60-TNFR)-specific TNF(R32W-S86T) showed a marked decrease in the percentage of differentiating cells in response to adipogenic factors as well as a reduction in peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) messenger RNA (mRNA) and glycerophosphate dehydrogenase (GPDH) activity, but increased endogenous TNF mRNA expression. |
| 14419 | 10875261 | Adipocyte precursor cells exposed to the 60-kDa TNF receptor (p60-TNFR)-specific TNF(R32W-S86T) showed a marked decrease in the percentage of differentiating cells in response to adipogenic factors as well as a reduction in peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) messenger RNA (mRNA) and glycerophosphate dehydrogenase (GPDH) activity, but increased endogenous TNF mRNA expression. |
| 14420 | 10875261 | Adipocyte precursor cells exposed to the 60-kDa TNF receptor (p60-TNFR)-specific TNF(R32W-S86T) showed a marked decrease in the percentage of differentiating cells in response to adipogenic factors as well as a reduction in peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) messenger RNA (mRNA) and glycerophosphate dehydrogenase (GPDH) activity, but increased endogenous TNF mRNA expression. |
| 14421 | 10875261 | Adipocyte precursor cells exposed to the 60-kDa TNF receptor (p60-TNFR)-specific TNF(R32W-S86T) showed a marked decrease in the percentage of differentiating cells in response to adipogenic factors as well as a reduction in peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) messenger RNA (mRNA) and glycerophosphate dehydrogenase (GPDH) activity, but increased endogenous TNF mRNA expression. |
| 14422 | 10875261 | We conclude that p60-TNFR mediates the antiadipogenic effect as well as the down-regulation of GLUT4 by TNF, thereby leading to long-term inhibition of insulin-stimulated glucose transport. |
| 14423 | 10875261 | We conclude that p60-TNFR mediates the antiadipogenic effect as well as the down-regulation of GLUT4 by TNF, thereby leading to long-term inhibition of insulin-stimulated glucose transport. |
| 14424 | 10875261 | We conclude that p60-TNFR mediates the antiadipogenic effect as well as the down-regulation of GLUT4 by TNF, thereby leading to long-term inhibition of insulin-stimulated glucose transport. |
| 14425 | 10875261 | We conclude that p60-TNFR mediates the antiadipogenic effect as well as the down-regulation of GLUT4 by TNF, thereby leading to long-term inhibition of insulin-stimulated glucose transport. |
| 14426 | 10871197 | Besides LPL overproduction, macrophages of diabetic patients exhibited an increase in basal and LPL-induced tumor necrosis factor (TNF)-alpha release. |
| 14427 | 10871197 | Besides LPL overproduction, macrophages of diabetic patients exhibited an increase in basal and LPL-induced tumor necrosis factor (TNF)-alpha release. |
| 14428 | 10871197 | Overall, these data demonstrate that macrophages of diabetic patients overexpress LPL and TNF-alpha and that peripheral factors dysregulated in diabetes are, at least in part, responsible for these alterations. |
| 14429 | 10871197 | Overall, these data demonstrate that macrophages of diabetic patients overexpress LPL and TNF-alpha and that peripheral factors dysregulated in diabetes are, at least in part, responsible for these alterations. |
| 14430 | 10868955 | In this study, the anti-inflammatory actions of the peroxisome proliferator-activated receptor (PPAR)-gamma agonists 15-deoxy-delta 12,14-prostaglandin J2 (15-d-delta 12,14-PGJ2) and troglitazone have been examined. |
| 14431 | 10868955 | Treatment of RAW 264.7 cells and CD-1 mouse peritoneal macrophages with lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) results in inducible nitric oxide synthase (iNOS), inducible cyclooxygenase (COX-2) and interleukin-1 (IL-1) expression, increased production of nitric oxide, and the release of IL-1. |
| 14432 | 10868955 | The inhibitory actions of 15-d-delta 12,14-PGJ2 on LPS + IFN-gamma-induced inflammatory events are not associated with the inhibition of iNOS enzymatic activity or macrophage cell death, but appear to result from an inhibition of iNOS and IL-1 transcription. |
| 14433 | 10868955 | In addition, the anti-inflammatory actions of 15-d-delta 12,14-PGJ2 are not limited to peritoneal macrophages, as 15-d-delta 12,14-PGJ2 prevents TNF-alpha + LPS-induced resident islet macrophage expression of IL-1beta and beta-cell expression of iNOS stimulated by the local release of IL-1 in rat islets. 15-d-delta 12,14-PGJ2 appears to be approximately 10-fold more effective at inhibiting resident islet macrophage activation (in response to TNF + LPS) than IL-1-induced nitrite production by beta-cells. |
| 14434 | 10868955 | Two mechanisms appear to be associated with the antiinflammatory actions of both 15-d-delta 12,14-PGJ2 and troglitazone: 1) the direct inhibition of cytokine- and endotoxin-stimulated iNOS and IL-1 transcription; and 2) the inhibition of IL-1 signaling, an event associated with PPAR-gamma agonist-induced activation of the heat shock response (as assayed by heat shock protein 70 expression). |
| 14435 | 10868955 | These findings indicate that the PPAR-gamma agonists, troglitazone and the J series of prostaglandins, are potent anti-inflammatory agents that prevent cytokine- and endotoxin-stimulated activation of peripheral and resident tissue macrophages and cytokine-induced iNOS expression by beta-cells by the inhibition of transcriptional activation and induction of the heat shock response. |
| 14436 | 10868954 | After a 24-h culture with IL-1beta (30 U/ml), beta-cells exhibited a lower expression of the beta-cell-specific protein transcription factor pancreatic and duodenal homeobox gene (PDX)-1, glucose transporter GLUT2, and proinsulin convertase PC2, with a marked reduction (60-70%) in glucose-induced insulin production and selective sensitivity to the toxins alloxan (ALX) and streptozotocin (STZ). |
| 14437 | 10868954 | On the other hand, the cells presented an increased expression of Mn-superoxide dismutase, heat shock protein 70, inducible heme oxygenase, and inducible nitrite oxide synthase. |
| 14438 | 10868954 | Exposure to IL-1beta can thus protect beta-cells against conditions that cause necrosis; however, it did not protect against apoptosis induced by the additional presence of interferon-gamma or tumor necrosis factor-alpha. |
| 14439 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 14440 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 14441 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 14442 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 14443 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 14444 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 14445 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 14446 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 14447 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 14448 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 14449 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 14450 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 14451 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 14452 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 14453 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 14454 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 14455 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 14456 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 14457 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 14458 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 14459 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 14460 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 14461 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 14462 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 14463 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 14464 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 14465 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 14466 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 14467 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 14468 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 14469 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 14470 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 14471 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 14472 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 14473 | 10842657 | However, the fat cells may still play an important role in insulin resistance and Syndrome X through, for instance, its endocrine functions (production of leptin, TNF alpha, PAI-1, etc.) and involvement in lipid metabolism (FFA release and hydrolysis of triglycerides). |
| 14474 | 10842657 | Examinations of the intracellular signaling mechanisms for insulin in fat cells from individuals with Type 2 diabetes revealed markedly lower insulin-stimulated PI3-kinase activity. |
| 14475 | 10842657 | Downstream activation and serine phosphorylation of PKB/Akt by insulin were also markedly reduced in Type 2 diabetes. |
| 14476 | 10842657 | Thus, these data show that both PI3-kinase and PKB activation by insulin are markedly reduced in Type 2 diabetes. |
| 14477 | 10842657 | We also examined whether an attenuated activation of PI3-kinase by insulin can be seen in non-diabetic insulin-resistant states. |
| 14478 | 10842657 | Thus, impaired IRS-1 expression and downstream signaling events in fat cells in response to insulin are associated with insulin resistance and Syndrome X. |
| 14479 | 10841005 | Polymorphism of the tumor necrosis factor-alpha receptor 2 gene is associated with obesity, leptin levels, and insulin resistance in young subjects and diet-treated type 2 diabetic patients. |
| 14480 | 10837498 | Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). |
| 14481 | 10837498 | Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). |
| 14482 | 10837498 | Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). |
| 14483 | 10837498 | The following observations supported that both NF-kappaB and AP-1 mediated enhanced TNFalpha transcription by CHG: 1) A 295-base pair fragment of the proximal TNFalpha promoter containing NF-kappaB and AP-1 sites reproduced the effects of CHG on TNFalpha transcription in a luciferase reporter assay, 2) mutational analyses of both NF-kappaB and the AP-1 sites abrogated 90% of the luciferase activity, 3) gel-shift analysis using the binding sites showed activation of NF-kappaB and AP-1 in CHG nuclear extracts, and 4) Western blot analyses demonstrated elevated nuclear levels of p65 and p50 and decreased cytosolic levels of IkappaBalpha in CHG-treated monocytes. |
| 14484 | 10837498 | The following observations supported that both NF-kappaB and AP-1 mediated enhanced TNFalpha transcription by CHG: 1) A 295-base pair fragment of the proximal TNFalpha promoter containing NF-kappaB and AP-1 sites reproduced the effects of CHG on TNFalpha transcription in a luciferase reporter assay, 2) mutational analyses of both NF-kappaB and the AP-1 sites abrogated 90% of the luciferase activity, 3) gel-shift analysis using the binding sites showed activation of NF-kappaB and AP-1 in CHG nuclear extracts, and 4) Western blot analyses demonstrated elevated nuclear levels of p65 and p50 and decreased cytosolic levels of IkappaBalpha in CHG-treated monocytes. |
| 14485 | 10837498 | The following observations supported that both NF-kappaB and AP-1 mediated enhanced TNFalpha transcription by CHG: 1) A 295-base pair fragment of the proximal TNFalpha promoter containing NF-kappaB and AP-1 sites reproduced the effects of CHG on TNFalpha transcription in a luciferase reporter assay, 2) mutational analyses of both NF-kappaB and the AP-1 sites abrogated 90% of the luciferase activity, 3) gel-shift analysis using the binding sites showed activation of NF-kappaB and AP-1 in CHG nuclear extracts, and 4) Western blot analyses demonstrated elevated nuclear levels of p65 and p50 and decreased cytosolic levels of IkappaBalpha in CHG-treated monocytes. |
| 14486 | 10837498 | That ROS acted as a key intermediate in the CHG pathway was supported by the following evidence: 1) increased superoxide levels similar to those observed with PMA or TNFalpha, 2) increased phosphorylation of stress-responsive mitogen-activated protein kinases p38 and JNK-1, 3) counteraction of the effects of CHG on TNFalpha production, the 295TNFluc reporter activity, activation of NF-kappaB, and repression of IkappaBalpha by antioxidants and p38 mitogen-activated protein kinase inhibitors. |
| 14487 | 10837498 | That ROS acted as a key intermediate in the CHG pathway was supported by the following evidence: 1) increased superoxide levels similar to those observed with PMA or TNFalpha, 2) increased phosphorylation of stress-responsive mitogen-activated protein kinases p38 and JNK-1, 3) counteraction of the effects of CHG on TNFalpha production, the 295TNFluc reporter activity, activation of NF-kappaB, and repression of IkappaBalpha by antioxidants and p38 mitogen-activated protein kinase inhibitors. |
| 14488 | 10837498 | That ROS acted as a key intermediate in the CHG pathway was supported by the following evidence: 1) increased superoxide levels similar to those observed with PMA or TNFalpha, 2) increased phosphorylation of stress-responsive mitogen-activated protein kinases p38 and JNK-1, 3) counteraction of the effects of CHG on TNFalpha production, the 295TNFluc reporter activity, activation of NF-kappaB, and repression of IkappaBalpha by antioxidants and p38 mitogen-activated protein kinase inhibitors. |
| 14489 | 10835296 | Cytokines and nitric oxide (NO) have been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 14490 | 10835296 | Our results demonstrate that PBN cotreatment prevents the generation of nitrite by RIN-5F cells induced by treatment with tumor necrosis factor-alpha, interleukin 1beta, and interferon-gamma in a dose-dependent fashion. |
| 14491 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 14492 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 14493 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 14494 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 14495 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 14496 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 14497 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 14498 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 14499 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 14500 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 14501 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 14502 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 14503 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 14504 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 14505 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 14506 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 14507 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 14508 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 14509 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 14510 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 14511 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 14512 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 14513 | 10825233 | Synergistic activation of NF-kappab and inducible isoform of nitric oxide synthase induction by interferon-gamma and tumor necrosis factor-alpha in INS-1 cells. |
| 14514 | 10825233 | Synergistic activation of NF-kappab and inducible isoform of nitric oxide synthase induction by interferon-gamma and tumor necrosis factor-alpha in INS-1 cells. |
| 14515 | 10825233 | Synergistic activation of NF-kappab and inducible isoform of nitric oxide synthase induction by interferon-gamma and tumor necrosis factor-alpha in INS-1 cells. |
| 14516 | 10825233 | Synergistic activation of NF-kappab and inducible isoform of nitric oxide synthase induction by interferon-gamma and tumor necrosis factor-alpha in INS-1 cells. |
| 14517 | 10825233 | Synergistic activation of NF-kappab and inducible isoform of nitric oxide synthase induction by interferon-gamma and tumor necrosis factor-alpha in INS-1 cells. |
| 14518 | 10825233 | In this study, we investigated signaling mechanisms mediating the effects of IFN-gamma in pancreatic beta-cells using a differentiated rat insulin-secreting cell line, INS-1, with special reference to the activation of transcription factors STAT (signal transducers and activators of transcription)1 and NF-kappaB. |
| 14519 | 10825233 | In this study, we investigated signaling mechanisms mediating the effects of IFN-gamma in pancreatic beta-cells using a differentiated rat insulin-secreting cell line, INS-1, with special reference to the activation of transcription factors STAT (signal transducers and activators of transcription)1 and NF-kappaB. |
| 14520 | 10825233 | In this study, we investigated signaling mechanisms mediating the effects of IFN-gamma in pancreatic beta-cells using a differentiated rat insulin-secreting cell line, INS-1, with special reference to the activation of transcription factors STAT (signal transducers and activators of transcription)1 and NF-kappaB. |
| 14521 | 10825233 | In this study, we investigated signaling mechanisms mediating the effects of IFN-gamma in pancreatic beta-cells using a differentiated rat insulin-secreting cell line, INS-1, with special reference to the activation of transcription factors STAT (signal transducers and activators of transcription)1 and NF-kappaB. |
| 14522 | 10825233 | In this study, we investigated signaling mechanisms mediating the effects of IFN-gamma in pancreatic beta-cells using a differentiated rat insulin-secreting cell line, INS-1, with special reference to the activation of transcription factors STAT (signal transducers and activators of transcription)1 and NF-kappaB. |
| 14523 | 10825233 | Exposure of INS-1 cells to 100 IU/ml IFN-gamma for 24 h resulted in significant inhibition of nutrient-induced insulin secretion associated with impaired metabolism. |
| 14524 | 10825233 | Exposure of INS-1 cells to 100 IU/ml IFN-gamma for 24 h resulted in significant inhibition of nutrient-induced insulin secretion associated with impaired metabolism. |
| 14525 | 10825233 | Exposure of INS-1 cells to 100 IU/ml IFN-gamma for 24 h resulted in significant inhibition of nutrient-induced insulin secretion associated with impaired metabolism. |
| 14526 | 10825233 | Exposure of INS-1 cells to 100 IU/ml IFN-gamma for 24 h resulted in significant inhibition of nutrient-induced insulin secretion associated with impaired metabolism. |
| 14527 | 10825233 | Exposure of INS-1 cells to 100 IU/ml IFN-gamma for 24 h resulted in significant inhibition of nutrient-induced insulin secretion associated with impaired metabolism. |
| 14528 | 10825233 | In combination with tumor necrosis factor-alpha (TNF-alpha) (50 ng/ml), IFN-gamma elicited severe cytotoxicity and induced the expression of the inducible isoform of nitric oxide synthase (iNOS) mRNA. |
| 14529 | 10825233 | In combination with tumor necrosis factor-alpha (TNF-alpha) (50 ng/ml), IFN-gamma elicited severe cytotoxicity and induced the expression of the inducible isoform of nitric oxide synthase (iNOS) mRNA. |
| 14530 | 10825233 | In combination with tumor necrosis factor-alpha (TNF-alpha) (50 ng/ml), IFN-gamma elicited severe cytotoxicity and induced the expression of the inducible isoform of nitric oxide synthase (iNOS) mRNA. |
| 14531 | 10825233 | In combination with tumor necrosis factor-alpha (TNF-alpha) (50 ng/ml), IFN-gamma elicited severe cytotoxicity and induced the expression of the inducible isoform of nitric oxide synthase (iNOS) mRNA. |
| 14532 | 10825233 | In combination with tumor necrosis factor-alpha (TNF-alpha) (50 ng/ml), IFN-gamma elicited severe cytotoxicity and induced the expression of the inducible isoform of nitric oxide synthase (iNOS) mRNA. |
| 14533 | 10825233 | IFN-gamma promoted tyrosine phosphorylation and DNA-binding of STAT1 through Janus kinase (JAK)1 activation without apparent phosphorylation of JAK2. |
| 14534 | 10825233 | IFN-gamma promoted tyrosine phosphorylation and DNA-binding of STAT1 through Janus kinase (JAK)1 activation without apparent phosphorylation of JAK2. |
| 14535 | 10825233 | IFN-gamma promoted tyrosine phosphorylation and DNA-binding of STAT1 through Janus kinase (JAK)1 activation without apparent phosphorylation of JAK2. |
| 14536 | 10825233 | IFN-gamma promoted tyrosine phosphorylation and DNA-binding of STAT1 through Janus kinase (JAK)1 activation without apparent phosphorylation of JAK2. |
| 14537 | 10825233 | IFN-gamma promoted tyrosine phosphorylation and DNA-binding of STAT1 through Janus kinase (JAK)1 activation without apparent phosphorylation of JAK2. |
| 14538 | 10825233 | TNF-alpha did not affect STAT1 activation, but stimulated DNA-binding and transcriptional activity of NF-kappaB, both of which were further increased by IFN-gamma. |
| 14539 | 10825233 | TNF-alpha did not affect STAT1 activation, but stimulated DNA-binding and transcriptional activity of NF-kappaB, both of which were further increased by IFN-gamma. |
| 14540 | 10825233 | TNF-alpha did not affect STAT1 activation, but stimulated DNA-binding and transcriptional activity of NF-kappaB, both of which were further increased by IFN-gamma. |
| 14541 | 10825233 | TNF-alpha did not affect STAT1 activation, but stimulated DNA-binding and transcriptional activity of NF-kappaB, both of which were further increased by IFN-gamma. |
| 14542 | 10825233 | TNF-alpha did not affect STAT1 activation, but stimulated DNA-binding and transcriptional activity of NF-kappaB, both of which were further increased by IFN-gamma. |
| 14543 | 10825233 | These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine resulted in the reduction of iNOS mRNA expression. |
| 14544 | 10825233 | These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine resulted in the reduction of iNOS mRNA expression. |
| 14545 | 10825233 | These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine resulted in the reduction of iNOS mRNA expression. |
| 14546 | 10825233 | These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine resulted in the reduction of iNOS mRNA expression. |
| 14547 | 10825233 | These effects of IFN-gamma and TNF-alpha seem physiologically relevant, because either inhibition of STAT1 by the tyrosine kinase inhibitor herbimycin A or that of NF-kappaB by sulfasalazine resulted in the reduction of iNOS mRNA expression. |
| 14548 | 10825233 | In conclusion, IFN-gamma activates STAT1 and potentiates TNF-alpha-induced NF-kappaB activation in INS-1 cells, thereby inducing iNOS and cell destruction. |
| 14549 | 10825233 | In conclusion, IFN-gamma activates STAT1 and potentiates TNF-alpha-induced NF-kappaB activation in INS-1 cells, thereby inducing iNOS and cell destruction. |
| 14550 | 10825233 | In conclusion, IFN-gamma activates STAT1 and potentiates TNF-alpha-induced NF-kappaB activation in INS-1 cells, thereby inducing iNOS and cell destruction. |
| 14551 | 10825233 | In conclusion, IFN-gamma activates STAT1 and potentiates TNF-alpha-induced NF-kappaB activation in INS-1 cells, thereby inducing iNOS and cell destruction. |
| 14552 | 10825233 | In conclusion, IFN-gamma activates STAT1 and potentiates TNF-alpha-induced NF-kappaB activation in INS-1 cells, thereby inducing iNOS and cell destruction. |
| 14553 | 10814778 | Hsp60 expression was found to be enhanced in response to cytokines as diverse as IL-1beta, TNF-alpha, IL-4, IL-6 and IL-10. |
| 14554 | 10814778 | Hsp60 expression was found to be enhanced in response to cytokines as diverse as IL-1beta, TNF-alpha, IL-4, IL-6 and IL-10. |
| 14555 | 10814778 | Upregulation of hsp27, however, was primarily induced by immunoregulatory cytokines like IL-4, IL-6 and TGF-beta whereas alphaB-crystallin expression was found to be enhanced by the pro-inflammatory cytokine TNF-alpha only. |
| 14556 | 10814778 | Upregulation of hsp27, however, was primarily induced by immunoregulatory cytokines like IL-4, IL-6 and TGF-beta whereas alphaB-crystallin expression was found to be enhanced by the pro-inflammatory cytokine TNF-alpha only. |
| 14557 | 10809183 | Tumor necrosis factor (TNF)-alpha-stimulated superoxide production and N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated aggregation in diabetic patients with triopathy were significantly greater than those in diabetics without triopathy. |
| 14558 | 10807946 | Down-regulation by troglitazone of hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes. |
| 14559 | 10807946 | Down-regulation by troglitazone of hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes. |
| 14560 | 10807946 | Down-regulation by troglitazone of hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes. |
| 14561 | 10807946 | Down-regulation by troglitazone of hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes. |
| 14562 | 10807946 | Down-regulation by troglitazone of hepatic tumor necrosis factor-alpha and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes. |
| 14563 | 10807946 | Troglitazone, a novel thiazolidinedione drug used to treat non-insulin-dependent diabetes mellitus, is a selective ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). |
| 14564 | 10807946 | Troglitazone, a novel thiazolidinedione drug used to treat non-insulin-dependent diabetes mellitus, is a selective ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). |
| 14565 | 10807946 | Troglitazone, a novel thiazolidinedione drug used to treat non-insulin-dependent diabetes mellitus, is a selective ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). |
| 14566 | 10807946 | Troglitazone, a novel thiazolidinedione drug used to treat non-insulin-dependent diabetes mellitus, is a selective ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). |
| 14567 | 10807946 | Troglitazone, a novel thiazolidinedione drug used to treat non-insulin-dependent diabetes mellitus, is a selective ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). |
| 14568 | 10807946 | At the end of treatment, hepatic expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA was quantitatively determined by kinetic polymerase chain reaction both under basal conditions and after stimulation with lipopolysaccharide (LPS). |
| 14569 | 10807946 | At the end of treatment, hepatic expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA was quantitatively determined by kinetic polymerase chain reaction both under basal conditions and after stimulation with lipopolysaccharide (LPS). |
| 14570 | 10807946 | At the end of treatment, hepatic expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA was quantitatively determined by kinetic polymerase chain reaction both under basal conditions and after stimulation with lipopolysaccharide (LPS). |
| 14571 | 10807946 | At the end of treatment, hepatic expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA was quantitatively determined by kinetic polymerase chain reaction both under basal conditions and after stimulation with lipopolysaccharide (LPS). |
| 14572 | 10807946 | At the end of treatment, hepatic expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA was quantitatively determined by kinetic polymerase chain reaction both under basal conditions and after stimulation with lipopolysaccharide (LPS). |
| 14573 | 10807946 | Both untreated lean and obese mice exhibited low levels of baseline TNF-alpha and IL-6 mRNA expression and responded with a dramatic increase in hepatic cytokine transcripts and TNF-alpha protein expression following a challenge with LPS. |
| 14574 | 10807946 | Both untreated lean and obese mice exhibited low levels of baseline TNF-alpha and IL-6 mRNA expression and responded with a dramatic increase in hepatic cytokine transcripts and TNF-alpha protein expression following a challenge with LPS. |
| 14575 | 10807946 | Both untreated lean and obese mice exhibited low levels of baseline TNF-alpha and IL-6 mRNA expression and responded with a dramatic increase in hepatic cytokine transcripts and TNF-alpha protein expression following a challenge with LPS. |
| 14576 | 10807946 | Both untreated lean and obese mice exhibited low levels of baseline TNF-alpha and IL-6 mRNA expression and responded with a dramatic increase in hepatic cytokine transcripts and TNF-alpha protein expression following a challenge with LPS. |
| 14577 | 10807946 | Both untreated lean and obese mice exhibited low levels of baseline TNF-alpha and IL-6 mRNA expression and responded with a dramatic increase in hepatic cytokine transcripts and TNF-alpha protein expression following a challenge with LPS. |
| 14578 | 10807946 | Similar to the effects on white adipose tissue, troglitazone not only down-regulated the baseline levels of hepatic TNF-alpha and IL-6, but also greatly attenuated the inducing effects of LPS. |
| 14579 | 10807946 | Similar to the effects on white adipose tissue, troglitazone not only down-regulated the baseline levels of hepatic TNF-alpha and IL-6, but also greatly attenuated the inducing effects of LPS. |
| 14580 | 10807946 | Similar to the effects on white adipose tissue, troglitazone not only down-regulated the baseline levels of hepatic TNF-alpha and IL-6, but also greatly attenuated the inducing effects of LPS. |
| 14581 | 10807946 | Similar to the effects on white adipose tissue, troglitazone not only down-regulated the baseline levels of hepatic TNF-alpha and IL-6, but also greatly attenuated the inducing effects of LPS. |
| 14582 | 10807946 | Similar to the effects on white adipose tissue, troglitazone not only down-regulated the baseline levels of hepatic TNF-alpha and IL-6, but also greatly attenuated the inducing effects of LPS. |
| 14583 | 10807946 | These data demonstrate that chronic administration of troglitazone is associated with a greatly attenuated responsiveness towards inducers of hepatic TNF-alpha and IL-6 production. |
| 14584 | 10807946 | These data demonstrate that chronic administration of troglitazone is associated with a greatly attenuated responsiveness towards inducers of hepatic TNF-alpha and IL-6 production. |
| 14585 | 10807946 | These data demonstrate that chronic administration of troglitazone is associated with a greatly attenuated responsiveness towards inducers of hepatic TNF-alpha and IL-6 production. |
| 14586 | 10807946 | These data demonstrate that chronic administration of troglitazone is associated with a greatly attenuated responsiveness towards inducers of hepatic TNF-alpha and IL-6 production. |
| 14587 | 10807946 | These data demonstrate that chronic administration of troglitazone is associated with a greatly attenuated responsiveness towards inducers of hepatic TNF-alpha and IL-6 production. |
| 14588 | 10803866 | Although MHC class II genes have a stronger association with type 1 diabetes than MHC class I genes, studies have shown that MHC class I molecules play an independent role in the etiology of type 1 diabetes, and the existence of susceptibility genes within a segment of MHC between the HLA-B and TNF genes has been predicted, where MHC class I chain-related gene A (MICA) resides. |
| 14589 | 10802155 | Inhibitory effect of troglitazone on TNF-alpha-induced expression of monocyte chemoattractant protein-1 (MCP-1) in human endothelial cells. |
| 14590 | 10802155 | Inhibitory effect of troglitazone on TNF-alpha-induced expression of monocyte chemoattractant protein-1 (MCP-1) in human endothelial cells. |
| 14591 | 10802155 | Inhibitory effect of troglitazone on TNF-alpha-induced expression of monocyte chemoattractant protein-1 (MCP-1) in human endothelial cells. |
| 14592 | 10802155 | HUVECs were treated with or without troglitazone (1 or 10 microM) in the presence or absence of various concentrations of tumor necrosis factor-alpha (TNF-alpha) (5, 50 or 500 ng/ml), and then the amounts of MCP-1 secreted from the HUVECs were measured. |
| 14593 | 10802155 | HUVECs were treated with or without troglitazone (1 or 10 microM) in the presence or absence of various concentrations of tumor necrosis factor-alpha (TNF-alpha) (5, 50 or 500 ng/ml), and then the amounts of MCP-1 secreted from the HUVECs were measured. |
| 14594 | 10802155 | HUVECs were treated with or without troglitazone (1 or 10 microM) in the presence or absence of various concentrations of tumor necrosis factor-alpha (TNF-alpha) (5, 50 or 500 ng/ml), and then the amounts of MCP-1 secreted from the HUVECs were measured. |
| 14595 | 10802155 | We found that TNF-alpha increased the secretions of MCP-1 119-fold vs. control, and that troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretions (19.4%). |
| 14596 | 10802155 | We found that TNF-alpha increased the secretions of MCP-1 119-fold vs. control, and that troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretions (19.4%). |
| 14597 | 10802155 | We found that TNF-alpha increased the secretions of MCP-1 119-fold vs. control, and that troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretions (19.4%). |
| 14598 | 10798271 | Under physiological conditions endothelium mediates vascular dilatation (formation of NO, PGI2, adenosine, hyperpolarizing factor), prevents platelet adhesion and activation (production of adenosine, NO and PGI2, removal of ADP), blocks thrombin formation (tissue factor pathway inhibitor, activation of protein C via thrombomodulin, activation of antithrombin III) and mitigates fibrin deposition (t- and scuplasminogen activator production). |
| 14599 | 10798271 | This prothrombotic, proinflammatory state is characterised by vaso-constriction, platelet and leukocyte activation and adhesion (externalization, expression and upregulation of von Willebrand factor, platelet activating factor, P-selectin, ICAM-1, IL-8, MCP-1, TNF alpha, etc.), promotion of thrombin formation, coagulation and fibrin deposition at the vascular wall (expression of tissue factor, PAI-1, phosphatidyl serine, etc.) and, in platelet-leukocyte coaggregates, additional inflammatory interactions via attachment of platelet CD40-ligand to endothelial, monocyte and B-cell CD40. |
| 14600 | 10780192 | Clinical manifestations seem to be related to the production of many interleukins, mainly IL-1, IL-6 and TNF. |
| 14601 | 10778531 | GLUT-4, tumour necrosis factor, essential fatty acids and daf-genes and their role in glucose homeostasis, insulin resistance, non-insulin dependent diabetes mellitus, and longevity. |
| 14602 | 10778531 | GLUT-4, tumour necrosis factor, essential fatty acids and daf-genes and their role in glucose homeostasis, insulin resistance, non-insulin dependent diabetes mellitus, and longevity. |
| 14603 | 10778531 | GLUT-4, tumour necrosis factor, essential fatty acids and daf-genes and their role in glucose homeostasis, insulin resistance, non-insulin dependent diabetes mellitus, and longevity. |
| 14604 | 10778531 | GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes seem to play an important and essential role in the maintenance of glucose homeostasis, and in the pathobiology of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 14605 | 10778531 | GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes seem to play an important and essential role in the maintenance of glucose homeostasis, and in the pathobiology of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 14606 | 10778531 | GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes seem to play an important and essential role in the maintenance of glucose homeostasis, and in the pathobiology of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 14607 | 10778531 | Daf-genes encode for proteins which are 35% identical to the human insulin receptor, a transforming growth factor-beta (TGF-beta) type signal and can also enhance the expression of superoxide dismutase (SOD). |
| 14608 | 10778531 | Daf-genes encode for proteins which are 35% identical to the human insulin receptor, a transforming growth factor-beta (TGF-beta) type signal and can also enhance the expression of superoxide dismutase (SOD). |
| 14609 | 10778531 | Daf-genes encode for proteins which are 35% identical to the human insulin receptor, a transforming growth factor-beta (TGF-beta) type signal and can also enhance the expression of superoxide dismutase (SOD). |
| 14610 | 10778531 | On the other hand, EFAs and their metabolites can increase the cell membrane fluidity and thus, enhance the expression of GLUT-4 and insulin receptors. |
| 14611 | 10778531 | On the other hand, EFAs and their metabolites can increase the cell membrane fluidity and thus, enhance the expression of GLUT-4 and insulin receptors. |
| 14612 | 10778531 | On the other hand, EFAs and their metabolites can increase the cell membrane fluidity and thus, enhance the expression of GLUT-4 and insulin receptors. |
| 14613 | 10778531 | In addition, EFAs can suppress TNF-alpha production and secretion and thus, are capable of reversing insulin resistance. |
| 14614 | 10778531 | In addition, EFAs can suppress TNF-alpha production and secretion and thus, are capable of reversing insulin resistance. |
| 14615 | 10778531 | In addition, EFAs can suppress TNF-alpha production and secretion and thus, are capable of reversing insulin resistance. |
| 14616 | 10778531 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 14617 | 10778531 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 14618 | 10778531 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 14619 | 10778531 | Hence, it is likely that there is a close interaction between GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin that may have relevance to the development of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 14620 | 10778531 | Hence, it is likely that there is a close interaction between GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin that may have relevance to the development of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 14621 | 10778531 | Hence, it is likely that there is a close interaction between GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin that may have relevance to the development of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 14622 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 14623 | 10773364 | The popliteal lymph node response to streptozotocin is under type 1, MHC class-I restricted, CD8(+) T-cell control. |
| 14624 | 10773364 | In order to determine whether PLN responses involve CD4(+) or CD8(+) T-cells, the effects of streptozotocin (STZ), a prototypic immunotoxic compound, were analyzed after injection into the hind footpad of C57 BL/6 mice and major histocompatibility complex (MHC) class I or II deficient mice. |
| 14625 | 10773364 | In order to determine whether PLN responses involve CD4(+) or CD8(+) T-cells, the effects of streptozotocin (STZ), a prototypic immunotoxic compound, were analyzed after injection into the hind footpad of C57 BL/6 mice and major histocompatibility complex (MHC) class I or II deficient mice. |
| 14626 | 10773364 | The involvement of type 1 or type 2 cell control on the production of cytokine mRNAs was analyzed in lymph node cells by quantitative RT-PCR, together with the analysis of a wide range of cytokine mRNAs after STZ injection (IL-1alpha, IL-1beta, TNF-alpha, IFN-gamma, IL-2, IL-2 receptor, IL-4, IL-5, IL-6, IL-10 and IL-12). |
| 14627 | 10773364 | The involvement of type 1 or type 2 cell control on the production of cytokine mRNAs was analyzed in lymph node cells by quantitative RT-PCR, together with the analysis of a wide range of cytokine mRNAs after STZ injection (IL-1alpha, IL-1beta, TNF-alpha, IFN-gamma, IL-2, IL-2 receptor, IL-4, IL-5, IL-6, IL-10 and IL-12). |
| 14628 | 10773364 | We have found that mice depleted in CD8(+) T-cells did not respond to STZ, whereas mice depleted in CD4(+) T-cells exhibited the expected positive PLN responses, with increased weight and cellularity indices. |
| 14629 | 10773364 | We have found that mice depleted in CD8(+) T-cells did not respond to STZ, whereas mice depleted in CD4(+) T-cells exhibited the expected positive PLN responses, with increased weight and cellularity indices. |
| 14630 | 10773364 | STZ induced a low production of interleukin (IL)-2 mRNAs, a mild increase in IL-1alpha and IL-6 mRNAs production, and a dramatic increase in IFN-gamma, IL-1beta, TNF-alpha, IL-12 and IL-2 receptor mRNAs, which correlated with positive PLN responses. |
| 14631 | 10773364 | STZ induced a low production of interleukin (IL)-2 mRNAs, a mild increase in IL-1alpha and IL-6 mRNAs production, and a dramatic increase in IFN-gamma, IL-1beta, TNF-alpha, IL-12 and IL-2 receptor mRNAs, which correlated with positive PLN responses. |
| 14632 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 14633 | 10773364 | No effects on IL-4, IL-5 and IL-10 mRNAs synthesis were noted. |
| 14634 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 14635 | 10773364 | In CD8(+) T-cell deficient mice, there was no production of IFN-gamma or IL-6 mRNAs. |
| 14636 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 14637 | 10773364 | These results suggest that PLN responses to STZ are under the control of type 1, MHC class-I-restricted, CD8(+) T-cells. |
| 14638 | 10773354 | Identification of four novel dinucleotide repeat polymorphisms in the TNF-alpha and TNF-beta genes. |
| 14639 | 10772656 | Moreover, we noted decreased generation of the proinflammatory cytokines TNF-alpha and IL-6 in gingival tissue, as well as decreased levels of matrix metalloproteinases. |
| 14640 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14641 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14642 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14643 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14644 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14645 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14646 | 10771998 | Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM. |
| 14647 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14648 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14649 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14650 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14651 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14652 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14653 | 10771998 | In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. |
| 14654 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14655 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14656 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14657 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14658 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14659 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14660 | 10771998 | We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. |
| 14661 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14662 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14663 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14664 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14665 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14666 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14667 | 10771998 | IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). |
| 14668 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14669 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14670 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14671 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14672 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14673 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14674 | 10771998 | IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. |
| 14675 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14676 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14677 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14678 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14679 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14680 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14681 | 10771998 | Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. |
| 14682 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14683 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14684 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14685 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14686 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14687 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14688 | 10771998 | The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). |
| 14689 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14690 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14691 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14692 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14693 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14694 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14695 | 10771998 | In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction. |
| 14696 | 10770222 | The -238 and -308 G-->A polymorphisms of the tumor necrosis factor alpha gene promoter are not associated with features of the insulin resistance syndrome or altered birth weight in Danish Caucasians. |
| 14697 | 10770222 | The -238 and -308 G-->A polymorphisms of the tumor necrosis factor alpha gene promoter are not associated with features of the insulin resistance syndrome or altered birth weight in Danish Caucasians. |
| 14698 | 10770222 | The -238 and -308 G-->A polymorphisms of the tumor necrosis factor alpha gene promoter are not associated with features of the insulin resistance syndrome or altered birth weight in Danish Caucasians. |
| 14699 | 10770222 | The objective of the present study was to investigate whether these genetic variants of TNF-alpha were associated with features of the insulin resistance syndrome or alterations in birth weight in two Danish study populations comprising 380 unrelated young healthy subjects and 249 glucose-tolerant relatives of type 2 diabetic patients, respectively. |
| 14700 | 10770222 | The objective of the present study was to investigate whether these genetic variants of TNF-alpha were associated with features of the insulin resistance syndrome or alterations in birth weight in two Danish study populations comprising 380 unrelated young healthy subjects and 249 glucose-tolerant relatives of type 2 diabetic patients, respectively. |
| 14701 | 10770222 | The objective of the present study was to investigate whether these genetic variants of TNF-alpha were associated with features of the insulin resistance syndrome or alterations in birth weight in two Danish study populations comprising 380 unrelated young healthy subjects and 249 glucose-tolerant relatives of type 2 diabetic patients, respectively. |
| 14702 | 10770222 | In conclusion, although the study was carried out on sufficiently large study samples, the study does not support a major role of the -308 or -238 substitutions of the TNF-alpha gene in the pathogenesis of insulin resistance or altered birth weight among Danish Caucasian subjects. |
| 14703 | 10770222 | In conclusion, although the study was carried out on sufficiently large study samples, the study does not support a major role of the -308 or -238 substitutions of the TNF-alpha gene in the pathogenesis of insulin resistance or altered birth weight among Danish Caucasian subjects. |
| 14704 | 10770222 | In conclusion, although the study was carried out on sufficiently large study samples, the study does not support a major role of the -308 or -238 substitutions of the TNF-alpha gene in the pathogenesis of insulin resistance or altered birth weight among Danish Caucasian subjects. |
| 14705 | 10760829 | Pancreatic cancer cells are usually resistant to apoptosis induced by cytotoxic drugs, by activation of surface receptors such as Fas and TNF receptor or by serum or growth factor withdrawal. |
| 14706 | 10760829 | Pancreatic cancer cells are usually resistant to apoptosis induced by cytotoxic drugs, by activation of surface receptors such as Fas and TNF receptor or by serum or growth factor withdrawal. |
| 14707 | 10760829 | Induction of apoptosis correlated with activation of the JNK/SAPK pathway and increased expression of Bax but not Bad or p53. |
| 14708 | 10760829 | Induction of apoptosis correlated with activation of the JNK/SAPK pathway and increased expression of Bax but not Bad or p53. |
| 14709 | 10760829 | PANC-1 cells were completely resistant to Fas antibody and TNF-alpha. |
| 14710 | 10760829 | PANC-1 cells were completely resistant to Fas antibody and TNF-alpha. |
| 14711 | 10760829 | EGF, FGF-2 and IGF-I did not protect PANC-1 cells from actD-mediated apoptosis. |
| 14712 | 10760829 | EGF, FGF-2 and IGF-I did not protect PANC-1 cells from actD-mediated apoptosis. |
| 14713 | 10760829 | Our observations suggest that actD may act via JNK/SAPK and Bax to promote apoptosis in PANC-1 cells and that it may inhibit the growth of other pancreatic cancer cell lines. |
| 14714 | 10760829 | Our observations suggest that actD may act via JNK/SAPK and Bax to promote apoptosis in PANC-1 cells and that it may inhibit the growth of other pancreatic cancer cell lines. |
| 14715 | 10756100 | cDNA cloning and mapping of a novel islet-brain/JNK-interacting protein. |
| 14716 | 10756100 | IB1/JIP-1 is a scaffold protein that regulates the c-Jun NH(2)-terminal kinase (JNK) signaling pathway, which is activated by environmental stresses and/or by treatment with proinflammatory cytokines including IL-1beta and TNF-alpha. |
| 14717 | 10756100 | Overall, both IB1 and IB2 proteins share a very similar organization, with a JNK-binding domain, a Src homology 3 domain, a phosphotyrosine-interacting domain, and polyacidic and polyproline stretches located at similar positions. |
| 14718 | 10756100 | Northern and RT-PCR analyses indicate that IB2 is expressed in brain and in pancreatic cells, including insulin-secreting cells. |
| 14719 | 10756100 | IB2 interacts with both JNK and the JNK-kinase MKK7. |
| 14720 | 10756100 | In addition, ectopic expression of the JNK-binding domain of IB2 decreases IL-1beta-induced pancreatic beta-cell death. |
| 14721 | 10756100 | These data establish IB2 as a novel scaffold protein that regulates the JNK signaling pathway in brain and pancreatic beta-cells and indicate that IB2 represents a novel candidate gene for diabetes. |
| 14722 | 10748653 | Carr suggests that such drugs should have this lipid-increasing effect because of their inhibition of low density lipoprotein-receptor-related protein, cytoplasmic retinoic-acid binding protein type 1 and P450 3A cytochrome. |
| 14723 | 10748653 | According to another hypothesis Tumor necrosis factor-alpha, through inhibition of lipoprotein-lipase, would determine high fat-storage in the adipose tissue. |
| 14724 | 10746656 | Thus, supernatants of islets from these mice contained increased levels of interleukin (IL)-4, IL-10, and, to a lesser extent, interferon-gamma and diminished levels of tumor necrosis factor-a compared with controls. |
| 14725 | 10746656 | Thus, supernatants of islets from these mice contained increased levels of interleukin (IL)-4, IL-10, and, to a lesser extent, interferon-gamma and diminished levels of tumor necrosis factor-a compared with controls. |
| 14726 | 10746656 | Because exogenous IL-4 and IL-10 exert antidiabetogenic effect in NOD mice and early blockade of endogenous tumor necrosis factor-alpha prevents NOD mouse diabetes, these phenomena may be causally related to the antidiabetogenic effect of HGG-pulsed DC treatment. |
| 14727 | 10746656 | Because exogenous IL-4 and IL-10 exert antidiabetogenic effect in NOD mice and early blockade of endogenous tumor necrosis factor-alpha prevents NOD mouse diabetes, these phenomena may be causally related to the antidiabetogenic effect of HGG-pulsed DC treatment. |
| 14728 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 14729 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 14730 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 14731 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 14732 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 14733 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 14734 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 14735 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 14736 | 10726910 | Leptin levels were significantly decreased, while tumor necrosis factor alpha (TNF-alpha) levels were not changed. |
| 14737 | 10722755 | The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307). |
| 14738 | 10722755 | The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307). |
| 14739 | 10722755 | The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307). |
| 14740 | 10722755 | The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307). |
| 14741 | 10722755 | Tumor necrosis factor alpha (TNFalpha) inhibits insulin action, in part, through serine phosphorylation of IRS proteins; however, the phosphorylation sites that mediate the inhibition are unknown. |
| 14742 | 10722755 | Tumor necrosis factor alpha (TNFalpha) inhibits insulin action, in part, through serine phosphorylation of IRS proteins; however, the phosphorylation sites that mediate the inhibition are unknown. |
| 14743 | 10722755 | Tumor necrosis factor alpha (TNFalpha) inhibits insulin action, in part, through serine phosphorylation of IRS proteins; however, the phosphorylation sites that mediate the inhibition are unknown. |
| 14744 | 10722755 | Tumor necrosis factor alpha (TNFalpha) inhibits insulin action, in part, through serine phosphorylation of IRS proteins; however, the phosphorylation sites that mediate the inhibition are unknown. |
| 14745 | 10722755 | TNFalpha promotes multipotential signal transduction cascades, including the activation of the Jun NH(2)-terminal kinase (JNK). |
| 14746 | 10722755 | TNFalpha promotes multipotential signal transduction cascades, including the activation of the Jun NH(2)-terminal kinase (JNK). |
| 14747 | 10722755 | TNFalpha promotes multipotential signal transduction cascades, including the activation of the Jun NH(2)-terminal kinase (JNK). |
| 14748 | 10722755 | TNFalpha promotes multipotential signal transduction cascades, including the activation of the Jun NH(2)-terminal kinase (JNK). |
| 14749 | 10722755 | Endogenous JNK associates with IRS-1 in Chinese hamster ovary cells. |
| 14750 | 10722755 | Endogenous JNK associates with IRS-1 in Chinese hamster ovary cells. |
| 14751 | 10722755 | Endogenous JNK associates with IRS-1 in Chinese hamster ovary cells. |
| 14752 | 10722755 | Endogenous JNK associates with IRS-1 in Chinese hamster ovary cells. |
| 14753 | 10722755 | Anisomycin, a strong activator of JNK in these cells, stimulates the activity of JNK bound to IRS-1 and inhibits the insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14754 | 10722755 | Anisomycin, a strong activator of JNK in these cells, stimulates the activity of JNK bound to IRS-1 and inhibits the insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14755 | 10722755 | Anisomycin, a strong activator of JNK in these cells, stimulates the activity of JNK bound to IRS-1 and inhibits the insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14756 | 10722755 | Anisomycin, a strong activator of JNK in these cells, stimulates the activity of JNK bound to IRS-1 and inhibits the insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14757 | 10722755 | Serine 307 is a major site of JNK phosphorylation in IRS-1. |
| 14758 | 10722755 | Serine 307 is a major site of JNK phosphorylation in IRS-1. |
| 14759 | 10722755 | Serine 307 is a major site of JNK phosphorylation in IRS-1. |
| 14760 | 10722755 | Serine 307 is a major site of JNK phosphorylation in IRS-1. |
| 14761 | 10722755 | Mutation of serine 307 to alanine eliminates phosphorylation of IRS-1 by JNK and abrogates the inhibitory effect of TNFalpha on insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14762 | 10722755 | Mutation of serine 307 to alanine eliminates phosphorylation of IRS-1 by JNK and abrogates the inhibitory effect of TNFalpha on insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14763 | 10722755 | Mutation of serine 307 to alanine eliminates phosphorylation of IRS-1 by JNK and abrogates the inhibitory effect of TNFalpha on insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14764 | 10722755 | Mutation of serine 307 to alanine eliminates phosphorylation of IRS-1 by JNK and abrogates the inhibitory effect of TNFalpha on insulin-stimulated tyrosine phosphorylation of IRS-1. |
| 14765 | 10722755 | These results suggest that phosphorylation of serine 307 might mediate, at least partially, the inhibitory effect of proinflammatory cytokines like TNFalpha on IRS-1 function. |
| 14766 | 10722755 | These results suggest that phosphorylation of serine 307 might mediate, at least partially, the inhibitory effect of proinflammatory cytokines like TNFalpha on IRS-1 function. |
| 14767 | 10722755 | These results suggest that phosphorylation of serine 307 might mediate, at least partially, the inhibitory effect of proinflammatory cytokines like TNFalpha on IRS-1 function. |
| 14768 | 10722755 | These results suggest that phosphorylation of serine 307 might mediate, at least partially, the inhibitory effect of proinflammatory cytokines like TNFalpha on IRS-1 function. |
| 14769 | 10720082 | No increased insulin sensitivity after a single intravenous administration of a recombinant human tumor necrosis factor receptor: Fc fusion protein in obese insulin-resistant patients. |
| 14770 | 10720082 | No increased insulin sensitivity after a single intravenous administration of a recombinant human tumor necrosis factor receptor: Fc fusion protein in obese insulin-resistant patients. |
| 14771 | 10720082 | No increased insulin sensitivity after a single intravenous administration of a recombinant human tumor necrosis factor receptor: Fc fusion protein in obese insulin-resistant patients. |
| 14772 | 10720082 | Inhibition of tumor necrosis factor (TNF)-alpha results in a marked increase in insulin sensitivity in obese rodents. |
| 14773 | 10720082 | Inhibition of tumor necrosis factor (TNF)-alpha results in a marked increase in insulin sensitivity in obese rodents. |
| 14774 | 10720082 | Inhibition of tumor necrosis factor (TNF)-alpha results in a marked increase in insulin sensitivity in obese rodents. |
| 14775 | 10720082 | We investigated the influence of a TNF antagonist [Ro 45-2081, a recombinant fusion protein that consists of the soluble TNF-receptor (p55) linked to the Fc portion of human IgG1] on insulin sensitivity of patients with android obesity. |
| 14776 | 10720082 | We investigated the influence of a TNF antagonist [Ro 45-2081, a recombinant fusion protein that consists of the soluble TNF-receptor (p55) linked to the Fc portion of human IgG1] on insulin sensitivity of patients with android obesity. |
| 14777 | 10720082 | We investigated the influence of a TNF antagonist [Ro 45-2081, a recombinant fusion protein that consists of the soluble TNF-receptor (p55) linked to the Fc portion of human IgG1] on insulin sensitivity of patients with android obesity. |
| 14778 | 10720082 | In conclusion, under the conditions of this study, no improvement in insulin sensitivity was observed in obese insulin-resistant patients following a single i.v. administration of a recombinant TNF receptor: Fc fusion protein. |
| 14779 | 10720082 | In conclusion, under the conditions of this study, no improvement in insulin sensitivity was observed in obese insulin-resistant patients following a single i.v. administration of a recombinant TNF receptor: Fc fusion protein. |
| 14780 | 10720082 | In conclusion, under the conditions of this study, no improvement in insulin sensitivity was observed in obese insulin-resistant patients following a single i.v. administration of a recombinant TNF receptor: Fc fusion protein. |
| 14781 | 10707937 | Sections from the pancreata of these injected mice were stained for cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], CD1d, interleukin 2 [IL-2], IL-4, IL-6, IL-10, and IL-12). |
| 14782 | 10707937 | The expression of IL-2 and IL-12 was very scarce. |
| 14783 | 10707936 | Neither the pancreata of normal BALB/c mice nor NOD mice at 2-16 weeks of age contained tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), IL-4, or IL-12. |
| 14784 | 10707936 | At 8 weeks of age, a few IL-2+ cells were found in the pancreas of one of three NOD mice. |
| 14785 | 10707567 | In muscle cells, the number of insulin receptor, the function of glucose transporter 4 and the activity of tyrosine kinase decrease. |
| 14786 | 10707567 | The rink of body fat accumulation and insulin resistance in muscle is thought through free fatty acid and tumor necrosis factor alpha secreted in adipose tissue. |
| 14787 | 10707560 | TNF-alpha causes insulin resistance through inhibition of the insulin signal transduction and TZDs have been shown to reduce insulin resistance by the suppression of the TNF-alpha gene expression. |
| 14788 | 10707552 | Tumor necrosis factor(TNF)-alpha is also synthesized by adipocytes, and is involved in the expression of peripheral insulin resistance. |
| 14789 | 10707552 | Tumor necrosis factor(TNF)-alpha is also synthesized by adipocytes, and is involved in the expression of peripheral insulin resistance. |
| 14790 | 10707552 | This review deals with molecular mechanisms of the TNF/TNF receptor system promoting insulin resistance, and its prevention by the insulin-sensitizing drugs, thiazolidinediones. |
| 14791 | 10707552 | This review deals with molecular mechanisms of the TNF/TNF receptor system promoting insulin resistance, and its prevention by the insulin-sensitizing drugs, thiazolidinediones. |
| 14792 | 10707549 | Since the molecular mechanism of insulin resistance is still unknown, insulin receptor dysfunction including abnormal IRS-1 phosphorylation is considered to be responsible for insulin resistance in some pathological states. |
| 14793 | 10707549 | Regarding the mechanism of insulin resistance related obesity, the increased expression of Tumor necrosis factor alpha and abnormality in PTPase in skeletal muscle are postulated. |
| 14794 | 10703602 | Analysis of tumor necrosis factor-alpha promoter polymorphism in type 1 diabetes: HLA-B and -DRB1 alleles are primarily associated with the disease in Japanese. |
| 14795 | 10703602 | Analysis of tumor necrosis factor-alpha promoter polymorphism in type 1 diabetes: HLA-B and -DRB1 alleles are primarily associated with the disease in Japanese. |
| 14796 | 10703602 | Since these TNF-alpha alleles are in linkage disequilibria with certain DRB1 and HLA-B alleles, two-locus analyses were carried out. |
| 14797 | 10703602 | Since these TNF-alpha alleles are in linkage disequilibria with certain DRB1 and HLA-B alleles, two-locus analyses were carried out. |
| 14798 | 10703602 | Because HLA-B and DRB1 genes were independently associated, both of these genes may be contributed primarily to the pathogenesis of type 1 diabetes in Japanese. |
| 14799 | 10703602 | Because HLA-B and DRB1 genes were independently associated, both of these genes may be contributed primarily to the pathogenesis of type 1 diabetes in Japanese. |
| 14800 | 10679090 | Several apoptotic pathways have been implicated in beta cell destruction, including Fas, perforin, and TNF-alpha. |
| 14801 | 10679090 | Evidence for Fas-mediated lysis of beta cells in the pathogenesis of IDDM in nonobese diabetic (NOD) mice includes: 1) Fas-deficient NOD mice bearing the lpr mutation (NOD-lpr/lpr) fail to develop IDDM; 2) transgenic expression of Fas ligand (FasL) on beta cells in NOD mice may result in accelerated IDDM; and 3) irradiated NOD-lpr/lpr mice are resistant to adoptive transfer of diabetes by cells from NOD mice. |
| 14802 | 10679090 | Here we present novel evidence for the role of Fas/FasL interactions in the progression of NOD diabetes using two newly derived mouse strains. |
| 14803 | 10679090 | We show that NOD mice heterozygous for the FasL mutation gld, which have reduced functional FasL expression on T cells but no lymphadenopathy, fail to develop IDDM. |
| 14804 | 10679090 | Further, we show that NOD-lpr/lpr mice bearing the scid mutation (NOD-lpr/lpr-scid/scid), which eliminates the enhanced FasL-mediated lytic activity induced by Fas deficiency, still have delayed onset and reduced incidence of IDDM after adoptive transfer of diabetogenic NOD spleen cells. |
| 14805 | 10679090 | These results provide evidence that Fas/FasL-mediated programmed cell death plays a significant role in the pathogenesis of autoimmune diabetes. |
| 14806 | 10690939 | Inhibitory effect of troglitazone on tumor necrosis factor alpha-induced expression of monocyte chemoattractant protein-1 in human mesangial cells. |
| 14807 | 10690939 | Inhibitory effect of troglitazone on tumor necrosis factor alpha-induced expression of monocyte chemoattractant protein-1 in human mesangial cells. |
| 14808 | 10690939 | Inhibitory effect of troglitazone on tumor necrosis factor alpha-induced expression of monocyte chemoattractant protein-1 in human mesangial cells. |
| 14809 | 10690939 | Inhibitory effect of troglitazone on tumor necrosis factor alpha-induced expression of monocyte chemoattractant protein-1 in human mesangial cells. |
| 14810 | 10690939 | HMCs were treated with or without troglitazone (1 or 10 micromol/L) in the presence or absence of tumor necrosis factor alpha (TNF-alpha) at various concentrations (50 or 500 ng/mL), and then MCP-1 secretion from the HMCs was measured. |
| 14811 | 10690939 | HMCs were treated with or without troglitazone (1 or 10 micromol/L) in the presence or absence of tumor necrosis factor alpha (TNF-alpha) at various concentrations (50 or 500 ng/mL), and then MCP-1 secretion from the HMCs was measured. |
| 14812 | 10690939 | HMCs were treated with or without troglitazone (1 or 10 micromol/L) in the presence or absence of tumor necrosis factor alpha (TNF-alpha) at various concentrations (50 or 500 ng/mL), and then MCP-1 secretion from the HMCs was measured. |
| 14813 | 10690939 | HMCs were treated with or without troglitazone (1 or 10 micromol/L) in the presence or absence of tumor necrosis factor alpha (TNF-alpha) at various concentrations (50 or 500 ng/mL), and then MCP-1 secretion from the HMCs was measured. |
| 14814 | 10690939 | We found that TNF-alpha increased the secretion of MCP-1 by 55-fold versus the control and troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretion (49.3%). |
| 14815 | 10690939 | We found that TNF-alpha increased the secretion of MCP-1 by 55-fold versus the control and troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretion (49.3%). |
| 14816 | 10690939 | We found that TNF-alpha increased the secretion of MCP-1 by 55-fold versus the control and troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretion (49.3%). |
| 14817 | 10690939 | We found that TNF-alpha increased the secretion of MCP-1 by 55-fold versus the control and troglitazone significantly inhibited this TNF-alpha-induced increase in MCP-1 secretion (49.3%). |
| 14818 | 10690939 | We demonstrated that alpha-tocopherol also inhibited TNF-alpha-induced MCP-1 production in HMCs, although its effects were not as strong as troglitazone. |
| 14819 | 10690939 | We demonstrated that alpha-tocopherol also inhibited TNF-alpha-induced MCP-1 production in HMCs, although its effects were not as strong as troglitazone. |
| 14820 | 10690939 | We demonstrated that alpha-tocopherol also inhibited TNF-alpha-induced MCP-1 production in HMCs, although its effects were not as strong as troglitazone. |
| 14821 | 10690939 | We demonstrated that alpha-tocopherol also inhibited TNF-alpha-induced MCP-1 production in HMCs, although its effects were not as strong as troglitazone. |
| 14822 | 10690898 | Interferon-gamma induces interleukin-1 converting enzyme expression in pancreatic islets by an interferon regulatory factor-1-dependent mechanism. |
| 14823 | 10690898 | The cysteine protease interleukin (IL)-1 converting enzyme (ICE) is a key proapoptotic caspase. |
| 14824 | 10690898 | ICE messenger RNA (mRNA) expression was highly up-regulated after 6-, 24-, and 72-h exposure of human islets to interferon (IFN)gamma, tumor necrosis factor (TNF)alpha + IFNgamma or IL-1beta + TNFalpha + IFNgamma, paralleled by increased iNOS (the inducible form of NO synthase) expression and NO production after exposure to the combined cytokines but not to IFNgamma or TNFalpha + IFNgamma. |
| 14825 | 10690898 | Cytokine-induced NO-independent ICE transcription was confirmed using iNOS inhibitors. |
| 14826 | 10690898 | Exposure of rat and mouse islets, or rat insulinoma cells, for 24 h to IFNgamma alone or in combination with the two other cytokines also resulted in a highly significant ICE mRNA expression. |
| 14827 | 10690898 | ICE transcription was not inducible in islets from IFN regulatory factor-1 knock-out mice, suggesting a key-role of this transcription-factor in cytokine-mediated ICE expression in pancreatic islets. |
| 14828 | 10690898 | In conclusion, cytokines and IFNgamma in particular increase ICE mRNA expression in pancreatic islet cells and beta-cell lines, independently of NO synthesis, suggesting that ICE up-regulation may be involved in cytokine-induced NO-independent apoptosis of human islets. |
| 14829 | 10688666 | Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. |
| 14830 | 10688666 | Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. |
| 14831 | 10688666 | Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. |
| 14832 | 10688666 | Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. |
| 14833 | 10688666 | Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. |
| 14834 | 10688666 | The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. |
| 14835 | 10688666 | The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. |
| 14836 | 10688666 | The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. |
| 14837 | 10688666 | The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. |
| 14838 | 10688666 | The stress-activated protein kinases (SAPKs, also called c-Jun NH(2)-terminal kinases) and the p38s, two mitogen-activated protein kinase (MAPK) subgroups activated by cytokines of the tumor necrosis factor (TNF) family, are pivotal to the de novo gene expression elicited as part of the inflammatory response. |
| 14839 | 10688666 | Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. |
| 14840 | 10688666 | Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. |
| 14841 | 10688666 | Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. |
| 14842 | 10688666 | Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. |
| 14843 | 10688666 | Apoptosis signal-regulating kinase 1 (ASK1) is a MAPK kinase kinase (MAP3K) that activates both the SAPKs and p38s in vivo. |
| 14844 | 10688666 | Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. |
| 14845 | 10688666 | Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. |
| 14846 | 10688666 | Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. |
| 14847 | 10688666 | Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. |
| 14848 | 10688666 | Here we show that TNF receptor (TNFR) associated factor 2 (TRAF2), an adapter protein that couples TNFRs to the SAPKs and p38s, can activate ASK1 in vivo and can interact in vivo with the amino- and carboxyl-terminal noncatalytic domains of the ASK1 polypeptide. |
| 14849 | 10688666 | Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. |
| 14850 | 10688666 | Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. |
| 14851 | 10688666 | Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. |
| 14852 | 10688666 | Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. |
| 14853 | 10688666 | Expression of the amino-terminal noncatalytic domain of ASK1 can inhibit TNF and TRAF2 activation of SAPK. |
| 14854 | 10688666 | TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. |
| 14855 | 10688666 | TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. |
| 14856 | 10688666 | TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. |
| 14857 | 10688666 | TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. |
| 14858 | 10688666 | TNF can stimulate the production of reactive oxygen species (ROS), and the redox-sensing enzyme thioredoxin (Trx) is an endogenous inhibitor of ASK1. |
| 14859 | 10688666 | We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. |
| 14860 | 10688666 | We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. |
| 14861 | 10688666 | We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. |
| 14862 | 10688666 | We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. |
| 14863 | 10688666 | We demonstrate that Trx significantly inhibits TRAF2 activation of SAPK and blocks the ASK1-TRAF2 interaction in a reaction reversed by oxidants. |
| 14864 | 10688666 | We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. |
| 14865 | 10688666 | We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. |
| 14866 | 10688666 | We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. |
| 14867 | 10688666 | We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. |
| 14868 | 10688666 | We show that expression of ASK1 with TRAF2 enhances in vivo ASK1 homo-oligomerization in a manner dependent, in part, upon the TRAF2 RING effector domain and the generation of ROS. |
| 14869 | 10688666 | Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization. |
| 14870 | 10688666 | Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization. |
| 14871 | 10688666 | Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization. |
| 14872 | 10688666 | Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization. |
| 14873 | 10688666 | Thus, activation of ASK1 by TNF requires the ROS-mediated dissociation of Trx possibly followed by the binding of TRAF2 and consequent ASK1 homo-oligomerization. |
| 14874 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 14875 | 10684857 | Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability. |
| 14876 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 14877 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 14878 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 14879 | 10684857 | We also found that costimulation with anti-CD3/CD40L resulted in enhanced production of interleukin (IL)-10, interferon gamma, and tumor necrosis factor alpha but not IL-2 or IL-6. |
| 14880 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 14881 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 14882 | 10681642 | In CRF patients, there is insulin resistance and high circulating levels of tumor necrosis factor and other cytokines. |
| 14883 | 10670906 | It has been suggested that cytokines released by monocytes/macrophages, including interleukin-1beta (IL-1beta), interleukin-12 (IL-12) and tumour necrosis factor-alpha (TNF-alpha) could have an initial role in islet B-cell damage. |
| 14884 | 10670906 | It has been suggested that cytokines released by monocytes/macrophages, including interleukin-1beta (IL-1beta), interleukin-12 (IL-12) and tumour necrosis factor-alpha (TNF-alpha) could have an initial role in islet B-cell damage. |
| 14885 | 10670906 | It has been suggested that cytokines released by monocytes/macrophages, including interleukin-1beta (IL-1beta), interleukin-12 (IL-12) and tumour necrosis factor-alpha (TNF-alpha) could have an initial role in islet B-cell damage. |
| 14886 | 10670906 | It has been suggested that cytokines released by monocytes/macrophages, including interleukin-1beta (IL-1beta), interleukin-12 (IL-12) and tumour necrosis factor-alpha (TNF-alpha) could have an initial role in islet B-cell damage. |
| 14887 | 10670906 | Cytokine levels (IL-1beta, IL-12, and TNF-alpha) in the supernatants of whole blood cultures incubated with PHA alone (10 microg/ml), or PHA + human insulin (50 microg/ml), or PHA + nicotinamide (100 micromol/l) were quantified by ELISA. |
| 14888 | 10670906 | Cytokine levels (IL-1beta, IL-12, and TNF-alpha) in the supernatants of whole blood cultures incubated with PHA alone (10 microg/ml), or PHA + human insulin (50 microg/ml), or PHA + nicotinamide (100 micromol/l) were quantified by ELISA. |
| 14889 | 10670906 | Cytokine levels (IL-1beta, IL-12, and TNF-alpha) in the supernatants of whole blood cultures incubated with PHA alone (10 microg/ml), or PHA + human insulin (50 microg/ml), or PHA + nicotinamide (100 micromol/l) were quantified by ELISA. |
| 14890 | 10670906 | Cytokine levels (IL-1beta, IL-12, and TNF-alpha) in the supernatants of whole blood cultures incubated with PHA alone (10 microg/ml), or PHA + human insulin (50 microg/ml), or PHA + nicotinamide (100 micromol/l) were quantified by ELISA. |
| 14891 | 10670906 | In the cultures with nicotinamide the concentration of IL-12 and TNF-alpha was significantly lower in the prediabetic group, diabetic patients, and the healthy controls than in the cultures with PHA only or with PHA + insulin. |
| 14892 | 10670906 | In the cultures with nicotinamide the concentration of IL-12 and TNF-alpha was significantly lower in the prediabetic group, diabetic patients, and the healthy controls than in the cultures with PHA only or with PHA + insulin. |
| 14893 | 10670906 | In the cultures with nicotinamide the concentration of IL-12 and TNF-alpha was significantly lower in the prediabetic group, diabetic patients, and the healthy controls than in the cultures with PHA only or with PHA + insulin. |
| 14894 | 10670906 | In the cultures with nicotinamide the concentration of IL-12 and TNF-alpha was significantly lower in the prediabetic group, diabetic patients, and the healthy controls than in the cultures with PHA only or with PHA + insulin. |
| 14895 | 10670906 | This suggests that nicotinamide could influence monocyte/macrophage function in peripheral blood by inhibiting production of IL-12 and TNF-alpha. |
| 14896 | 10670906 | This suggests that nicotinamide could influence monocyte/macrophage function in peripheral blood by inhibiting production of IL-12 and TNF-alpha. |
| 14897 | 10670906 | This suggests that nicotinamide could influence monocyte/macrophage function in peripheral blood by inhibiting production of IL-12 and TNF-alpha. |
| 14898 | 10670906 | This suggests that nicotinamide could influence monocyte/macrophage function in peripheral blood by inhibiting production of IL-12 and TNF-alpha. |
| 14899 | 10668912 | The role of TNF-alpha in human adipose tissue: prevention of weight gain at the expense of insulin resistance? |
| 14900 | 10668912 | This antiadipogenic property is accompanied by suppression of developmental and metabolic markers of fat cell differentiation, such as peroxisome proliferator-activated receptor (PPAR)-gamma2, lipoprotein lipase (LPL), glycerol-3-phosphate dehydrogenase (GPDH) and GLUT4. |
| 14901 | 10657556 | IL-6 decreases lipoprotein lipase (LPL) activity and monomeric LPL levels in plasma, which increases macrophage uptake of lipids. |
| 14902 | 10657556 | In fatty streaks and in the atheromatous 'cap' and 'shoulder' regions, macrophage foam cells and smooth muscle cells (SMC) express IL-6, suggesting a role for this cytokine along with interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha), in the progression of atherosclerosis. |
| 14903 | 10657556 | Furthermore, circulating IL-6 stimulates the hypothalamic-pituitary-adrenal (HPA) axis, activation of which is associated with central obesity, hypertension and insulin resistance. |
| 14904 | 10654615 | Tumor necrosis factor-alpha-induced insulin resistance in adipocytes. |
| 14905 | 10654615 | Tumor necrosis factor-alpha-induced insulin resistance in adipocytes. |
| 14906 | 10654615 | Tumor necrosis factor-alpha-induced insulin resistance in adipocytes. |
| 14907 | 10654615 | Tumor necrosis factor-alpha-induced insulin resistance in adipocytes. |
| 14908 | 10654615 | Recent studies examining the link between insulin resistance and the development of obesity and noninsulin-dependent diabetes mellitus are consistent with the involvement of tumor necrosis factor-alpha (TNF-alpha) as a central mediator. |
| 14909 | 10654615 | Recent studies examining the link between insulin resistance and the development of obesity and noninsulin-dependent diabetes mellitus are consistent with the involvement of tumor necrosis factor-alpha (TNF-alpha) as a central mediator. |
| 14910 | 10654615 | Recent studies examining the link between insulin resistance and the development of obesity and noninsulin-dependent diabetes mellitus are consistent with the involvement of tumor necrosis factor-alpha (TNF-alpha) as a central mediator. |
| 14911 | 10654615 | Recent studies examining the link between insulin resistance and the development of obesity and noninsulin-dependent diabetes mellitus are consistent with the involvement of tumor necrosis factor-alpha (TNF-alpha) as a central mediator. |
| 14912 | 10654615 | In insulin resistant obese mouse models, neutralization of TNF-alpha in circulation has been demonstrated to restore insulin-mediated glucose uptake. |
| 14913 | 10654615 | In insulin resistant obese mouse models, neutralization of TNF-alpha in circulation has been demonstrated to restore insulin-mediated glucose uptake. |
| 14914 | 10654615 | In insulin resistant obese mouse models, neutralization of TNF-alpha in circulation has been demonstrated to restore insulin-mediated glucose uptake. |
| 14915 | 10654615 | In insulin resistant obese mouse models, neutralization of TNF-alpha in circulation has been demonstrated to restore insulin-mediated glucose uptake. |
| 14916 | 10654615 | Mechanistic studies in cell culture have suggested that TNF-alpha functions to render cells insulin resistant through regulation of the synthesis of the insulin responsive glucose transporter as well as through interference with insulin signaling. |
| 14917 | 10654615 | Mechanistic studies in cell culture have suggested that TNF-alpha functions to render cells insulin resistant through regulation of the synthesis of the insulin responsive glucose transporter as well as through interference with insulin signaling. |
| 14918 | 10654615 | Mechanistic studies in cell culture have suggested that TNF-alpha functions to render cells insulin resistant through regulation of the synthesis of the insulin responsive glucose transporter as well as through interference with insulin signaling. |
| 14919 | 10654615 | Mechanistic studies in cell culture have suggested that TNF-alpha functions to render cells insulin resistant through regulation of the synthesis of the insulin responsive glucose transporter as well as through interference with insulin signaling. |
| 14920 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 14921 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 14922 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 14923 | 10637268 | Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8(+) T cells. |
| 14924 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 14925 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 14926 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 14927 | 10637268 | Here we show that TNF-alpha promotes autoaggression of both effector CD4(+) and CD8(+) T cells. |
| 14928 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 14929 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 14930 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 14931 | 10637268 | Whereas CD8(+) T cells are critical for diabetes progression, CD4(+) T cells play a lesser role. |
| 14932 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 14933 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 14934 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 14935 | 10637268 | TNF-alpha-mediated diabetes development was not dependent on CD154-CD40 signals or activated CD4(+) T cells. |
| 14936 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 14937 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 14938 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 14939 | 10637268 | Instead, it appears that TNF-alpha can promote cross-presentation of islet antigen to CD8(+) T cells using a unique CD40-CD154-independent pathway. |
| 14940 | 10623855 | Activation of peroxisome proliferator-activated receptor gamma does not inhibit IL-6 or TNF-alpha responses of macrophages to lipopolysaccharide in vitro or in vivo. |
| 14941 | 10623855 | Activation of peroxisome proliferator-activated receptor gamma does not inhibit IL-6 or TNF-alpha responses of macrophages to lipopolysaccharide in vitro or in vivo. |
| 14942 | 10623855 | Activation of peroxisome proliferator-activated receptor gamma does not inhibit IL-6 or TNF-alpha responses of macrophages to lipopolysaccharide in vitro or in vivo. |
| 14943 | 10623855 | Although 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) at micromolar concentrations significantly inhibited the production of TNF-alpha and IL-6, four other high affinity PPARgamma ligands failed to affect cytokine production. |
| 14944 | 10623855 | Although 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) at micromolar concentrations significantly inhibited the production of TNF-alpha and IL-6, four other high affinity PPARgamma ligands failed to affect cytokine production. |
| 14945 | 10623855 | Although 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) at micromolar concentrations significantly inhibited the production of TNF-alpha and IL-6, four other high affinity PPARgamma ligands failed to affect cytokine production. |
| 14946 | 10623855 | Rather, their blood levels of TNF-alpha and IL-6 were elevated beyond the levels observed in control db/db mice challenged with LPS. |
| 14947 | 10623855 | Rather, their blood levels of TNF-alpha and IL-6 were elevated beyond the levels observed in control db/db mice challenged with LPS. |
| 14948 | 10623855 | Rather, their blood levels of TNF-alpha and IL-6 were elevated beyond the levels observed in control db/db mice challenged with LPS. |
| 14949 | 10623794 | Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex. |
| 14950 | 10623794 | Both the induction of TNF-alpha and NO formation were found dependent on a functional Tlr4 whereas stimulation of macrophages by CpG DNA was Tlr4 independent. |
| 14951 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14952 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14953 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14954 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14955 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14956 | 10618409 | A mouse CD8 T cell-mediated acute autoimmune diabetes independent of the perforin and Fas cytotoxic pathways: possible role of membrane TNF. |
| 14957 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14958 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14959 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14960 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14961 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14962 | 10618409 | Double transgenic mice [rat insulin promoter (RIP)-tumor necrosis factor (TNF) and RIP-CD80] whose pancreatic beta cells release TNF and bear CD80 all develop an acute early (6 wk) and lethal diabetes mediated by CD8 T cells. |
| 14963 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14964 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14965 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14966 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14967 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14968 | 10618409 | Such double transgenic mice were made defective in either the perforin, Fas, or TNF pathways. |
| 14969 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14970 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14971 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14972 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14973 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14974 | 10618409 | Mice lacking TNF receptor (TNFR) II had no or late diabetes, but only a minority had severe insulitis. |
| 14975 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14976 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14977 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14978 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14979 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14980 | 10618409 | Mice lacking the TNF-lymphotoxin (LTalpha) locus (whose sole source of TNF are the beta cells) all had insulitis comparable to that of nondefective mice, but no diabetes or a retarded and milder form, with lesions suggesting different mechanisms of injury. |
| 14981 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14982 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14983 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14984 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14985 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14986 | 10618409 | Because both TNFR II and TNF-LTalpha mutations have complex effects on the immune system, these data do not formally incriminate membrane TNF as the major T cell mediator of this acute autoimmune diabetes; nevertheless, in the absence of involvement of the perforin or Fas cytotoxic pathways, membrane TNF appears to be the likeliest candidate. |
| 14987 | 10615948 | Their secretion of different pro-inflammatory cytokines such as interleukin (IL)-1beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha affects beta-cell function. |
| 14988 | 10615948 | Here we report that a combination of these cytokines inhibits insulin release, stimulates inducible nitric oxide synthase (iNOS), and upregulates the surface expression of Fas in NIT-1 beta-cells and intact mouse islets. |
| 14989 | 10615948 | Using iNOS-deficient and Fas-deficient islets, respectively, we investigated the relative contribution of NO and Fas upregulation in cytokine-induced beta-cell damage. |
| 14990 | 10615948 | The lack of NO production partially protected islets from cytokine-induced apoptosis but had no effect on cell death induced by cell surface cross-linking of Fas with soluble Fas ligand (FasL). |
| 14991 | 10615948 | In conclusion, pro-inflammatory cytokines exert a cytotoxic effect on beta-cells via an NO-dependent pathway and, in parallel, render beta-cells susceptible to Fas:FasL-mediated, NO-independent cell death triggered by activated T-cells. |
| 14992 | 10614913 | The mechanisms whereby smoking affects eye disease are widely unknown, cytokines (INF-gamma, TNF-alpha, IL-1), receptors and receptor antagonists have probably a crucial role. |
| 14993 | 10607745 | Agents such as perforin and granzymes, CD95 ligand and tumor necrosis factor-alpha, or cytokines and free-radicals have all been shown to cause beta cell apoptosis. |
| 14994 | 10600783 | To investigate in vivo adipose tissue production of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and their soluble receptors: TNF receptor type I (sTNFR-I), TNF receptor type II (sTNFR-II), and IL-6 receptor (sIL-6R), we determined arteriovenous differences in their levels across abdominal subcutaneous adipose tissue in obese subjects. |
| 14995 | 10599887 | Allele typing of human TNFA 5'-flanking region using polymerase chain reaction-preferential homoduplex formation assay (PCR-PHFA): linkage disequilibrium with HLA class I and class II genes in Japanese. |
| 14996 | 10599887 | Allele typing of human TNFA 5'-flanking region using polymerase chain reaction-preferential homoduplex formation assay (PCR-PHFA): linkage disequilibrium with HLA class I and class II genes in Japanese. |
| 14997 | 10599887 | Allele typing of human TNFA 5'-flanking region using polymerase chain reaction-preferential homoduplex formation assay (PCR-PHFA): linkage disequilibrium with HLA class I and class II genes in Japanese. |
| 14998 | 10599887 | Allele typing of human TNFA 5'-flanking region using polymerase chain reaction-preferential homoduplex formation assay (PCR-PHFA): linkage disequilibrium with HLA class I and class II genes in Japanese. |
| 14999 | 10599887 | Allele typing of human TNFA 5'-flanking region using polymerase chain reaction-preferential homoduplex formation assay (PCR-PHFA): linkage disequilibrium with HLA class I and class II genes in Japanese. |
| 15000 | 10599887 | Tumor necrosis factor alpha plays a substantial role in a number of conditions such as inflammation, autoimmunity, insulin resistance and sleep. |
| 15001 | 10599887 | Tumor necrosis factor alpha plays a substantial role in a number of conditions such as inflammation, autoimmunity, insulin resistance and sleep. |
| 15002 | 10599887 | Tumor necrosis factor alpha plays a substantial role in a number of conditions such as inflammation, autoimmunity, insulin resistance and sleep. |
| 15003 | 10599887 | Tumor necrosis factor alpha plays a substantial role in a number of conditions such as inflammation, autoimmunity, insulin resistance and sleep. |
| 15004 | 10599887 | Tumor necrosis factor alpha plays a substantial role in a number of conditions such as inflammation, autoimmunity, insulin resistance and sleep. |
| 15005 | 10599887 | Based on HLA-A, -B and -DRB1 genotypes together with TNFA genotypes, multi-locus haplotypes were analyzed. |
| 15006 | 10599887 | Based on HLA-A, -B and -DRB1 genotypes together with TNFA genotypes, multi-locus haplotypes were analyzed. |
| 15007 | 10599887 | Based on HLA-A, -B and -DRB1 genotypes together with TNFA genotypes, multi-locus haplotypes were analyzed. |
| 15008 | 10599887 | Based on HLA-A, -B and -DRB1 genotypes together with TNFA genotypes, multi-locus haplotypes were analyzed. |
| 15009 | 10599887 | Based on HLA-A, -B and -DRB1 genotypes together with TNFA genotypes, multi-locus haplotypes were analyzed. |
| 15010 | 10599887 | Interestingly, TNFA alleles previously shown to have a higher promoter activity (U02, U03) were found to form haplotypes with certain DRB1 alleles associated with T helper 1 (Th1)-dominant diseases such as rheumatoid arthritis, insulin dependent diabetes mellitus and Crohn's disease in Japanese. |
| 15011 | 10599887 | Interestingly, TNFA alleles previously shown to have a higher promoter activity (U02, U03) were found to form haplotypes with certain DRB1 alleles associated with T helper 1 (Th1)-dominant diseases such as rheumatoid arthritis, insulin dependent diabetes mellitus and Crohn's disease in Japanese. |
| 15012 | 10599887 | Interestingly, TNFA alleles previously shown to have a higher promoter activity (U02, U03) were found to form haplotypes with certain DRB1 alleles associated with T helper 1 (Th1)-dominant diseases such as rheumatoid arthritis, insulin dependent diabetes mellitus and Crohn's disease in Japanese. |
| 15013 | 10599887 | Interestingly, TNFA alleles previously shown to have a higher promoter activity (U02, U03) were found to form haplotypes with certain DRB1 alleles associated with T helper 1 (Th1)-dominant diseases such as rheumatoid arthritis, insulin dependent diabetes mellitus and Crohn's disease in Japanese. |
| 15014 | 10599887 | Interestingly, TNFA alleles previously shown to have a higher promoter activity (U02, U03) were found to form haplotypes with certain DRB1 alleles associated with T helper 1 (Th1)-dominant diseases such as rheumatoid arthritis, insulin dependent diabetes mellitus and Crohn's disease in Japanese. |
| 15015 | 10599887 | In contrast, TNFA allele with a low promoter activity (U01) is in linkage disequilibrium with the DRB1 alleles associated with T helper 2 (Th2)-dominant diseases such as atopic dermatitis and ulcerative colitis. |
| 15016 | 10599887 | In contrast, TNFA allele with a low promoter activity (U01) is in linkage disequilibrium with the DRB1 alleles associated with T helper 2 (Th2)-dominant diseases such as atopic dermatitis and ulcerative colitis. |
| 15017 | 10599887 | In contrast, TNFA allele with a low promoter activity (U01) is in linkage disequilibrium with the DRB1 alleles associated with T helper 2 (Th2)-dominant diseases such as atopic dermatitis and ulcerative colitis. |
| 15018 | 10599887 | In contrast, TNFA allele with a low promoter activity (U01) is in linkage disequilibrium with the DRB1 alleles associated with T helper 2 (Th2)-dominant diseases such as atopic dermatitis and ulcerative colitis. |
| 15019 | 10599887 | In contrast, TNFA allele with a low promoter activity (U01) is in linkage disequilibrium with the DRB1 alleles associated with T helper 2 (Th2)-dominant diseases such as atopic dermatitis and ulcerative colitis. |
| 15020 | 10580421 | Most likely, this discrepancy was not due to age-dependent differences in the immunological responses of NOD mice to rhIL-11 because staphylococcus aureus enterotoxin B-induced tumor necrosis factor (TNF) and IL-12 production were equally suppressed by rhIL-11 in 12- and 25-week-old NOD mice. |
| 15021 | 10580421 | Most likely, this discrepancy was not due to age-dependent differences in the immunological responses of NOD mice to rhIL-11 because staphylococcus aureus enterotoxin B-induced tumor necrosis factor (TNF) and IL-12 production were equally suppressed by rhIL-11 in 12- and 25-week-old NOD mice. |
| 15022 | 10580421 | Relative to controls, NOD mice pretreated with rhIL-11 also showed significantly diminished blood levels of TNF, interferon-gamma, and IL-12 induced by anti-CD3 antibody and/or lipopolysaccharide. |
| 15023 | 10580421 | Relative to controls, NOD mice pretreated with rhIL-11 also showed significantly diminished blood levels of TNF, interferon-gamma, and IL-12 induced by anti-CD3 antibody and/or lipopolysaccharide. |
| 15024 | 10567588 | The pronounced proteasome defect results in defective production and activation of the transcription factor NF-kappaB, which plays an important role in immune and inflammatory responses as well as in preventing apoptosis induced by tumor necrosis factor alpha. |
| 15025 | 10567588 | The defect in proteasome function in NOD mouse splenocytes was evident from impaired NF-kappaB subunit p50 and p52 generation by proteolytic processing and impaired degradation of the NF-kappaB-inhibitory protein IkappaBalpha. |
| 15026 | 10567588 | These data suggest that NOD proteasome dysfunction is due to a tissue- and developmental-stage-specific defect in expression of the MHC-linked Lmp2 gene, resulting in altered transcription factor NF-kappaB activity, and that this defect contributes to pathogenesis in NOD mice. |
| 15027 | 10566598 | Influence of TNF microsatellite polymorphisms (TNFa) on age-at-onset of insulin-dependent diabetes mellitus. |
| 15028 | 10566598 | Influence of TNF microsatellite polymorphisms (TNFa) on age-at-onset of insulin-dependent diabetes mellitus. |
| 15029 | 10566598 | Influence of TNF microsatellite polymorphisms (TNFa) on age-at-onset of insulin-dependent diabetes mellitus. |
| 15030 | 10566598 | Influence of TNF microsatellite polymorphisms (TNFa) on age-at-onset of insulin-dependent diabetes mellitus. |
| 15031 | 10566598 | Influence of TNF microsatellite polymorphisms (TNFa) on age-at-onset of insulin-dependent diabetes mellitus. |
| 15032 | 10566598 | The TNF-alpha gene is located in the HLA region and has been implicated in the pathogenesis of Type I (insulin-dependent) diabetes mellitus (IDDM). |
| 15033 | 10566598 | The TNF-alpha gene is located in the HLA region and has been implicated in the pathogenesis of Type I (insulin-dependent) diabetes mellitus (IDDM). |
| 15034 | 10566598 | The TNF-alpha gene is located in the HLA region and has been implicated in the pathogenesis of Type I (insulin-dependent) diabetes mellitus (IDDM). |
| 15035 | 10566598 | The TNF-alpha gene is located in the HLA region and has been implicated in the pathogenesis of Type I (insulin-dependent) diabetes mellitus (IDDM). |
| 15036 | 10566598 | The TNF-alpha gene is located in the HLA region and has been implicated in the pathogenesis of Type I (insulin-dependent) diabetes mellitus (IDDM). |
| 15037 | 10566598 | We investigated the frequency of TNFa microsatellite alleles in 76 young-onset IDDM patients, 65 adult-onset IDDM patients, and 90 control subjects. |
| 15038 | 10566598 | We investigated the frequency of TNFa microsatellite alleles in 76 young-onset IDDM patients, 65 adult-onset IDDM patients, and 90 control subjects. |
| 15039 | 10566598 | We investigated the frequency of TNFa microsatellite alleles in 76 young-onset IDDM patients, 65 adult-onset IDDM patients, and 90 control subjects. |
| 15040 | 10566598 | We investigated the frequency of TNFa microsatellite alleles in 76 young-onset IDDM patients, 65 adult-onset IDDM patients, and 90 control subjects. |
| 15041 | 10566598 | We investigated the frequency of TNFa microsatellite alleles in 76 young-onset IDDM patients, 65 adult-onset IDDM patients, and 90 control subjects. |
| 15042 | 10566598 | We also examined the association of these TNFa alleles with HLA-DRB1 alleles, HLA-class I alleles, and TNF-alpha production. |
| 15043 | 10566598 | We also examined the association of these TNFa alleles with HLA-DRB1 alleles, HLA-class I alleles, and TNF-alpha production. |
| 15044 | 10566598 | We also examined the association of these TNFa alleles with HLA-DRB1 alleles, HLA-class I alleles, and TNF-alpha production. |
| 15045 | 10566598 | We also examined the association of these TNFa alleles with HLA-DRB1 alleles, HLA-class I alleles, and TNF-alpha production. |
| 15046 | 10566598 | We also examined the association of these TNFa alleles with HLA-DRB1 alleles, HLA-class I alleles, and TNF-alpha production. |
| 15047 | 10566598 | These results suggest that TNFa polymorphisms are associated with age-at-onset of IDDM and influence the inflammatory process of pancreatic beta cell destruction in the development of IDDM. |
| 15048 | 10566598 | These results suggest that TNFa polymorphisms are associated with age-at-onset of IDDM and influence the inflammatory process of pancreatic beta cell destruction in the development of IDDM. |
| 15049 | 10566598 | These results suggest that TNFa polymorphisms are associated with age-at-onset of IDDM and influence the inflammatory process of pancreatic beta cell destruction in the development of IDDM. |
| 15050 | 10566598 | These results suggest that TNFa polymorphisms are associated with age-at-onset of IDDM and influence the inflammatory process of pancreatic beta cell destruction in the development of IDDM. |
| 15051 | 10566598 | These results suggest that TNFa polymorphisms are associated with age-at-onset of IDDM and influence the inflammatory process of pancreatic beta cell destruction in the development of IDDM. |
| 15052 | 10561528 | We investigated the induction of adhesion molecules such as L-selectin, E-selectin, ICAM-1, VCAM-1 and Mac-1 on Schwann cells by proinflammatory cytokines. |
| 15053 | 10561528 | We investigated the induction of adhesion molecules such as L-selectin, E-selectin, ICAM-1, VCAM-1 and Mac-1 on Schwann cells by proinflammatory cytokines. |
| 15054 | 10561528 | We investigated the induction of adhesion molecules such as L-selectin, E-selectin, ICAM-1, VCAM-1 and Mac-1 on Schwann cells by proinflammatory cytokines. |
| 15055 | 10561528 | Incubation of human Schwann cells with TNFalpha, IFNgamma and IL-1beta induces the expression of ICAM-1 starting at 6 h and reaching a peak at 24 h on more than 90% of cells. |
| 15056 | 10561528 | Incubation of human Schwann cells with TNFalpha, IFNgamma and IL-1beta induces the expression of ICAM-1 starting at 6 h and reaching a peak at 24 h on more than 90% of cells. |
| 15057 | 10561528 | Incubation of human Schwann cells with TNFalpha, IFNgamma and IL-1beta induces the expression of ICAM-1 starting at 6 h and reaching a peak at 24 h on more than 90% of cells. |
| 15058 | 10561528 | VCAM-1 expression was induced after 6 h of treatment with TNFalpha and IL-1beta on almost 100% of Schwann cells. |
| 15059 | 10561528 | VCAM-1 expression was induced after 6 h of treatment with TNFalpha and IL-1beta on almost 100% of Schwann cells. |
| 15060 | 10561528 | VCAM-1 expression was induced after 6 h of treatment with TNFalpha and IL-1beta on almost 100% of Schwann cells. |
| 15061 | 10561528 | Surprisingly, stimulation with TNFalpha, IFNgamma and IL-1beta also induced the expression of L-selectin on fetal and diabetic Schwann cells, but not on normal adult cells. |
| 15062 | 10561528 | Surprisingly, stimulation with TNFalpha, IFNgamma and IL-1beta also induced the expression of L-selectin on fetal and diabetic Schwann cells, but not on normal adult cells. |
| 15063 | 10561528 | Surprisingly, stimulation with TNFalpha, IFNgamma and IL-1beta also induced the expression of L-selectin on fetal and diabetic Schwann cells, but not on normal adult cells. |
| 15064 | 10561528 | E-selectin, an adhesion molecule classically upregulated during inflammation, as well as Mac-1, a ligand for ICAM-1, were not expressed on human Schwann cells at basal condition or after treatment with cytokines. |
| 15065 | 10561528 | E-selectin, an adhesion molecule classically upregulated during inflammation, as well as Mac-1, a ligand for ICAM-1, were not expressed on human Schwann cells at basal condition or after treatment with cytokines. |
| 15066 | 10561528 | E-selectin, an adhesion molecule classically upregulated during inflammation, as well as Mac-1, a ligand for ICAM-1, were not expressed on human Schwann cells at basal condition or after treatment with cytokines. |
| 15067 | 10561528 | No ICAM-1, VCAM-1 and L-selectin expression was found on unstimulated Schwann cells. |
| 15068 | 10561528 | No ICAM-1, VCAM-1 and L-selectin expression was found on unstimulated Schwann cells. |
| 15069 | 10561528 | No ICAM-1, VCAM-1 and L-selectin expression was found on unstimulated Schwann cells. |
| 15070 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15071 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15072 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15073 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15074 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15075 | 10540181 | Platelet expression of tumour necrosis factor-alpha (TNF-alpha), TNF receptors and intercellular adhesion molecule-1 (ICAM-1) in patients with proliferative diabetic retinopathy. |
| 15076 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15077 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15078 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15079 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15080 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15081 | 10540181 | Microvascular complications of insulin-dependent diabetes mellitus (IDDM) have been strongly associated with platelet abnormalities, whilst TNF-alpha has been implicated in the pathogenesis of this condition. |
| 15082 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15083 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15084 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15085 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15086 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15087 | 10540181 | However, at present it is not clear whether human circulating platelets express TNF-alpha or TNF receptors (TNF-R) or whether impaired expression of these molecules and of the TNF-reactive adhesion molecule ICAM-1 may be associated with platelet abnormalities in patients with IDDM. |
| 15088 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15089 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15090 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15091 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15092 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15093 | 10540181 | We observed that the proportion of platelets staining for TNF-alpha was significantly higher in IDDM patients with active PDR than in patients without microvascular complications (P = 0.0078), quiescent PDR (P = 0.003) or healthy subjects (P = 0.0013). |
| 15094 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15095 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15096 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15097 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15098 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15099 | 10540181 | There was a direct correlation between platelet expression of TNF-alpha and that of TNF-R in PDR patients, indicating that platelet staining for TNF-alpha may be due to binding of this cytokine to its receptors. |
| 15100 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15101 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15102 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15103 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15104 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15105 | 10540181 | The results suggest that increased platelet expression of TNF-alpha, TNF-R and ICAM-1 in IDDM patients may constitute important markers of thrombocyte abnormalities during the development of microvascular complications of diabetes mellitus. |
| 15106 | 10549054 | Transrepression results from the inhibitory interaction between the GR and other transcription factors like AP-1 and NF-kappa B. |
| 15107 | 10549054 | Since AP-1 and NF-kappa B DNA binding sites have been mapped to the promoter regions of many genes coding for proinflammatory mediators (IL-1, 2, 5, 6, 8, 13, TNF-alpha, RANTES, Eotaxin, GM-CSF, metalloproteinases, ICAM-1 ...), this interaction may be an important aspect of the GC anti-inflammatory properties. |
| 15108 | 10545284 | In conclusion, data presented suggest that insulin might regulate superoxide generation and TNF-alpha release by leukocytes upon exposure to LPS in vivo. |
| 15109 | 10542046 | Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. |
| 15110 | 10542046 | Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. |
| 15111 | 10542046 | Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. |
| 15112 | 10542046 | Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. |
| 15113 | 10542046 | Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. |
| 15114 | 10542046 | Tumour necrosis factor (TNF) and nonesterified fatty acids have been proposed to be crucial factors in the development of the insulin-resistant state. |
| 15115 | 10542046 | Tumour necrosis factor (TNF) and nonesterified fatty acids have been proposed to be crucial factors in the development of the insulin-resistant state. |
| 15116 | 10542046 | Tumour necrosis factor (TNF) and nonesterified fatty acids have been proposed to be crucial factors in the development of the insulin-resistant state. |
| 15117 | 10542046 | Tumour necrosis factor (TNF) and nonesterified fatty acids have been proposed to be crucial factors in the development of the insulin-resistant state. |
| 15118 | 10542046 | Tumour necrosis factor (TNF) and nonesterified fatty acids have been proposed to be crucial factors in the development of the insulin-resistant state. |
| 15119 | 10542046 | We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. |
| 15120 | 10542046 | We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. |
| 15121 | 10542046 | We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. |
| 15122 | 10542046 | We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. |
| 15123 | 10542046 | We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. |
| 15124 | 10542046 | Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. |
| 15125 | 10542046 | Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. |
| 15126 | 10542046 | Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. |
| 15127 | 10542046 | Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. |
| 15128 | 10542046 | Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. |
| 15129 | 10542046 | In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. |
| 15130 | 10542046 | In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. |
| 15131 | 10542046 | In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. |
| 15132 | 10542046 | In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. |
| 15133 | 10542046 | In contrast, the nonesterified fatty acid palmitate inhibited insulin-induced signalling cascades not only at the level of IR and IRS-1 phosphorylation, but also at the level protein kinase B (PKB/Akt), which is thought to be directly involved in the insulin-induced translocation of GLUT4, and inhibited insulin-induced glucose uptake. |
| 15134 | 10542046 | Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. |
| 15135 | 10542046 | Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. |
| 15136 | 10542046 | Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. |
| 15137 | 10542046 | Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. |
| 15138 | 10542046 | Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. |
| 15139 | 10542046 | Our data illustrate the complexity of the mechanisms governing insulin resistance of skeletal muscle, questioning the role of TNF as a direct inhibitor of glucose homoeostasis in this tissue and shedding new light on an as yet unrecognized multifunctional role for the predominant nonesterified fatty acid palmitate in this process. |
| 15140 | 10542046 | Our data illustrate the complexity of the mechanisms governing insulin resistance of skeletal muscle, questioning the role of TNF as a direct inhibitor of glucose homoeostasis in this tissue and shedding new light on an as yet unrecognized multifunctional role for the predominant nonesterified fatty acid palmitate in this process. |
| 15141 | 10542046 | Our data illustrate the complexity of the mechanisms governing insulin resistance of skeletal muscle, questioning the role of TNF as a direct inhibitor of glucose homoeostasis in this tissue and shedding new light on an as yet unrecognized multifunctional role for the predominant nonesterified fatty acid palmitate in this process. |
| 15142 | 10542046 | Our data illustrate the complexity of the mechanisms governing insulin resistance of skeletal muscle, questioning the role of TNF as a direct inhibitor of glucose homoeostasis in this tissue and shedding new light on an as yet unrecognized multifunctional role for the predominant nonesterified fatty acid palmitate in this process. |
| 15143 | 10542046 | Our data illustrate the complexity of the mechanisms governing insulin resistance of skeletal muscle, questioning the role of TNF as a direct inhibitor of glucose homoeostasis in this tissue and shedding new light on an as yet unrecognized multifunctional role for the predominant nonesterified fatty acid palmitate in this process. |
| 15144 | 10536488 | The increase of these "cardiovascular risk factors" levels will be probably induced by higher activity of inflammatory cytokines IL-1 beta and/or TNF alpha in NIDDM patients, because both are inducers of orosomucoid fibrinogen and PAI-1 synthesis. |
| 15145 | 10536488 | The increase of these "cardiovascular risk factors" levels will be probably induced by higher activity of inflammatory cytokines IL-1 beta and/or TNF alpha in NIDDM patients, because both are inducers of orosomucoid fibrinogen and PAI-1 synthesis. |
| 15146 | 10536488 | Both cytoadhesive molecules are produced by endothelial cells which are influenced by IL-1 beta and/or TNF alpha. |
| 15147 | 10536488 | Both cytoadhesive molecules are produced by endothelial cells which are influenced by IL-1 beta and/or TNF alpha. |
| 15148 | 10528229 | Noninsulin-dependent diabetes mellitus occurs in mice ectopically expressing the human Axl tyrosine kinase receptor. |
| 15149 | 10528229 | We addressed this question by generating transgenic mice possessing constitutive ectopic expression of human axl throughout cells of the myeloid hematopoietic lineage through the use of the granulocyte colony-stimulating factor (GCSF) receptor promoter. |
| 15150 | 10528229 | Axl transgenic animals expressed elevated serum tumor necrosis factor (TNF)-alpha levels that were further enhanced upon in vitro lipopolysaccharide (LPS) stimulation of peripheral blood. |
| 15151 | 10527399 | Singaporean Chinese with insulin-dependent diabetes mellitus (IDDM) have previously been shown to be associated with the DRB1*0301 haplotype and the joint occurrence of DRB1*0301/*0901 and DRB1*0301/*04. |
| 15152 | 10527399 | Singaporean Chinese with insulin-dependent diabetes mellitus (IDDM) have previously been shown to be associated with the DRB1*0301 haplotype and the joint occurrence of DRB1*0301/*0901 and DRB1*0301/*04. |
| 15153 | 10527399 | Singaporean Chinese with insulin-dependent diabetes mellitus (IDDM) have previously been shown to be associated with the DRB1*0301 haplotype and the joint occurrence of DRB1*0301/*0901 and DRB1*0301/*04. |
| 15154 | 10527399 | The present study extended previous HLA associations by investigating the HLA region using four microsatellites (TNFa, D6S273, TAP1, DQCARII). |
| 15155 | 10527399 | The present study extended previous HLA associations by investigating the HLA region using four microsatellites (TNFa, D6S273, TAP1, DQCARII). |
| 15156 | 10527399 | The present study extended previous HLA associations by investigating the HLA region using four microsatellites (TNFa, D6S273, TAP1, DQCARII). |
| 15157 | 10527399 | Our findings reinforce the notion that susceptibility to and protection against IDDM may include TNF region. |
| 15158 | 10527399 | Our findings reinforce the notion that susceptibility to and protection against IDDM may include TNF region. |
| 15159 | 10527399 | Our findings reinforce the notion that susceptibility to and protection against IDDM may include TNF region. |
| 15160 | 10527399 | In the present study, TNFa*12 seemed to be the primary association in the DRB1*0405 haplotype and may play an independent role in the pathogenesis of IDDM through TNF-alpha function. |
| 15161 | 10527399 | In the present study, TNFa*12 seemed to be the primary association in the DRB1*0405 haplotype and may play an independent role in the pathogenesis of IDDM through TNF-alpha function. |
| 15162 | 10527399 | In the present study, TNFa*12 seemed to be the primary association in the DRB1*0405 haplotype and may play an independent role in the pathogenesis of IDDM through TNF-alpha function. |
| 15163 | 10526261 | Depot-specific release of leptin from subcutaneous and omental adipocytes in suspension culture: effect of tumor necrosis factor-alpha and transforming growth factor-beta1. |
| 15164 | 10522817 | After the administration of mAbs directed against LFA-1, ICAM-1, murine VCAM-1, VLA-4, MadCAM or alpha4,beta7-integrin prior to the cell transfer we could demonstrate a significant decrease of donor lymphocyte adherence in islets (P<0.01). |
| 15165 | 10522817 | Therefore we pretreated the recipients with antibodies to cytokines or silica. mAb IFN-gamma, pAb TNF-alpha, pAb IL-1alpha or silica reduced lymphocyte adherence to islet endothelium significantly (P<0.01). |
| 15166 | 10512379 | Tumor necrosis factor-alpha-238 and -308 polymorphisms do not associated with traits related to obesity and insulin resistance. |
| 15167 | 10512379 | Tumor necrosis factor-alpha-238 and -308 polymorphisms do not associated with traits related to obesity and insulin resistance. |
| 15168 | 10512379 | Tumor necrosis factor-alpha-238 and -308 polymorphisms do not associated with traits related to obesity and insulin resistance. |
| 15169 | 10512379 | Tumor necrosis factor-alpha (TNF-alpha) is expressed primarily in adipocytes, and elevated levels of this cytokine have been linked to obesity and insulin resistance. |
| 15170 | 10512379 | Tumor necrosis factor-alpha (TNF-alpha) is expressed primarily in adipocytes, and elevated levels of this cytokine have been linked to obesity and insulin resistance. |
| 15171 | 10512379 | Tumor necrosis factor-alpha (TNF-alpha) is expressed primarily in adipocytes, and elevated levels of this cytokine have been linked to obesity and insulin resistance. |
| 15172 | 10512379 | The purpose of this investigation was to test whether the TNF-alpha-308 polymorphism (previously linked to insulin resistance and increased leptin levels) and the TNF-alpha-238 polymorphism (linked to decreased insulin resistance) were associated with insulin resistance or obesity-related traits in 424 subjects self-referred to the Johns Hopkins Weight Management Center (JHWMC). |
| 15173 | 10512379 | The purpose of this investigation was to test whether the TNF-alpha-308 polymorphism (previously linked to insulin resistance and increased leptin levels) and the TNF-alpha-238 polymorphism (linked to decreased insulin resistance) were associated with insulin resistance or obesity-related traits in 424 subjects self-referred to the Johns Hopkins Weight Management Center (JHWMC). |
| 15174 | 10512379 | The purpose of this investigation was to test whether the TNF-alpha-308 polymorphism (previously linked to insulin resistance and increased leptin levels) and the TNF-alpha-238 polymorphism (linked to decreased insulin resistance) were associated with insulin resistance or obesity-related traits in 424 subjects self-referred to the Johns Hopkins Weight Management Center (JHWMC). |
| 15175 | 10510538 | [Relation between plasma levels of IGF-I, leptin and TNF-alpha in diabetics]. |
| 15176 | 10503944 | Recent investigations suggest that cytotoxic cytokines such as tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta or free radicals play an essential role in destruction of pancreatic beta cells in Type 1 diabetes and that, therefore, anti-oxidant or anti-TNF alpha and IL-1beta therapy could prevent the development of Type I diabetes. |
| 15177 | 10503944 | Recent investigations suggest that cytotoxic cytokines such as tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta or free radicals play an essential role in destruction of pancreatic beta cells in Type 1 diabetes and that, therefore, anti-oxidant or anti-TNF alpha and IL-1beta therapy could prevent the development of Type I diabetes. |
| 15178 | 10503944 | Troglitazone belongs to a novel class of antidiabetic agent possessing the ability to enhance insulin action provably through activating PPAR gamma and to scavenge free radicals. |
| 15179 | 10503944 | Troglitazone belongs to a novel class of antidiabetic agent possessing the ability to enhance insulin action provably through activating PPAR gamma and to scavenge free radicals. |
| 15180 | 10503944 | TNF alpha (10 pg/ml) and IL-1beta (1 pg/ml) addition to hamster insulinoma cell line HIT-T15 for 7 days in vitro decreased insulin secretion and cell viability. |
| 15181 | 10503944 | TNF alpha (10 pg/ml) and IL-1beta (1 pg/ml) addition to hamster insulinoma cell line HIT-T15 for 7 days in vitro decreased insulin secretion and cell viability. |
| 15182 | 10480607 | These purified human islet MVEC (HI-MVEC) express von Willebrand factor, take up high levels of acetylated LDL, and upregulate endothelial cell leukocyte adhesion molecule 1 in response to tumor necrosis factor-alpha. |
| 15183 | 10480607 | We also demonstrate that alpha-1 proteinase inhibitor (Api) is expressed on HI-MVEC and specifically located at the area of cell-cell junctions. |
| 15184 | 10480594 | Animal studies have shown that interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma affect type 1 diabetes development profoundly. |
| 15185 | 10479531 | Messenger RNA expression of several inflammatory cytokines, including interleukin-1beta (IL-1beta), IL-2, IL-10, interferon-gamma, and tumor necrosis factor-alpha was detected in the submandibular glands of both NOD and BALB/c mice by the reverse transcription polymerase chain reaction. |
| 15186 | 10477397 | Combinations of cytokines, including interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma), induce nitric oxide (NO) production and cell death in pancreatic islet cells. |
| 15187 | 10477397 | These cells were exposed for different time points to IL-1beta (50 U/mI), IFN-gamma (1,000 U/ml) and/or TNF-alpha (1,000 U/ml) before being harvested for determination of viability (by nuclear dyes) and mRNA expression (by RT-PCR with specific primers). |
| 15188 | 10477397 | Following a 24 hours exposure to IL-1beta or IL-1beta + IFN-gamma, pancreatic islets isolated from IRF-1-/- mice presented a 30-50% reduction in medium nitrite accumulation and inducible NO-synthase (iNOS) expression. |
| 15189 | 10477397 | Interestingly, both wt and IRF-1-/- purified beta-cells failed to produce NO in response to IL-1beta alone, but presented a similar increase in nitrite accumulation and iNOS expression following exposure to IL-1beta + IFN-gamma. |
| 15190 | 10477397 | IL-1beta induced serine protease inhibitor-3 (SPI-3; a putative cellular "defense" protein) mRNA expression in both wt and IRF-1-/- islets or beta-cells. |
| 15191 | 10477397 | IFN-gamma decreased the IL-1beta-induced SPI-3 expression in wt islets or beta-cells, but induced a 5-fold increase in the expression of this mRNA in IRF-1-/- islets cells, suggesting that IRF-1 mediates an inhibitory effect of IFN-gamma on SPI-3 expression. |
| 15192 | 10477397 | Treatment of whole islets for 3 days with IL-1beta + IFN-gamma induced significantly more islet cell death in wt than in IRF-1-/- mice (respectively 85 +/- 3% versus 31 +/- 4% dead cells). |
| 15193 | 10477397 | In conclusion, IRF-1 contributes to cytokine-induced islet iNOS expression and cell death. |
| 15194 | 10469241 | Expression of vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) in the pancreas was assessed using immunohistochemistry. |
| 15195 | 10469241 | Pretreatment of recipients with antibodies to cytokines or silica reduced lymphocyte adherence to islet endothelium from 2.04% (goat immunoglobulin G; IgG) or 1.82% (rat IgG) to 0.47, 0.58, 0.39 or 0. 19% for monoclonal antibody (mAb) interferon-gamma (IFN-gamma), polyclonal antibody (pAb) tumour necrosis factor-alpha (TNF-alpha), pAb interleukin (IL)-1alpha or silica, respectively. |
| 15196 | 10469241 | Reduced adhesion was associated with a decreased expression of VCAM-1 and ICAM-1 in islets of treated recipients compared with mice treated with 5 mg/kg STZ alone. |
| 15197 | 10469241 | Prevention of increased expression of ICAM-1 or VCAM-1 and reduction of lymphocyte adhesion in islets by silica or antibody indicate an involvement of macrophages and macrophage derived cytokines in the generation of this immune response. |
| 15198 | 10469238 | Previously, pretreatment with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infection. |
| 15199 | 10469238 | Previously, pretreatment with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infection. |
| 15200 | 10469238 | Previously, pretreatment with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infection. |
| 15201 | 10469238 | Previously, pretreatment with IL-1beta and tumour necrosis factor-alpha (TNF-alpha) protected C3H/HeJ mice from lethal bacterial infection. |
| 15202 | 10469238 | Therefore the effects of pretreatment with IL-1beta and TNF-alpha or antimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. |
| 15203 | 10469238 | Therefore the effects of pretreatment with IL-1beta and TNF-alpha or antimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. |
| 15204 | 10469238 | Therefore the effects of pretreatment with IL-1beta and TNF-alpha or antimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. |
| 15205 | 10469238 | Therefore the effects of pretreatment with IL-1beta and TNF-alpha or antimurine IL-10 antibody i.p. 1 hr before this infection in both strains of C3H mice were examined. |
| 15206 | 10469238 | Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. |
| 15207 | 10469238 | Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. |
| 15208 | 10469238 | Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. |
| 15209 | 10469238 | Pretreatment with TNF-alpha or anti-IL-10 antibody enhanced the survival of both strains of mice. |
| 15210 | 10469238 | TNF-alpha, in combination with IL-1beta, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. |
| 15211 | 10469238 | TNF-alpha, in combination with IL-1beta, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. |
| 15212 | 10469238 | TNF-alpha, in combination with IL-1beta, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. |
| 15213 | 10469238 | TNF-alpha, in combination with IL-1beta, enhanced the survival and bacterial clearance better than single pretreatment in C3H/HeJ mice. |
| 15214 | 10465670 | Tumor necrosis factor-alpha: a continuum of liability between insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus and carcinoma (review). |
| 15215 | 10465670 | Tumor necrosis factor-alpha: a continuum of liability between insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus and carcinoma (review). |
| 15216 | 10465670 | Tumor necrosis factor-alpha: a continuum of liability between insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus and carcinoma (review). |
| 15217 | 10465670 | Tumor necrosis factor-alpha: a continuum of liability between insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus and carcinoma (review). |
| 15218 | 10465670 | In this review, tumor necrosis factor-alpha (TNF-alpha) is identified as the uniting principle linking the pathogenesis of insulin-dependent diabetes mellitus (IDDM), non-insulin dependent diabetes mellitus (NIDDM) and carcinoma. |
| 15219 | 10465670 | In this review, tumor necrosis factor-alpha (TNF-alpha) is identified as the uniting principle linking the pathogenesis of insulin-dependent diabetes mellitus (IDDM), non-insulin dependent diabetes mellitus (NIDDM) and carcinoma. |
| 15220 | 10465670 | In this review, tumor necrosis factor-alpha (TNF-alpha) is identified as the uniting principle linking the pathogenesis of insulin-dependent diabetes mellitus (IDDM), non-insulin dependent diabetes mellitus (NIDDM) and carcinoma. |
| 15221 | 10465670 | In this review, tumor necrosis factor-alpha (TNF-alpha) is identified as the uniting principle linking the pathogenesis of insulin-dependent diabetes mellitus (IDDM), non-insulin dependent diabetes mellitus (NIDDM) and carcinoma. |
| 15222 | 10465670 | Elevated TNF-alpha initially increases, and then inhibits, the activity of a number of key enzymes involved in energy metabolism and major histocompatibility (MHC) class I molecule expression. |
| 15223 | 10465670 | Elevated TNF-alpha initially increases, and then inhibits, the activity of a number of key enzymes involved in energy metabolism and major histocompatibility (MHC) class I molecule expression. |
| 15224 | 10465670 | Elevated TNF-alpha initially increases, and then inhibits, the activity of a number of key enzymes involved in energy metabolism and major histocompatibility (MHC) class I molecule expression. |
| 15225 | 10465670 | Elevated TNF-alpha initially increases, and then inhibits, the activity of a number of key enzymes involved in energy metabolism and major histocompatibility (MHC) class I molecule expression. |
| 15226 | 10465670 | These enzymes include: protein-tyrosine kinase (PTKase) and protein-tyrosine phosphatase (PTPase--enzymes involved in energy metabolism, cell proliferation and stimulation of the MHC class I molecule pathway. |
| 15227 | 10465670 | These enzymes include: protein-tyrosine kinase (PTKase) and protein-tyrosine phosphatase (PTPase--enzymes involved in energy metabolism, cell proliferation and stimulation of the MHC class I molecule pathway. |
| 15228 | 10465670 | These enzymes include: protein-tyrosine kinase (PTKase) and protein-tyrosine phosphatase (PTPase--enzymes involved in energy metabolism, cell proliferation and stimulation of the MHC class I molecule pathway. |
| 15229 | 10465670 | These enzymes include: protein-tyrosine kinase (PTKase) and protein-tyrosine phosphatase (PTPase--enzymes involved in energy metabolism, cell proliferation and stimulation of the MHC class I molecule pathway. |
| 15230 | 10465670 | Of primary importance is the inhibiting effect of TNF-alpha on PTKase, since this induces insulin resistance in NIDDM and carcinoma, and PTPase, which inhibits MHC class I molecule expression. |
| 15231 | 10465670 | Of primary importance is the inhibiting effect of TNF-alpha on PTKase, since this induces insulin resistance in NIDDM and carcinoma, and PTPase, which inhibits MHC class I molecule expression. |
| 15232 | 10465670 | Of primary importance is the inhibiting effect of TNF-alpha on PTKase, since this induces insulin resistance in NIDDM and carcinoma, and PTPase, which inhibits MHC class I molecule expression. |
| 15233 | 10465670 | Of primary importance is the inhibiting effect of TNF-alpha on PTKase, since this induces insulin resistance in NIDDM and carcinoma, and PTPase, which inhibits MHC class I molecule expression. |
| 15234 | 10465670 | Conversely, carcinoma is associated with an inhibition of PTPase activity, which reduces the expression of MHC class I antigen expression on the cell surface thereby allowing malignant cells to escape immune surveillance. |
| 15235 | 10465670 | Conversely, carcinoma is associated with an inhibition of PTPase activity, which reduces the expression of MHC class I antigen expression on the cell surface thereby allowing malignant cells to escape immune surveillance. |
| 15236 | 10465670 | Conversely, carcinoma is associated with an inhibition of PTPase activity, which reduces the expression of MHC class I antigen expression on the cell surface thereby allowing malignant cells to escape immune surveillance. |
| 15237 | 10465670 | Conversely, carcinoma is associated with an inhibition of PTPase activity, which reduces the expression of MHC class I antigen expression on the cell surface thereby allowing malignant cells to escape immune surveillance. |
| 15238 | 10455420 | Lentivirus-mediated Bcl-2 expression in betaTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. |
| 15239 | 10455420 | In this study we genetically engineered betaTC-tet cells with the anti-apoptotic gene Bcl-2 using new lentiviral vectors and showed that it protected this cell line against apoptosis induced by hypoxia, staurosporine and a mixture of cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 15240 | 10455420 | Expression of Bcl-2, however, did not inter- fere either with the intrinsic mechanism of growth arrest present in the betaTC-tet cells or with their normal glucose dose-dependent insulin secretory activity. |
| 15241 | 10455420 | Furthermore, Bcl-2 expressing betaTC-tet cells retained their capacity to secrete insulin under mild hypoxia. |
| 15242 | 10450504 | In the past decade, a wealth of information has accumulated through studies in non-obese diabetic (NOD) mice regarding the molecular and cellular events that participate in the progression to diabetes in insulin-dependent diabetes mellitus (IDDM). |
| 15243 | 10450504 | In the past decade, a wealth of information has accumulated through studies in non-obese diabetic (NOD) mice regarding the molecular and cellular events that participate in the progression to diabetes in insulin-dependent diabetes mellitus (IDDM). |
| 15244 | 10450504 | In the past decade, a wealth of information has accumulated through studies in non-obese diabetic (NOD) mice regarding the molecular and cellular events that participate in the progression to diabetes in insulin-dependent diabetes mellitus (IDDM). |
| 15245 | 10450504 | Here we describe a new NOD model for analyzing the role of TNF-alpha in IDDM, TNF-alpha-NOD mice. |
| 15246 | 10450504 | Here we describe a new NOD model for analyzing the role of TNF-alpha in IDDM, TNF-alpha-NOD mice. |
| 15247 | 10450504 | Here we describe a new NOD model for analyzing the role of TNF-alpha in IDDM, TNF-alpha-NOD mice. |
| 15248 | 10450504 | Although adoptive transfer studies demonstrated that TNF-alpha can enhance presentation of islet antigen to both effector CD4+ and CD8+ T cells, further investigations in TNF-alpha-NOD mice deficient in either CD4+ or CD8+ T cells demonstrated that diabetes progression is dependent on CD8+ T cells, with CD4+ T cells playing a lesser role. |
| 15249 | 10450504 | Although adoptive transfer studies demonstrated that TNF-alpha can enhance presentation of islet antigen to both effector CD4+ and CD8+ T cells, further investigations in TNF-alpha-NOD mice deficient in either CD4+ or CD8+ T cells demonstrated that diabetes progression is dependent on CD8+ T cells, with CD4+ T cells playing a lesser role. |
| 15250 | 10450504 | Although adoptive transfer studies demonstrated that TNF-alpha can enhance presentation of islet antigen to both effector CD4+ and CD8+ T cells, further investigations in TNF-alpha-NOD mice deficient in either CD4+ or CD8+ T cells demonstrated that diabetes progression is dependent on CD8+ T cells, with CD4+ T cells playing a lesser role. |
| 15251 | 10450504 | The data accumulating from TNF-alpha-NOD mice, described in this review, indicates novel pathways by which inflammatory stimuli can precipitate autoimmunity, and suggests newer approaches in the design of therapeutic treatments that prevent beta-cell destruction in IDDM. |
| 15252 | 10450504 | The data accumulating from TNF-alpha-NOD mice, described in this review, indicates novel pathways by which inflammatory stimuli can precipitate autoimmunity, and suggests newer approaches in the design of therapeutic treatments that prevent beta-cell destruction in IDDM. |
| 15253 | 10450504 | The data accumulating from TNF-alpha-NOD mice, described in this review, indicates novel pathways by which inflammatory stimuli can precipitate autoimmunity, and suggests newer approaches in the design of therapeutic treatments that prevent beta-cell destruction in IDDM. |
| 15254 | 10440223 | Activation of the AP-1 transcription factor by inflammatory cytokines of the TNF family. |
| 15255 | 10440223 | Activation of the AP-1 transcription factor by inflammatory cytokines of the TNF family. |
| 15256 | 10440223 | This review will discuss what is known of how cytokines of the TNF family, acting at the cell surface, recruit two mitogen-activated protein kinase (MAPK) subfamilies, the stress-activated protein kinases (SAPKs, also called JNKs) and the p38s, to transduce signals to AP-1. |
| 15257 | 10440223 | This review will discuss what is known of how cytokines of the TNF family, acting at the cell surface, recruit two mitogen-activated protein kinase (MAPK) subfamilies, the stress-activated protein kinases (SAPKs, also called JNKs) and the p38s, to transduce signals to AP-1. |
| 15258 | 10437623 | The phosphodiesterase inhibitor IBMX suppresses TNF-alpha expression in human adipocyte precursor cells: a possible explanation for its adipogenic effect. |
| 15259 | 10436260 | Soluble tumor necrosis factor receptors in sera from patients with insulin-dependent diabetes mellitus: relations to duration and complications of disease. |
| 15260 | 10436260 | Soluble tumor necrosis factor receptors in sera from patients with insulin-dependent diabetes mellitus: relations to duration and complications of disease. |
| 15261 | 10436260 | Soluble tumor necrosis factor receptors in sera from patients with insulin-dependent diabetes mellitus: relations to duration and complications of disease. |
| 15262 | 10436260 | Concentrations of soluble receptors for tumor necrosis factor (p55 and p75) strongly correlate with clinical stage and progression of infectious diseases, and may be useful in monitoring autoimmune diseases. |
| 15263 | 10436260 | Concentrations of soluble receptors for tumor necrosis factor (p55 and p75) strongly correlate with clinical stage and progression of infectious diseases, and may be useful in monitoring autoimmune diseases. |
| 15264 | 10436260 | Concentrations of soluble receptors for tumor necrosis factor (p55 and p75) strongly correlate with clinical stage and progression of infectious diseases, and may be useful in monitoring autoimmune diseases. |
| 15265 | 10436260 | However, the role of soluble TNF receptors in insulin-dependent diabetes mellitus (type 1 DM) is not clear. |
| 15266 | 10436260 | However, the role of soluble TNF receptors in insulin-dependent diabetes mellitus (type 1 DM) is not clear. |
| 15267 | 10436260 | However, the role of soluble TNF receptors in insulin-dependent diabetes mellitus (type 1 DM) is not clear. |
| 15268 | 10436260 | We have compared levels of p55 and p75 in sera from different groups of type 1 DM patients. |
| 15269 | 10436260 | We have compared levels of p55 and p75 in sera from different groups of type 1 DM patients. |
| 15270 | 10436260 | We have compared levels of p55 and p75 in sera from different groups of type 1 DM patients. |
| 15271 | 10436260 | Both p55 and p75 increased with severity of type 1 DM complications (P < 0.00001). |
| 15272 | 10436260 | Both p55 and p75 increased with severity of type 1 DM complications (P < 0.00001). |
| 15273 | 10436260 | Both p55 and p75 increased with severity of type 1 DM complications (P < 0.00001). |
| 15274 | 10436260 | These results indicate that type 1 DM without complications is associated with lower serum levels of p55 than in healthy controls, and that type 1 DM complications increase the p55 and p75 levels. |
| 15275 | 10436260 | These results indicate that type 1 DM without complications is associated with lower serum levels of p55 than in healthy controls, and that type 1 DM complications increase the p55 and p75 levels. |
| 15276 | 10436260 | These results indicate that type 1 DM without complications is associated with lower serum levels of p55 than in healthy controls, and that type 1 DM complications increase the p55 and p75 levels. |
| 15277 | 10436260 | In addition, the results suggest that increased serum levels of p55 and p75 in type 1 DM patients may be early markers of type 1 DM complications. |
| 15278 | 10436260 | In addition, the results suggest that increased serum levels of p55 and p75 in type 1 DM patients may be early markers of type 1 DM complications. |
| 15279 | 10436260 | In addition, the results suggest that increased serum levels of p55 and p75 in type 1 DM patients may be early markers of type 1 DM complications. |
| 15280 | 10436179 | Epistatic effects of genes encoding tumor necrosis factor-alpha, immunoglobulin allotypes, and HLA antigens on susceptibility to non-insulin-dependent (type 2) diabetes mellitus. |
| 15281 | 10433099 | CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. |
| 15282 | 10433099 | However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic beta-cells that do not express MHC (major histocompatibility complex) class II molecules. |
| 15283 | 10433099 | Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic beta-cells are destroyed by CD4+ T lymphocytes. |
| 15284 | 10433099 | IFN (interferon)-gamma, tumor necrosis factor-alpha, interleukin-1 and their combinations failed to enhance Fas expression. |
| 15285 | 10433099 | Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-gamma-treated MIN6N8 cells with FasL upregulation. |
| 15286 | 10426368 | Accordingly, splenic lymphoid cells (SLC) from hIL-13-treated mice secreted less interferon (IFN)-gamma upon ex vivo stimulation with Concanavalin A than controls, and anti-CD3 monoclonal antibody-induced activation of T-cells in vivo resulted in lower blood levels of IFN-gamma and tumor necrosis factor-alpha and augmented blood levels of IL-4 in NOD mice pretreated with hIL-13. hIL-13 treatment also increased the blood levels of IgE and inhibited the transfer of type 1 diabetes by spleen cells from a diabetic donor to irradiated recipients. |
| 15287 | 10426368 | Taken together, these data add hIL-13 to the list of cytokines capable of downregulating immunoinflammatory diabetogenic pathways in NOD mice, and further support the concept that IL-4-related anti-inflammatory cytokines might have a role in the prevention of type 1 diabetes. |
| 15288 | 10422520 | [Relation between cytokines (TNF-alpha, IL-1 and 6) and homocysteine in android obesity and the phenomenon of insulin resistance syndromes]. |
| 15289 | 10422520 | [Relation between cytokines (TNF-alpha, IL-1 and 6) and homocysteine in android obesity and the phenomenon of insulin resistance syndromes]. |
| 15290 | 10422520 | [Relation between cytokines (TNF-alpha, IL-1 and 6) and homocysteine in android obesity and the phenomenon of insulin resistance syndromes]. |
| 15291 | 10422520 | [Relation between cytokines (TNF-alpha, IL-1 and 6) and homocysteine in android obesity and the phenomenon of insulin resistance syndromes]. |
| 15292 | 10422520 | TNF-alpha (so-called cachectin), IL-1 and 6 are important regulating agents in the homeostasis of energy in the organism, as among others they control processes of apoptosis and thus also the volume of adipose and muscular tissues. |
| 15293 | 10422520 | TNF-alpha (so-called cachectin), IL-1 and 6 are important regulating agents in the homeostasis of energy in the organism, as among others they control processes of apoptosis and thus also the volume of adipose and muscular tissues. |
| 15294 | 10422520 | TNF-alpha (so-called cachectin), IL-1 and 6 are important regulating agents in the homeostasis of energy in the organism, as among others they control processes of apoptosis and thus also the volume of adipose and muscular tissues. |
| 15295 | 10422520 | TNF-alpha (so-called cachectin), IL-1 and 6 are important regulating agents in the homeostasis of energy in the organism, as among others they control processes of apoptosis and thus also the volume of adipose and muscular tissues. |
| 15296 | 10422520 | By acting on phosphorylation of IRS-1 and PI-3 kinase TNF-alpha promotes significantly insulin resistance, causes deterioration of diabetes, as well as elevated body temperature, sleepiness and anorexia. |
| 15297 | 10422520 | By acting on phosphorylation of IRS-1 and PI-3 kinase TNF-alpha promotes significantly insulin resistance, causes deterioration of diabetes, as well as elevated body temperature, sleepiness and anorexia. |
| 15298 | 10422520 | By acting on phosphorylation of IRS-1 and PI-3 kinase TNF-alpha promotes significantly insulin resistance, causes deterioration of diabetes, as well as elevated body temperature, sleepiness and anorexia. |
| 15299 | 10422520 | By acting on phosphorylation of IRS-1 and PI-3 kinase TNF-alpha promotes significantly insulin resistance, causes deterioration of diabetes, as well as elevated body temperature, sleepiness and anorexia. |
| 15300 | 10422520 | In a group of 65 patients, mostly with android obesity, in hyperleptinaemic and insulin resistant probands with coronarographically confirmed microvascular angina pectoris (n = 22) or IHD, mostly after a myocardial infarction (n = 43) with one or more significant stenoses on the epicardial coronary arteries in half the patients positive or elevated TNF-alpha was found and in 28% also IL-6. |
| 15301 | 10422520 | In a group of 65 patients, mostly with android obesity, in hyperleptinaemic and insulin resistant probands with coronarographically confirmed microvascular angina pectoris (n = 22) or IHD, mostly after a myocardial infarction (n = 43) with one or more significant stenoses on the epicardial coronary arteries in half the patients positive or elevated TNF-alpha was found and in 28% also IL-6. |
| 15302 | 10422520 | In a group of 65 patients, mostly with android obesity, in hyperleptinaemic and insulin resistant probands with coronarographically confirmed microvascular angina pectoris (n = 22) or IHD, mostly after a myocardial infarction (n = 43) with one or more significant stenoses on the epicardial coronary arteries in half the patients positive or elevated TNF-alpha was found and in 28% also IL-6. |
| 15303 | 10422520 | In a group of 65 patients, mostly with android obesity, in hyperleptinaemic and insulin resistant probands with coronarographically confirmed microvascular angina pectoris (n = 22) or IHD, mostly after a myocardial infarction (n = 43) with one or more significant stenoses on the epicardial coronary arteries in half the patients positive or elevated TNF-alpha was found and in 28% also IL-6. |
| 15304 | 10416955 | IL-6 is released by a range of tissues in response to stimulation by the monocyte-derived cytokines interleukin-1 and tumor necrosis factor; by suppressing production of these cytokines, fish oil, alpha-linolenic acid, and pentoxifylline can reduce IL-6 synthesis. |
| 15305 | 10415614 | Treatment of Balb/c male mice for two weeks resulted in the increase of IL-4, and the decrease of TNF-alpha, IFN-gamma, and IL-2 release from stimulated splenocytes, suggesting that UK-114 modulates the Th1/Th2 cytokine profile toward Th2. |
| 15306 | 10415018 | Islet inflammation begins as peripheral benign Th2 type insulitis and progresses to destructive Th1 type insulitis, which is driven by the innate immune system via secretion of IL-12 and IL-18. |
| 15307 | 10415018 | In IL-18-treated animals, we detected significantly lower intraislet infiltration (p < 0.05) and concomitantly an impaired progression from Th2 insulitis to Th1-dependent insulitis, as evidenced from IFN-gamma and IL-10 mRNA levels in tissue. |
| 15308 | 10415018 | The deficient progression was probably due to lesser mRNA expression of the Th1 driving cytokines IL-12 and IL-18 by the innate immune system (p < 0.05). |
| 15309 | 10415018 | Cultivation of islets with IL-18 affected NO production or mitochondrial activity and did not protect from the toxicity mediated by IL-1beta, TNF-alpha, and IFN-gamma. |
| 15310 | 10405788 | Hypertension and insulin resistance: role of peroxisome proliferator-activated receptor gamma. |
| 15311 | 10405788 | Hypertension and insulin resistance: role of peroxisome proliferator-activated receptor gamma. |
| 15312 | 10405788 | Recently, a new class of antidiabetic agents, thiazolidinediones (TZD) has been developed and has been shown to improve insulin resistance by binding and activating a nuclear receptor, peroxisome proliferator-activated receptor (PPAR) gamma. 3. cDNA of rat PPAR gamma 1 and gamma 2 were cloned and gene regulation of PPAR gamma in rat mature adipocytes was examined. |
| 15313 | 10405788 | Recently, a new class of antidiabetic agents, thiazolidinediones (TZD) has been developed and has been shown to improve insulin resistance by binding and activating a nuclear receptor, peroxisome proliferator-activated receptor (PPAR) gamma. 3. cDNA of rat PPAR gamma 1 and gamma 2 were cloned and gene regulation of PPAR gamma in rat mature adipocytes was examined. |
| 15314 | 10405788 | Hydrogen peroxide, an oxygen radical, which is recognized to be the common intracellular signal for multiple risk factors, potently down-regulated PPAR gamma mRNA expression in rat mature adipocytes. 4. |
| 15315 | 10405788 | Hydrogen peroxide, an oxygen radical, which is recognized to be the common intracellular signal for multiple risk factors, potently down-regulated PPAR gamma mRNA expression in rat mature adipocytes. 4. |
| 15316 | 10405788 | Tumour necrosis factor (TNF)-alpha, which is considered to play a role in obesity-induced non-insulin-dependent diabetes mellitus and to augment oxidative stress, also suppressed PPAR gamma expression. 5. |
| 15317 | 10405788 | Tumour necrosis factor (TNF)-alpha, which is considered to play a role in obesity-induced non-insulin-dependent diabetes mellitus and to augment oxidative stress, also suppressed PPAR gamma expression. 5. |
| 15318 | 10405788 | Thiazolidinediones dose-dependently recovered TNF-alpha-induced down-regulation of PPAR gamma mRNA expression. 6. |
| 15319 | 10405788 | Thiazolidinediones dose-dependently recovered TNF-alpha-induced down-regulation of PPAR gamma mRNA expression. 6. |
| 15320 | 10405788 | The modulation of PPAR gamma expression by TZD can be one mechanism for the improvement of insulin resistance by TZD. 7. |
| 15321 | 10405788 | The modulation of PPAR gamma expression by TZD can be one mechanism for the improvement of insulin resistance by TZD. 7. |
| 15322 | 10405788 | The PPAR gamma gene transcript was detected in cultured endothelial cells. 8. |
| 15323 | 10405788 | The PPAR gamma gene transcript was detected in cultured endothelial cells. 8. |
| 15324 | 10395191 | The role of TNFalpha and TNF receptors in obesity and insulin resistance. |
| 15325 | 10395191 | Earlier studies have indicated that quantitative regulation of the insulin sensitive glucose transporters (Glut-4) and insulin receptors themselves may contribute to this disorder, however, these two factors are probably inadequate to explain the extent of insulin resistance. |
| 15326 | 10393700 | Human beta-cell preparations were cultured for 48 or 72 hours with or without IL-1beta, TNF-alpha, or IFN-gamma, alone or in combination. |
| 15327 | 10393700 | Cytokine combinations, in particular IL-1beta plus IFN-gamma, disproportionately elevated medium proinsulin levels. |
| 15328 | 10393700 | The delay in proinsulin conversion can be attributed to lower expression of PC1 and PC2 convertases. |
| 15329 | 10389841 | Activation of the sphingomyelin/ceramide pathway may mediate interleukin-1-induced beta-cell death (Welsh, N: Interleuken-1beta-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF-2 in the insulin-producing cell line RINm5F. |
| 15330 | 10389841 | The ceramide effect on cell viability mimicked the effect of the cytokines TNF-alpha, IL-1beta, and IFN-gamma, reported stimulators of sphingomyelin hydrolysis. |
| 15331 | 10385418 | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. |
| 15332 | 10385418 | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. |
| 15333 | 10385418 | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. |
| 15334 | 10385418 | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. |
| 15335 | 10385418 | Tumor necrosis factor-alpha (TNFalpha) is a potential mediator of beta cell destruction in insulin-dependent diabetes mellitus. |
| 15336 | 10385418 | Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). |
| 15337 | 10385418 | Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). |
| 15338 | 10385418 | Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). |
| 15339 | 10385418 | Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). |
| 15340 | 10385418 | Primary beta cells express low levels of the type I TNF receptor (TNFR1) but do not express the type 2 receptor (TNFR2). |
| 15341 | 10385418 | Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. |
| 15342 | 10385418 | Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. |
| 15343 | 10385418 | Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. |
| 15344 | 10385418 | Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. |
| 15345 | 10385418 | Evidence for TNFR1 expression on beta cells came from flow cytometry using monoclonal antibodies specific for TNFR1 and TNFR2 and from RT-PCR of beta cell RNA. |
| 15346 | 10385418 | TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. |
| 15347 | 10385418 | TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. |
| 15348 | 10385418 | TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. |
| 15349 | 10385418 | TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. |
| 15350 | 10385418 | TNF induced NF-kappaB activation in both primary islet cells and NIT-1 cells. |
| 15351 | 10385418 | Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). |
| 15352 | 10385418 | Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). |
| 15353 | 10385418 | Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). |
| 15354 | 10385418 | Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). |
| 15355 | 10385418 | Apoptosis in response to TNFalpha was observed in NIT-1 cells whereas apoptosis of primary beta cells required both TNFalpha and interferon-gamma (IFNgamma). |
| 15356 | 10385418 | Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). |
| 15357 | 10385418 | Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). |
| 15358 | 10385418 | Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). |
| 15359 | 10385418 | Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). |
| 15360 | 10385418 | Apoptosis could be prevented in NIT-1 cells by expression of dominant negative Fas-associating protein with death domain (dnFADD). |
| 15361 | 10385418 | Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. |
| 15362 | 10385418 | Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. |
| 15363 | 10385418 | Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. |
| 15364 | 10385418 | Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. |
| 15365 | 10385418 | Apoptosis in NIT-1 cells was increased by coincubation with IFNgamma, which also increased caspase 1 expression. |
| 15366 | 10385418 | Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. |
| 15367 | 10385418 | Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. |
| 15368 | 10385418 | Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. |
| 15369 | 10385418 | Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. |
| 15370 | 10385418 | Caspase activation is the dominant pathway of TNF-induced cell death in NIT-1 cells and may be an important mechanism of beta cell damage in insulin-dependent diabetes mellitus. |
| 15371 | 10382275 | We also show that serum lipids cause a generalized decrease in macrophage cytokine production using interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-beta 1) as marker cytokines. |
| 15372 | 10369924 | The central MHC gene IKBL carries a structural polymorphism that is associated with HLA-A3,B7,DR15. |
| 15373 | 10369924 | The central MHC gene IKBL carries a structural polymorphism that is associated with HLA-A3,B7,DR15. |
| 15374 | 10369924 | Susceptibility to several disorders, including insulin-dependent diabetes mellitus and multiple sclerosis, has been associated with alleles of HLA class II genes and loci in the TNF cluster in the central major histocompatibility complex (MHC) region. |
| 15375 | 10369924 | Susceptibility to several disorders, including insulin-dependent diabetes mellitus and multiple sclerosis, has been associated with alleles of HLA class II genes and loci in the TNF cluster in the central major histocompatibility complex (MHC) region. |
| 15376 | 10369924 | Here we address the IKBL gene, which lies near the TNF cluster at the telomeric end of the central MHC. |
| 15377 | 10369924 | Here we address the IKBL gene, which lies near the TNF cluster at the telomeric end of the central MHC. |
| 15378 | 10369924 | The latter (IKBL+738) was present in multiple examples of the 7.1 haplotype [HLA-A3, B7, DR2 (DR15)] and resulted in a cysteine to arginine substitution in a predicted protein kinase C phosphorylation site. |
| 15379 | 10369924 | The latter (IKBL+738) was present in multiple examples of the 7.1 haplotype [HLA-A3, B7, DR2 (DR15)] and resulted in a cysteine to arginine substitution in a predicted protein kinase C phosphorylation site. |
| 15380 | 10369423 | It has recently been indicated that tumor necrosis factor-alpha (TNF-alpha) production is increased under chronic hyperglycemia and TNF-alpha has harmful effects on insulin sensitivity and possibly on chronic diabetic complications. |
| 15381 | 10362456 | Peroxisome proliferator activated receptor-gamma, leptin and tumor necrosis factor-alpha mRNA expression during very low calorie diet in subcutaneous adipose tissue in obese women. |
| 15382 | 10358748 | These results suggest the involvement of TNF-alpha in the damage of the insulin producing cells and thus an immunity-related inflammatory process. |
| 15383 | 10342808 | The bcl-2-transfected beta-cells were fully protected from impaired insulin secretion and destruction resulting from incubation for 5 days with the cytokine combination of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. |
| 15384 | 10342486 | We have analyzed rat and human islet responses in parallel, 48 h after exposure to the nitric oxide donor S-nitrosoglutathione, the mixed donor 3-morpholinosydnonimine, hypoxanthine/xanthine oxidase, peroxynitrite, and combined cytokines (interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma). |
| 15385 | 10342486 | Rat islet insulin secretion was reduced by S-nitrosoglutathione or combined cytokines, but unexpectedly increased by peroxynitrite or hypoxanthine/xanthine oxidase. |
| 15386 | 10339629 | Changes in exercise habits, body habitus, leptin, amylin, tumor necrosis factor alpha, and nitric oxide all play a role in the pathogenesis of age-related insulin resistance. |
| 15387 | 10334320 | These included cholecystokinin A and B receptors (CCK-AR and CCK-BR), glucagon-like peptide 1 receptor (GLP-1R), the LIM/homeodomain islet-1 gene (Isl-1), the caudal-type homeodomain 3 (CDX-3), the uncoupling protein 1 (UCP-1), the beta3-adrenoceptor (beta3-AR), the fatty acid-binding protein 2 (FABP-2), the hormone-sensitive lipase (HSL), the lipoprotein lipase (LPL), the apoprotein-C2 (apo-C2), the insulin receptor substrate-1 (IRS-1), the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and the liver carnitine palmitoyltransferase-1 (CPT-1). |
| 15388 | 10334320 | Phenotypes related to obesity such as BMI, adult life body weight gain, fasting leptin, insulin, fasting glycerol, and free fatty acids were used for nonparametric sib-pair analyses. |
| 15389 | 10334320 | Moreover, a suggestive indication for linkage was found between the Isl-1 locus and BMI and leptin values (P = 0.001 and 0.0003, respectively) and leptin adjusted for BMI (P = 0.0001). |
| 15390 | 10334320 | Multipoint analyses for leptin trait with Isl-1 and two flanking markers (D5S418 and D5S407) showed that the logarithm of odds (LOD) score is 1.73, coinciding with the Isl-1 locus. |
| 15391 | 10334320 | Although marginally positive indications for linkage in subgroups of families were found with IRS-1, CPT-1, and HSL loci, our data suggested that these genes are not major contributors to obesity. |
| 15392 | 10331417 | Tumor necrosis factor system activity is associated with insulin resistance and dyslipidemia in myotonic dystrophy. |
| 15393 | 10331417 | In a recent study, plasma soluble tumor necrosis factor receptor (sTNFR)2 levels were found to be associated with muscle tissue mass and insulin resistance. |
| 15394 | 10330425 | Leukocyte 12-lipoxygenase (12-LO) gene expression in pancreatic beta cells is upregulated by cytotoxic cytokines like IL-1beta. |
| 15395 | 10330425 | Isolated pancreatic islets were treated with IL-1beta, TNF-alpha, and IFN-gamma for 18 hours. |
| 15396 | 10330425 | Isolated peritoneal macrophages were stimulated for 48 hours with IFN-gamma + LPS and compared for nitrate/nitrite generation. 12-LO KO macrophages generated 50% less nitrate/nitrite when compared with C57BL/6 macrophages. |
| 15397 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15398 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15399 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15400 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15401 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15402 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15403 | 10328964 | Tumor necrosis factor-alpha and basic fibroblast growth factor differentially inhibit the insulin-like growth factor-I induced expression of myogenin in C2C12 myoblasts. |
| 15404 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15405 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15406 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15407 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15408 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15409 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15410 | 10328964 | Tumor necrosis factor-alpha (TNF-alpha) plays a role in several disease states such as sepsis, cachexia, and non-insulin-dependent diabetes. |
| 15411 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15412 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15413 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15414 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15415 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15416 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15417 | 10328964 | TNF-alpha interferes with insulin signaling and inhibits differentiation-specific gene expression in adipose tissue and skeletal muscle. |
| 15418 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15419 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15420 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15421 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15422 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15423 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15424 | 10328964 | We have examined the mechanisms by which TNF-alpha, in comparison to basic fibroblast growth factor (bFGF), inhibits the insulin-like growth factor-I (IGF-I)-induced differentiation of C2C12 myoblasts. |
| 15425 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15426 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15427 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15428 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15429 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15430 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15431 | 10328964 | Adhesion of quiescent, suspended myoblasts to collagen in high concentrations of IGF-I (10 nM) induced these cells to proliferate during the initial 24 h postplating and in so doing transiently inhibited the expression of myogenin, an essential transcription factor controlling myoblast differentiation. |
| 15432 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15433 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15434 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15435 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15436 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15437 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15438 | 10328964 | Low doses of IGF-I (1 nM) were minimally mitogenic and enhanced muscle-specific gene expression. |
| 15439 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15440 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15441 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15442 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15443 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15444 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15445 | 10328964 | Quiescent myoblasts treated with bFGF in combination with IGF-I did not express myogenin, but expressed proliferating cell nuclear antigen and underwent DNA synthesis. |
| 15446 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15447 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15448 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15449 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15450 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15451 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15452 | 10328964 | In contrast, TNF-alpha in the presence or absence of 1 nM IGF-I, did not stimulate DNA synthesis in myoblasts. |
| 15453 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15454 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15455 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15456 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15457 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15458 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15459 | 10328964 | However, TNF-alpha inhibited myogenin mRNA and protein expression. |
| 15460 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15461 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15462 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15463 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15464 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15465 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15466 | 10328964 | Expression of the cyclin-dependent kinase inhibitor p21 correlated with myogenin expression and myoblast differentiation, but not with growth arrest. |
| 15467 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15468 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15469 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15470 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15471 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15472 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15473 | 10328964 | These results indicate that both TNF-alpha and bFGF inhibit myogenin expression but differentially influence myoblast proliferation. |
| 15474 | 10320053 | It has been known for some time that down-regulation and reduced kinase activity of the insulin receptor play a role in insulin resistance; however, it has recently emerged that defects in the intracellular responses to insulin are also very important. |
| 15475 | 10320053 | We found that the insulin-stimulated activation of MAP kinase was defective in obese, insulin-resistant mice. |
| 15476 | 10320053 | Similarly, we investigated insulin-stimulated PI3-kinase activation in the isolated soleus muscle of lean and obese mice, and found a marked reduction in the PI3-kinase activation of obese animals. |
| 15477 | 10320053 | The magnitude of the effect was greater than the reduction in insulin receptor activation, suggesting that impairment of PI3-kinase activation is a very important element in the development of insulin resistance in obese mice. |
| 15478 | 10320053 | In keeping with this, we found that the defect in PI3-kinase activation developed in young obese mice before the emergence of overt insulin resistance. |
| 15479 | 10320053 | In adipocytes from young obese mice in which insulin resistance had not yet developed, we found that there were already marked defects in IRS-1 tyrosine phosphorylation. |
| 15480 | 10320053 | Such a process could contribute to the defective IRS-1 tyrosine phosphorylation in insulin-resistant animals. |
| 15481 | 10320053 | We found that brief exposure of 3T3-L1 adipocytes to platelet-derived growth factor led to IRS-1 serine/threonine phosphorylation through a PI3-kinase-dependent pathway, and that this prevented phosphorylation of the tyrosine residues of IRS-1. |
| 15482 | 10320053 | Such a mechanism, induced by growth factors, TNF-alpha or some other agent, may play an important role in the development of insulin resistance in obese mice. |
| 15483 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15484 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15485 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15486 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15487 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15488 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15489 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15490 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15491 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15492 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 15493 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15494 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15495 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15496 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15497 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15498 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15499 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15500 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15501 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15502 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 15503 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15504 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15505 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15506 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15507 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15508 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15509 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15510 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15511 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15512 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 15513 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15514 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15515 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15516 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15517 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15518 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15519 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15520 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15521 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15522 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 15523 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15524 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15525 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15526 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15527 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15528 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15529 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15530 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15531 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15532 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 15533 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15534 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15535 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15536 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15537 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15538 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15539 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15540 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15541 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15542 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 15543 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15544 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15545 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15546 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15547 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15548 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15549 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15550 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15551 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15552 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 15553 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15554 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15555 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15556 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15557 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15558 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15559 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15560 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15561 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15562 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 15563 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15564 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15565 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15566 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15567 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15568 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15569 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15570 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15571 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15572 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 15573 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15574 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15575 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15576 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15577 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15578 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15579 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15580 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15581 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15582 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 15583 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 15584 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 15585 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 15586 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 15587 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 15588 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 15589 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 15590 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 15591 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 15592 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 15593 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 15594 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 15595 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 15596 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 15597 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 15598 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 15599 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 15600 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 15601 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 15602 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 15603 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 15604 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 15605 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 15606 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 15607 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 15608 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 15609 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 15610 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 15611 | 10221665 | Systemic levels of cytokines and GAD-specific autoantibodies isotypes in Chinese IDDM patients. |
| 15612 | 10221665 | It is not clear if a Th1/Th2 imbalance in Type 1 diabetes (insulin-dependent diabetes mellitus, IDDM) would lead to a particular antigen-specific IgG subclass dominant as had been shown in the mouse model. |
| 15613 | 10221665 | With high-sensitivity ELISA systems that measure sub-picogram cytokine concentrations, 26 of the 41 patients (63.4%) had at least one of the pro-inflammatory Th1 cytokines (TNF-alpha, IFN-gamma and IL-12) detected. |
| 15614 | 10212230 | Treatment of rat islets with poly(IC) + interferon-gamma (IFN-gamma) stimulates the time- and concentration-dependent expression of iNOS and production of nitrite by rat islets. iNOS expression and nitrite production by rat islets in response to poly(IC) + IFN-gamma correlate with an inhibition of insulin secretion and islet degeneration, effects that are prevented by the iNOS inhibitor aminoguanidine (AG). |
| 15615 | 10212230 | We have previously shown that poly(IC) + IFN-gamma activates resident macrophages, stimulating iNOS expression, nitric oxide production and interleukin-1 (IL-1) release. |
| 15616 | 10212230 | In addition, in response to tumor necrosis factor-alpha (TNF-alpha) + lipopolysaccharide, activated resident macrophages mediate beta-cell damage via intraislet IL-1 release followed by IL-1-induced iNOS expression by beta-cells. |
| 15617 | 10212230 | Treatment of macrophage-depleted rat islets for 40 h with poly(IC) + IFN-gamma results in the expression of iNOS, production of nitrite, and inhibition of insulin secretion. |
| 15618 | 10212230 | Poly IC + IFN-gamma stimulates iNOS expression and inhibits insulin secretion by primary beta-cells purified by fluorescence-activated cell sorting. |
| 15619 | 10212230 | In addition, AG prevents the inhibitory effects of poly(IC) + IFN-gamma on glucose-stimulated insulin secretion by beta-cells. |
| 15620 | 10212230 | These results indicate that dsRNA + IFN-gamma interacts directly with beta-cells stimulating iNOS expression and inhibiting insulin secretion in a nitric oxide-dependent manner. |
| 15621 | 10202048 | These changes occurred contemporaneously with a shift in the profile of circulating cytokines from a Th1-dominant (IFN-gamma) to Th2-dominant (IL-4, IL-10) phenotype. |
| 15622 | 10202048 | No significant changes in either circulating IL-1beta, IL-6, or TNF-alpha levels were observed in infected mice. |
| 15623 | 10201999 | To address the question of whether the cell death-inducing cytokines TNF and lymphotoxin alpha are involved in this process, we generated nonobese diabetic (NOD) mice that are deficient for TNF receptor 1 (TNFR1 or TNFRp55). |
| 15624 | 10201999 | To address the question of whether the cell death-inducing cytokines TNF and lymphotoxin alpha are involved in this process, we generated nonobese diabetic (NOD) mice that are deficient for TNF receptor 1 (TNFR1 or TNFRp55). |
| 15625 | 10201999 | To address the question of whether the cell death-inducing cytokines TNF and lymphotoxin alpha are involved in this process, we generated nonobese diabetic (NOD) mice that are deficient for TNF receptor 1 (TNFR1 or TNFRp55). |
| 15626 | 10201999 | Since this was probably due to the complex immunomodulatory effects of TNF and lymphotoxin alpha signaled via TNFR1 on lymphohemopoietic cells, adoptive transfer experiments with spleen cells from diabetic NOD mice were conducted. |
| 15627 | 10201999 | Since this was probably due to the complex immunomodulatory effects of TNF and lymphotoxin alpha signaled via TNFR1 on lymphohemopoietic cells, adoptive transfer experiments with spleen cells from diabetic NOD mice were conducted. |
| 15628 | 10201999 | Since this was probably due to the complex immunomodulatory effects of TNF and lymphotoxin alpha signaled via TNFR1 on lymphohemopoietic cells, adoptive transfer experiments with spleen cells from diabetic NOD mice were conducted. |
| 15629 | 10201999 | Together with the described expression patterns of perforin and TNF in the mononuclear islet infiltrates of NOD mice, these results indicate that two diabetogenic effector mechanisms are delivered by distinct cell populations: CD8+ T cells lyse beta cells via perforin-dependent cytotoxicity, whereas CD4+ T cells, macrophages, and dendritic cells contribute to diabetes development via TNFR1-dependent beta cell toxicity. |
| 15630 | 10201999 | Together with the described expression patterns of perforin and TNF in the mononuclear islet infiltrates of NOD mice, these results indicate that two diabetogenic effector mechanisms are delivered by distinct cell populations: CD8+ T cells lyse beta cells via perforin-dependent cytotoxicity, whereas CD4+ T cells, macrophages, and dendritic cells contribute to diabetes development via TNFR1-dependent beta cell toxicity. |
| 15631 | 10201999 | Together with the described expression patterns of perforin and TNF in the mononuclear islet infiltrates of NOD mice, these results indicate that two diabetogenic effector mechanisms are delivered by distinct cell populations: CD8+ T cells lyse beta cells via perforin-dependent cytotoxicity, whereas CD4+ T cells, macrophages, and dendritic cells contribute to diabetes development via TNFR1-dependent beta cell toxicity. |
| 15632 | 10199144 | The increase of both the influx of free fatty acid to liver and the production of TNF-alpha in adipose tissue may play an important role in mechanism of insulin resistance associated with central obesity. |
| 15633 | 10199144 | Exercise training also improves insulin sensitivity via increased oxidative enzymes, glucose transporters (GLUT4) and capillarity in muscle as well as by reducing abdominal fat. |
| 15634 | 10199140 | In the presence of diabetes or persistent hyperglycemia, many cytokines including growth factors such as PDGF, HB-EGF, IL-1 beta and TNF alpha are upregulated in intimal cells of the arterial or aortic wall. |
| 15635 | 10199140 | In addition, diabetes causes abnormal responsibility to HB-EGF, PDGF and TGF-beta in medial smooth muscle cells leading to the elevated activity to their proliferation and migration into the intima. |
| 15636 | 10199130 | Regarding mechanism of obesity-induced insulin resistance, the increased expression of Tumor necrosis factor alpha and abnormality in PTPase are postulated. |
| 15637 | 10195925 | C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? |
| 15638 | 10195925 | C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? |
| 15639 | 10195925 | C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? |
| 15640 | 10195925 | C-reactive protein, a hepatic acute phase protein largely regulated by circulating levels of interleukin-6, predicts coronary heart disease incidence in healthy subjects. |
| 15641 | 10195925 | C-reactive protein, a hepatic acute phase protein largely regulated by circulating levels of interleukin-6, predicts coronary heart disease incidence in healthy subjects. |
| 15642 | 10195925 | C-reactive protein, a hepatic acute phase protein largely regulated by circulating levels of interleukin-6, predicts coronary heart disease incidence in healthy subjects. |
| 15643 | 10195925 | In this study we have sought associations of levels of C-reactive protein and interleukin-6 with measures of obesity and of chronic infection as their putative determinants. |
| 15644 | 10195925 | In this study we have sought associations of levels of C-reactive protein and interleukin-6 with measures of obesity and of chronic infection as their putative determinants. |
| 15645 | 10195925 | In this study we have sought associations of levels of C-reactive protein and interleukin-6 with measures of obesity and of chronic infection as their putative determinants. |
| 15646 | 10195925 | We have also related levels of C-reactive protein and interleukin-6 to markers of the insulin resistance syndrome and of endothelial dysfunction. |
| 15647 | 10195925 | We have also related levels of C-reactive protein and interleukin-6 to markers of the insulin resistance syndrome and of endothelial dysfunction. |
| 15648 | 10195925 | We have also related levels of C-reactive protein and interleukin-6 to markers of the insulin resistance syndrome and of endothelial dysfunction. |
| 15649 | 10195925 | We performed a cross-sectional study in 107 nondiabetic subjects: (1) Levels of C-reactive protein, and concentrations of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, were related to all measures of obesity, but titers of antibodies to Helicobacter pylori were only weakly and those of Chlamydia pneumoniae and cytomegalovirus were not significantly correlated with levels of these molecules. |
| 15650 | 10195925 | We performed a cross-sectional study in 107 nondiabetic subjects: (1) Levels of C-reactive protein, and concentrations of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, were related to all measures of obesity, but titers of antibodies to Helicobacter pylori were only weakly and those of Chlamydia pneumoniae and cytomegalovirus were not significantly correlated with levels of these molecules. |
| 15651 | 10195925 | We performed a cross-sectional study in 107 nondiabetic subjects: (1) Levels of C-reactive protein, and concentrations of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, were related to all measures of obesity, but titers of antibodies to Helicobacter pylori were only weakly and those of Chlamydia pneumoniae and cytomegalovirus were not significantly correlated with levels of these molecules. |
| 15652 | 10195925 | Levels of C-reactive protein were significantly related to those of interleukin-6 (r=0.37, P<0.0005) and tumor necrosis factor-alpha (r=0.46, P<0.0001). (2) Concentrations of C-reactive protein were related to insulin resistance as calculated from the homoeostasis model assessment model, blood pressure, HDL, and triglyceride, and to markers of endothelial dysfunction (plasma levels of von Willebrand factor, tissue plasminogen activator, and cellular fibronectin). |
| 15653 | 10195925 | Levels of C-reactive protein were significantly related to those of interleukin-6 (r=0.37, P<0.0005) and tumor necrosis factor-alpha (r=0.46, P<0.0001). (2) Concentrations of C-reactive protein were related to insulin resistance as calculated from the homoeostasis model assessment model, blood pressure, HDL, and triglyceride, and to markers of endothelial dysfunction (plasma levels of von Willebrand factor, tissue plasminogen activator, and cellular fibronectin). |
| 15654 | 10195925 | Levels of C-reactive protein were significantly related to those of interleukin-6 (r=0.37, P<0.0005) and tumor necrosis factor-alpha (r=0.46, P<0.0001). (2) Concentrations of C-reactive protein were related to insulin resistance as calculated from the homoeostasis model assessment model, blood pressure, HDL, and triglyceride, and to markers of endothelial dysfunction (plasma levels of von Willebrand factor, tissue plasminogen activator, and cellular fibronectin). |
| 15655 | 10195925 | These data suggest that adipose tissue is an important determinant of a low level, chronic inflammatory state as reflected by levels of interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, and that infection with H pylori, C pneumoniae, and cytomegalovirus is not. |
| 15656 | 10195925 | These data suggest that adipose tissue is an important determinant of a low level, chronic inflammatory state as reflected by levels of interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, and that infection with H pylori, C pneumoniae, and cytomegalovirus is not. |
| 15657 | 10195925 | These data suggest that adipose tissue is an important determinant of a low level, chronic inflammatory state as reflected by levels of interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, and that infection with H pylori, C pneumoniae, and cytomegalovirus is not. |
| 15658 | 10193411 | TNF-alpha has been implicated in the pathogenesis of insulin- dependent diabetes mellitus (IDDM). |
| 15659 | 10193411 | TNF-alpha has been implicated in the pathogenesis of insulin- dependent diabetes mellitus (IDDM). |
| 15660 | 10193411 | TNF-alpha has been implicated in the pathogenesis of insulin- dependent diabetes mellitus (IDDM). |
| 15661 | 10193411 | We investigated serum levels of sTNF receptors (sTNF-RI and sTNF-RII) in IDDM patients with or without PDR, and related these to the in vitro production of TNF-alpha upon activation of whole blood and isolated mononuclear cells (MNC). |
| 15662 | 10193411 | We investigated serum levels of sTNF receptors (sTNF-RI and sTNF-RII) in IDDM patients with or without PDR, and related these to the in vitro production of TNF-alpha upon activation of whole blood and isolated mononuclear cells (MNC). |
| 15663 | 10193411 | We investigated serum levels of sTNF receptors (sTNF-RI and sTNF-RII) in IDDM patients with or without PDR, and related these to the in vitro production of TNF-alpha upon activation of whole blood and isolated mononuclear cells (MNC). |
| 15664 | 10193411 | Inhibition of TNF-alpha by TNF-R in plasma supernatants of activated blood from PDR patients was demonstrated by increase of TNF-alpha activity in the presence of anti-TNF-RI and anti-TNF-RII antibodies. |
| 15665 | 10193411 | Inhibition of TNF-alpha by TNF-R in plasma supernatants of activated blood from PDR patients was demonstrated by increase of TNF-alpha activity in the presence of anti-TNF-RI and anti-TNF-RII antibodies. |
| 15666 | 10193411 | Inhibition of TNF-alpha by TNF-R in plasma supernatants of activated blood from PDR patients was demonstrated by increase of TNF-alpha activity in the presence of anti-TNF-RI and anti-TNF-RII antibodies. |
| 15667 | 10190896 | Of these, interleukin 1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma are perhaps the most important. |
| 15668 | 10190896 | Of these, interleukin 1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma are perhaps the most important. |
| 15669 | 10190896 | We found that islets deficient in Fas, IFN-gamma receptor, or inducible nitric oxide synthase had normal diabetes development; however, the specific lack of TNF- alpha receptor 1 (p55) afforded islets a profound protection from disease by altering the ability of islet-reactive, CD4(+) T cells to establish insulitis and subsequently destroy islet beta cells. |
| 15670 | 10190896 | We found that islets deficient in Fas, IFN-gamma receptor, or inducible nitric oxide synthase had normal diabetes development; however, the specific lack of TNF- alpha receptor 1 (p55) afforded islets a profound protection from disease by altering the ability of islet-reactive, CD4(+) T cells to establish insulitis and subsequently destroy islet beta cells. |
| 15671 | 10189559 | Elevated concentrations of the fibrinolytic inhibitor plasminogen activator inhibitor-1 are associated with insulin resistance. |
| 15672 | 10189559 | In experimental systems, increased expression and secretion of plasminogen activator inhibitor-1 by hepatocyte and endothelial cell lines can be induced by insulin, proinsulin-like molecules, triglyceride-rich lipoproteins and oxidized LDL, as well as by inducing insulin resistance in isolated hepatocytes. |
| 15673 | 10189559 | Concentrations of the endothelial cell protein von Willebrand factor are elevated in insulin-resistant states, suggesting that abnormalities of capillary endothelium, as well as those reported for endothelium-dependent vasodilatation, may play a role in the etiology of insulin resistance. |
| 15674 | 10189559 | It is proposed that the recent observations of secretion of interleukin-6 by adipose tissue, combined with the actions of adipose tissue-expressed tumor necrosis factor-alpha in obesity-induced insulin resistance, could underlie the associations of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease. |
| 15675 | 10102704 | Treatment of the cells with cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin-1beta, or with growth factors, such as platelet-derived growth factor, insulin-like growth factor-I, and epidermal growth factor, all led to NF-kappaB activation in cells cultured in both NG and HG. |
| 15676 | 10102704 | Treatment of the cells with cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin-1beta, or with growth factors, such as platelet-derived growth factor, insulin-like growth factor-I, and epidermal growth factor, all led to NF-kappaB activation in cells cultured in both NG and HG. |
| 15677 | 10102704 | The augmented TNF-alpha-induced NF-kappaB activation in HG was associated with increased TNF-alpha-mediated transcriptional activation of the vascular cell adhesion molecule-1 promoter. |
| 15678 | 10102704 | The augmented TNF-alpha-induced NF-kappaB activation in HG was associated with increased TNF-alpha-mediated transcriptional activation of the vascular cell adhesion molecule-1 promoter. |
| 15679 | 10102704 | HG-induced NF-kappaB activation was inhibited by a protein kinase C inhibitor, calphostin C. |
| 15680 | 10102704 | HG-induced NF-kappaB activation was inhibited by a protein kinase C inhibitor, calphostin C. |
| 15681 | 10051652 | We report here that the hyperleptinemia depletes adipocyte fat while profoundly down-regulating lipogenic enzymes and their transcription factor, peroxisome proliferator-activated receptor (PPAR)gamma in epididymal fat; enzymes of fatty acid oxidation and their transcription factor, PPARalpha, normally low in adipocytes, are up-regulated, as are uncoupling proteins 1 and 2. |
| 15682 | 10051652 | This transformation of adipocytes from cells that store triglycerides to fatty acid-oxidizing cells is accompanied by loss of the adipocyte markers, adipocyte fatty acid-binding protein 2, tumor necrosis factor alpha, and leptin, and by the appearance of the preadipocyte marker Pref-1. |
| 15683 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 15684 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 15685 | 10047431 | Both CD4(+)and CD8(+)T cells are required for IFN-gamma gene expression in pancreatic islets and autoimmune diabetes development in biobreeding rats. |
| 15686 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 15687 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 15688 | 10047431 | To study the relative roles of CD4(+)and CD8(+)T cells and their cytokine products in autoimmune diabetes development, we selectively depleted CD4(+)and CD8(+)T cells in autoimmune diabetes-prone (DP) biobreeding (BB) rats, by administrations of anti-CD2 and anti-CD8 monoclonal antibody (mAb) respectively. |
| 15689 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 15690 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 15691 | 10047431 | Depletion of CD4(+)T cells (by anti-CD2 mAb) in blood, spleen and islets prevented diabetes development in DP-BB rats, and depletion of CD8(+)T cells (by anti-CD8 mAb) delayed and significantly decreased diabetes incidence. |
| 15692 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 15693 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 15694 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells completely prevented IFN-gamma mRNA upregulation in islets of DP-BB rats above the low level expressed in islets of diabetes-resistant (DR) BB rats. |
| 15695 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 15696 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 15697 | 10047431 | Also, IL-10 mRNA levels in islets of DP-BB rats were significantly decreased by depletion of either CD4(+)or CD8(+)T cells, whereas the effects of the anti-T cell mAb on mRNA levels of other cytokines in islets (IL-2, IL-4, IL-12p40, and TNF-alpha) were discordant. |
| 15698 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 15699 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 15700 | 10047431 | In contrast, both mAb treatments significantly upregulated IL-4 and TNF-alpha mRNA levels in spleens of DP-BB rats. |
| 15701 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 15702 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 15703 | 10047431 | These results demonstrate that islet infiltration by both CD4(+)and CD8(+)T cells is required for IFN-gamma and IL-10 production in islets and beta-cell destruction. |
| 15704 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 15705 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 15706 | 10047431 | Depletion of either CD4(+)or CD8(+)T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically. |
| 15707 | 9933106 | Insulin-dependent diabetes mellitus (IDDM) is not a disease of unbridled destruction. |
| 15708 | 9933106 | The monokines IL-18, IL-12 and TNF-alpha were pivotal, their induction occurring almost immediately and their coordinate action being required for the onset of aggression. |
| 15709 | 9933106 | Other cytokines with direct toxicity for beta cells, including IL-1 -beta, IL-6 and IFN-gamma, were subsequently induced; in contrast, there was no cellular or molecular evidence of cell contact-mediated mechanisms of beta cell death. |
| 15710 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15711 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15712 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15713 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15714 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15715 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15716 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15717 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15718 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15719 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 15720 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15721 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15722 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15723 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15724 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15725 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15726 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15727 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15728 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15729 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 15730 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15731 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15732 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15733 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15734 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15735 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15736 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15737 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15738 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15739 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 15740 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15741 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15742 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15743 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15744 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15745 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15746 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15747 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15748 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15749 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 15750 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15751 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15752 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15753 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15754 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15755 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15756 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15757 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15758 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15759 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 15760 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15761 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15762 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15763 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15764 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15765 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15766 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15767 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15768 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15769 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 15770 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15771 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15772 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15773 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15774 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15775 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15776 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15777 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15778 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15779 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 15780 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15781 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15782 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15783 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15784 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15785 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15786 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15787 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15788 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15789 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 15790 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15791 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15792 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15793 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15794 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15795 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15796 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15797 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15798 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15799 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 15800 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15801 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15802 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15803 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15804 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15805 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15806 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15807 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15808 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15809 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 15810 | 9930944 | In this study, we investigated whether drugs such as currently used in islet-transplanted patients inhibit the release of IL-1beta, TNFalpha, and superoxide from mononuclear blood cells in vitro. |
| 15811 | 9930944 | In this study, we investigated whether drugs such as currently used in islet-transplanted patients inhibit the release of IL-1beta, TNFalpha, and superoxide from mononuclear blood cells in vitro. |
| 15812 | 9930944 | In this study, we investigated whether drugs such as currently used in islet-transplanted patients inhibit the release of IL-1beta, TNFalpha, and superoxide from mononuclear blood cells in vitro. |
| 15813 | 9930944 | In this study, we investigated whether drugs such as currently used in islet-transplanted patients inhibit the release of IL-1beta, TNFalpha, and superoxide from mononuclear blood cells in vitro. |
| 15814 | 9930944 | In this study, we investigated whether drugs such as currently used in islet-transplanted patients inhibit the release of IL-1beta, TNFalpha, and superoxide from mononuclear blood cells in vitro. |
| 15815 | 9930944 | Methylprednisolone (10 microg/ml) inhibited the release of IL-1beta and TNFalpha, but had no effect on superoxide generation. |
| 15816 | 9930944 | Methylprednisolone (10 microg/ml) inhibited the release of IL-1beta and TNFalpha, but had no effect on superoxide generation. |
| 15817 | 9930944 | Methylprednisolone (10 microg/ml) inhibited the release of IL-1beta and TNFalpha, but had no effect on superoxide generation. |
| 15818 | 9930944 | Methylprednisolone (10 microg/ml) inhibited the release of IL-1beta and TNFalpha, but had no effect on superoxide generation. |
| 15819 | 9930944 | Methylprednisolone (10 microg/ml) inhibited the release of IL-1beta and TNFalpha, but had no effect on superoxide generation. |
| 15820 | 9930944 | Both pentoxifylline (66 microg/ml) and cyclosporin A (300 ng/ml) slightly inhibited TNFalpha release without affecting IL-1beta or superoxide generation. |
| 15821 | 9930944 | Both pentoxifylline (66 microg/ml) and cyclosporin A (300 ng/ml) slightly inhibited TNFalpha release without affecting IL-1beta or superoxide generation. |
| 15822 | 9930944 | Both pentoxifylline (66 microg/ml) and cyclosporin A (300 ng/ml) slightly inhibited TNFalpha release without affecting IL-1beta or superoxide generation. |
| 15823 | 9930944 | Both pentoxifylline (66 microg/ml) and cyclosporin A (300 ng/ml) slightly inhibited TNFalpha release without affecting IL-1beta or superoxide generation. |
| 15824 | 9930944 | Both pentoxifylline (66 microg/ml) and cyclosporin A (300 ng/ml) slightly inhibited TNFalpha release without affecting IL-1beta or superoxide generation. |
| 15825 | 9930944 | Nicotinamide (0.25 mM) did not interfere with the generation TNFalpha or superoxide and only slightly inhibited IL-1beta production. |
| 15826 | 9930944 | Nicotinamide (0.25 mM) did not interfere with the generation TNFalpha or superoxide and only slightly inhibited IL-1beta production. |
| 15827 | 9930944 | Nicotinamide (0.25 mM) did not interfere with the generation TNFalpha or superoxide and only slightly inhibited IL-1beta production. |
| 15828 | 9930944 | Nicotinamide (0.25 mM) did not interfere with the generation TNFalpha or superoxide and only slightly inhibited IL-1beta production. |
| 15829 | 9930944 | Nicotinamide (0.25 mM) did not interfere with the generation TNFalpha or superoxide and only slightly inhibited IL-1beta production. |
| 15830 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 15831 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 15832 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 15833 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 15834 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 15835 | 9925347 | The role of tumor necrosis factor-alpha in insulin resistance has been studied in 59 patients with Type 2 diabetes, 28 with android type obesity and 35 healthy lean controls. |
| 15836 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15837 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15838 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15839 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15840 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15841 | 9920095 | Recent research suggests that tumor necrosis factor-alpha (TNF alpha) may play an important role in obesity-associated insulin resistance and diabetes. |
| 15842 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15843 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15844 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15845 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15846 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15847 | 9920095 | We studied the relationship between TNF alpha and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM). |
| 15848 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15849 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15850 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15851 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15852 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15853 | 9920095 | Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF alpha were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. |
| 15854 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15855 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15856 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15857 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15858 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15859 | 9920095 | There were moderate, but statistically significant, correlations between TNF alpha and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23-0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. |
| 15860 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15861 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15862 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15863 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15864 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15865 | 9920095 | We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. |
| 15866 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15867 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15868 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15869 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15870 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15871 | 9920095 | The data suggest a possible role for TNF alpha in the pathophysiology of insulin resistance. |
| 15872 | 9916130 | However, p38 kinase activation by mannitol or tumor necrosis factor-alpha was not inhibited by GF109203X. |
| 15873 | 9892227 | The heightened hepatic insulin sensitivity is supported by the decrease in gene expression of both glucose-6-phosphatase and PEPCK and by physiological hyperinsulinemia in VF- but not VF+ rats. |
| 15874 | 9892227 | The improvement in hepatic insulin sensitivity in VF- rats was also supported by a approximately 70% decrease in the plasma levels of insulin-like growth factor binding protein-1, a marker of insulin's transcription regulation in the liver. |
| 15875 | 9892227 | The removal of VF pads also resulted in marked decreases in the gene expression of tumor necrosis factor-alpha (by 72%) and leptin (by 60%) in subcutaneous fat. |
| 15876 | 9892218 | A mechanism of autoimmune destruction of islet beta-cells in type 1 diabetes has been proposed to be the binding of Fas ligand (FasL) on T-cells to Fas receptors on beta-cells. |
| 15877 | 9892218 | A mechanism of autoimmune destruction of islet beta-cells in type 1 diabetes has been proposed to be the binding of Fas ligand (FasL) on T-cells to Fas receptors on beta-cells. |
| 15878 | 9892218 | We investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice. |
| 15879 | 9892218 | We investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice. |
| 15880 | 9892218 | Two-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice. |
| 15881 | 9892218 | Two-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice. |
| 15882 | 9892218 | In contrast, Fas was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from diabetic mice, but it was nearly or totally absent on these cells in islet grafts from normoglycemic mice. |
| 15883 | 9892218 | In contrast, Fas was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from diabetic mice, but it was nearly or totally absent on these cells in islet grafts from normoglycemic mice. |
| 15884 | 9892218 | Also, mRNA levels of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were significantly lower in islet grafts from normoglycemic mice. |
| 15885 | 9892218 | Also, mRNA levels of interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were significantly lower in islet grafts from normoglycemic mice. |
| 15886 | 9892218 | Finally, Fas was induced on NOD islet cells by incubation with IL-1beta, IFN-gamma, and the combination of IL-1beta, TNF-alpha, and IFN-gamma. |
| 15887 | 9892218 | Finally, Fas was induced on NOD islet cells by incubation with IL-1beta, IFN-gamma, and the combination of IL-1beta, TNF-alpha, and IFN-gamma. |
| 15888 | 9892218 | These findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves. |
| 15889 | 9892218 | These findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves. |
| 15890 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15891 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15892 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15893 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15894 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15895 | 9882452 | The cytokine tumor necrosis factor-alpha (TNFalpha) contributes to metabolic changes in disease states such as insulin resistance. |
| 15896 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15897 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15898 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15899 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15900 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15901 | 9882452 | These changes coincided with a decrease in endothelin-1-induced phosphatidylinositol (PI) cycle activity in 3T3-L1 adipocytes chronically exposed to TNFalpha. |
| 15902 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15903 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15904 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15905 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15906 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15907 | 9882452 | Endothelin-1-induced mobilization of calcium from intracellular stores was also diminished by TNFalpha. |
| 15908 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15909 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15910 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15911 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15912 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15913 | 9882452 | The effect of TNFalpha on endothelin-1-induced PI cycle activity and calcium mobilization was not due to a decrease in endothelin receptors. |
| 15914 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15915 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15916 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15917 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15918 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15919 | 9882452 | However, TNFalpha did cause a moderate decrease in phosphatidylinositol 4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) activity in 3T3-L1 adipocytes. |
| 15920 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15921 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15922 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15923 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15924 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15925 | 9882452 | Combined, a decrease in phosphoinositide production and PIP2-specific PLC activity could be responsible for altering PI cycle activity and the generation of the second messenger myo-inositol 1,4,5-trisphosphate, thereby reducing calcium mobilization. |
| 15926 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15927 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15928 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15929 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15930 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15931 | 9882452 | Such changes in intracellular signaling may contribute to the pathophysiology of insulin resistance associated with TNFalpha. |
| 15932 | 9867218 | Sustained antibody-mediated inhibition of tumor necrosis factor (TNF) activity offers protection against Type I (insulin-dependent) diabetes mellitus in non-obese diabetic (NOD) mice. |
| 15933 | 9862421 | TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28. |
| 15934 | 9862421 | TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28. |
| 15935 | 9862421 | TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28. |
| 15936 | 9862421 | TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28. |
| 15937 | 9862421 | TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28. |
| 15938 | 9862421 | Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. |
| 15939 | 9862421 | Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. |
| 15940 | 9862421 | Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. |
| 15941 | 9862421 | Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. |
| 15942 | 9862421 | Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. |
| 15943 | 9862421 | We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. |
| 15944 | 9862421 | We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. |
| 15945 | 9862421 | We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. |
| 15946 | 9862421 | We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. |
| 15947 | 9862421 | We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. |
| 15948 | 9862421 | TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. |
| 15949 | 9862421 | TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. |
| 15950 | 9862421 | TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. |
| 15951 | 9862421 | TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. |
| 15952 | 9862421 | TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. |
| 15953 | 9862421 | Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells. |
| 15954 | 9862421 | Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells. |
| 15955 | 9862421 | Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells. |
| 15956 | 9862421 | Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells. |
| 15957 | 9862421 | Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells. |
| 15958 | 9853588 | Enhancement of MHC class II antigen expression by islets using TNFalpha and IFNgamma did not increase their stimulatory capacity in the islet cocultures, which may have been due to a corresponding absence of B7 expression. |
| 15959 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15960 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15961 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15962 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15963 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15964 | 9832430 | An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha. |
| 15965 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15966 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15967 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15968 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15969 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15970 | 9832430 | Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. |
| 15971 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15972 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15973 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15974 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15975 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15976 | 9832430 | The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. |
| 15977 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15978 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15979 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15980 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15981 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15982 | 9832430 | These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. |
| 15983 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15984 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15985 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15986 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15987 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15988 | 9832430 | TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. |
| 15989 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15990 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15991 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15992 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15993 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15994 | 9832430 | In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes. |
| 15995 | 9832419 | Functional analysis of tumor necrosis factor (TNF) receptors in TNF-alpha-mediated insulin resistance in genetic obesity. |
| 15996 | 9832419 | Functional analysis of tumor necrosis factor (TNF) receptors in TNF-alpha-mediated insulin resistance in genetic obesity. |
| 15997 | 9832419 | Functional analysis of tumor necrosis factor (TNF) receptors in TNF-alpha-mediated insulin resistance in genetic obesity. |
| 15998 | 9832419 | Functional analysis of tumor necrosis factor (TNF) receptors in TNF-alpha-mediated insulin resistance in genetic obesity. |
| 15999 | 9832419 | Functional analysis of tumor necrosis factor (TNF) receptors in TNF-alpha-mediated insulin resistance in genetic obesity. |
| 16000 | 9832419 | Tumor necrosis factor-alpha (TNF-alpha) is overexpressed in obesity and is a candidate mediator of obesity-induced insulin resistance. |
| 16001 | 9832419 | Tumor necrosis factor-alpha (TNF-alpha) is overexpressed in obesity and is a candidate mediator of obesity-induced insulin resistance. |
| 16002 | 9832419 | Tumor necrosis factor-alpha (TNF-alpha) is overexpressed in obesity and is a candidate mediator of obesity-induced insulin resistance. |
| 16003 | 9832419 | Tumor necrosis factor-alpha (TNF-alpha) is overexpressed in obesity and is a candidate mediator of obesity-induced insulin resistance. |
| 16004 | 9832419 | Tumor necrosis factor-alpha (TNF-alpha) is overexpressed in obesity and is a candidate mediator of obesity-induced insulin resistance. |
| 16005 | 9832419 | Complete lack of TNF-alpha function through targeted mutations in TNF-alpha gene or both of its receptors results in significant improvement of insulin sensitivity in dietary, chemical, or genetic models of rodent obesity. |
| 16006 | 9832419 | Complete lack of TNF-alpha function through targeted mutations in TNF-alpha gene or both of its receptors results in significant improvement of insulin sensitivity in dietary, chemical, or genetic models of rodent obesity. |
| 16007 | 9832419 | Complete lack of TNF-alpha function through targeted mutations in TNF-alpha gene or both of its receptors results in significant improvement of insulin sensitivity in dietary, chemical, or genetic models of rodent obesity. |
| 16008 | 9832419 | Complete lack of TNF-alpha function through targeted mutations in TNF-alpha gene or both of its receptors results in significant improvement of insulin sensitivity in dietary, chemical, or genetic models of rodent obesity. |
| 16009 | 9832419 | Complete lack of TNF-alpha function through targeted mutations in TNF-alpha gene or both of its receptors results in significant improvement of insulin sensitivity in dietary, chemical, or genetic models of rodent obesity. |
| 16010 | 9832419 | In this study, we have analyzed the in vivo role of TNF signaling from p55 [TNF receptor (TNFR) 1] and p75 (TNFR 2) TNFR in the development of insulin resistance by generating genetically obese mice (ob/ob) lacking p55 or p75 TNFRs. |
| 16011 | 9832419 | In this study, we have analyzed the in vivo role of TNF signaling from p55 [TNF receptor (TNFR) 1] and p75 (TNFR 2) TNFR in the development of insulin resistance by generating genetically obese mice (ob/ob) lacking p55 or p75 TNFRs. |
| 16012 | 9832419 | In this study, we have analyzed the in vivo role of TNF signaling from p55 [TNF receptor (TNFR) 1] and p75 (TNFR 2) TNFR in the development of insulin resistance by generating genetically obese mice (ob/ob) lacking p55 or p75 TNFRs. |
| 16013 | 9832419 | In this study, we have analyzed the in vivo role of TNF signaling from p55 [TNF receptor (TNFR) 1] and p75 (TNFR 2) TNFR in the development of insulin resistance by generating genetically obese mice (ob/ob) lacking p55 or p75 TNFRs. |
| 16014 | 9832419 | In this study, we have analyzed the in vivo role of TNF signaling from p55 [TNF receptor (TNFR) 1] and p75 (TNFR 2) TNFR in the development of insulin resistance by generating genetically obese mice (ob/ob) lacking p55 or p75 TNFRs. |
| 16015 | 9832419 | In the ob/ob mice, the absence of p55 caused a significant improvement in insulin sensitivity. p75 deficiency alone did not affect insulin sensitivity but might potentiate the effects of p55 deficiency in animals lacking both TNFRs. |
| 16016 | 9832419 | In the ob/ob mice, the absence of p55 caused a significant improvement in insulin sensitivity. p75 deficiency alone did not affect insulin sensitivity but might potentiate the effects of p55 deficiency in animals lacking both TNFRs. |
| 16017 | 9832419 | In the ob/ob mice, the absence of p55 caused a significant improvement in insulin sensitivity. p75 deficiency alone did not affect insulin sensitivity but might potentiate the effects of p55 deficiency in animals lacking both TNFRs. |
| 16018 | 9832419 | In the ob/ob mice, the absence of p55 caused a significant improvement in insulin sensitivity. p75 deficiency alone did not affect insulin sensitivity but might potentiate the effects of p55 deficiency in animals lacking both TNFRs. |
| 16019 | 9832419 | In the ob/ob mice, the absence of p55 caused a significant improvement in insulin sensitivity. p75 deficiency alone did not affect insulin sensitivity but might potentiate the effects of p55 deficiency in animals lacking both TNFRs. |
| 16020 | 9832419 | These results indicate that TNF-alpha is a component of insulin resistance in the ob/ob model of murine obesity and p55 TNFR is the predominant receptor mediating its actions. |
| 16021 | 9832419 | These results indicate that TNF-alpha is a component of insulin resistance in the ob/ob model of murine obesity and p55 TNFR is the predominant receptor mediating its actions. |
| 16022 | 9832419 | These results indicate that TNF-alpha is a component of insulin resistance in the ob/ob model of murine obesity and p55 TNFR is the predominant receptor mediating its actions. |
| 16023 | 9832419 | These results indicate that TNF-alpha is a component of insulin resistance in the ob/ob model of murine obesity and p55 TNFR is the predominant receptor mediating its actions. |
| 16024 | 9832419 | These results indicate that TNF-alpha is a component of insulin resistance in the ob/ob model of murine obesity and p55 TNFR is the predominant receptor mediating its actions. |
| 16025 | 9832415 | In nondiabetic muscle cells, acute (90-min) exposure to TNF alpha (5 ng/ml) stimulated glucose uptake (73 +/- 14% increase) to a greater extent than insulin (37 +/- 4%; P < 0.02). |
| 16026 | 9832415 | In nondiabetic muscle cells, acute (90-min) exposure to TNF alpha (5 ng/ml) stimulated glucose uptake (73 +/- 14% increase) to a greater extent than insulin (37 +/- 4%; P < 0.02). |
| 16027 | 9832415 | In nondiabetic muscle cells, acute (90-min) exposure to TNF alpha (5 ng/ml) stimulated glucose uptake (73 +/- 14% increase) to a greater extent than insulin (37 +/- 4%; P < 0.02). |
| 16028 | 9832415 | The acute uptake response to TNF alpha in diabetic cells (51 +/- 6% increase) was also greater than that to insulin (31 +/- 3%; P < 0.05). |
| 16029 | 9832415 | The acute uptake response to TNF alpha in diabetic cells (51 +/- 6% increase) was also greater than that to insulin (31 +/- 3%; P < 0.05). |
| 16030 | 9832415 | The acute uptake response to TNF alpha in diabetic cells (51 +/- 6% increase) was also greater than that to insulin (31 +/- 3%; P < 0.05). |
| 16031 | 9832415 | Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. |
| 16032 | 9832415 | Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. |
| 16033 | 9832415 | Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. |
| 16034 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16035 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16036 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16037 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16038 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16039 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16040 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16041 | 9820807 | Treating 3T3-L1 adipocytes with TNF-alpha decreases Na+/myo-inositol co-transporter (SMIT) mRNA levels and myo-inositol accumulation in a concentration-and time-dependent manner. |
| 16042 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16043 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16044 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16045 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16046 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16047 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16048 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16049 | 9820807 | Studies with actinomycin D suggest that RNA synthesis is required for the TNF-alpha-induced effect on SMIT mRNA levels. |
| 16050 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16051 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16052 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16053 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16054 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16055 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16056 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16057 | 9820807 | In contrast with the effect of TNF-alpha, hyperosmolarity increases SMIT mRNA levels and myo-inositol accumulation in 3T3-L1 adipocytes. |
| 16058 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16059 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16060 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16061 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16062 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16063 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16064 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16065 | 9820807 | In 3T3-L1 adipocytes, both TNF-alpha and hyperosmolarity increase mitogen-activated protein kinase kinase pathway activity; however, with the possible exception of c-Jun N-terminal kinase, this pathway does not seem to regulate SMIT mRNA levels or myo-inositol accumulation. |
| 16066 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16067 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16068 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16069 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16070 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16071 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16072 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16073 | 9820807 | TNF-alpha activates nuclear factor kappaB (NF-kappaB) in 3T3-L1 adipocytes but, unlike the effect of TNF-alpha on cultured endothelial cells, NF-kappaB does not seem to contribute to the regulation by TNF-alpha of SMIT gene expression in 3T3-L1 adipocytes. |
| 16074 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16075 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16076 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16077 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16078 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16079 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16080 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16081 | 9820807 | Therefore other signal transduction pathways must be considered in the regulation by TNF-alpha of SMIT mRNA levels and activity. |
| 16082 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16083 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16084 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16085 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16086 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16087 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16088 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16089 | 9820807 | Thus TNF-alpha and hyperosmolarity have opposing effects on SMIT mRNA levels and activity in 3T3-L1 adipocytes. |
| 16090 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16091 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16092 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16093 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16094 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16095 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16096 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16097 | 9820807 | Because myo-inositol in the form of phosphoinositides is an important component of membranes and signal transduction pathways, the regulation of myo-inositol metabolism by TNF-alpha might represent another mechanism by which TNF-alpha regulates adipocyte function. |
| 16098 | 9797040 | In addition to its anti-diabetic effects it acts as a perixosome proliferator activated receptor-gamma (PPAR-gamma) agonist and has anti-inflammatory properties by inhibiting macrophage tumour necrosis factor-alpha (TNF-alpha) secretion. |
| 16099 | 9792545 | Plasma levels of the soluble fraction of tumor necrosis factor receptor 2 and insulin resistance. |
| 16100 | 9792545 | Plasma levels of the soluble fraction of tumor necrosis factor receptor 2 and insulin resistance. |
| 16101 | 9792545 | Recent studies have shown that the tumor necrosis factor (TNF) system is implicated in the insulin resistance of human obesity. |
| 16102 | 9792545 | Recent studies have shown that the tumor necrosis factor (TNF) system is implicated in the insulin resistance of human obesity. |
| 16103 | 9792545 | These findings support TNF-alpha as a system regulating insulin action in human obesity. |
| 16104 | 9792545 | These findings support TNF-alpha as a system regulating insulin action in human obesity. |
| 16105 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 16106 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 16107 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 16108 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 16109 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 16110 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 16111 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 16112 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 16113 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 16114 | 9787233 | Detection of vascular endothelial growth factor and tumor necrosis factor alpha in epiretinal membranes of proliferative diabetic retinopathy, proliferative vitreoretinopathy and macular pucker. |
| 16115 | 9784493 | Overexpression of the nuclear form of sterol regulatory element-binding protein-1c (nSREBP-1c/ADD1) in cultured 3T3-L1 preadipocytes was shown previously to promote adipocyte differentiation. |
| 16116 | 9784493 | Here, we produced transgenic mice that overexpress nSREBP-1c in adipose tissue under the control of the adipocyte-specific aP2 enhancer/promoter. |
| 16117 | 9784493 | Levels of mRNA encoding adipocyte differentiation markers (C/EBPalpha, PPARgamma, adipsin, leptin, UCP1) were reduced, but levels of Pref-1 and TNFalpha were increased. (2) Marked insulin resistance with 60-fold elevation in plasma insulin. (3) Diabetes mellitus with elevated blood glucose (>300 mg/dl) that failed to decline when insulin was injected. (4) Fatty liver from birth and elevated plasma triglyceride levels later in life. |
| 16118 | 9776712 | Poly I:C, an inducer of IFN-alpha and other cytokines, has been used to study the development of diabetes in both the BioBreeding (BB) diabetes prone rat and non-obese diabetic (NOD) mouse animal models of insulin-dependent diabetes mellitus (IDDM). |
| 16119 | 9776712 | The administration of poly-0.05, but not poly-5.0, decreased TNF-alpha mRNA and IL-10 mRNA content in spleen cells. |
| 16120 | 9773752 | Elevated serum tumor necrosis factor-alpha and endothelin 1 levels correlate with increased C-peptide concentration in android type obesity. |
| 16121 | 9764597 | We measured production of monokines (IL-6 and tumour necrosis factor-alpha (TNF-alpha)), active NO and reactive oxygen intermediates (ROIs), as well as expression of several cell surface adhesion molecules (Mac-1, -2 and -3, intercellular adhesion molecule-1 (ICAM-1) and Fc gammaRII), by thioglycollate medium-induced peritoneal macrophages of normoglycaemic and alloxan diabetic CBA/J mice (blood glucose level in the range 300 or 500 mg/dl). |
| 16122 | 9764597 | We measured production of monokines (IL-6 and tumour necrosis factor-alpha (TNF-alpha)), active NO and reactive oxygen intermediates (ROIs), as well as expression of several cell surface adhesion molecules (Mac-1, -2 and -3, intercellular adhesion molecule-1 (ICAM-1) and Fc gammaRII), by thioglycollate medium-induced peritoneal macrophages of normoglycaemic and alloxan diabetic CBA/J mice (blood glucose level in the range 300 or 500 mg/dl). |
| 16123 | 9764597 | Macrophages of animals with moderate diabetes (300 mg/dl) produced significantly more IL-6 and TNF-alpha and ROIs than cells of control mice and showed an increased expression of all cell surface molecules, except Mac-3. |
| 16124 | 9764597 | Macrophages of animals with moderate diabetes (300 mg/dl) produced significantly more IL-6 and TNF-alpha and ROIs than cells of control mice and showed an increased expression of all cell surface molecules, except Mac-3. |
| 16125 | 9748273 | Insulin-like growth factor-I inhibits the stress-activated protein kinase/c-Jun N-terminal kinase. |
| 16126 | 9748273 | The pathways involved in the cellular responses to the insulin-like growth factors (IGFs) are numerous and vary according to cell type. |
| 16127 | 9748273 | In this study, we analyzed the IGF-I effect on the stress-activated protein kinase/c-Jun N-terminal kinase (JNK) activity using human embryonic kidney 293 cells, 293 cells transiently expressing hemagglutinin-JNK, and 293 cells stably expressing a hemagglutinin-JNK transgene. |
| 16128 | 9748273 | In all cell types, endogenous or transfected JNK activity was strongly stimulated by anisomycin or tumor necrosis factor-alpha, and 10 nM IGF-I pretreatment suppressed the induced JNK activity. |
| 16129 | 9748273 | To determine whether the effect of IGF-I on JNK activity involves the mitogen-activated protein kinase or PI3'K pathway, we used the specific MEK1 inhibitor PD098059 and the PI3'K inhibitor LY 294002. |
| 16130 | 9748273 | PD098059 did not alter the IGF-I suppressive effect on stressor-induced JNK activity, but LY 294002 suppressed the IGF-I effect. |
| 16131 | 9748273 | Moreover, in transiently transfected parental 293 cells expressing dominant-negative Akt, anisomycin-increased JNK activity was not suppressed by pretreatment with IGF-I. |
| 16132 | 9748273 | Our results demonstrate that the action of IGF-I on JNK in these cells is via PI3'K and Akt. |
| 16133 | 9748221 | Here, we show that the PPARalpha and PPARgamma forms are expressed in differentiated human monocyte-derived macrophages, which participate in inflammation control and atherosclerotic plaque formation. |
| 16134 | 9748221 | Whereas PPARalpha is already present in undifferentiated monocytes, PPARgamma expression is induced upon differentiation into macrophages. |
| 16135 | 9748221 | Immunocytochemistry analysis demonstrates that PPARalpha resides constitutively in the cytoplasm, whereas PPARgamma is predominantly nuclear localized. |
| 16136 | 9748221 | Transient transfection experiments indicate that PPARalpha and PPARgamma are transcriptionally active after ligand stimulation. |
| 16137 | 9748221 | Ligand activation of PPARgamma, but not of PPARalpha, results in apoptosis induction of unactivated differentiated macrophages as measured by the TUNEL assay and the appearance of the active proteolytic subunits of the cell death protease caspase-3. |
| 16138 | 9748221 | However, both PPARalpha and PPARgamma ligands induce apoptosis of macrophages activated with tumor necrosis factor alpha/interferon gamma. |
| 16139 | 9748221 | Finally, PPARgamma inhibits the transcriptional activity of the NFkappaB p65/RelA subunit, suggesting that PPAR activators induce macrophage apoptosis by negatively interfering with the anti-apoptotic NFkappaB signaling pathway. |
| 16140 | 9727063 | Insulin-dependent diabetes mellitus in humans is linked with specific HLA class II genes, e.g., HLA-DQA1*0301/ DQB1*0302 (DQ8). |
| 16141 | 9727063 | Two GAD peptide-specific (247-266 and 509-528), DQ8 restricted Th1 CD4(+) T cell lines, were generated from immunized DQ8(+)/I-Abo mice. |
| 16142 | 9727063 | In addition to CD4, islet mRNA from these mice also showed expression of CD8, IFNgamma, TNFalpha, Fas, and Fas ligand. |
| 16143 | 9726225 | In contrast to the marked site-related expression of leptin, genes encoding lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and adipsin were not consistently differentially expressed. |
| 16144 | 9726225 | In contrast to the marked site-related expression of leptin, genes encoding lipoprotein lipase (LPL), hormone-sensitive lipase (HSL), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), tumor necrosis factor-alpha (TNF-alpha), and adipsin were not consistently differentially expressed. |
| 16145 | 9726225 | Of note, a highly significant inverse correlation between adipocyte PPAR-gamma expression and BMI (r = -0.7, P = 0.0005) was found. |
| 16146 | 9726225 | Of note, a highly significant inverse correlation between adipocyte PPAR-gamma expression and BMI (r = -0.7, P = 0.0005) was found. |
| 16147 | 9726225 | Because cIAP2 may be involved in the regulation of TNF-alpha signaling, this raises the possibility that depot-specific differences may exist in the regulation of adipocyte apoptosis. |
| 16148 | 9726225 | Because cIAP2 may be involved in the regulation of TNF-alpha signaling, this raises the possibility that depot-specific differences may exist in the regulation of adipocyte apoptosis. |
| 16149 | 9726225 | Given the importance of PPAR-gamma in adipocyte development and insulin sensitivity, the inverse correlation between adipocyte PPAR-gamma mRNA levels and adiposity may represent a local regulatory mechanism restraining fat accumulation and/or may be related to the reduction of insulin sensitivity that occurs with increasing fat mass. |
| 16150 | 9726225 | Given the importance of PPAR-gamma in adipocyte development and insulin sensitivity, the inverse correlation between adipocyte PPAR-gamma mRNA levels and adiposity may represent a local regulatory mechanism restraining fat accumulation and/or may be related to the reduction of insulin sensitivity that occurs with increasing fat mass. |
| 16151 | 9725204 | Autoimmunity without diabetes in transgenic mice expressing beta cell-specific CD86, but not CD80: parameters that trigger progression to diabetes. |
| 16152 | 9725204 | To define more clearly the roles of CD80 (RIP-CD80) and CD86 (RIP-CD86) in the activation of autoreactive T cells in vivo, we generated transgenic mice expressing either or both costimulatory molecules on the beta cells of the pancreas. |
| 16153 | 9725204 | While RIP-CD80 mice do not show any sign of autoimmunity, at the age of 7 mo RIP-CD86 transgenic mice develop a lymphoid infiltrate with both IFN-gamma- and IL-4-positive cells in the vicinity of the islets; these mice, however, never progress to diabetes. |
| 16154 | 9725204 | This fundamental difference in the ability of CD80 and CD86 to activate self-reactive T cells in vivo is, however, obliterated when the level of TCR signaling is increased by either TNF-alpha or transgenic MHC class II expression. |
| 16155 | 9725204 | These results support the suggestion that CD80 and CD86 mainly differ at the level of the intensity of the signals they deliver. |
| 16156 | 9722689 | PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. |
| 16157 | 9722689 | PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. |
| 16158 | 9722689 | PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. |
| 16159 | 9722689 | PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. |
| 16160 | 9722689 | PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. |
| 16161 | 9722689 | We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. |
| 16162 | 9722689 | We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. |
| 16163 | 9722689 | We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. |
| 16164 | 9722689 | We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. |
| 16165 | 9722689 | We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. |
| 16166 | 9722689 | Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. |
| 16167 | 9722689 | Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. |
| 16168 | 9722689 | Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. |
| 16169 | 9722689 | Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. |
| 16170 | 9722689 | Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. |
| 16171 | 9722689 | Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. |
| 16172 | 9722689 | Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. |
| 16173 | 9722689 | Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. |
| 16174 | 9722689 | Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. |
| 16175 | 9722689 | Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. |
| 16176 | 9722689 | Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. |
| 16177 | 9722689 | Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. |
| 16178 | 9722689 | Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. |
| 16179 | 9722689 | Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. |
| 16180 | 9722689 | Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. |
| 16181 | 9722689 | Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). |
| 16182 | 9722689 | Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). |
| 16183 | 9722689 | Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). |
| 16184 | 9722689 | Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). |
| 16185 | 9722689 | Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). |
| 16186 | 9722687 | Based on our clinical observations that patients with insulin-dependent diabetes mellitus (IDDM) are subject to periodontal disease, we developed the hypothesis that hyper- or hypoglycemia might contribute to the pathogenesis of diabetic periodontitis. |
| 16187 | 9722687 | Hyperglycemia progressively glycates body proteins, forming advanced glycation end products (AGE), which stimulate phagocytes to release inflammatory cytokines such as TNF-alpha and IL-6. |
| 16188 | 9719467 | Insulin-dependent diabetes mellitus (IDDM) is a disease that results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans. |
| 16189 | 9719467 | Insulin-dependent diabetes mellitus (IDDM) is a disease that results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans. |
| 16190 | 9719467 | Type 1 cytokines--interleukin 2 (IL-2), interferon gamma (IFNgamma), and tumor necrosis factor beta (TNFbeta), dominate over an immunoregulatory (suppressor) Th2 subset of T cells and their cytokine products, i.e. |
| 16191 | 9719467 | Type 1 cytokines--interleukin 2 (IL-2), interferon gamma (IFNgamma), and tumor necrosis factor beta (TNFbeta), dominate over an immunoregulatory (suppressor) Th2 subset of T cells and their cytokine products, i.e. |
| 16192 | 9719467 | Type 2 cytokines--IL-4 and IL-10. |
| 16193 | 9719467 | Type 2 cytokines--IL-4 and IL-10. |
| 16194 | 9719467 | Type 1 cytokines activate (1) cytotoxic T cells that interact specifically with beta-cells and destroy them, and (2) macrophages to produce proinflammatory cytokines (IL-1 and TNFalpha), and oxygen and nitrogen free radicals that are highly toxic to islet beta-cells. |
| 16195 | 9719467 | Type 1 cytokines activate (1) cytotoxic T cells that interact specifically with beta-cells and destroy them, and (2) macrophages to produce proinflammatory cytokines (IL-1 and TNFalpha), and oxygen and nitrogen free radicals that are highly toxic to islet beta-cells. |
| 16196 | 9719467 | Furthermore, the cytokines IL-1, TNFalpha, and IFNgamma are cytotoxic to beta-cells, in large part by inducing the formation of oxygen free radicals, nitric oxide, and peroxynitrite in the beta-cells themselves. |
| 16197 | 9719467 | Furthermore, the cytokines IL-1, TNFalpha, and IFNgamma are cytotoxic to beta-cells, in large part by inducing the formation of oxygen free radicals, nitric oxide, and peroxynitrite in the beta-cells themselves. |
| 16198 | 9716913 | It was found that strain-related susceptibility to diabetes induction correlated with a higher level of IL-2, IFN-gamma, and TNF-alpha production, whereas such differences were not observed when IL-1 and NO production by macrophages were analyzed; elimination of immunoregulatory RT6+T cells that increases IFN-gamma production, enhances susceptibility to MLD-STZ-induced diabetes; mercury-induced Th-2 cells down-regulated the disease; IFN-gamma-mediated macrophage activation to produce proinflammatory cytokines rather than NO is an important event in early diabetogenic effects of invading macrophages; inhibition of IL-1 activity downregulates diabetes induction; and generation of NO in beta cells appears to be important for diabetogenic effects. |
| 16199 | 9714125 | Relation between plasma tumor necrosis factor-alpha and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus. |
| 16200 | 9714125 | Relation between plasma tumor necrosis factor-alpha and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus. |
| 16201 | 9714125 | Relation between plasma tumor necrosis factor-alpha and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus. |
| 16202 | 9714125 | Relation between plasma tumor necrosis factor-alpha and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus. |
| 16203 | 9714125 | Relation between plasma tumor necrosis factor-alpha and insulin sensitivity in elderly men with non-insulin-dependent diabetes mellitus. |
| 16204 | 9714125 | TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. |
| 16205 | 9714125 | TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. |
| 16206 | 9714125 | TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. |
| 16207 | 9714125 | TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. |
| 16208 | 9714125 | TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. |
| 16209 | 9714125 | In this study, we analyzed plasma levels of TNF-alpha in 40 70-year-old men with newly detected non-insulin-dependent diabetes mellitus and in 20 age-matched controls. |
| 16210 | 9714125 | In this study, we analyzed plasma levels of TNF-alpha in 40 70-year-old men with newly detected non-insulin-dependent diabetes mellitus and in 20 age-matched controls. |
| 16211 | 9714125 | In this study, we analyzed plasma levels of TNF-alpha in 40 70-year-old men with newly detected non-insulin-dependent diabetes mellitus and in 20 age-matched controls. |
| 16212 | 9714125 | In this study, we analyzed plasma levels of TNF-alpha in 40 70-year-old men with newly detected non-insulin-dependent diabetes mellitus and in 20 age-matched controls. |
| 16213 | 9714125 | In this study, we analyzed plasma levels of TNF-alpha in 40 70-year-old men with newly detected non-insulin-dependent diabetes mellitus and in 20 age-matched controls. |
| 16214 | 9714125 | The plasma levels of TNF-alpha were higher in patients (4.00+/-1.53 pg/mL in moderately insulin resistant and 4.91+/-1.43 pg/mL in severely insulin resistant subjects) than in controls (3.27+/-0.79 pg/mL, P<0.001). |
| 16215 | 9714125 | The plasma levels of TNF-alpha were higher in patients (4.00+/-1.53 pg/mL in moderately insulin resistant and 4.91+/-1.43 pg/mL in severely insulin resistant subjects) than in controls (3.27+/-0.79 pg/mL, P<0.001). |
| 16216 | 9714125 | The plasma levels of TNF-alpha were higher in patients (4.00+/-1.53 pg/mL in moderately insulin resistant and 4.91+/-1.43 pg/mL in severely insulin resistant subjects) than in controls (3.27+/-0.79 pg/mL, P<0.001). |
| 16217 | 9714125 | The plasma levels of TNF-alpha were higher in patients (4.00+/-1.53 pg/mL in moderately insulin resistant and 4.91+/-1.43 pg/mL in severely insulin resistant subjects) than in controls (3.27+/-0.79 pg/mL, P<0.001). |
| 16218 | 9714125 | The plasma levels of TNF-alpha were higher in patients (4.00+/-1.53 pg/mL in moderately insulin resistant and 4.91+/-1.43 pg/mL in severely insulin resistant subjects) than in controls (3.27+/-0.79 pg/mL, P<0.001). |
| 16219 | 9714125 | The finding of an association between high plasma levels of TNF-alpha and several metabolic abnormalities characteristic for the insulin resistance syndrome suggests that TNF-alpha may be involved in the pathogenesis of non-insulin-dependent diabetes mellitus. |
| 16220 | 9714125 | The finding of an association between high plasma levels of TNF-alpha and several metabolic abnormalities characteristic for the insulin resistance syndrome suggests that TNF-alpha may be involved in the pathogenesis of non-insulin-dependent diabetes mellitus. |
| 16221 | 9714125 | The finding of an association between high plasma levels of TNF-alpha and several metabolic abnormalities characteristic for the insulin resistance syndrome suggests that TNF-alpha may be involved in the pathogenesis of non-insulin-dependent diabetes mellitus. |
| 16222 | 9714125 | The finding of an association between high plasma levels of TNF-alpha and several metabolic abnormalities characteristic for the insulin resistance syndrome suggests that TNF-alpha may be involved in the pathogenesis of non-insulin-dependent diabetes mellitus. |
| 16223 | 9714125 | The finding of an association between high plasma levels of TNF-alpha and several metabolic abnormalities characteristic for the insulin resistance syndrome suggests that TNF-alpha may be involved in the pathogenesis of non-insulin-dependent diabetes mellitus. |
| 16224 | 9712898 | Tumor necrosis factor signaling to stress-activated protein kinase (SAPK)/Jun NH2-terminal kinase (JNK) and p38. |
| 16225 | 9712898 | Tumor necrosis factor signaling to stress-activated protein kinase (SAPK)/Jun NH2-terminal kinase (JNK) and p38. |
| 16226 | 9712898 | Germinal center kinase couples TRAF2 to mitogen-activated protein kinase/ERK kinase kinase 1 and SAPK while receptor interacting protein associates with a mitogen-activated protein kinase kinase kinase upstream of MKK6 and p38. |
| 16227 | 9712898 | Germinal center kinase couples TRAF2 to mitogen-activated protein kinase/ERK kinase kinase 1 and SAPK while receptor interacting protein associates with a mitogen-activated protein kinase kinase kinase upstream of MKK6 and p38. |
| 16228 | 9712898 | Tumor necrosis factor (TNF) elicits a diverse array of inflammatory responses through engagement of its type-1 receptor (TNFR1). |
| 16229 | 9712898 | Tumor necrosis factor (TNF) elicits a diverse array of inflammatory responses through engagement of its type-1 receptor (TNFR1). |
| 16230 | 9712898 | Many of these responses require de novo gene expression mediated by the activator protein-1 (AP-1) transcription factor. |
| 16231 | 9712898 | Many of these responses require de novo gene expression mediated by the activator protein-1 (AP-1) transcription factor. |
| 16232 | 9712898 | We investigated the mechanism by which TNFR1 recruits the stress-activated protein kinases (SAPKs) and the p38s, two mitogen-activated protein kinase (MAPK) families that together regulate AP-1. |
| 16233 | 9712898 | We investigated the mechanism by which TNFR1 recruits the stress-activated protein kinases (SAPKs) and the p38s, two mitogen-activated protein kinase (MAPK) families that together regulate AP-1. |
| 16234 | 9712898 | We show that the human SPS1 homologue germinal center kinase (GCK) can interact in vivo with the TNFR1 signal transducer TNFR-associated factor-2 (TRAF2) and with MAPK/ERK kinase kinase 1 (MEKK1), a MAPK kinase kinase (MAPKKK) upstream of the SAPKs, thereby coupling TRAF2 to the SAPKs. |
| 16235 | 9712898 | We show that the human SPS1 homologue germinal center kinase (GCK) can interact in vivo with the TNFR1 signal transducer TNFR-associated factor-2 (TRAF2) and with MAPK/ERK kinase kinase 1 (MEKK1), a MAPK kinase kinase (MAPKKK) upstream of the SAPKs, thereby coupling TRAF2 to the SAPKs. |
| 16236 | 9712898 | Receptor interacting protein (RIP) is a second TNFR signal transducer which can bind TRAF2. |
| 16237 | 9712898 | Receptor interacting protein (RIP) is a second TNFR signal transducer which can bind TRAF2. |
| 16238 | 9712898 | We show that RIP activates both p38 and SAPK; and that TRAF2 activation of p38 requires RIP. |
| 16239 | 9712898 | We show that RIP activates both p38 and SAPK; and that TRAF2 activation of p38 requires RIP. |
| 16240 | 9712898 | We also demonstrate that the RIP noncatalytic intermediate domain associates in vivo with an endogenous MAPKKK that can activate the p38 pathway in vitro. |
| 16241 | 9712898 | We also demonstrate that the RIP noncatalytic intermediate domain associates in vivo with an endogenous MAPKKK that can activate the p38 pathway in vitro. |
| 16242 | 9712898 | Thus, TRAF2 initiates SAPK and p38 activation by binding two proximal protein kinases: GCK and RIP. |
| 16243 | 9712898 | Thus, TRAF2 initiates SAPK and p38 activation by binding two proximal protein kinases: GCK and RIP. |
| 16244 | 9712898 | GCK and RIP, in turn, signal by binding MAPKKKs upstream of the SAPKs and p38s. |
| 16245 | 9712898 | GCK and RIP, in turn, signal by binding MAPKKKs upstream of the SAPKs and p38s. |
| 16246 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16247 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16248 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16249 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16250 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16251 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16252 | 9691088 | The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. |
| 16253 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16254 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16255 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16256 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16257 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16258 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16259 | 9691088 | Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. |
| 16260 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16261 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16262 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16263 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16264 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16265 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16266 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 16267 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16268 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16269 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16270 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16271 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16272 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16273 | 9691088 | Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. |
| 16274 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16275 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16276 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16277 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16278 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16279 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16280 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 16281 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16282 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16283 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16284 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16285 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16286 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16287 | 9691088 | Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. |
| 16288 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16289 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16290 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16291 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16292 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16293 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16294 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 16295 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16296 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16297 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16298 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16299 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16300 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16301 | 9691088 | Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. |
| 16302 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16303 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16304 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16305 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16306 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16307 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16308 | 9691088 | These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells. |
| 16309 | 9685802 | [Tumor necrosis factor-alpha; a possible pathogenic factor in obesity in insulin resistant and non-insulin-dependent diabetes mellitus?]. |
| 16310 | 9685802 | [Tumor necrosis factor-alpha; a possible pathogenic factor in obesity in insulin resistant and non-insulin-dependent diabetes mellitus?]. |
| 16311 | 9685802 | [Tumor necrosis factor-alpha; a possible pathogenic factor in obesity in insulin resistant and non-insulin-dependent diabetes mellitus?]. |
| 16312 | 9685802 | The role of tumor necrosis factor (TNF)-alpha in the development of insulin resistance has repeatedly been emphasized in the past few years. |
| 16313 | 9685802 | The role of tumor necrosis factor (TNF)-alpha in the development of insulin resistance has repeatedly been emphasized in the past few years. |
| 16314 | 9685802 | The role of tumor necrosis factor (TNF)-alpha in the development of insulin resistance has repeatedly been emphasized in the past few years. |
| 16315 | 9685802 | The present paper summarizes the data (including the authors' observations as well) focusing on the potential role of TNF-alpha in the pathogenesis of obesity and non-insulin-dependent diabetes mellitus: alteration of insulin receptor function, lipid metabolism, expression of sulphonylurea receptors, all of them suggested to be related to the TNF-alpha. |
| 16316 | 9685802 | The present paper summarizes the data (including the authors' observations as well) focusing on the potential role of TNF-alpha in the pathogenesis of obesity and non-insulin-dependent diabetes mellitus: alteration of insulin receptor function, lipid metabolism, expression of sulphonylurea receptors, all of them suggested to be related to the TNF-alpha. |
| 16317 | 9685802 | The present paper summarizes the data (including the authors' observations as well) focusing on the potential role of TNF-alpha in the pathogenesis of obesity and non-insulin-dependent diabetes mellitus: alteration of insulin receptor function, lipid metabolism, expression of sulphonylurea receptors, all of them suggested to be related to the TNF-alpha. |
| 16318 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16319 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16320 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16321 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16322 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16323 | 9679667 | Correlation studies between cytokines expressed in islets and autoimmune diabetes development in NOD mice and BB rats have demonstrated that beta-cell destructive insulitis is associated with increased expression of proinflammatory cytokines (IL-1, TNF alpha, and IFN alpha) and type 1 cytokines (IFN gamma, TNF beta, IL-2 and IL-12), whereas non-destructive (benign) insulitis is associated with increased expression of type 2 cytokines (IL-4 and IL-10) and the type 3 cytokine (TGF beta). |
| 16324 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16325 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16326 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16327 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16328 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16329 | 9679667 | Cytokines (IL-1, TNF alpha, TNF beta and IFN gamma) may be directly cytotoxic to beta-cells by inducing nitric oxide and oxygen free radicals in the beta-cells. |
| 16330 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16331 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16332 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16333 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16334 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16335 | 9679667 | In addition, cytokines may sensitize beta-cells to T-cell-mediated cytotoxicity in vivo by upregulating MHC class I expression on the beta-cells (an action of IFN gamma), and inducing Fas (CD95) expression on beta-cells (actions of IL-1, and possibly TNF alpha and IFN gamma). |
| 16336 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16337 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16338 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16339 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16340 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16341 | 9679667 | Transgenic expression of cytokines in beta-cells of non-diabetes-prone mice and NOD mice has suggested pathogenic roles for IFN alpha, IFN gamma, IL-2 and IL-10 in insulin-dependent diabetes mellitus (IDDM) development, and protective roles for IL-4, IL-6 and TNF alpha. |
| 16342 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16343 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16344 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16345 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16346 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16347 | 9679667 | Islet-reactive CD4+ T-cell lines and clones that adoptively transfer IDDM into young NOD mice have a Th1 phenotype (IFN gamma-producing), but other islet-specific Th1 clones that produce TGF beta can adoptively transfer protection against IDDM in NOD mice. |
| 16348 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16349 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16350 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16351 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16352 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16353 | 9679667 | NOD mice with targeted deletions of IL-12 and IFN gamma genes still develop IDDM, albeit delayed and slightly less often. |
| 16354 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16355 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16356 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16357 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16358 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16359 | 9679667 | In contrast, post-natal deletions of IL-12 and IFN gamma, also IL-1, TNF alpha, IL-2, and IL-6--by systemic administrations of neutralizing antibodies, soluble receptors and receptor antagonists, and receptor-targeted cytotoxic drugs--significantly decrease IDDM incidence in NOD mice and/or BB rats. |
| 16360 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16361 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16362 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16363 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16364 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16365 | 9679667 | These cytokine deletion studies have provided the best evidence for pathologic roles for proinflammatory cytokines (IL-1, TNF alpha, and IL-6) and type 1 cytokines (IFN gamma, IL-2 and IL-12) in IDDM development. |
| 16366 | 9664082 | TNF-alpha may play a role in mediating insulin resistance associated with obesity. |
| 16367 | 9664082 | TNF-alpha may play a role in mediating insulin resistance associated with obesity. |
| 16368 | 9664082 | TNF-alpha may play a role in mediating insulin resistance associated with obesity. |
| 16369 | 9664082 | TNF elicits cellular responses via two receptors called p55 and p75. |
| 16370 | 9664082 | TNF elicits cellular responses via two receptors called p55 and p75. |
| 16371 | 9664082 | TNF elicits cellular responses via two receptors called p55 and p75. |
| 16372 | 9664082 | In addition, high-fat diet-fed p75(-)/- mice had the lowest body weights and leptin levels, and improved insulin sensitivity. |
| 16373 | 9664082 | In addition, high-fat diet-fed p75(-)/- mice had the lowest body weights and leptin levels, and improved insulin sensitivity. |
| 16374 | 9664082 | In addition, high-fat diet-fed p75(-)/- mice had the lowest body weights and leptin levels, and improved insulin sensitivity. |
| 16375 | 9664082 | Our data do not support the concept that TNF, acting via its receptors, is a major contributor to obesity-associated insulin resistance. |
| 16376 | 9664082 | Our data do not support the concept that TNF, acting via its receptors, is a major contributor to obesity-associated insulin resistance. |
| 16377 | 9664082 | Our data do not support the concept that TNF, acting via its receptors, is a major contributor to obesity-associated insulin resistance. |
| 16378 | 9645700 | Dehydroepiandrosterone decreases serum tumor necrosis factor-alpha and restores insulin sensitivity: independent effect from secondary weight reduction in genetically obese Zucker fatty rats. |
| 16379 | 9645700 | Dehydroepiandrosterone decreases serum tumor necrosis factor-alpha and restores insulin sensitivity: independent effect from secondary weight reduction in genetically obese Zucker fatty rats. |
| 16380 | 9645700 | Dehydroepiandrosterone decreases serum tumor necrosis factor-alpha and restores insulin sensitivity: independent effect from secondary weight reduction in genetically obese Zucker fatty rats. |
| 16381 | 9645700 | Serum concentration of tumor necrosis factor (TNF)-alpha, one of cytokines causing insulin resistance, was also reduced significantly in DHEA-treated, but not in pair-fed obese rats. |
| 16382 | 9645700 | Serum concentration of tumor necrosis factor (TNF)-alpha, one of cytokines causing insulin resistance, was also reduced significantly in DHEA-treated, but not in pair-fed obese rats. |
| 16383 | 9645700 | Serum concentration of tumor necrosis factor (TNF)-alpha, one of cytokines causing insulin resistance, was also reduced significantly in DHEA-treated, but not in pair-fed obese rats. |
| 16384 | 9645700 | In conclusion, our results suggest that DHEA treatment reduces body weight and serum TNF-alpha independently, and that both may ameliorate insulin resistance in obese Zucker fatty rats. |
| 16385 | 9645700 | In conclusion, our results suggest that DHEA treatment reduces body weight and serum TNF-alpha independently, and that both may ameliorate insulin resistance in obese Zucker fatty rats. |
| 16386 | 9645700 | In conclusion, our results suggest that DHEA treatment reduces body weight and serum TNF-alpha independently, and that both may ameliorate insulin resistance in obese Zucker fatty rats. |
| 16387 | 9576755 | We addressed the role of hyperglycemia in leukocyte-endothelium interaction under flow conditions by exposing human umbilical vein endothelial cells for 24 h to normal (5 mM), high concentration of glucose (30 mM), advanced glycosylation end product-albumin (100 microg/ml), or hyperglycemic (174-316 mg/dl) sera from patients with diabetes and abnormal hemoglobin A1c (8.1+/-1.4%). |
| 16388 | 9576755 | Sera from diabetic patients significantly (P < 0.01) enhanced leukocyte adhesion as compared with controls, despite normal levels of IL-1beta and TNFalpha in these sera. |
| 16389 | 9614356 | In addition, the in situ expression of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), monocyte-chemotactic protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) were studied by immunohistochemistry. |
| 16390 | 9614356 | In addition, the in situ expression of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), monocyte-chemotactic protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) were studied by immunohistochemistry. |
| 16391 | 9614356 | In addition, the in situ expression of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), monocyte-chemotactic protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) were studied by immunohistochemistry. |
| 16392 | 9614356 | Further in vitro studies consisted of measurement of the production of thyroxine (T4), triiodothyronine (T3), thyroglobulin, IL-6, TNF-alpha and MCP-1 by the thyroid follicles. |
| 16393 | 9614356 | Further in vitro studies consisted of measurement of the production of thyroxine (T4), triiodothyronine (T3), thyroglobulin, IL-6, TNF-alpha and MCP-1 by the thyroid follicles. |
| 16394 | 9614356 | Further in vitro studies consisted of measurement of the production of thyroxine (T4), triiodothyronine (T3), thyroglobulin, IL-6, TNF-alpha and MCP-1 by the thyroid follicles. |
| 16395 | 9614356 | There was no noteworthy difference in production of thyroglobulin and MCP-1 between BB-DP and Wistar follicles at any age. |
| 16396 | 9614356 | There was no noteworthy difference in production of thyroglobulin and MCP-1 between BB-DP and Wistar follicles at any age. |
| 16397 | 9614356 | There was no noteworthy difference in production of thyroglobulin and MCP-1 between BB-DP and Wistar follicles at any age. |
| 16398 | 9614356 | MCP-1 and TNF-alpha were expressed only when infiltrates were present in BB-DP thyroids (restricted to leucocytes, ages > 18 weeks). |
| 16399 | 9614356 | MCP-1 and TNF-alpha were expressed only when infiltrates were present in BB-DP thyroids (restricted to leucocytes, ages > 18 weeks). |
| 16400 | 9614356 | MCP-1 and TNF-alpha were expressed only when infiltrates were present in BB-DP thyroids (restricted to leucocytes, ages > 18 weeks). |
| 16401 | 9609135 | The functional state of APCs during preferential stimulation of Th1 reactivities (APC1 state) is characterized by the release of TNFalpha, IL-12 and/or IL-18. |
| 16402 | 9609113 | Protein phosphatase-1 and insulin action. |
| 16403 | 9609113 | Protein Phosphatase-1 (PP-1) appears to be the key component of the insulin signalling pathway which is responsible for bridging the initial insulin-simulated phosphorylation cascade with the ultimate dephosphorylation of insulin sensitive substrates. |
| 16404 | 9609113 | Dephosphorylations catalyzed by PP-1 activate glycogen synthase (GS) and simultaneously inactivate phosphorylase a and phosphorylase kinase promoting glycogen synthesis. |
| 16405 | 9609113 | Our in vivo studies using L6 rat skeletal muscle cells and freshly isolated adipocytes indicate that insulin stimulates PP-1 by increasing the phosphorylation status of its regulatory subunit (PP-1G). |
| 16406 | 9609113 | PP-1 activation is accompanied by an inactivation of Protein Phosphatase-2A (PP-2A) activity. |
| 16407 | 9609113 | To gain insight into the upstream kinases that mediate insulin-stimulated PP-1G phosphorylation, we employed inhibitors of the ras/MAPK, PI3-kinase, and PKC signalling pathways. |
| 16408 | 9609113 | These inhibitor studies suggest that PP-1G phosphorylation is mediated via a complex, cell type specific mechanism involving PI3-kinase/PKC/PKB and/or the ras/MAP kinase/Rsk kinase cascade. cAMP agonists such as SpcAMP (via PKA) and TNF-alpha (recently identified as endogenous inhibitor of insulin action via ceramide) block insulin-stimulated PP-1G phosphorylation with a parallel decrease of PP-1 activity, presumably due to the dissociation of the PP-1 catalytic subunit from the regulatory G-subunit. |
| 16409 | 9609113 | It appears that any agent or condition which interferes with the insulin-induced phosphorylation and activation of PP-1, will decrease the magnitude of insulin's effect on downstream metabolic processes. |
| 16410 | 9609113 | Therefore, regulation of the PP-1G subunit by site-specific phosphorylation plays an important role in insulin signal transduction in target cells. |
| 16411 | 9609113 | Mechanistic and functional studies with cell lines expressing PP-1G subunit site-specific mutations will help clarify the exact role and regulation of PP-1G site-specific phosphorylations on PP-1 catalytic function. |
| 16412 | 9608925 | By altering the TNF and IL-1 cytokines, leukocytic activation can be controlled. |
| 16413 | 9608925 | Other cytokines (IL-4, IL-10) have an immunosuppressive action and reduce the formation of TF. |
| 16414 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16415 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16416 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16417 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16418 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16419 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16420 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16421 | 9538268 | Tumor necrosis factor-alpha regulates the gene expression of macrophage migration inhibitory factor through tyrosine kinase-dependent pathway in 3T3-L1 adipocytes. |
| 16422 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16423 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16424 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16425 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16426 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16427 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16428 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16429 | 9538268 | We have recently identified the expression of MIF in adipocytes and found that tumor necrosis factor (TNF)-alpha stimulates its secretion from 3T3-L1 adipocytes. |
| 16430 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16431 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16432 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16433 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16434 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16435 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16436 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16437 | 9538268 | Since adipocytes are regarded as a potential source of various biologically active substances, we examined in more detail the effect of TNF-alpha on MIF expression in 3T3-L1 adipocytes in the present study. |
| 16438 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16439 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16440 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16441 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16442 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16443 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16444 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16445 | 9538268 | We found that TNF-alpha induced MIF mRNA in dose- and time-dependent manners. |
| 16446 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16447 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16448 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16449 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16450 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16451 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16452 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16453 | 9538268 | After stimulation with TNF-alpha, the amount of intracellular MIF protein was unchanged or slightly decreased, concomitant with increased release of this protein into the extracellular space. |
| 16454 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16455 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16456 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16457 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16458 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16459 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16460 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16461 | 9538268 | This observation indicates that TNF-alpha stimulates MIF secretion from the constitutively expressed intracellular pool of 3T3-L1 adipocytes and promotes de novo synthesis of MIF. |
| 16462 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16463 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16464 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16465 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16466 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16467 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16468 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16469 | 9538268 | From evaluation of the mechanism of MIF gene expression, we found that tyrosine kinase inhibitors, either genistein or herbimycin A, suppressed the MIF mRNA induction by TNF-alpha. |
| 16470 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16471 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16472 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16473 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16474 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16475 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16476 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16477 | 9538268 | The results suggest the possibility that upregulation of MIF mRNA expression by TNF-alpha is mediated by a tyrosine kinase-dependent pathway. |
| 16478 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16479 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16480 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16481 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16482 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16483 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16484 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16485 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16486 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16487 | 9588442 | Short-term exposure to tumor necrosis factor-alpha does not affect insulin-stimulated glucose uptake in skeletal muscle. |
| 16488 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16489 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16490 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16491 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16492 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16493 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16494 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16495 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16496 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16497 | 9588442 | It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. |
| 16498 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16499 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16500 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16501 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16502 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16503 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16504 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16505 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16506 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16507 | 9588442 | Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. |
| 16508 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16509 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16510 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16511 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16512 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16513 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16514 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16515 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16516 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16517 | 9588442 | Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. |
| 16518 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16519 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16520 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16521 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16522 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16523 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16524 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16525 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16526 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16527 | 9588442 | TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. |
| 16528 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16529 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16530 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16531 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16532 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16533 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16534 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16535 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16536 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16537 | 9588442 | Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. |
| 16538 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16539 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16540 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16541 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16542 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16543 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16544 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16545 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16546 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16547 | 9588442 | We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. |
| 16548 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16549 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16550 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16551 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16552 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16553 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16554 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16555 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16556 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16557 | 9588442 | Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. |
| 16558 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16559 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16560 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16561 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16562 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16563 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16564 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16565 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16566 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16567 | 9588442 | Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. |
| 16568 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16569 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16570 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16571 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16572 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16573 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16574 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16575 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16576 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16577 | 9588442 | We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. |
| 16578 | 9583742 | Insulin-dependent diabetes mellitus (IDDM) is caused by the progressive autoimmune destruction of insulin-producing pancreatic beta cells. |
| 16579 | 9583742 | The presentation of beta cell-specific autoantigens by macrophages and/or dendritic cells to CD4+ T helper cells, in association with MHC class II molecules, is considered the initial step in the development of autoimmune IDDM. |
| 16580 | 9583742 | The CD4+ T cells secrete IFN-gamma and IL-2. |
| 16581 | 9583742 | IFN-gamma activates other resting macrophages, which, in turn, release cytokines, such as IL-1beta, TNF-alpha, and free radicals, which are toxic to beta cells. |
| 16582 | 9583742 | During this process, IL-2 and other cytokines induce the migration of CD8+ peripheral T cells to the inflamed islets, perhaps by inducing the expression of a specific homing receptor. |
| 16583 | 9583742 | The precytotoxic CD8+ T cells that bear beta cell-specific autoantigen receptors differentiate into cytotoxic effector T cells upon recognition of the beta cell-specific peptide bound to MHC class I molecules in the presence of beta cell-specific CD4+ T helper cells. |
| 16584 | 9583742 | In this way, macrophages, CD4+ T cells, and CD8+ T cells synergistically destroy beta cells, resulting in the onset of autoimmune IDDM. |
| 16585 | 9568706 | BRL 49653 blocks the lipolytic actions of tumor necrosis factor-alpha: a potential new insulin-sensitizing mechanism for thiazolidinediones. |
| 16586 | 9568706 | BRL 49653 blocks the lipolytic actions of tumor necrosis factor-alpha: a potential new insulin-sensitizing mechanism for thiazolidinediones. |
| 16587 | 9568706 | BRL 49653 blocks the lipolytic actions of tumor necrosis factor-alpha: a potential new insulin-sensitizing mechanism for thiazolidinediones. |
| 16588 | 9568706 | BRL 49653 blocks the lipolytic actions of tumor necrosis factor-alpha: a potential new insulin-sensitizing mechanism for thiazolidinediones. |
| 16589 | 9568706 | Adipocyte production of TNF-alpha is proposed to play a role in the development of insulin resistance, and because BRL 49653 has been shown to antagonize some of the effects of TNF-alpha, we examined the effects of TNF-alpha and BRL 49653 on adipocyte lipolysis. |
| 16590 | 9568706 | Adipocyte production of TNF-alpha is proposed to play a role in the development of insulin resistance, and because BRL 49653 has been shown to antagonize some of the effects of TNF-alpha, we examined the effects of TNF-alpha and BRL 49653 on adipocyte lipolysis. |
| 16591 | 9568706 | Adipocyte production of TNF-alpha is proposed to play a role in the development of insulin resistance, and because BRL 49653 has been shown to antagonize some of the effects of TNF-alpha, we examined the effects of TNF-alpha and BRL 49653 on adipocyte lipolysis. |
| 16592 | 9568706 | Adipocyte production of TNF-alpha is proposed to play a role in the development of insulin resistance, and because BRL 49653 has been shown to antagonize some of the effects of TNF-alpha, we examined the effects of TNF-alpha and BRL 49653 on adipocyte lipolysis. |
| 16593 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 16594 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 16595 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 16596 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 16597 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 16598 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 16599 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 16600 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 16601 | 9568689 | Inhibition of IL-12 and IFN-gamma secretion was demonstrated in macrophages activated with lipopolysaccharide or T-cells stimulated through the CD3/T-cell receptor complex, respectively. |
| 16602 | 9568689 | Tumor necrosis factor-alpha was also inhibited, but IL-4 was less sensitive to suppression. |
| 16603 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16604 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16605 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16606 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16607 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16608 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16609 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16610 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16611 | 9568681 | Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. |
| 16612 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16613 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16614 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16615 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16616 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16617 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16618 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16619 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16620 | 9568681 | Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. |
| 16621 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16622 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16623 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16624 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16625 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16626 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16627 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16628 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16629 | 9568681 | This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. |
| 16630 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16631 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16632 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16633 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16634 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16635 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16636 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16637 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16638 | 9568681 | Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. |
| 16639 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16640 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16641 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16642 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16643 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16644 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16645 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16646 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16647 | 9568681 | Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. |
| 16648 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16649 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16650 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16651 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16652 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16653 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16654 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16655 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16656 | 9568681 | The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. |
| 16657 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16658 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16659 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16660 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16661 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16662 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16663 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16664 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16665 | 9568681 | The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. |
| 16666 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16667 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16668 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16669 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16670 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16671 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16672 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16673 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16674 | 9568681 | An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. |
| 16675 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16676 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16677 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16678 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16679 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16680 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16681 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16682 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16683 | 9568681 | These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. |
| 16684 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16685 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16686 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16687 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16688 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16689 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16690 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16691 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16692 | 9568681 | We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR. |
| 16693 | 9562347 | Tumour necrosis factor-alpha (TNF alpha) expression is linked with insulin resistance, and is under strong genetic control. |
| 16694 | 9562347 | Tumour necrosis factor-alpha (TNF alpha) expression is linked with insulin resistance, and is under strong genetic control. |
| 16695 | 9562347 | We examined the relationship between insulin resistance and two polymorphisms of the TNF alpha promoter region (positions -238 and -308). |
| 16696 | 9562347 | We examined the relationship between insulin resistance and two polymorphisms of the TNF alpha promoter region (positions -238 and -308). |
| 16697 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 16698 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 16699 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 16700 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 16701 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 16702 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 16703 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 16704 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 16705 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 16706 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 16707 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 16708 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 16709 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 16710 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 16711 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 16712 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 16713 | 9541176 | Healthy family members of patients with insulin-dependent diabetes mellitus (IDDM) are known to share a number of immunological abnormalities with their affected relatives. |
| 16714 | 9541176 | We report that circulating tumour necrosis factor-alpha (TNF-alpha) and soluble interleukin-2 (sIL-2) receptor were present in increased amounts in non-diabetic family members at levels similar to those found in the diabetic children (duration of disease 3 months-5 years). |
| 16715 | 9541164 | In order to evaluate the relationship between tumour necrosis factor-alpha (TNF-alpha) level in muscle and metabolic abnormalities in obesity and diabetes mellitus, pioglitazone, a novel insulin-sensitizing agent, was administered to Wistar fatty rats and time-dependent changes in muscle TNF-alpha content and plasma indicators of diabetes and obesity were measured. |
| 16716 | 9531322 | The nonobese diabetic (NOD) mouse spontaneously develops autoimmune insulin-dependent diabetes mellitus (IDDM) and serves as an animal model for human type I diabetes. |
| 16717 | 9531322 | TNF-alpha is known to be produced by islet-infiltrating mononuclear cells during insulitis and subsequent beta cell destruction and has been implicated in the pathogenesis of IDDM. |
| 16718 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 16719 | 9526909 | Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1beta), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). |
| 16720 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 16721 | 9526909 | Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1beta. |
| 16722 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16723 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16724 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16725 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16726 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16727 | 9510167 | Treatment of freshly isolated rat islets with TNF-alpha and LPS results in a potent inhibition of glucose-stimulated insulin secretion. |
| 16728 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16729 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16730 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16731 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16732 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16733 | 9510167 | The inhibitory actions of TNF + LPS are mediated by the intraislet production and release of IL-1 followed by IL-1-induced inducible nitric oxide synthase (iNOS) expression by beta cells. |
| 16734 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16735 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16736 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16737 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16738 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16739 | 9510167 | The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. |
| 16740 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16741 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16742 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16743 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16744 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16745 | 9510167 | Resident macrophages appear to be the source of IL-1, as a 7-day culture of rat islets at 24 degrees C (conditions known to deplete islets of lymphoid cells) prevents TNF + LPS-induced iNOS expression, nitrite production, and the inhibitory effects on insulin secretion. |
| 16746 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16747 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16748 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16749 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16750 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16751 | 9510167 | In addition, macrophage depletion also inhibits TNF + LPS-induced IL-1alpha and IL-1beta mRNA expression in rat islets. |
| 16752 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16753 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16754 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16755 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16756 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16757 | 9510167 | IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. |
| 16758 | 9506740 | To clarify the significance of the serum levels of tumor necrosis factor-alpha (TNF-alpha) in the mechanism of insulin resistance, we studied 12 obese patients with noninsulin-dependent diabetes mellitus (NIDDM). |
| 16759 | 9506740 | To clarify the significance of the serum levels of tumor necrosis factor-alpha (TNF-alpha) in the mechanism of insulin resistance, we studied 12 obese patients with noninsulin-dependent diabetes mellitus (NIDDM). |
| 16760 | 9506740 | To clarify the significance of the serum levels of tumor necrosis factor-alpha (TNF-alpha) in the mechanism of insulin resistance, we studied 12 obese patients with noninsulin-dependent diabetes mellitus (NIDDM). |
| 16761 | 9506740 | We evaluated the relationship of TNF-alpha levels with the visceral, subcutaneous, and total fat areas measured by computed tomography (CT), and with insulin resistance evaluated by the glucose infusion rate (GIR) observed during an euglycemic hyperinsulinemic clamp study. |
| 16762 | 9506740 | We evaluated the relationship of TNF-alpha levels with the visceral, subcutaneous, and total fat areas measured by computed tomography (CT), and with insulin resistance evaluated by the glucose infusion rate (GIR) observed during an euglycemic hyperinsulinemic clamp study. |
| 16763 | 9506740 | We evaluated the relationship of TNF-alpha levels with the visceral, subcutaneous, and total fat areas measured by computed tomography (CT), and with insulin resistance evaluated by the glucose infusion rate (GIR) observed during an euglycemic hyperinsulinemic clamp study. |
| 16764 | 9506740 | These results suggest that serum TNF-alpha levels may play an important role in mechanism of insulin resistance associated with obesity. |
| 16765 | 9506740 | These results suggest that serum TNF-alpha levels may play an important role in mechanism of insulin resistance associated with obesity. |
| 16766 | 9506740 | These results suggest that serum TNF-alpha levels may play an important role in mechanism of insulin resistance associated with obesity. |
| 16767 | 9505147 | Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. |
| 16768 | 9505147 | Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. |
| 16769 | 9505147 | Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. |
| 16770 | 9505147 | Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. |
| 16771 | 9505147 | During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). |
| 16772 | 9505147 | During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). |
| 16773 | 9505147 | During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). |
| 16774 | 9505147 | During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). |
| 16775 | 9505147 | Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. |
| 16776 | 9505147 | Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. |
| 16777 | 9505147 | Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. |
| 16778 | 9505147 | Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. |
| 16779 | 9505147 | Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels. |
| 16780 | 9505147 | Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels. |
| 16781 | 9505147 | Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels. |
| 16782 | 9505147 | Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels. |
| 16783 | 9480725 | Non-obese diabetic (NOD) mice spontaneously develop insulin-dependent (type 1) diabetes mellitus (IDDM) caused by T cells which destroy the insulin-producing islet beta-cells. |
| 16784 | 9480725 | Since cytokines are involved in this auto-immune beta-cell damage, we used an ELISPOT assay to enumerate the islet-associated T cells that secreted interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) or interleukin-4 (IL-4). |
| 16785 | 9480725 | We found that NOD females, more susceptible than males to IDDM, accumulated islet IFN-gamma producers more rapidly with age than did the males. |
| 16786 | 9480725 | Acceleration of male IDDM by cyclophosphamide led to a marked increase in IFN-gamma secreting islet T cells. |
| 16787 | 9495610 | The aim of the present study was to monitor clinical, microbiological, medical, and immunological effects of non-surgical periodontal therapy in diabetics and healthy controls. 20 IDDM (insulin dependent, n = 7) or NIDDM (non-insulin dependent, n = 13) diabetic patients (median duration 11.5 years, range of HbA1C: 4.4-10.6%) with moderate to advanced periodontal disease and 20 matched healthy control patients, were subjected to supragingival pretreatment and subsequent subgingival therapy. |
| 16788 | 9495610 | Periodontal examinations (API, PBI, BOP, PPD, PAL), microbiological examinations (culture), medical routine examinations, and immunological examinations (oxidative burst response of PMNs to TNF-alpha and FMLP) were performed at baseline, 2 weeks after supragingival, and 4 months after subgingival therapy. 4 months after completion of non-surgical therapy, the following compared to baseline significant (p < or = 0.05) changes (delta) of clinical parameters (median) were found in diabetic patients versus control patients: deltaAPI (30.4% versus 36.3%), deltaPBI (22.9% versus 24.2%), deltaBOP (39.5% versus 46.9%). |
| 16789 | 9421467 | GAD-reactive CD4+ Th1 cells induce diabetes in NOD/SCID mice. |
| 16790 | 9421467 | Although glutamic acid decarboxylase (GAD) has been implicated in IDDM, there is no direct evidence showing GAD-reactive T cells are diabetogenic in vivo. |
| 16791 | 9421467 | Splenocytes from this mouse showed a proliferative response to purified GAD, and were used to generate a CD4+ T cell line, designated 5A, that expresses TCRs encoding Vbeta2 and Vbeta12. 5A T cells exhibit a MHC restricted proliferative response to purified GAD, as well as GAD65 peptide 524-543. |
| 16792 | 9421467 | After antigen-specific stimulation, 5A T cells secrete IFNgamma and TNFalpha/beta, but not IL-4. |
| 16793 | 9421467 | We conclude that GAD injection in young NOD mice may, in some cases, provoke diabetes due to the activation of diabetogenic T cells reactive to GAD65 peptides. |
| 16794 | 9421467 | Our data provide direct evidence that GAD65 autoimmunity may be a critical event in the pathogenesis of IDDM. |
| 16795 | 9432636 | The activated lymphocytes have been shown to secrete a number of cytokines including tumour necrosis factor-alpha, interleukin-1 and interferon-gamma. |
| 16796 | 9432636 | The activated lymphocytes have been shown to secrete a number of cytokines including tumour necrosis factor-alpha, interleukin-1 and interferon-gamma. |
| 16797 | 9432636 | It was found that pentoxifylline (Ptx) was able to inhibit significantly the HLA-DR expression and glycosaminoglycan synthesis induced by inflammatory cytokines including TNF-alpha, IFN-gamma and IL-1. |
| 16798 | 9432636 | It was found that pentoxifylline (Ptx) was able to inhibit significantly the HLA-DR expression and glycosaminoglycan synthesis induced by inflammatory cytokines including TNF-alpha, IFN-gamma and IL-1. |
| 16799 | 9432636 | TNF-alpha, anti-TSH-receptor, anti-eye muscle, anti-thyroglobulin and anti-thyroid peroxidase antibodies in the patients'sera. |
| 16800 | 9432636 | TNF-alpha, anti-TSH-receptor, anti-eye muscle, anti-thyroglobulin and anti-thyroid peroxidase antibodies in the patients'sera. |
| 16801 | 9451599 | In order to study cytokine production profile (IFN-gamma, IL-4 and TNF-alpha) and TCRBV-gene usage of peripheral autoreactive T cells from IDDM patients, we have generated antigen-specific T cell lines with either tetanus toxoid, insulinoma membranes or a single beta-cell protein, recombinant ICA69, which has been shown to be a target of both autoantibodies and T cells in IDDM. |
| 16802 | 9451599 | In order to study cytokine production profile (IFN-gamma, IL-4 and TNF-alpha) and TCRBV-gene usage of peripheral autoreactive T cells from IDDM patients, we have generated antigen-specific T cell lines with either tetanus toxoid, insulinoma membranes or a single beta-cell protein, recombinant ICA69, which has been shown to be a target of both autoantibodies and T cells in IDDM. |
| 16803 | 9451599 | T cell responses against beta-cell antigens and tetanus toxoid (TT) were shown to be associated with IFN-gamma and TNF-alpha production, suggestive of a Th1-like phenotype of the T-cell lines. |
| 16804 | 9451599 | T cell responses against beta-cell antigens and tetanus toxoid (TT) were shown to be associated with IFN-gamma and TNF-alpha production, suggestive of a Th1-like phenotype of the T-cell lines. |
| 16805 | 9443093 | In order to investigate the status of some circulating factors in nephrotic syndrome, we examined the secretion of monocyte chemotactic peptide (MCP)-1, tumor necrosis factor (TNF) alpha or fibronectin in sera or by peripheral blood mononuclear cells (PBMC) from patients with membranous nephropathy (MN), diabetic nephropathy (DN) or minimal change disease (MCD). |
| 16806 | 9443093 | In order to investigate the status of some circulating factors in nephrotic syndrome, we examined the secretion of monocyte chemotactic peptide (MCP)-1, tumor necrosis factor (TNF) alpha or fibronectin in sera or by peripheral blood mononuclear cells (PBMC) from patients with membranous nephropathy (MN), diabetic nephropathy (DN) or minimal change disease (MCD). |
| 16807 | 9443093 | When MC were cultured with PBMC supernatants from patients, TNF alpha levels in PBMC supernatants correlated with production of MCP-1 or fibronectin by MC. |
| 16808 | 9443093 | When MC were cultured with PBMC supernatants from patients, TNF alpha levels in PBMC supernatants correlated with production of MCP-1 or fibronectin by MC. |
| 16809 | 9438411 | Abnormalities in tumor necrosis factor alpha expression have been noted in each of the above comorbid conditions, so leptin deficiency could promote these complications if leptin had immunoregulatory activity. |
| 16810 | 9428419 | Tumor necrosis factor-alpha (TNF-alpha), a cytokine whose synthesis is up-regulated in the diabetic uterus, did not induce nuclear fragmentation nor clusterin expression but increased the incidence of TUNEL-positive nuclei. |
| 16811 | 9421371 | Previous studies have shown that anti-gamma-interferon (IFN-gamma) antibody reduces the frequency of autoimmune IDDM in the DP-BB rat. |
| 16812 | 9421371 | Unexpectedly, IFN-gamma markedly reduced the incidence of IDDM as compared with control rats when administered six times per week at a dosage of 280,000 U between ages 30-35 to 105 days or ages 60-64 to 105 days. |
| 16813 | 9421371 | However, long-lasting protection against IDDM development over the 1-year study period was achieved only by the highest dosage of IFN-gamma administered from age 30 to 105 days. |
| 16814 | 9421371 | Ex vivo production of tumor necrosis factor-alpha from splenic lymphoid cells (SLCs) and peritoneal macrophages of the rats treated with IFN-gamma was comparable with that of controls; however, SLCs from the IFN-gamma-treated animals secreted lower amounts of IFN-gamma after stimulation with concanavalin A. |
| 16815 | 9421371 | IFN-gamma treatment also markedly reduced the frequency of phenotypically activated SLC-expressing class II antigens and interleukin-2 receptor. |
| 16816 | 9421371 | Finally, in agreement with the observed antidiabetogenic effects, exogenously administered IFN-gamma induced neither insulitis nor IDDM development in DR-BB rats, a subline of DP-BB rats in which autoimmune diabetes rarely occurs spontaneously but can be induced by administration of polyinosinic-polycytidilic acid. |
| 16817 | 9421370 | Effects of cell-permeable ceramides and tumor necrosis factor-alpha on insulin signaling and glucose uptake in 3T3-L1 adipocytes. |
| 16818 | 9421370 | Effects of cell-permeable ceramides and tumor necrosis factor-alpha on insulin signaling and glucose uptake in 3T3-L1 adipocytes. |
| 16819 | 9421370 | Effects of cell-permeable ceramides and tumor necrosis factor-alpha on insulin signaling and glucose uptake in 3T3-L1 adipocytes. |
| 16820 | 9421370 | Long-term increases in PI 3-kinase activity associated with insulin receptor substrate 1 (IRS-1) increased GLUT1 and GLUT4 concentrations in plasma membranes. |
| 16821 | 9421370 | Long-term increases in PI 3-kinase activity associated with insulin receptor substrate 1 (IRS-1) increased GLUT1 and GLUT4 concentrations in plasma membranes. |
| 16822 | 9421370 | Long-term increases in PI 3-kinase activity associated with insulin receptor substrate 1 (IRS-1) increased GLUT1 and GLUT4 concentrations in plasma membranes. |
| 16823 | 9421370 | This together with increased GLUT1 (but not GLUT4) synthesis explains the increase in non-insulin-dependent glucose uptake. |
| 16824 | 9421370 | This together with increased GLUT1 (but not GLUT4) synthesis explains the increase in non-insulin-dependent glucose uptake. |
| 16825 | 9421370 | This together with increased GLUT1 (but not GLUT4) synthesis explains the increase in non-insulin-dependent glucose uptake. |
| 16826 | 9421370 | C2-ceramide inhibited insulin-stimulated glucose uptake after 2 h by decreasing insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. |
| 16827 | 9421370 | C2-ceramide inhibited insulin-stimulated glucose uptake after 2 h by decreasing insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. |
| 16828 | 9421370 | C2-ceramide inhibited insulin-stimulated glucose uptake after 2 h by decreasing insulin-induced translocation of GLUT1 and GLUT4 to plasma membranes. |
| 16829 | 9421370 | Incubation for 24 h with tumor necrosis factor-alpha (TNF-alpha) but not C2-ceramide decreased the concentration and insulin-induced tyrosine phosphorylation of IRS-1 in this experimental system. |
| 16830 | 9421370 | Incubation for 24 h with tumor necrosis factor-alpha (TNF-alpha) but not C2-ceramide decreased the concentration and insulin-induced tyrosine phosphorylation of IRS-1 in this experimental system. |
| 16831 | 9421370 | Incubation for 24 h with tumor necrosis factor-alpha (TNF-alpha) but not C2-ceramide decreased the concentration and insulin-induced tyrosine phosphorylation of IRS-1 in this experimental system. |
| 16832 | 9421370 | Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo. |
| 16833 | 9421370 | Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo. |
| 16834 | 9421370 | Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo. |
| 16835 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16836 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16837 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16838 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16839 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16840 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16841 | 9396242 | [Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure]. |
| 16842 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16843 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16844 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16845 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16846 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16847 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16848 | 9396242 | Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. |
| 16849 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16850 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16851 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16852 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16853 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16854 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16855 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 16856 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16857 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16858 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16859 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16860 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16861 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16862 | 9396242 | Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. |
| 16863 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16864 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16865 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16866 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16867 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16868 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16869 | 9396242 | A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). |
| 16870 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16871 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16872 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16873 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16874 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16875 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16876 | 9396242 | LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. |
| 16877 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16878 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16879 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16880 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16881 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16882 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16883 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 16884 | 9392477 | Furthermore, TNF-alpha has distinct effects on adipose tissue including induction of insulin resistance, induction of leptin production, stimulation of lipolysis, suppression of lipogenesis, induction of adipocyte dedifferentiation, and impairment of preadipocyte differentiation in vitro. |
| 16885 | 9392477 | Furthermore, TNF-alpha has distinct effects on adipose tissue including induction of insulin resistance, induction of leptin production, stimulation of lipolysis, suppression of lipogenesis, induction of adipocyte dedifferentiation, and impairment of preadipocyte differentiation in vitro. |
| 16886 | 9392477 | Taken together, these effects all tend to decrease adipocyte volume and number and suggest a role for TNF-alpha in limiting increase in fat mass. |
| 16887 | 9392477 | Taken together, these effects all tend to decrease adipocyte volume and number and suggest a role for TNF-alpha in limiting increase in fat mass. |
| 16888 | 9392135 | [TNF gene polymorphism and IDDM]. |
| 16889 | 9356012 | TNF-alpha-induced insulin resistance in vivo and its prevention by troglitazone. |
| 16890 | 9356012 | TNF-alpha-induced insulin resistance in vivo and its prevention by troglitazone. |
| 16891 | 9356012 | TNF-alpha-induced insulin resistance in vivo and its prevention by troglitazone. |
| 16892 | 9356012 | TNF-alpha-induced insulin resistance in vivo and its prevention by troglitazone. |
| 16893 | 9356012 | Tumor necrosis factor (TNF)-alpha may play a role in the insulin resistance of obesity and NIDDM. |
| 16894 | 9356012 | Tumor necrosis factor (TNF)-alpha may play a role in the insulin resistance of obesity and NIDDM. |
| 16895 | 9356012 | Tumor necrosis factor (TNF)-alpha may play a role in the insulin resistance of obesity and NIDDM. |
| 16896 | 9356012 | Tumor necrosis factor (TNF)-alpha may play a role in the insulin resistance of obesity and NIDDM. |
| 16897 | 9356012 | To determine whether this drug could prevent the development of TNF-alpha-induced insulin resistance, glucose turnover was assessed in rats infused with cytokine and pretreated with troglitazone. |
| 16898 | 9356012 | To determine whether this drug could prevent the development of TNF-alpha-induced insulin resistance, glucose turnover was assessed in rats infused with cytokine and pretreated with troglitazone. |
| 16899 | 9356012 | To determine whether this drug could prevent the development of TNF-alpha-induced insulin resistance, glucose turnover was assessed in rats infused with cytokine and pretreated with troglitazone. |
| 16900 | 9356012 | To determine whether this drug could prevent the development of TNF-alpha-induced insulin resistance, glucose turnover was assessed in rats infused with cytokine and pretreated with troglitazone. |
| 16901 | 9356012 | TNF-alpha infusion resulted in a pronounced reduction in submaximal insulin-stimulated glucose disposal rate (GDR) (97 +/- 10 vs. 141 +/- 4 micromol x kg[-1] x min[-1], P < 0.05), maximal GDR (175 +/- 8 vs. 267 +/- 6 micromol x kg[-1] x min[-1], P < 0.01), and in insulin receptor-tyrosine kinase activity (IR-TKA) (248 +/- 39 vs. 406 +/- 32 fmol ATP/fmol IR, P < 0.05). |
| 16902 | 9356012 | TNF-alpha infusion resulted in a pronounced reduction in submaximal insulin-stimulated glucose disposal rate (GDR) (97 +/- 10 vs. 141 +/- 4 micromol x kg[-1] x min[-1], P < 0.05), maximal GDR (175 +/- 8 vs. 267 +/- 6 micromol x kg[-1] x min[-1], P < 0.01), and in insulin receptor-tyrosine kinase activity (IR-TKA) (248 +/- 39 vs. 406 +/- 32 fmol ATP/fmol IR, P < 0.05). |
| 16903 | 9356012 | TNF-alpha infusion resulted in a pronounced reduction in submaximal insulin-stimulated glucose disposal rate (GDR) (97 +/- 10 vs. 141 +/- 4 micromol x kg[-1] x min[-1], P < 0.05), maximal GDR (175 +/- 8 vs. 267 +/- 6 micromol x kg[-1] x min[-1], P < 0.01), and in insulin receptor-tyrosine kinase activity (IR-TKA) (248 +/- 39 vs. 406 +/- 32 fmol ATP/fmol IR, P < 0.05). |
| 16904 | 9356012 | TNF-alpha infusion resulted in a pronounced reduction in submaximal insulin-stimulated glucose disposal rate (GDR) (97 +/- 10 vs. 141 +/- 4 micromol x kg[-1] x min[-1], P < 0.05), maximal GDR (175 +/- 8 vs. 267 +/- 6 micromol x kg[-1] x min[-1], P < 0.01), and in insulin receptor-tyrosine kinase activity (IR-TKA) (248 +/- 39 vs. 406 +/- 32 fmol ATP/fmol IR, P < 0.05). |
| 16905 | 9329377 | Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. |
| 16906 | 9329377 | Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. |
| 16907 | 9329377 | Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. |
| 16908 | 9329377 | Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. |
| 16909 | 9329377 | Leptin concentrations in relation to body mass index and the tumor necrosis factor-alpha system in humans. |
| 16910 | 9329377 | The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. |
| 16911 | 9329377 | The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. |
| 16912 | 9329377 | The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. |
| 16913 | 9329377 | The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. |
| 16914 | 9329377 | The expression of leptin, an adipocyte-derived protein whose circulating levels reflect energy stores, can be induced by tumor necrosis factor (TNF)alpha in rodents, but an association between the TNF alpha system and leptin levels has not been reported in humans. |
| 16915 | 9329377 | To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. |
| 16916 | 9329377 | To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. |
| 16917 | 9329377 | To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. |
| 16918 | 9329377 | To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. |
| 16919 | 9329377 | To evaluate the potential association between serum leptin and the TNF alpha system, we measured the levels of soluble TNF alpha-receptor (sTNF alpha-R55), which has been validated as a sensitive indicator of activation of the TNF alpha system. |
| 16920 | 9329377 | By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. |
| 16921 | 9329377 | By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. |
| 16922 | 9329377 | By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. |
| 16923 | 9329377 | By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. |
| 16924 | 9329377 | By simple regression analysis in controls, there was a strong positive association between leptin and 3 parameters: body mass index, sTNF alpha-R55, and insulin levels. |
| 16925 | 9329377 | In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. |
| 16926 | 9329377 | In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. |
| 16927 | 9329377 | In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. |
| 16928 | 9329377 | In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. |
| 16929 | 9329377 | In a multiple regression analysis model, leptin remained significantly and strongly associated with body mass index, and the association of leptin with both insulin and sTNF alpha-R55, although weakened, remained significant. |
| 16930 | 9329377 | These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. |
| 16931 | 9329377 | These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. |
| 16932 | 9329377 | These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. |
| 16933 | 9329377 | These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. |
| 16934 | 9329377 | These data are consistent with the hypothesis that the TNF alpha system plays a role in regulating leptin levels in humans. |
| 16935 | 9329377 | Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans. |
| 16936 | 9329377 | Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans. |
| 16937 | 9329377 | Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans. |
| 16938 | 9329377 | Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans. |
| 16939 | 9329377 | Further elucidation of a possible role of the TNF alpha system in leptin expression and circulating levels may have important implications for our understanding of obesity and cachexia in humans. |
| 16940 | 9324360 | Here we demonstrate that transgenic mice expressing both TNFalpha and the Leishmania major LACK antigen in the pancreas (RIP-TNFalpha/RIP-LACK) exhibit an impaired ability to mount a CD4+ T cell response against LACK. |
| 16941 | 9324360 | In addition, peripheral CD4+ T cells from TCR transgenic mice (TCR-LACK/RIP-TNFalpha/RIP-LACK) produced reduced interleukin-2 but elevated levels of T helper 2 cytokines in response to LACK peptide in vitro. |
| 16942 | 9342542 | Influence of metabolic and genetic factors on tumour necrosis factor-alpha and lymphotoxin-alpha production in insulin-dependent diabetes mellitus. |
| 16943 | 9342542 | Influence of metabolic and genetic factors on tumour necrosis factor-alpha and lymphotoxin-alpha production in insulin-dependent diabetes mellitus. |
| 16944 | 9342542 | Influence of metabolic and genetic factors on tumour necrosis factor-alpha and lymphotoxin-alpha production in insulin-dependent diabetes mellitus. |
| 16945 | 9342542 | The potential role of tumour necrosis factors (TNFs) in autoimmunity and insulin-dependent diabetes mellitus (IDDM) led us to determine in vitro TNF-alpha and lymphotoxin-alpha (LT-alpha, TNF-beta) production in IDDM patients according to TNF polymorphism. |
| 16946 | 9342542 | The potential role of tumour necrosis factors (TNFs) in autoimmunity and insulin-dependent diabetes mellitus (IDDM) led us to determine in vitro TNF-alpha and lymphotoxin-alpha (LT-alpha, TNF-beta) production in IDDM patients according to TNF polymorphism. |
| 16947 | 9342542 | The potential role of tumour necrosis factors (TNFs) in autoimmunity and insulin-dependent diabetes mellitus (IDDM) led us to determine in vitro TNF-alpha and lymphotoxin-alpha (LT-alpha, TNF-beta) production in IDDM patients according to TNF polymorphism. |
| 16948 | 9342542 | A study of the microsatellite TNFa region close to the LTA gene showed that the presence of the TNFa1 allele in HLA-(DR3) subjects was associated with increased risk of IDDM. |
| 16949 | 9342542 | A study of the microsatellite TNFa region close to the LTA gene showed that the presence of the TNFa1 allele in HLA-(DR3) subjects was associated with increased risk of IDDM. |
| 16950 | 9342542 | A study of the microsatellite TNFa region close to the LTA gene showed that the presence of the TNFa1 allele in HLA-(DR3) subjects was associated with increased risk of IDDM. |
| 16951 | 9342542 | These results indicate that low LT-alpha production is an additional risk factor for IDDM and that poor glycaemic control in patients is associated with enhanced PBMC TNF-alpha production which causes an imbalance between TNF-alpha and LT-alpha production in IDDM patient. |
| 16952 | 9342542 | These results indicate that low LT-alpha production is an additional risk factor for IDDM and that poor glycaemic control in patients is associated with enhanced PBMC TNF-alpha production which causes an imbalance between TNF-alpha and LT-alpha production in IDDM patient. |
| 16953 | 9342542 | These results indicate that low LT-alpha production is an additional risk factor for IDDM and that poor glycaemic control in patients is associated with enhanced PBMC TNF-alpha production which causes an imbalance between TNF-alpha and LT-alpha production in IDDM patient. |
| 16954 | 9342538 | Is leptin the link between obesity and insulin resistance? |
| 16955 | 9342538 | Insulin and glucocorticoids increase leptin expression, whereas catecholamines, via beta-adrenergic receptors and cAMP, and long-chain fatty acids (and thiazolidinediones), via PPARy, inhibit leptin expression. |
| 16956 | 9342538 | Leptin is a cytokine that binds to transmembrane receptors similar to the receptors of cytokine family (type IL-6), and transmit their information inside the cell, after dimerisation. |
| 16957 | 9342538 | Then leptin binds to a long-form of leptin receptor in the hypothalamus (with a cytoplasmic domain of 302 amino residues) and decreases the production of neuropeptide Y, a neuromediator of food intake. |
| 16958 | 9342538 | The long-form of leptin receptor, transmits its information via the Janus Kinases (JAK) who subsequently phosphorylate transcription factors of the STAT family. |
| 16959 | 9342538 | Recent studies have shown that leptin inhibits insulin secretion and have anti-insulin effects on liver and adipose tissue. |
| 16960 | 9342538 | If these effects are confirmed, leptin could play a role similar to TNF alpha and could participate in the insulin-resistance of obesity and type II diabetes. |
| 16961 | 9326333 | Using both parametric and nonparametric methods, we found no evidence of linkage of obesity to any of nine candidate genes/regions, including the Prader-Willi chromosomal region (PWS), the human homologue of the mouse agouti gene (ASP), and the genes for leptin (OB), the leptin receptor (OBR/DB), the beta3-adrenergic receptor (ADRB3), lipoprotein lipase (LPL), hepatic lipase (LIPC), glycogen synthase (GYS), and tumor necrosis factor alpha (TNFA). |
| 16962 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16963 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16964 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16965 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16966 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16967 | 9335502 | Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. |
| 16968 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16969 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16970 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16971 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16972 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16973 | 9335502 | It has been suggested that tumour necrosis factor (TNF)-alpha is a candidate mediator of insulin resistance in obesity, as it is overexpressed in the adipose tissues of rodents and humans and it blocks the action of insulin in cultured cells and whole animals. |
| 16974 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16975 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16976 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16977 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16978 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16979 | 9335502 | To investigate the role of TNF-alpha in obesity and insulin resistance, we have generated obese mice with a targeted null mutation in the gene encoding TNF-alpha and those encoding the two receptors for TNF-alpha. |
| 16980 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16981 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16982 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16983 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16984 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16985 | 9335502 | The absence of TNF-alpha resulted in significantly improved insulin sensitivity in both diet-induced obesity and that resulting for the ob/ob model of obesity. |
| 16986 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16987 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16988 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16989 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16990 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16991 | 9335502 | The TNFalpha-deficient obese mice had lower levels of circulating free fatty acids, and were protected from the obesity-related reduction in the insulin receptor signalling in muscle and fat tissues. |
| 16992 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16993 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16994 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16995 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16996 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16997 | 9335502 | These results indicate that TNF-alpha is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action. |
| 16998 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 16999 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 17000 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 17001 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 17002 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 17003 | 9312188 | Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling. |
| 17004 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17005 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17006 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17007 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17008 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17009 | 9312188 | TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. |
| 17010 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17011 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17012 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17013 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17014 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17015 | 9312188 | Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. |
| 17016 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17017 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17018 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17019 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17020 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17021 | 9312188 | Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). |
| 17022 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17023 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17024 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17025 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17026 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17027 | 9312188 | The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. |
| 17028 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17029 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17030 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17031 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17032 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17033 | 9312188 | These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. |
| 17034 | 9275207 | Because type I autoimmune diabetes destroys islets by mechanisms that involve class I MHC and TNF-alpha, we investigated whether the entire cassette of Ad E3 genes might prevent the onset of diabetes in a well studied lymphocytic choriomeningitis viral (LCMV) murine model of virus-induced autoimmune diabetes. |
| 17035 | 9275207 | Because type I autoimmune diabetes destroys islets by mechanisms that involve class I MHC and TNF-alpha, we investigated whether the entire cassette of Ad E3 genes might prevent the onset of diabetes in a well studied lymphocytic choriomeningitis viral (LCMV) murine model of virus-induced autoimmune diabetes. |
| 17036 | 9275207 | Although the decrease in class I MHC in islets by Ad genes was demonstrated in these in vivo studies, the relative importance of this process and the control of TNF-alpha cytolysis must await further genetic dissection of the introduced Ad genes. |
| 17037 | 9275207 | Although the decrease in class I MHC in islets by Ad genes was demonstrated in these in vivo studies, the relative importance of this process and the control of TNF-alpha cytolysis must await further genetic dissection of the introduced Ad genes. |
| 17038 | 9287059 | To address the hypothesis that tumor necrosis factor (TNF)-alpha has a role in obesity-associated insulin resistance or the regulation of in vivo lipid metabolism, mice with targeted disruption of the TNF-alpha gene were generated and studied. |
| 17039 | 9287059 | To address the hypothesis that tumor necrosis factor (TNF)-alpha has a role in obesity-associated insulin resistance or the regulation of in vivo lipid metabolism, mice with targeted disruption of the TNF-alpha gene were generated and studied. |
| 17040 | 9287059 | Fed plasma insulin levels decreased 47% (28 weeks), triglyceride levels decreased (all three ages; maximum 35% at 19 weeks), and fed plasma leptin decreased 33% (28 weeks). |
| 17041 | 9287059 | Fed plasma insulin levels decreased 47% (28 weeks), triglyceride levels decreased (all three ages; maximum 35% at 19 weeks), and fed plasma leptin decreased 33% (28 weeks). |
| 17042 | 9287059 | We conclude 1) that TNF-alpha functions to regulate plasma triglycerides and body adiposity and 2) that although TNF-alpha contributes to reduced insulin sensitivity in older or obese mice, the absence of TNF-alpha is not sufficient to substantially protect against insulin resistance in the GTG hyperphagic model of rodent obesity. |
| 17043 | 9287059 | We conclude 1) that TNF-alpha functions to regulate plasma triglycerides and body adiposity and 2) that although TNF-alpha contributes to reduced insulin sensitivity in older or obese mice, the absence of TNF-alpha is not sufficient to substantially protect against insulin resistance in the GTG hyperphagic model of rodent obesity. |
| 17044 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17045 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17046 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17047 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17048 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17049 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17050 | 9287048 | The TNF-alpha gene Nco I polymorphism influences the relationship among insulin resistance, percent body fat, and increased serum leptin levels. |
| 17051 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17052 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17053 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17054 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17055 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17056 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17057 | 9287048 | Tumor necrosis factor-alpha (TNF-alpha), acting as a modulator of gene expression in adipocytes, is implicated in the development of insulin resistance and obesity. |
| 17058 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17059 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17060 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17061 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17062 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17063 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17064 | 9287048 | The aim of this study was to investigate whether the Nco I polymorphism of the TNF-alpha gene influences the relationship among insulin resistance, percent body fat, and serum leptin levels. |
| 17065 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17066 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17067 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17068 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17069 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17070 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17071 | 9287048 | Basal serum insulin was greater (14.2 +/- 2 vs. 9.2 +/- 0.9 mU/l, P = 0.041) in the TNF-2 group in the presence of comparable serum glucose concentration. |
| 17072 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17073 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17074 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17075 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17076 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17077 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17078 | 9287048 | The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). |
| 17079 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17080 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17081 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17082 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17083 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17084 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17085 | 9287048 | TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). |
| 17086 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17087 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17088 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17089 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17090 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17091 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17092 | 9287048 | Paralleling the known relationship between insulin and leptin levels, serum leptin concentration was clearly increased in the TNF-2 group (19.6 +/- 3.4 vs. 11.1 +/- 1.5 ng/ml, P = 0.03). |
| 17093 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17094 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17095 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17096 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17097 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17098 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17099 | 9287048 | Results of the present study suggest that TNF-alphaNco I polymorphism may exacerbate the alterations in leptin levels normally found among insulin-resistant subjects. |
| 17100 | 15989661 | These include influence on insulin receptor kinase activity, control of insulin receptor phosphorylation, change in number of insulin receptors, quantity and activity of GLUT-4, modulation of tumour necrosis factor (TNF) activity, activation of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and alteration of hepatic glucose metabolism. |
| 17101 | 9293394 | Human serum albumin minimally-modified by methylglyoxal (MGmin-HSA) stimulated the synthesis and secretion of tumour necrosis factor-alpha (TNF-alpha) from human monocytic THP-1 cells in vitro. |
| 17102 | 9293394 | Human serum albumin minimally-modified by methylglyoxal (MGmin-HSA) stimulated the synthesis and secretion of tumour necrosis factor-alpha (TNF-alpha) from human monocytic THP-1 cells in vitro. |
| 17103 | 9293394 | Human serum albumin minimally-modified by glucose-derived advanced glycation endproducts (AGEmin-HSA) and human serum albumin highly-modified by glucose-derived advanced glycation endproducts (AGE-HSA) stimulated markedly lower synthesis and secretion of TNF-alpha from THP-1 cells than did MGmin-HSA. |
| 17104 | 9293394 | Human serum albumin minimally-modified by glucose-derived advanced glycation endproducts (AGEmin-HSA) and human serum albumin highly-modified by glucose-derived advanced glycation endproducts (AGE-HSA) stimulated markedly lower synthesis and secretion of TNF-alpha from THP-1 cells than did MGmin-HSA. |
| 17105 | 9288574 | Pioglitazone and metformin reverse insulin resistance induced by tumor necrosis factor-alpha in liver cells. |
| 17106 | 9288574 | Pioglitazone and metformin reverse insulin resistance induced by tumor necrosis factor-alpha in liver cells. |
| 17107 | 9288574 | Pioglitazone and metformin reverse insulin resistance induced by tumor necrosis factor-alpha in liver cells. |
| 17108 | 9288574 | Pioglitazone and metformin reverse insulin resistance induced by tumor necrosis factor-alpha in liver cells. |
| 17109 | 9288574 | Tumor necrosis factor-alpha (TNF-alpha) has recently been implicated as a cause of insulin resistance (IR) in obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 17110 | 9288574 | Tumor necrosis factor-alpha (TNF-alpha) has recently been implicated as a cause of insulin resistance (IR) in obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 17111 | 9288574 | Tumor necrosis factor-alpha (TNF-alpha) has recently been implicated as a cause of insulin resistance (IR) in obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 17112 | 9288574 | Tumor necrosis factor-alpha (TNF-alpha) has recently been implicated as a cause of insulin resistance (IR) in obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 17113 | 9288574 | To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. |
| 17114 | 9288574 | To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. |
| 17115 | 9288574 | To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. |
| 17116 | 9288574 | To examine mechanisms involved, we induced IR induced IR in H-411 E cells with graded doses of TNF-alpha and measured the ability of insulin (INS) to stimulate both calmodulin (CaM) mRNA and glucose utilization. |
| 17117 | 9288574 | With TNF-alpha concentration at 1 ng/ml and 10(4) muU/ml INS, metformin 10 microM and pioglitazone 1.5 microM, reversed the IR induced by TNF-alpha restoring biologic response to 100% of INS effect alone. |
| 17118 | 9288574 | With TNF-alpha concentration at 1 ng/ml and 10(4) muU/ml INS, metformin 10 microM and pioglitazone 1.5 microM, reversed the IR induced by TNF-alpha restoring biologic response to 100% of INS effect alone. |
| 17119 | 9288574 | With TNF-alpha concentration at 1 ng/ml and 10(4) muU/ml INS, metformin 10 microM and pioglitazone 1.5 microM, reversed the IR induced by TNF-alpha restoring biologic response to 100% of INS effect alone. |
| 17120 | 9288574 | With TNF-alpha concentration at 1 ng/ml and 10(4) muU/ml INS, metformin 10 microM and pioglitazone 1.5 microM, reversed the IR induced by TNF-alpha restoring biologic response to 100% of INS effect alone. |
| 17121 | 9245742 | The TNF-beta gene Nco I polymorphism is not associated with hypertriglyceridemia or insulin resistance in lean and obese subjects. |
| 17122 | 9245742 | Interindividual differences in TNF-alpha monocyte responses can be accounted for by genetic polymorphisms at the TNF-beta locus defined by the Nco I restriction enzyme. |
| 17123 | 9245742 | Higher triglyceride levels in non-insulin-dependent diabetic patients homozygous at the 10.5-kb fragment of the TNF-beta gene have been described. |
| 17124 | 9245742 | The aim of this study was to investigate whether the Ncol polymorphism of the TNF-beta gene influences the relationship between insulin resistance and triglyceride levels. |
| 17125 | 9245742 | In summary, the 10.5-kb homozygous genotype of the TNF-beta locus does not contribute to differences in triglyceride levels or insulin sensitivity among nondiabetic subjects. |
| 17126 | 9258512 | The capsule membrane permeability to IgG (150 kDa), Transferrin (81 kDa), Tumor necrosis factor (TNF, 51 kDa), Interleukin-1 beta (IL-1 beta, 17.5 kDa), and insulin (5.8 kDa) was estimated by measuring the binding of 125I-labeled proteins to the encapsulated antibody coated Dynabeads. |
| 17127 | 9258512 | The capsule membrane permeability to IgG (150 kDa), Transferrin (81 kDa), Tumor necrosis factor (TNF, 51 kDa), Interleukin-1 beta (IL-1 beta, 17.5 kDa), and insulin (5.8 kDa) was estimated by measuring the binding of 125I-labeled proteins to the encapsulated antibody coated Dynabeads. |
| 17128 | 9258512 | The capsule membrane permeability to IgG (150 kDa), Transferrin (81 kDa), Tumor necrosis factor (TNF, 51 kDa), Interleukin-1 beta (IL-1 beta, 17.5 kDa), and insulin (5.8 kDa) was estimated by measuring the binding of 125I-labeled proteins to the encapsulated antibody coated Dynabeads. |
| 17129 | 9258512 | The high-G capsules, however, could be made impermeable to TNF and still allowed transferrin to pass. |
| 17130 | 9258512 | The high-G capsules, however, could be made impermeable to TNF and still allowed transferrin to pass. |
| 17131 | 9258512 | The high-G capsules, however, could be made impermeable to TNF and still allowed transferrin to pass. |
| 17132 | 9258512 | The permeability of these capsules to IL-1 beta, but not to TNF was confirmed in an assay where mouse islets of Langerhans were incubated with TNF and IL-1 beta, and comparing the IL-6 for encapsulated and non-encapsulated islets. |
| 17133 | 9258512 | The permeability of these capsules to IL-1 beta, but not to TNF was confirmed in an assay where mouse islets of Langerhans were incubated with TNF and IL-1 beta, and comparing the IL-6 for encapsulated and non-encapsulated islets. |
| 17134 | 9258512 | The permeability of these capsules to IL-1 beta, but not to TNF was confirmed in an assay where mouse islets of Langerhans were incubated with TNF and IL-1 beta, and comparing the IL-6 for encapsulated and non-encapsulated islets. |
| 17135 | 9224423 | High levels of adipose tissue-derived tumor necrosis factor-alpha (AT-TNF) mRNA and protein have previously been associated with genetic models of obesity and insulin resistance. |
| 17136 | 9224423 | High levels of adipose tissue-derived tumor necrosis factor-alpha (AT-TNF) mRNA and protein have previously been associated with genetic models of obesity and insulin resistance. |
| 17137 | 9224423 | Since TNF has been shown to affect several key genes in tissue culture, mRNA for lipoprotein lipase, hormone-sensitive lipase, and Glut4 were measured. |
| 17138 | 9224423 | Since TNF has been shown to affect several key genes in tissue culture, mRNA for lipoprotein lipase, hormone-sensitive lipase, and Glut4 were measured. |
| 17139 | 9200658 | The production of tumor necrosis factor-alpha (TNF-alpha) was investigated in uterine explants from normal, diabetic, or insulin-treated diabetic pregnant rats. |
| 17140 | 9200658 | The production of tumor necrosis factor-alpha (TNF-alpha) was investigated in uterine explants from normal, diabetic, or insulin-treated diabetic pregnant rats. |
| 17141 | 9200658 | Daily insulin administration failed to normalize uterine TNF-alpha secretion despite correction of glycemia in the diabetic rats. |
| 17142 | 9200658 | Daily insulin administration failed to normalize uterine TNF-alpha secretion despite correction of glycemia in the diabetic rats. |
| 17143 | 9200487 | Measurement of the macrophage-derived cytokines IL-12, TNF-alpha, and IL-1beta revealed a selective increase of their expression, after KRV infection, in the splenic lymphocytes and the pancreatic islets. |
| 17144 | 9200487 | Measurement of CD4+ T cell-derived cytokines revealed that IL-2 and IFN-gamma cytokine gene expression closely correlates with an elevation of IL-12, but IL-4 and IL-10 do not change. |
| 17145 | 9198233 | Subsequent RT-PCR and in situ hybridization studies suggest that the increased plasma PAI-1 originates primarily from the adipocyte in response to chronically elevated levels of tumor necrosis factor-alpha (TNF-alpha), insulin, and transforming growth factor-beta (TGF-beta). |
| 17146 | 9185518 | Interleukin-1beta and tumor necrosis factor-alpha significantly upregulate expression of BSC2 mRNA and protein in human umbilical vein endothelial cells, a response that is inhibited by pretreatment with interferon-gamma. |
| 17147 | 9185518 | In vivo, BSC2 mRNA is upregulated after intraperitoneal administration of bacterial endotoxin (LPS) in murine lung and kidney, but not in cardiac tissue. |
| 17148 | 9196042 | Identification of macrophage migration inhibitory factor in adipose tissue and its induction by tumor necrosis factor-alpha. |
| 17149 | 9196042 | Identification of macrophage migration inhibitory factor in adipose tissue and its induction by tumor necrosis factor-alpha. |
| 17150 | 9196042 | Identification of macrophage migration inhibitory factor in adipose tissue and its induction by tumor necrosis factor-alpha. |
| 17151 | 9196042 | Northern and Western blot analyses revealed the expression of MIF mRNA and MIF protein, respectively, in both the fat pad and the adipocyte cell line. |
| 17152 | 9196042 | Northern and Western blot analyses revealed the expression of MIF mRNA and MIF protein, respectively, in both the fat pad and the adipocyte cell line. |
| 17153 | 9196042 | Northern and Western blot analyses revealed the expression of MIF mRNA and MIF protein, respectively, in both the fat pad and the adipocyte cell line. |
| 17154 | 9196042 | The results showed that MIF content was 1.6 +/- 0.48 ng/ml (mean +/- SD) after 24 hr culture, and the content was increased up to 9.7 +/- 2.8 ng/ml by stimulation with TNF-alpha (50 nM). |
| 17155 | 9196042 | The results showed that MIF content was 1.6 +/- 0.48 ng/ml (mean +/- SD) after 24 hr culture, and the content was increased up to 9.7 +/- 2.8 ng/ml by stimulation with TNF-alpha (50 nM). |
| 17156 | 9196042 | The results showed that MIF content was 1.6 +/- 0.48 ng/ml (mean +/- SD) after 24 hr culture, and the content was increased up to 9.7 +/- 2.8 ng/ml by stimulation with TNF-alpha (50 nM). |
| 17157 | 9196042 | Since TNF-alpha produced in adipocytes is known to induce insulin resistance, the results suggest the possibility that MIF plays an important role in the mechanism of insulin resistance often observed in obesity and diabetes via regulation of TNF-alpha expression. |
| 17158 | 9196042 | Since TNF-alpha produced in adipocytes is known to induce insulin resistance, the results suggest the possibility that MIF plays an important role in the mechanism of insulin resistance often observed in obesity and diabetes via regulation of TNF-alpha expression. |
| 17159 | 9196042 | Since TNF-alpha produced in adipocytes is known to induce insulin resistance, the results suggest the possibility that MIF plays an important role in the mechanism of insulin resistance often observed in obesity and diabetes via regulation of TNF-alpha expression. |
| 17160 | 9218757 | Protection of NIT-1 pancreatic beta-cells from immune attack by inhibition of NF-kappaB. |
| 17161 | 9218757 | Protection of NIT-1 pancreatic beta-cells from immune attack by inhibition of NF-kappaB. |
| 17162 | 9218757 | We have recently observed that inhibition of NF-kappaB in NIT-1 insulinoma cells protects them from tumour necrosis factor (TNF)-induced cell death in vitro, possibly because expression of interleukin-1 (IL-1)beta-converting enzyme (ICE), a member of the cysteine protease pathway of cell death, is decreased. |
| 17163 | 9218757 | We have recently observed that inhibition of NF-kappaB in NIT-1 insulinoma cells protects them from tumour necrosis factor (TNF)-induced cell death in vitro, possibly because expression of interleukin-1 (IL-1)beta-converting enzyme (ICE), a member of the cysteine protease pathway of cell death, is decreased. |
| 17164 | 9218757 | In the current study we have examined the effect of the same inhibitor of NF-kappaB on class I major histocompatibility complex (MHC) protein expression in NIT-1 cells and shown that inhibition of NF-kappaB activation decreased basal and TNF-induced class I MHC levels. |
| 17165 | 9218757 | In the current study we have examined the effect of the same inhibitor of NF-kappaB on class I major histocompatibility complex (MHC) protein expression in NIT-1 cells and shown that inhibition of NF-kappaB activation decreased basal and TNF-induced class I MHC levels. |
| 17166 | 9218757 | Although inducible nitric oxide synthase (iNOS) may also be inhibited by inhibition of NF-kappaB, this could not be demonstrated in NIT-1/delta sp cells because wild-type NIT-1 cells express very little iNOS. |
| 17167 | 9218757 | Although inducible nitric oxide synthase (iNOS) may also be inhibited by inhibition of NF-kappaB, this could not be demonstrated in NIT-1/delta sp cells because wild-type NIT-1 cells express very little iNOS. |
| 17168 | 9218757 | When NIT-1/delta sp12 cells, expressing high levels of the NF-kappaB inhibitor, are transplanted into immunodeficient NOD/scid mice, tumorigenesis and death by hypoglycemia proceed similarly to untransfected NIT-1 cells. |
| 17169 | 9218757 | When NIT-1/delta sp12 cells, expressing high levels of the NF-kappaB inhibitor, are transplanted into immunodeficient NOD/scid mice, tumorigenesis and death by hypoglycemia proceed similarly to untransfected NIT-1 cells. |
| 17170 | 9218757 | In conclusion, inhibition of NF-kappaB is likely to suppress several different pathways of immune-mediated cell death in beta-cells and protects NIT-1 cells from immune attack by diabetogenic T cells in vivo. |
| 17171 | 9218757 | In conclusion, inhibition of NF-kappaB is likely to suppress several different pathways of immune-mediated cell death in beta-cells and protects NIT-1 cells from immune attack by diabetogenic T cells in vivo. |
| 17172 | 9148940 | Cdc42Hs, but not Rac1, inhibits serum-stimulated cell cycle progression at G1/S through a mechanism requiring p38/RK. |
| 17173 | 9148940 | Antimitogenic stimuli such as environmental or genotoxic stress, transforming growth factor-beta, and the inflammatory cytokines tumor necrosis factor and interleukin-1 activate two extracellular signal-regulated kinase (ERK)-based signaling pathways: the stress-activated protein kinase (SAPK/JNK) pathway and the p38 pathway. |
| 17174 | 9148940 | Activated p38 phosphorylates transcription factors important in the regulation of cell growth and apoptosis, including activating transcription factor 2 (ATF2), Max, cAMP response element-binding protein-homologous protein/growth arrest DNA damage 153 (CHDP/GADD153). |
| 17175 | 9148940 | In turn, p38 lies downstream of the Rho family GTPases Cdc42Hs and Rac1, as well as at least three mitogen-activated protein kinase (MAPK)/ERK-kinases (MEKs): MAPK kinases-3, -6, and SAPK/ERK-kinase-1. |
| 17176 | 9148940 | Using a quantitative microinjection approach, we show here that Cdc42Hs, but not Rac1 or RhoA, can inhibit cell cycle progression at G1/S through a mechanism requiring activation of p38. |
| 17177 | 9148940 | Furthermore, these results suggest that although both Cdc42Hs and Rac1 can activate p38 in situ, the effects of Cdc42Hs and Rac1 on cell cycle progression are, in fact, quite distinct. |
| 17178 | 9151895 | Repeated injections of adult mice with recombinant murine TNF prolong the survival of NZB/W F1 mice, and suppress type I insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice. |
| 17179 | 9151895 | Repeated injections of adult mice with recombinant murine TNF prolong the survival of NZB/W F1 mice, and suppress type I insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice. |
| 17180 | 9151895 | Furthermore, T cell responses of HNT-TCR transgenic mice also expressing the human TNF-globin transgene were markedly reduced compared to HNT-TCR single transgenic littermates, indicating that sustained p55 TNF-R signaling is sufficient to suppress T cell function in vivo. |
| 17181 | 9151895 | Furthermore, T cell responses of HNT-TCR transgenic mice also expressing the human TNF-globin transgene were markedly reduced compared to HNT-TCR single transgenic littermates, indicating that sustained p55 TNF-R signaling is sufficient to suppress T cell function in vivo. |
| 17182 | 9411420 | [Monitoring of changes in levels of endogenous TNF alpha in patients with uncontrolled insulin dependent diabetes mellitus]. |
| 17183 | 9174153 | Polymorphisms of tumor necrosis factor receptor 2 are not associated with insulin-dependent diabetes mellitus or Graves' disease. |
| 17184 | 9174153 | Polymorphisms of tumor necrosis factor receptor 2 are not associated with insulin-dependent diabetes mellitus or Graves' disease. |
| 17185 | 9174153 | Insulin-dependent diabetes mellitus (IDDM) and Graves' disease (GD) are autoimmune endocrinopathies and associated with distinct HLA-DR and -DQ alleles as well as several tumor necrosis factor alpha (TNF-alpha) and beta (TNF-beta) alleles. |
| 17186 | 9174153 | Insulin-dependent diabetes mellitus (IDDM) and Graves' disease (GD) are autoimmune endocrinopathies and associated with distinct HLA-DR and -DQ alleles as well as several tumor necrosis factor alpha (TNF-alpha) and beta (TNF-beta) alleles. |
| 17187 | 9174153 | TNF-alpha and TNF-beta interact with TNF receptor (TNF-R), of which two subtypes have been described: TNF-R1 and TNF-R2. |
| 17188 | 9174153 | TNF-alpha and TNF-beta interact with TNF receptor (TNF-R), of which two subtypes have been described: TNF-R1 and TNF-R2. |
| 17189 | 9174153 | We investigated TNF-R2 alleles in 90 patients with IDDM, 101 with GD and 70 healthy controls. |
| 17190 | 9174153 | We investigated TNF-R2 alleles in 90 patients with IDDM, 101 with GD and 70 healthy controls. |
| 17191 | 9174153 | In conclusion, the studied polymorphism of TNF-R2 was associated with neither IDDM nor GD in a German population. |
| 17192 | 9174153 | In conclusion, the studied polymorphism of TNF-R2 was associated with neither IDDM nor GD in a German population. |
| 17193 | 9174152 | HLA-DQB1*0304-DRB1*0408 haplotype associated with insulin-dependent diabetes mellitus in populations in the eastern Baltic region. |
| 17194 | 9174152 | The rare HLA-DQB1*0304 allele was found increased among IDDM patients in the populations of the eastern Baltic region. |
| 17195 | 9174152 | HLA-DQB1*0304 in these populations was associated with DRB1*0408, and the haplotype was further characterized by a B35 allele and a typical combination of microsatellite markers from the TNF gene region. |
| 17196 | 9133556 | Plasminogen activator inhibitor type 1 (PAI-1) contributes to the pathogenesis of atherothrombosis. |
| 17197 | 9133556 | Its plasma level is strongly correlated with parameters that define the insulin resistance syndrome, in particular with BMI and visceral accumulation of body fat, suggesting that PAI-1 may be an adipose tissue-derived circulating peptide. |
| 17198 | 9133556 | PAI-1 protein detected by immunolocalization was present at the stromal and adipocyte levels. |
| 17199 | 9133556 | Transforming growth factor-beta1 significantly increased PAI-1 antigen production by the adipocyte fraction, whereas tumor necrosis factor-alpha did not have any effect. |
| 17200 | 9133556 | Interestingly, after 5 h of incubation, omental tissue explants produced significantly more PAI-1 antigen than did subcutaneous tissue from the same individual, whereas similar production of leptin by the two territories was observed. |
| 17201 | 9127018 | Immunohistochemistry studies show that IL-10/Fc treatment inhibits expression of TNF-alpha, proinflammatory cytokine, as well as Th1-type cytokines, IL-2 and IFN-gamma, but promotes expression of IL-4 and IL-10, Th2-type cytokines, by islet-infiltrating leukocytes. |
| 17202 | 9094680 | When we examined the expression of the soluble mediators interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) in the pancreatic islets, we found that these mediators were clearly expressed at an early stage of insulitis and that this expression was evident until the development of diabetes. |
| 17203 | 9094680 | When we examined the expression of the soluble mediators interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and inducible nitric oxide synthase (iNOS) in the pancreatic islets, we found that these mediators were clearly expressed at an early stage of insulitis and that this expression was evident until the development of diabetes. |
| 17204 | 9094680 | Mice treated with antibody against IL-1beta or TNF-alpha or with the iNOS inhibitor aminoguanidine exhibited a significant decrease in the incidence of diabetes. |
| 17205 | 9094680 | Mice treated with antibody against IL-1beta or TNF-alpha or with the iNOS inhibitor aminoguanidine exhibited a significant decrease in the incidence of diabetes. |
| 17206 | 9185876 | The cell recruitment phase, between 6 and 12 weeks of age, is predominated by production of the monokines IL-1alpha, IL-6, and TNF After stimulation IFN-gamma and occasional IL-10 and GM-CSF producing cells could also be observed. |
| 17207 | 9185876 | The cell recruitment phase, between 6 and 12 weeks of age, is predominated by production of the monokines IL-1alpha, IL-6, and TNF After stimulation IFN-gamma and occasional IL-10 and GM-CSF producing cells could also be observed. |
| 17208 | 9185876 | During the effector phase, between 4 and 6 months, there is a characteristic Th1 cytokine profile with lymphocytes producing IL-2, IFN-gamma and TNF, supposedly TNF-beta. |
| 17209 | 9185876 | During the effector phase, between 4 and 6 months, there is a characteristic Th1 cytokine profile with lymphocytes producing IL-2, IFN-gamma and TNF, supposedly TNF-beta. |
| 17210 | 9185876 | No IL-4 production could be detected and IL-10 was very rarely found, indicating the absence of a Th2 response. |
| 17211 | 9185876 | No IL-4 production could be detected and IL-10 was very rarely found, indicating the absence of a Th2 response. |
| 17212 | 9178025 | The aim of the present study was the estimation of in vitro production of macrophage-derived cytokines: IL-1 beta, TNF-alpha, IL-12 by peripheral blood in high risk IDDM first degree relatives, since it could reflect early events leading to the development of type 1 diabetes in humans. |
| 17213 | 9178025 | The aim of the present study was the estimation of in vitro production of macrophage-derived cytokines: IL-1 beta, TNF-alpha, IL-12 by peripheral blood in high risk IDDM first degree relatives, since it could reflect early events leading to the development of type 1 diabetes in humans. |
| 17214 | 9178025 | The aim of the present study was the estimation of in vitro production of macrophage-derived cytokines: IL-1 beta, TNF-alpha, IL-12 by peripheral blood in high risk IDDM first degree relatives, since it could reflect early events leading to the development of type 1 diabetes in humans. |
| 17215 | 9178025 | The aim of the present study was the estimation of in vitro production of macrophage-derived cytokines: IL-1 beta, TNF-alpha, IL-12 by peripheral blood in high risk IDDM first degree relatives, since it could reflect early events leading to the development of type 1 diabetes in humans. |
| 17216 | 9178025 | IL-1 beta, TNF-alpha and IL-12 concentrations in supernatants of whole blood cultures with PHA (10 micrograms/ml) were quantified by ELISA. |
| 17217 | 9178025 | IL-1 beta, TNF-alpha and IL-12 concentrations in supernatants of whole blood cultures with PHA (10 micrograms/ml) were quantified by ELISA. |
| 17218 | 9178025 | IL-1 beta, TNF-alpha and IL-12 concentrations in supernatants of whole blood cultures with PHA (10 micrograms/ml) were quantified by ELISA. |
| 17219 | 9178025 | IL-1 beta, TNF-alpha and IL-12 concentrations in supernatants of whole blood cultures with PHA (10 micrograms/ml) were quantified by ELISA. |
| 17220 | 9178025 | In the ICA positive relatives of IDDM subjects levels of IL-12 were significantly higher as compared with the control group, both at 48 h (p < 0.02) and at 72 h (p < 0.05) of incubation and positively correlated with TNF-alpha and IL-1 beta (R = 0.46, p < 0.02 and R = 0.32, p < 0.05). |
| 17221 | 9178025 | In the ICA positive relatives of IDDM subjects levels of IL-12 were significantly higher as compared with the control group, both at 48 h (p < 0.02) and at 72 h (p < 0.05) of incubation and positively correlated with TNF-alpha and IL-1 beta (R = 0.46, p < 0.02 and R = 0.32, p < 0.05). |
| 17222 | 9178025 | In the ICA positive relatives of IDDM subjects levels of IL-12 were significantly higher as compared with the control group, both at 48 h (p < 0.02) and at 72 h (p < 0.05) of incubation and positively correlated with TNF-alpha and IL-1 beta (R = 0.46, p < 0.02 and R = 0.32, p < 0.05). |
| 17223 | 9178025 | In the ICA positive relatives of IDDM subjects levels of IL-12 were significantly higher as compared with the control group, both at 48 h (p < 0.02) and at 72 h (p < 0.05) of incubation and positively correlated with TNF-alpha and IL-1 beta (R = 0.46, p < 0.02 and R = 0.32, p < 0.05). |
| 17224 | 9178025 | We did not observe statistical differences in in vitro production of TNF-alpha and IL-1 beta between the study groups. |
| 17225 | 9178025 | We did not observe statistical differences in in vitro production of TNF-alpha and IL-1 beta between the study groups. |
| 17226 | 9178025 | We did not observe statistical differences in in vitro production of TNF-alpha and IL-1 beta between the study groups. |
| 17227 | 9178025 | We did not observe statistical differences in in vitro production of TNF-alpha and IL-1 beta between the study groups. |
| 17228 | 9178025 | If the involvement of Th1 cells is confirmed in the destruction of islet beta-cells, it is possible that IL-12 antagonists will have a role in the future prevention of insulin dependent diabetes mellitus. |
| 17229 | 9178025 | If the involvement of Th1 cells is confirmed in the destruction of islet beta-cells, it is possible that IL-12 antagonists will have a role in the future prevention of insulin dependent diabetes mellitus. |
| 17230 | 9178025 | If the involvement of Th1 cells is confirmed in the destruction of islet beta-cells, it is possible that IL-12 antagonists will have a role in the future prevention of insulin dependent diabetes mellitus. |
| 17231 | 9178025 | If the involvement of Th1 cells is confirmed in the destruction of islet beta-cells, it is possible that IL-12 antagonists will have a role in the future prevention of insulin dependent diabetes mellitus. |
| 17232 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17233 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17234 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17235 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17236 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17237 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17238 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17239 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17240 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 17241 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17242 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17243 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17244 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17245 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17246 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17247 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17248 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17249 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 17250 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17251 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17252 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17253 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17254 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17255 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17256 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17257 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17258 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 17259 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17260 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17261 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17262 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17263 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17264 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17265 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17266 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17267 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 17268 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17269 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17270 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17271 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17272 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17273 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17274 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17275 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17276 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 17277 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17278 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17279 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17280 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17281 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17282 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17283 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17284 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17285 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 17286 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17287 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17288 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17289 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17290 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17291 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17292 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17293 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17294 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 17295 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17296 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17297 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17298 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17299 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17300 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17301 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17302 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17303 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 17304 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17305 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17306 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17307 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17308 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17309 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17310 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17311 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17312 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 17313 | 9112337 | Interleukin 1 beta, tumour necrosis factor-alpha and interleukin 1 receptor antagonist in newly diagnosed insulin-dependent diabetes mellitus: comparison to long-standing diabetes and healthy individuals. |
| 17314 | 9112337 | Interleukin 1 beta, tumour necrosis factor-alpha and interleukin 1 receptor antagonist in newly diagnosed insulin-dependent diabetes mellitus: comparison to long-standing diabetes and healthy individuals. |
| 17315 | 9112337 | Interleukin 1 beta, tumour necrosis factor-alpha and interleukin 1 receptor antagonist in newly diagnosed insulin-dependent diabetes mellitus: comparison to long-standing diabetes and healthy individuals. |
| 17316 | 9112337 | Interleukin 1 beta (IL-1) and tumour necrosis factor alpha (TNF) are important for the beta cell lysis in insulin-dependent diabetes mellitus (IDDM), while IL-1 receptor antagonist (IL-1ra) is considered protective by blocking the effects of IL-1. |
| 17317 | 9112337 | Interleukin 1 beta (IL-1) and tumour necrosis factor alpha (TNF) are important for the beta cell lysis in insulin-dependent diabetes mellitus (IDDM), while IL-1 receptor antagonist (IL-1ra) is considered protective by blocking the effects of IL-1. |
| 17318 | 9112337 | Interleukin 1 beta (IL-1) and tumour necrosis factor alpha (TNF) are important for the beta cell lysis in insulin-dependent diabetes mellitus (IDDM), while IL-1 receptor antagonist (IL-1ra) is considered protective by blocking the effects of IL-1. |
| 17319 | 9112337 | Serum concentrations and ex-vivo production of IL-1, TNF and IL-1ra were examined in 10 newly diagnosed IDDM (ND-IDDM) patients, and compared with 11 long-standing IDDM (LS-IDDM) patients and 14 healthy volunteers. |
| 17320 | 9112337 | Serum concentrations and ex-vivo production of IL-1, TNF and IL-1ra were examined in 10 newly diagnosed IDDM (ND-IDDM) patients, and compared with 11 long-standing IDDM (LS-IDDM) patients and 14 healthy volunteers. |
| 17321 | 9112337 | Serum concentrations and ex-vivo production of IL-1, TNF and IL-1ra were examined in 10 newly diagnosed IDDM (ND-IDDM) patients, and compared with 11 long-standing IDDM (LS-IDDM) patients and 14 healthy volunteers. |
| 17322 | 9112337 | Ex-vivo LPS-stimulated production of IL-1 in ND-IDDM patients was significantly increased compared with LS-IDDM patients and healthy controls, while TNF and IL-1ra synthesis did not differ significantly. |
| 17323 | 9112337 | Ex-vivo LPS-stimulated production of IL-1 in ND-IDDM patients was significantly increased compared with LS-IDDM patients and healthy controls, while TNF and IL-1ra synthesis did not differ significantly. |
| 17324 | 9112337 | Ex-vivo LPS-stimulated production of IL-1 in ND-IDDM patients was significantly increased compared with LS-IDDM patients and healthy controls, while TNF and IL-1ra synthesis did not differ significantly. |
| 17325 | 9112337 | IL-1ra/IL-1 ratio was significantly decreased in ND-IDDM, and returned to normal values in the LS-IDDM group. |
| 17326 | 9112337 | IL-1ra/IL-1 ratio was significantly decreased in ND-IDDM, and returned to normal values in the LS-IDDM group. |
| 17327 | 9112337 | IL-1ra/IL-1 ratio was significantly decreased in ND-IDDM, and returned to normal values in the LS-IDDM group. |
| 17328 | 9105558 | The basal and LPS-stimulated levels of interleukin-1 beta and tumour necrosis factor alpha (TNF alpha) and the basal level of interleukin-1-receptor antagonist (IL-1RA) were identical for the 3 groups. |
| 17329 | 9105558 | The basal and LPS-stimulated levels of interleukin-1 beta and tumour necrosis factor alpha (TNF alpha) and the basal level of interleukin-1-receptor antagonist (IL-1RA) were identical for the 3 groups. |
| 17330 | 9105558 | After vitamin E, TNF alpha dropped in controls and smokers, and IL-1RA in smokers only. |
| 17331 | 9105558 | After vitamin E, TNF alpha dropped in controls and smokers, and IL-1RA in smokers only. |
| 17332 | 10684070 | [Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. |
| 17333 | 10684070 | [Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. |
| 17334 | 10684070 | [Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. |
| 17335 | 10684070 | [Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. |
| 17336 | 10684070 | Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. |
| 17337 | 10684070 | Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. |
| 17338 | 10684070 | Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. |
| 17339 | 10684070 | Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. |
| 17340 | 10684070 | The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. |
| 17341 | 10684070 | The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. |
| 17342 | 10684070 | The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. |
| 17343 | 10684070 | The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. |
| 17344 | 10684070 | It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies. |
| 17345 | 10684070 | It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies. |
| 17346 | 10684070 | It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies. |
| 17347 | 10684070 | It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies. |
| 17348 | 9137980 | The cytokine tumor necrosis factor alpha (TNF alpha) was proposed to mediate obesity related insulin resistance upon production in fat cells and to participate in tissue remodelling leading to vascular complications upon being released by macrophages. |
| 17349 | 9137980 | The cytokine tumor necrosis factor alpha (TNF alpha) was proposed to mediate obesity related insulin resistance upon production in fat cells and to participate in tissue remodelling leading to vascular complications upon being released by macrophages. |
| 17350 | 9137980 | Neither body mass index nor glycosylated hemoglobin correlated with TNF alpha in any of the groups. |
| 17351 | 9137980 | Neither body mass index nor glycosylated hemoglobin correlated with TNF alpha in any of the groups. |
| 17352 | 9127142 | Interestingly, DQ alleles with which these DR alleles are in linkage dysequilibrium, DQ1 and DQ2 and 3, were also associated with high and low IFN-gamma production, respectively. |
| 17353 | 9127142 | TNF-alpha production was significantly higher in DR3-positive than in DR3-negative subjects, in accord with previous studies. |
| 17354 | 9127142 | The finding of HLA allele-related polymorphism of IFN-gamma production corroborates other lines of evidence that regulation of IFN-gamma expression contributes to HLA-associated susceptibility to immunoinflammatory diseases, in particular insulin-dependent diabetes and multiple sclerosis. |
| 17355 | 9067916 | Epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) beta 1, TGF-beta 2 and TGF-beta 3, and tumor necrosis factor (TNF)-alpha and TNF-beta candidate genes were selected for analysis due to their putative roles in diabetic renal disease and chronic glomerulonephritis. |
| 17356 | 9067916 | The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. |
| 17357 | 9032102 | Differential regulation of the p80 tumor necrosis factor receptor in human obesity and insulin resistance. |
| 17358 | 9032102 | Differential regulation of the p80 tumor necrosis factor receptor in human obesity and insulin resistance. |
| 17359 | 9032102 | Differential regulation of the p80 tumor necrosis factor receptor in human obesity and insulin resistance. |
| 17360 | 9032102 | Differential regulation of the p80 tumor necrosis factor receptor in human obesity and insulin resistance. |
| 17361 | 9032102 | Previous studies have shown that tumor necrosis factor (TNF)-alpha production from adipose tissue is elevated in rodent and human obesity and plays an important role in insulin resistance in experimental animal models. |
| 17362 | 9032102 | Previous studies have shown that tumor necrosis factor (TNF)-alpha production from adipose tissue is elevated in rodent and human obesity and plays an important role in insulin resistance in experimental animal models. |
| 17363 | 9032102 | Previous studies have shown that tumor necrosis factor (TNF)-alpha production from adipose tissue is elevated in rodent and human obesity and plays an important role in insulin resistance in experimental animal models. |
| 17364 | 9032102 | Previous studies have shown that tumor necrosis factor (TNF)-alpha production from adipose tissue is elevated in rodent and human obesity and plays an important role in insulin resistance in experimental animal models. |
| 17365 | 9032102 | In this study, we examined the adipose expression of both TNF receptors (TNFR1 and TNFR2) in human obesity and demonstrated that obese female subjects express approximately twofold more TNFR2 mRNA in fat tissue and approximately sixfold more soluble TNFR2 in circulation relative to lean control subjects. |
| 17366 | 9032102 | In this study, we examined the adipose expression of both TNF receptors (TNFR1 and TNFR2) in human obesity and demonstrated that obese female subjects express approximately twofold more TNFR2 mRNA in fat tissue and approximately sixfold more soluble TNFR2 in circulation relative to lean control subjects. |
| 17367 | 9032102 | In this study, we examined the adipose expression of both TNF receptors (TNFR1 and TNFR2) in human obesity and demonstrated that obese female subjects express approximately twofold more TNFR2 mRNA in fat tissue and approximately sixfold more soluble TNFR2 in circulation relative to lean control subjects. |
| 17368 | 9032102 | In this study, we examined the adipose expression of both TNF receptors (TNFR1 and TNFR2) in human obesity and demonstrated that obese female subjects express approximately twofold more TNFR2 mRNA in fat tissue and approximately sixfold more soluble TNFR2 in circulation relative to lean control subjects. |
| 17369 | 9032102 | TNFR2 expression levels in adipose tissue were strongly correlated with BMI (r = 0.65, P < 0.001) and level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance, as well as level of TNF-alpha mRNA expression in fat tissue (r = 0.56, P < 0.001). |
| 17370 | 9032102 | TNFR2 expression levels in adipose tissue were strongly correlated with BMI (r = 0.65, P < 0.001) and level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance, as well as level of TNF-alpha mRNA expression in fat tissue (r = 0.56, P < 0.001). |
| 17371 | 9032102 | TNFR2 expression levels in adipose tissue were strongly correlated with BMI (r = 0.65, P < 0.001) and level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance, as well as level of TNF-alpha mRNA expression in fat tissue (r = 0.56, P < 0.001). |
| 17372 | 9032102 | TNFR2 expression levels in adipose tissue were strongly correlated with BMI (r = 0.65, P < 0.001) and level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance, as well as level of TNF-alpha mRNA expression in fat tissue (r = 0.56, P < 0.001). |
| 17373 | 9032102 | These results suggest that TNFR2 might play a role in human obesity by modulating the actions of TNF-alpha. |
| 17374 | 9032102 | These results suggest that TNFR2 might play a role in human obesity by modulating the actions of TNF-alpha. |
| 17375 | 9032102 | These results suggest that TNFR2 might play a role in human obesity by modulating the actions of TNF-alpha. |
| 17376 | 9032102 | These results suggest that TNFR2 might play a role in human obesity by modulating the actions of TNF-alpha. |
| 17377 | 9000700 | Cells from IDDM patients (n = 53) produced significantly higher amounts of Th1 cytokines gamma-interferon (IFN-gamma) (P = 0.028) and tumor necrosis factor alpha (TNF-alpha) (P = 0.007) than normal control subjects (n = 56), while Th2 cytokine levels (interleukin [IL]-4, IL-10) were similar. |
| 17378 | 9000700 | Cells from IDDM patients (n = 53) produced significantly higher amounts of Th1 cytokines gamma-interferon (IFN-gamma) (P = 0.028) and tumor necrosis factor alpha (TNF-alpha) (P = 0.007) than normal control subjects (n = 56), while Th2 cytokine levels (interleukin [IL]-4, IL-10) were similar. |
| 17379 | 9000700 | Cells from IDDM patients (n = 53) produced significantly higher amounts of Th1 cytokines gamma-interferon (IFN-gamma) (P = 0.028) and tumor necrosis factor alpha (TNF-alpha) (P = 0.007) than normal control subjects (n = 56), while Th2 cytokine levels (interleukin [IL]-4, IL-10) were similar. |
| 17380 | 9000700 | Antibodies to GAD, ICA512, or insulin did not correlate with individual cytokine profiles. |
| 17381 | 9000700 | Antibodies to GAD, ICA512, or insulin did not correlate with individual cytokine profiles. |
| 17382 | 9000700 | Antibodies to GAD, ICA512, or insulin did not correlate with individual cytokine profiles. |
| 17383 | 9000700 | Conversely, whole blood cultures from patients with Graves' disease (n = 18) produced significantly less TNF-alpha and IL-4 than normal subjects (P = 0.001-0.006). |
| 17384 | 9000700 | Conversely, whole blood cultures from patients with Graves' disease (n = 18) produced significantly less TNF-alpha and IL-4 than normal subjects (P = 0.001-0.006). |
| 17385 | 9000700 | Conversely, whole blood cultures from patients with Graves' disease (n = 18) produced significantly less TNF-alpha and IL-4 than normal subjects (P = 0.001-0.006). |
| 17386 | 9000700 | However, when the balance between Th1 and Th2 cytokine production was analyzed in individuals, the ratio between IFN-gamma or TNF-alpha and IL-4 or IL-10 was clearly biased toward Th1 reactivity in patients with IDDM (P = 0.0001), while a dominance of Th2 cytokine production was seen in Graves' disease (P = 0.0001). |
| 17387 | 9000700 | However, when the balance between Th1 and Th2 cytokine production was analyzed in individuals, the ratio between IFN-gamma or TNF-alpha and IL-4 or IL-10 was clearly biased toward Th1 reactivity in patients with IDDM (P = 0.0001), while a dominance of Th2 cytokine production was seen in Graves' disease (P = 0.0001). |
| 17388 | 9000700 | However, when the balance between Th1 and Th2 cytokine production was analyzed in individuals, the ratio between IFN-gamma or TNF-alpha and IL-4 or IL-10 was clearly biased toward Th1 reactivity in patients with IDDM (P = 0.0001), while a dominance of Th2 cytokine production was seen in Graves' disease (P = 0.0001). |
| 17389 | 9006895 | Actin-binding protein-280 binds the stress-activated protein kinase (SAPK) activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells. |
| 17390 | 9006895 | Actin-binding protein-280 binds the stress-activated protein kinase (SAPK) activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells. |
| 17391 | 9006895 | Actin-binding protein-280 binds the stress-activated protein kinase (SAPK) activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells. |
| 17392 | 9006895 | Actin-binding protein-280 binds the stress-activated protein kinase (SAPK) activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells. |
| 17393 | 9006895 | Actin-binding protein-280 binds the stress-activated protein kinase (SAPK) activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells. |
| 17394 | 9006895 | SEK-1, a dual specificity protein kinase that serves as one of the immediate upstream activators of the stress-activated protein kinases (SAPKs), associates specifically with the actin-binding protein, ABP-280, in vitro and in situ. |
| 17395 | 9006895 | SEK-1, a dual specificity protein kinase that serves as one of the immediate upstream activators of the stress-activated protein kinases (SAPKs), associates specifically with the actin-binding protein, ABP-280, in vitro and in situ. |
| 17396 | 9006895 | SEK-1, a dual specificity protein kinase that serves as one of the immediate upstream activators of the stress-activated protein kinases (SAPKs), associates specifically with the actin-binding protein, ABP-280, in vitro and in situ. |
| 17397 | 9006895 | SEK-1, a dual specificity protein kinase that serves as one of the immediate upstream activators of the stress-activated protein kinases (SAPKs), associates specifically with the actin-binding protein, ABP-280, in vitro and in situ. |
| 17398 | 9006895 | SEK-1, a dual specificity protein kinase that serves as one of the immediate upstream activators of the stress-activated protein kinases (SAPKs), associates specifically with the actin-binding protein, ABP-280, in vitro and in situ. |
| 17399 | 9006895 | SEK-1 binds to the carboxyl-terminal rod segment of ABP-280, upstream of the ABP carboxyl-terminal dimerization domain. |
| 17400 | 9006895 | SEK-1 binds to the carboxyl-terminal rod segment of ABP-280, upstream of the ABP carboxyl-terminal dimerization domain. |
| 17401 | 9006895 | SEK-1 binds to the carboxyl-terminal rod segment of ABP-280, upstream of the ABP carboxyl-terminal dimerization domain. |
| 17402 | 9006895 | SEK-1 binds to the carboxyl-terminal rod segment of ABP-280, upstream of the ABP carboxyl-terminal dimerization domain. |
| 17403 | 9006895 | SEK-1 binds to the carboxyl-terminal rod segment of ABP-280, upstream of the ABP carboxyl-terminal dimerization domain. |
| 17404 | 9006895 | Activation of SEK-1 in situ increases the SEK-1 activity bound to ABP-280 without changing the amount of SEK-1 polypeptide bound. |
| 17405 | 9006895 | Activation of SEK-1 in situ increases the SEK-1 activity bound to ABP-280 without changing the amount of SEK-1 polypeptide bound. |
| 17406 | 9006895 | Activation of SEK-1 in situ increases the SEK-1 activity bound to ABP-280 without changing the amount of SEK-1 polypeptide bound. |
| 17407 | 9006895 | Activation of SEK-1 in situ increases the SEK-1 activity bound to ABP-280 without changing the amount of SEK-1 polypeptide bound. |
| 17408 | 9006895 | Activation of SEK-1 in situ increases the SEK-1 activity bound to ABP-280 without changing the amount of SEK-1 polypeptide bound. |
| 17409 | 9006895 | The influence of ABP-280 on SAPK regulation was evaluated in human melanoma cells that lack ABP-280 expression, and in stable transformants of these cells expressing wild type ABP, or an actin-binding but dimerization-deficient mutant ABP (ABPDeltaCT109). |
| 17410 | 9006895 | The influence of ABP-280 on SAPK regulation was evaluated in human melanoma cells that lack ABP-280 expression, and in stable transformants of these cells expressing wild type ABP, or an actin-binding but dimerization-deficient mutant ABP (ABPDeltaCT109). |
| 17411 | 9006895 | The influence of ABP-280 on SAPK regulation was evaluated in human melanoma cells that lack ABP-280 expression, and in stable transformants of these cells expressing wild type ABP, or an actin-binding but dimerization-deficient mutant ABP (ABPDeltaCT109). |
| 17412 | 9006895 | The influence of ABP-280 on SAPK regulation was evaluated in human melanoma cells that lack ABP-280 expression, and in stable transformants of these cells expressing wild type ABP, or an actin-binding but dimerization-deficient mutant ABP (ABPDeltaCT109). |
| 17413 | 9006895 | The influence of ABP-280 on SAPK regulation was evaluated in human melanoma cells that lack ABP-280 expression, and in stable transformants of these cells expressing wild type ABP, or an actin-binding but dimerization-deficient mutant ABP (ABPDeltaCT109). |
| 17414 | 9006895 | ABP-280-deficient cells show an activation of SAPK in response to most stimuli that is comparable to that seen in ABP-280-replete cells; ABP-280-deficient cells, however, fail to show the brisk tumor necrosis factor-alpha (TNF-alpha) activation of SAPK seen in ABP-replete cells and have an 80% reduction in SAPK activation by lysophosphatidic acid. |
| 17415 | 9006895 | ABP-280-deficient cells show an activation of SAPK in response to most stimuli that is comparable to that seen in ABP-280-replete cells; ABP-280-deficient cells, however, fail to show the brisk tumor necrosis factor-alpha (TNF-alpha) activation of SAPK seen in ABP-replete cells and have an 80% reduction in SAPK activation by lysophosphatidic acid. |
| 17416 | 9006895 | ABP-280-deficient cells show an activation of SAPK in response to most stimuli that is comparable to that seen in ABP-280-replete cells; ABP-280-deficient cells, however, fail to show the brisk tumor necrosis factor-alpha (TNF-alpha) activation of SAPK seen in ABP-replete cells and have an 80% reduction in SAPK activation by lysophosphatidic acid. |
| 17417 | 9006895 | ABP-280-deficient cells show an activation of SAPK in response to most stimuli that is comparable to that seen in ABP-280-replete cells; ABP-280-deficient cells, however, fail to show the brisk tumor necrosis factor-alpha (TNF-alpha) activation of SAPK seen in ABP-replete cells and have an 80% reduction in SAPK activation by lysophosphatidic acid. |
| 17418 | 9006895 | ABP-280-deficient cells show an activation of SAPK in response to most stimuli that is comparable to that seen in ABP-280-replete cells; ABP-280-deficient cells, however, fail to show the brisk tumor necrosis factor-alpha (TNF-alpha) activation of SAPK seen in ABP-replete cells and have an 80% reduction in SAPK activation by lysophosphatidic acid. |
| 17419 | 9006895 | Expression of the dimerization-deficient mutant ABP-280 fails to correct the defective SAPK response to lysophosphatidic acid, but essentially normalizes the TNF-alpha activation of SAPK. |
| 17420 | 9006895 | Expression of the dimerization-deficient mutant ABP-280 fails to correct the defective SAPK response to lysophosphatidic acid, but essentially normalizes the TNF-alpha activation of SAPK. |
| 17421 | 9006895 | Expression of the dimerization-deficient mutant ABP-280 fails to correct the defective SAPK response to lysophosphatidic acid, but essentially normalizes the TNF-alpha activation of SAPK. |
| 17422 | 9006895 | Expression of the dimerization-deficient mutant ABP-280 fails to correct the defective SAPK response to lysophosphatidic acid, but essentially normalizes the TNF-alpha activation of SAPK. |
| 17423 | 9006895 | Expression of the dimerization-deficient mutant ABP-280 fails to correct the defective SAPK response to lysophosphatidic acid, but essentially normalizes the TNF-alpha activation of SAPK. |
| 17424 | 9006895 | Thus, a lack of ABP-280 in melanoma cells causes a defect in the regulation of SAPK that is selective for TNF-alpha and is attributable to the lack of ABP-280 polypeptide itself rather than to the disordered actin cytoskeleton that results therefrom. |
| 17425 | 9006895 | Thus, a lack of ABP-280 in melanoma cells causes a defect in the regulation of SAPK that is selective for TNF-alpha and is attributable to the lack of ABP-280 polypeptide itself rather than to the disordered actin cytoskeleton that results therefrom. |
| 17426 | 9006895 | Thus, a lack of ABP-280 in melanoma cells causes a defect in the regulation of SAPK that is selective for TNF-alpha and is attributable to the lack of ABP-280 polypeptide itself rather than to the disordered actin cytoskeleton that results therefrom. |
| 17427 | 9006895 | Thus, a lack of ABP-280 in melanoma cells causes a defect in the regulation of SAPK that is selective for TNF-alpha and is attributable to the lack of ABP-280 polypeptide itself rather than to the disordered actin cytoskeleton that results therefrom. |
| 17428 | 9006895 | Thus, a lack of ABP-280 in melanoma cells causes a defect in the regulation of SAPK that is selective for TNF-alpha and is attributable to the lack of ABP-280 polypeptide itself rather than to the disordered actin cytoskeleton that results therefrom. |
| 17429 | 9006895 | ABP-280 participates in TNF-alpha signal transduction to SAPKs, in part through the binding of SEK-1. |
| 17430 | 9006895 | ABP-280 participates in TNF-alpha signal transduction to SAPKs, in part through the binding of SEK-1. |
| 17431 | 9006895 | ABP-280 participates in TNF-alpha signal transduction to SAPKs, in part through the binding of SEK-1. |
| 17432 | 9006895 | ABP-280 participates in TNF-alpha signal transduction to SAPKs, in part through the binding of SEK-1. |
| 17433 | 9006895 | ABP-280 participates in TNF-alpha signal transduction to SAPKs, in part through the binding of SEK-1. |
| 17434 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17435 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17436 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17437 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17438 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17439 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17440 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17441 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17442 | 8995390 | Tumor necrosis factor-alpha-induced insulin resistance in 3T3-L1 adipocytes is accompanied by a loss of insulin receptor substrate-1 and GLUT4 expression without a loss of insulin receptor-mediated signal transduction. |
| 17443 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17444 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17445 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17446 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17447 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17448 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17449 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17450 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17451 | 8995390 | A number of studies have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is associated with profound insulin resistance in adipocytes and may also play a critical role in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus. |
| 17452 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17453 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17454 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17455 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17456 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17457 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17458 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17459 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17460 | 8995390 | GLUT4 down-regulation has been implicated as a possible cause of insulin resistance as has been the reduced kinase function of the insulin receptor. |
| 17461 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17462 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17463 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17464 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17465 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17466 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17467 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17468 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17469 | 8995390 | Here we examine the effects of tumor necrosis factor on the protein components thought to be involved in insulin-stimulated glucose transport in adipocytes, namely the insulin receptor, its major substrate IRS-1, and the insulin responsive glucose transporter GLUT4. |
| 17470 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17471 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17472 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17473 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17474 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17475 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17476 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17477 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17478 | 8995390 | Prolonged exposure (72-96 h) of 3T3-L1 adipocytes to TNF-alpha causes a substantial reduction (>80%) in IRS-1 and GLUT4 mRNA and protein as well as a lesser reduction (>50%) in the amount of the insulin receptor. |
| 17479 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17480 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17481 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17482 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17483 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17484 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17485 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17486 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17487 | 8995390 | Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure. |
| 17488 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17489 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17490 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17491 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17492 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17493 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17494 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17495 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17496 | 8995390 | Furthermore, the ability of the insulin receptor to phosphorylate exogenous substrate in the test tube is also normal following its isolation from TNF-alpha-treated cells. |
| 17497 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17498 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17499 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17500 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17501 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17502 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17503 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17504 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17505 | 8995390 | These results are confirmed by the reduced but obvious level of insulin-dependent glucose transport and GLUT4 translocation observed in TNF-alpha-treated adipocytes. |
| 17506 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17507 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17508 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17509 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17510 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17511 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17512 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17513 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17514 | 8995390 | We conclude that the insulin resistance of glucose transport in 3T3-L1 adipocytes exposed to TNF-alpha for 72-96 h results from a reduced amount in requisite proteins involved in insulin action. |
| 17515 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17516 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17517 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17518 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17519 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17520 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17521 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17522 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17523 | 8995390 | These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes. |
| 17524 | 9543185 | In comparison to isografts from non-CP injected mice, isografts from CP-treated mice showed increased expression of IFN-gamma, TNF-alpha, TNF-beta, IL-5, and eotaxin but no increase in IL-10 expression. |
| 17525 | 9275009 | It has been suggested that tumor necrosis factor-alpha (TNF-alpha) is a key mediator of insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17526 | 9275009 | It has been suggested that tumor necrosis factor-alpha (TNF-alpha) is a key mediator of insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17527 | 9275009 | These results suggest that KB-R7785 exerts its antidiabetic effect by ameliorating insulin sensitivity through the inhibition of TNF-alpha production. |
| 17528 | 9275009 | These results suggest that KB-R7785 exerts its antidiabetic effect by ameliorating insulin sensitivity through the inhibition of TNF-alpha production. |
| 17529 | 9187938 | Increased blood plasminogen activator inhibitor-1 and intercellular adhesion molecule-1 as possible risk factors of atherosclerosis in Werner syndrome. |
| 17530 | 9187938 | PAI-1 is a potent inhibitor of tissue plasminogen activator and a possible risk factor of atherosclerosis. |
| 17531 | 9187938 | One of the well-known physiological substances that induce the PAI-1 gene is tumor necrosis factor-alpha, which also induces other possible risk factors of atherosclerosis, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1. |
| 17532 | 9187938 | We conclude that high concentrations of PAI-1 and ICAM-1 in blood may be one of the potent causes of severe atherosclerosis in Werner syndrome. |
| 17533 | 9144026 | These results suggest a protective effect of glutathione on beta-cell cytotoxicity induced by tumor necrosis factor-alpha and encourage the use of glutathione in trials aimed at reducing the beta-cell damage occurring in insulin-dependent diabetes. |
| 17534 | 9049792 | Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. |
| 17535 | 9049792 | Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. |
| 17536 | 9049792 | Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. |
| 17537 | 9049792 | Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. |
| 17538 | 9049792 | The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. |
| 17539 | 9049792 | The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. |
| 17540 | 9049792 | The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. |
| 17541 | 9049792 | The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. |
| 17542 | 9049792 | In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. |
| 17543 | 9049792 | In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. |
| 17544 | 9049792 | In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. |
| 17545 | 9049792 | In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. |
| 17546 | 9049792 | In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients. |
| 17547 | 9049792 | In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients. |
| 17548 | 9049792 | In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients. |
| 17549 | 9049792 | In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients. |
| 17550 | 9022027 | Prevention of autoimmune diabetes mellitus in NOD mice by transgenic expression of soluble tumor necrosis factor receptor p55. |
| 17551 | 9022027 | This protection is associated with a marked decrease in the severity and incidence of insulitis and in the expression of the adhesion molecules MAdCAM-1 and ICAM-1 on the venules of pancreatic islets. |
| 17552 | 9022027 | These data suggest a central role for TNF-alpha in the mediation of insulitis and of the subsequent destruction of insulin-secreting beta-cells observed in NOD mice. |
| 17553 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17554 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17555 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17556 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17557 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17558 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 17559 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17560 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17561 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17562 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17563 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17564 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 17565 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17566 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17567 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17568 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17569 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17570 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 17571 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17572 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17573 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17574 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17575 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17576 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 17577 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17578 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17579 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17580 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17581 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17582 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 17583 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17584 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17585 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17586 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17587 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17588 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 17589 | 8986132 | Ebselen and cytokine-induced nitric oxide synthase expression in insulin-producing cells. |
| 17590 | 8986132 | Interleukin-1 (IL-1) may be a mediator of beta-cell damage in insulin-dependent diabetes mellitus (IDDM). |
| 17591 | 8986132 | The IL-1 mechanism of action on insulin-producing cells probably includes activation of the transcription nuclear factor kappa B (NF-kappa B), increased transcription of the inducible form of nitric oxide synthase (iNOS) and the subsequent production of nitric oxide (NO). |
| 17592 | 8986132 | However, ebselen failed to prevent the increase in nitrite production and the decrease in glucose oxidation and insulin release by rat islets exposed to IL-1 beta for 24 hr. |
| 17593 | 8986132 | Ebselen prevented the increase in nitrite production by human islets exposed for 14 hr to a combination of cytokines (IL-1 beta, tumor necrosis factor-alpha and interferon-gamma). |
| 17594 | 8986132 | In RIN cells, ebselen counteracted both the expression of iNOS mRNA and the increase in nitrite production induced by 6 hr exposure to IL-beta but failed to block IL-1 beta-induced iNOS expression following 24 hr exposure to the cytokine. |
| 17595 | 8986132 | Moreover, ebselen did not prevent IL-1 beta-induced NF-kappa B activation. |
| 17596 | 8986132 | As a whole, these data indicate that ebselen partially counteracts cytokine-induced NOS activation in pancreatic beta-cells, an effect not associated with inhibition of NF-kappa B activation. |
| 17597 | 9048875 | Using lipopolysaccharide (LPS)-stimulated cells, sulphatide increased the IL-2 production (163 +/- 17% of controls without sulphatide, p = 0.02), and gal-cer increased the IL-1 alpha production (145 +/- 13%, p = 0.006), whereas neither gal-cer nor sulphatide had an effect on the production of IL-6, IL-10 or TNF alpha. |
| 17598 | 9048875 | Using lipopolysaccharide (LPS)-stimulated cells, sulphatide increased the IL-2 production (163 +/- 17% of controls without sulphatide, p = 0.02), and gal-cer increased the IL-1 alpha production (145 +/- 13%, p = 0.006), whereas neither gal-cer nor sulphatide had an effect on the production of IL-6, IL-10 or TNF alpha. |
| 17599 | 9048875 | Using lipopolysaccharide (LPS)-stimulated cells, sulphatide increased the IL-2 production (163 +/- 17% of controls without sulphatide, p = 0.02), and gal-cer increased the IL-1 alpha production (145 +/- 13%, p = 0.006), whereas neither gal-cer nor sulphatide had an effect on the production of IL-6, IL-10 or TNF alpha. |
| 17600 | 9048875 | When stimulating cells with phytohaemagglutinin (PHA), sulphatide decreased the production of IL-6 (88 +/- 5%, p = 0.009), IL-10 (66 +/- 3%, p = 0.000003), and TNF alpha (75 +/- 9% p = 0.02). |
| 17601 | 9048875 | When stimulating cells with phytohaemagglutinin (PHA), sulphatide decreased the production of IL-6 (88 +/- 5%, p = 0.009), IL-10 (66 +/- 3%, p = 0.000003), and TNF alpha (75 +/- 9% p = 0.02). |
| 17602 | 9048875 | When stimulating cells with phytohaemagglutinin (PHA), sulphatide decreased the production of IL-6 (88 +/- 5%, p = 0.009), IL-10 (66 +/- 3%, p = 0.000003), and TNF alpha (75 +/- 9% p = 0.02). |
| 17603 | 9048875 | Gal-cer, however, increased the production of IL-6 (188 +/- 13% p = 0.000006), and decreased the production of TNF beta (80 +/- 6%, p = 0.007). |
| 17604 | 9048875 | Gal-cer, however, increased the production of IL-6 (188 +/- 13% p = 0.000006), and decreased the production of TNF beta (80 +/- 6%, p = 0.007). |
| 17605 | 9048875 | Gal-cer, however, increased the production of IL-6 (188 +/- 13% p = 0.000006), and decreased the production of TNF beta (80 +/- 6%, p = 0.007). |
| 17606 | 9048875 | Neither gal-cer nor sulphatide had an effect on the production of IL-2 or IFN gamma from PHA-stimulated cells. |
| 17607 | 9048875 | Neither gal-cer nor sulphatide had an effect on the production of IL-2 or IFN gamma from PHA-stimulated cells. |
| 17608 | 9048875 | Neither gal-cer nor sulphatide had an effect on the production of IL-2 or IFN gamma from PHA-stimulated cells. |
| 17609 | 9034609 | Endothelial cells can be activated by several stimuli, including cytokines such as tumor necrosis factor-alpha and interleukin-1. |
| 17610 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17611 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17612 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17613 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17614 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17615 | 9013754 | Circulating TNF-alpha and leptin levels in offspring of NIDDM patients do not correlate to individual insulin sensitivity. |
| 17616 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17617 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17618 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17619 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17620 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17621 | 9013754 | TNF-alpha and leptin, which are overproduced in fat tissue of obese insulin resistant animal models and in obese humans, might mediate such an inhibitory effect on insulin signalling in skeletal muscle. |
| 17622 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17623 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17624 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17625 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17626 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17627 | 9013754 | The aim of the present study was to evaluate whether circulating TNF-alpha and leptin correlates to the individual skeletal muscle insulin sensitivity in individuals with different degrees of obesity and insulin resistance. |
| 17628 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17629 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17630 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17631 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17632 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17633 | 9013754 | We measured circulating TNF-alpha and leptin values in non diabetic offsprings of NIDDM patients. 36 German and 47 Finnish subjects participated in the study. |
| 17634 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17635 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17636 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17637 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17638 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17639 | 9013754 | In contrast, leptin levels did not correlate with GDR and TNF-alpha. |
| 17640 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17641 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17642 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17643 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17644 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17645 | 9013754 | In summary, even though, in a few insulin resistant subjects, higher circulating TNF-alpha or leptin levels with the individual insulin sensitivity can be demonstrated, the data suggest that the circulating pool of TNF-alpha and leptin in blood is unlikely to be a major contributing factor for obesity induced insulin resistance in the vast majority of individuals at high risk to develop NIDDM. |
| 17646 | 9009565 | Interleukin-1-beta, tumour necrosis factor-alpha, islet-cell antibody, and insulin secretion in children with thalassemia major on long-term blood transfusion. |
| 17647 | 9009565 | Interleukin-1-beta, tumour necrosis factor-alpha, islet-cell antibody, and insulin secretion in children with thalassemia major on long-term blood transfusion. |
| 17648 | 9009565 | Interleukin-1-beta, tumour necrosis factor-alpha, islet-cell antibody, and insulin secretion in children with thalassemia major on long-term blood transfusion. |
| 17649 | 9009565 | In vitro, cytokines like interleukin-1-beta (IL-1-B) and tumour necrosis factor-alpha (TNF-A) inhibit insulin release and can destroy islet B-cells. |
| 17650 | 9009565 | In vitro, cytokines like interleukin-1-beta (IL-1-B) and tumour necrosis factor-alpha (TNF-A) inhibit insulin release and can destroy islet B-cells. |
| 17651 | 9009565 | In vitro, cytokines like interleukin-1-beta (IL-1-B) and tumour necrosis factor-alpha (TNF-A) inhibit insulin release and can destroy islet B-cells. |
| 17652 | 9009565 | We measured blood levels of IL-1-B, TNF-A, and islet cell antibody (ICA) in 20 children with IDDM, 20 of their non-diabetic siblings, 20 children with thalassemia major on long-term hypertransfusion therapy and iron chelation, and 10 normal age-matched children. |
| 17653 | 9009565 | We measured blood levels of IL-1-B, TNF-A, and islet cell antibody (ICA) in 20 children with IDDM, 20 of their non-diabetic siblings, 20 children with thalassemia major on long-term hypertransfusion therapy and iron chelation, and 10 normal age-matched children. |
| 17654 | 9009565 | We measured blood levels of IL-1-B, TNF-A, and islet cell antibody (ICA) in 20 children with IDDM, 20 of their non-diabetic siblings, 20 children with thalassemia major on long-term hypertransfusion therapy and iron chelation, and 10 normal age-matched children. |
| 17655 | 9009565 | Circulating IL-1-B and TNF-A concentrations were significantly higher in IDDM-siblings (33.7 +/- 12.7 pg/ml and 655 +/- 165 pg/ml, respectively) v. normal children (21.1 +/- 6.4 pg/ml and 383 +/- 122 pg/ml, respectively). |
| 17656 | 9009565 | Circulating IL-1-B and TNF-A concentrations were significantly higher in IDDM-siblings (33.7 +/- 12.7 pg/ml and 655 +/- 165 pg/ml, respectively) v. normal children (21.1 +/- 6.4 pg/ml and 383 +/- 122 pg/ml, respectively). |
| 17657 | 9009565 | Circulating IL-1-B and TNF-A concentrations were significantly higher in IDDM-siblings (33.7 +/- 12.7 pg/ml and 655 +/- 165 pg/ml, respectively) v. normal children (21.1 +/- 6.4 pg/ml and 383 +/- 122 pg/ml, respectively). |
| 17658 | 8971540 | The effect of TNF*B gene polymorphism on TNF-alpha and -beta secretion levels in patients with insulin-dependent diabetes mellitus and healthy controls. |
| 17659 | 8971540 | The effect of TNF*B gene polymorphism on TNF-alpha and -beta secretion levels in patients with insulin-dependent diabetes mellitus and healthy controls. |
| 17660 | 8971540 | The effect of TNF*B gene polymorphism on TNF-alpha and -beta secretion levels in patients with insulin-dependent diabetes mellitus and healthy controls. |
| 17661 | 8971540 | It has been suggested that inter-individual differences in the secretion levels of these cytokines may contribute to the predisposition of certain individuals to the development of diseases such as insulin-dependent diabetes mellitus (IDDM). |
| 17662 | 8971540 | It has been suggested that inter-individual differences in the secretion levels of these cytokines may contribute to the predisposition of certain individuals to the development of diseases such as insulin-dependent diabetes mellitus (IDDM). |
| 17663 | 8971540 | It has been suggested that inter-individual differences in the secretion levels of these cytokines may contribute to the predisposition of certain individuals to the development of diseases such as insulin-dependent diabetes mellitus (IDDM). |
| 17664 | 8971540 | We have investigated whether a diallelic TNF*B polymorphism detected using the enzyme Ncol influences the TNF-alpha and/or -beta secretory capacity of peripheral blood mononuclear cells (PBMC) from PHA stimulated healthy individuals and IDDM patients. |
| 17665 | 8971540 | We have investigated whether a diallelic TNF*B polymorphism detected using the enzyme Ncol influences the TNF-alpha and/or -beta secretory capacity of peripheral blood mononuclear cells (PBMC) from PHA stimulated healthy individuals and IDDM patients. |
| 17666 | 8971540 | We have investigated whether a diallelic TNF*B polymorphism detected using the enzyme Ncol influences the TNF-alpha and/or -beta secretory capacity of peripheral blood mononuclear cells (PBMC) from PHA stimulated healthy individuals and IDDM patients. |
| 17667 | 8971540 | We have shown that the level of TNF-beta secreted correlates with the TNF*B genotype in healthy individuals: those with the TNF B*2 allele secreted significantly higher levels of TNF-beta (P = 0.025) than those with the TNF*B1 allele. |
| 17668 | 8971540 | We have shown that the level of TNF-beta secreted correlates with the TNF*B genotype in healthy individuals: those with the TNF B*2 allele secreted significantly higher levels of TNF-beta (P = 0.025) than those with the TNF*B1 allele. |
| 17669 | 8971540 | We have shown that the level of TNF-beta secreted correlates with the TNF*B genotype in healthy individuals: those with the TNF B*2 allele secreted significantly higher levels of TNF-beta (P = 0.025) than those with the TNF*B1 allele. |
| 17670 | 8971540 | In IDDM patients, the reverse situation was observed, with those patients with the TNF*B1 allele secreting higher levels of TNF-beta than those with the TNF*B2 allele. |
| 17671 | 8971540 | In IDDM patients, the reverse situation was observed, with those patients with the TNF*B1 allele secreting higher levels of TNF-beta than those with the TNF*B2 allele. |
| 17672 | 8971540 | In IDDM patients, the reverse situation was observed, with those patients with the TNF*B1 allele secreting higher levels of TNF-beta than those with the TNF*B2 allele. |
| 17673 | 8971540 | Furthermore, when IDDM patients and controls were matched for TNF*B genotype, the IDDM patients with the TNF*B2 allele secreted significantly lower levels of TNF-beta than controls with this allele. |
| 17674 | 8971540 | Furthermore, when IDDM patients and controls were matched for TNF*B genotype, the IDDM patients with the TNF*B2 allele secreted significantly lower levels of TNF-beta than controls with this allele. |
| 17675 | 8971540 | Furthermore, when IDDM patients and controls were matched for TNF*B genotype, the IDDM patients with the TNF*B2 allele secreted significantly lower levels of TNF-beta than controls with this allele. |
| 17676 | 8971540 | Thus, the extended haplotype Bw62-DR4-TNF*B2/2 rather than IDDM per se is almost certainly responsible for the depressed TNF-beta secretion found in the IDDM-TNF*B2 homozygous cohort. |
| 17677 | 8971540 | Thus, the extended haplotype Bw62-DR4-TNF*B2/2 rather than IDDM per se is almost certainly responsible for the depressed TNF-beta secretion found in the IDDM-TNF*B2 homozygous cohort. |
| 17678 | 8971540 | Thus, the extended haplotype Bw62-DR4-TNF*B2/2 rather than IDDM per se is almost certainly responsible for the depressed TNF-beta secretion found in the IDDM-TNF*B2 homozygous cohort. |
| 17679 | 8940348 | The cytokine combination of interleukin-1beta (10 U/ml), tumor necrosis factor-alpha (10(3) U/ml), and interferon-gamma (10(3) U/ml), and the oxidant, t-butylhydroperoxide, induced significant increases in islet levels of the same aldehydes: butanal, pentanal, 4-hydroxynonenal (4-HNE), and hexanal. |
| 17680 | 8940348 | In contrast, N(G)-monomethyl-L-arginine, an inhibitor of nitric oxide synthase, prevented cytokine-induced nitrite production, but did not prevent cytokine-induced increases in 4-HNE, hexanal, and MDA or decreases in insulin and DNA in the islets. |
| 17681 | 8910278 | Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein. |
| 17682 | 8910278 | Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein. |
| 17683 | 8910278 | Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. |
| 17684 | 8910278 | Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. |
| 17685 | 8910278 | These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha. |
| 17686 | 8910278 | These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha. |
| 17687 | 8950668 | Previously our case-control study in the Belgian population showed significant association between IDDM and certain HLA class II alleles, in particular Lys71+, encoding DRB1 alleles. |
| 17688 | 8950668 | In the present study, 81 Danish multiplex IDDM families and 82 healthy Danish controls were examined for polymorphisms in the HLA-DRB genes and 54 of the 81 families for polymorphisms in HLA-B, -DQA1, -DQB1, -TNFA, and -TNFB genes. |
| 17689 | 8950668 | Linkage between IDDM and DRB1 alleles that encode Lys71+ was shown by affected zib pair analysis which showed strong linkage (p < 1 x 10(-6). |
| 17690 | 8932996 | Mouse islet cell lysis mediated by interleukin-1-induced Fas. |
| 17691 | 8932996 | This study was conducted to investigate the possible involvement of Fas in beta-cell death in insulitis of Type 1 (insulin-dependent) diabetes mellitus. |
| 17692 | 8932996 | Although primary cultured Balb/c mouse islet cells did not express Fas mRNA, 4-12 hours of treatment with 10(2)-10(3) U/l of mouse interleukin-1 alpha (IL-1 alpha) induced the expression of Fas mRNA. |
| 17693 | 8932996 | Surface Fas expression was detected by immunofluorescence flow cytometry using a non-cytolytic anti-Fas monoclonal antibody after 6 or 12 h of incubation with 10(3) U/l of IL-1 alpha. |
| 17694 | 8932996 | Since the Fas antibody showed no cross-reactive activity of tumour necrosis factor (TNF), the cytotoxic effect was not mediated by TNF receptors. |
| 17695 | 8932996 | The Fas-mediated killing of islet cells was not L-arginine-dependent, or blocked by N(G)-monomethyl-L-arginine. beta-TC1 cells also expressed Fas mRNA when exposed to IL-1 alpha or IL-1 alpha plus interferon-gamma. |
| 17696 | 8920883 | To analyze the effects of TNF alpha in insulin-dependent diabetes mellitus (IDDM), we have generated nonobese diabetic (NOD) transgenic mice expressing TNF alpha under the control of the rat insulin II promoter (RIP). |
| 17697 | 8920883 | To analyze the effects of TNF alpha in insulin-dependent diabetes mellitus (IDDM), we have generated nonobese diabetic (NOD) transgenic mice expressing TNF alpha under the control of the rat insulin II promoter (RIP). |
| 17698 | 8920883 | To analyze the effects of TNF alpha in insulin-dependent diabetes mellitus (IDDM), we have generated nonobese diabetic (NOD) transgenic mice expressing TNF alpha under the control of the rat insulin II promoter (RIP). |
| 17699 | 8920883 | To analyze the effects of TNF alpha in insulin-dependent diabetes mellitus (IDDM), we have generated nonobese diabetic (NOD) transgenic mice expressing TNF alpha under the control of the rat insulin II promoter (RIP). |
| 17700 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 17701 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 17702 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 17703 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 17704 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 17705 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 17706 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 17707 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 17708 | 8920883 | Diabetes was induced however, in the RIP-TNF alpha transgenic mice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively transferred to these mice. |
| 17709 | 8920883 | Diabetes was induced however, in the RIP-TNF alpha transgenic mice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively transferred to these mice. |
| 17710 | 8920883 | Diabetes was induced however, in the RIP-TNF alpha transgenic mice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively transferred to these mice. |
| 17711 | 8920883 | Diabetes was induced however, in the RIP-TNF alpha transgenic mice when CD8+ diabetogenic cloned T cells or splenic cells from diabetic NOD mice were adoptively transferred to these mice. |
| 17712 | 8895359 | Lisofylline, an inhibitor of unsaturated phosphatidic acid generation, ameliorates interleukin-1 beta-induced dysfunction in cultured rat islets. |
| 17713 | 8895359 | Interleukin-1 beta (IL-1 beta) causes rat islet cell dysfunction through mechanisms that involve inducible nitric oxide synthase (iNOS). |
| 17714 | 8895359 | Lisofylline (LSF), a water-soluble, nontoxic, selective inhibitor of the PA-1 alpha subspecies, which is stimulated by IL-1 beta and tumor necrosis factor-alpha, has been shown to prevent cytokine-induced cytotoxicity in in vivo animal models. |
| 17715 | 8895359 | To evaluate the effect of LSF on acute IL-1 beta-induced islet dysfunction, rat islets were exposed to IL-1 beta (0.1 ng/ml) with or without LSF (100 microM) for 24 h, followed by 25 mM glucose (G) stimulation, measurement of rat insulin by RIA, and calculation of the insulin secretion rate. |
| 17716 | 8895359 | Islets were also exposed to IL-1 beta with or without LSF, and Western immunoblots were performed to evaluate the effect of LSF on iNOS protein expression. |
| 17717 | 8895359 | IL-1 beta caused a 44% decrease in islet G-stimulated insulin secretion compared to that in untreated islets (P < 0.0005), which was totally reversed by LSF. |
| 17718 | 8895359 | In addition, IL-1 beta decreased the G-stimulated medium insulin content by 75% at 24 h (P = 0.0004) and 86% at 48 h compared to that in control islets (P < 0.0001). |
| 17719 | 8895359 | IL-1 beta-induced expression of iNOS was unchanged with the addition of LSF. |
| 17720 | 8933279 | Differential expression of ICAM-1 and LFA-1 versus L-selectin and VCAM-1 in autoimmune insulitis of NOD mice and association with both Th1- and Th2-type infiltrates. |
| 17721 | 8933279 | NOD mouse islets did not show the expression of ICAM-1, LFA-1, L-selectin and VCAM-1 prior to infiltration by mononuclear cells. |
| 17722 | 8933279 | ICAM-1 and LFA-1 were first demonstrable in islets with strong periinsular infiltrates (insulitis grade 2) while L-selectin and VCAM-1 were only seen in islets with mild or strong intraislet infiltration (grade 3-4). |
| 17723 | 8933279 | Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.). |
| 17724 | 8933279 | ICAM-1 and LFA-1 expression is seen prior to L-selectin and VCAM-1. |
| 17725 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 17726 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 17727 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 17728 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 17729 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 17730 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 17731 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 17732 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 17733 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 17734 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 17735 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 17736 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 17737 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 17738 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 17739 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 17740 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 17741 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 17742 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 17743 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 17744 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 17745 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 17746 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 17747 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 17748 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 17749 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 17750 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 17751 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 17752 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 17753 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 17754 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 17755 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 17756 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 17757 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 17758 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 17759 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 17760 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 17761 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 17762 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 17763 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 17764 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 17765 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 17766 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 17767 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 17768 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 17769 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 17770 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 17771 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 17772 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 17773 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 17774 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 17775 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 17776 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 17777 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 17778 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 17779 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 17780 | 8905209 | Their activation leads to an increased release of cytokines and growth factors including PDGF, interleukins, TNF-alpha, and TGF-beta, all of which may act concomitantly in the disease process. |
| 17781 | 8843187 | The expression of GLUT4 mRNA and its protein level in adipose and muscle tissues and tumor necrosis factor alpha (TNF-alpha) protein in adipose tissue were not significantly different between group D and group C of both strains. |
| 17782 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 17783 | 8826970 | Both CD4+ and CD8+ T-cells in syngeneic islet grafts in NOD mice produce interferon-gamma during beta-cell destruction. |
| 17784 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 17785 | 8826970 | Islet grafts from CFA-injected mice contained fewer CD4+ and CD8+ cells and more B cells; also fewer interferon gamma (IFN-gamma), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha)-positive cells and more IL-4 and IL-10 positive cells. |
| 17786 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 17787 | 8826970 | By performing two-color immunostaining of cell surface antigens and intracellular IFN-gamma, we found that IFN-gamma positive cells in islet grafts from CFA- and PBS-injected mice were approximately equally divided between CD4+ and CD8+ T-cell subsets. |
| 17788 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 17789 | 8826970 | Also, the frequencies of both CD4+ IFN-gamma + and CD8+ IFN-gamma + cells were decreased in islet grafts from CFA-injected mice. |
| 17790 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 17791 | 8826970 | These findings suggest that destruction of beta-cells in syngeneic islets transplanted into NOD mice is promoted by cells producing Th1-type cytokines (IFN-gamma, IL-2, and TNF-alpha) and prevented by cells producing TH2-type cytokines (IL-4 and IL-10). |
| 17792 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 17793 | 8826970 | Furthermore, both CD4+ and CD8+ IFN-gamma-producing T-cells in the islet grafts appear to be involved in beta-cell destruction and diabetes recurrence. |
| 17794 | 8872171 | From the analysis of TNFabc on extended haplotype fragments, and assuming that the fragments arose by ancient homologous crossing over, it was possible to "map" TNF and how that it was somewhat closer to HLA-B than the complement region, corresponding to the physical map of this region. |
| 17795 | 8872171 | From the analysis of TNFabc on extended haplotype fragments, and assuming that the fragments arose by ancient homologous crossing over, it was possible to "map" TNF and how that it was somewhat closer to HLA-B than the complement region, corresponding to the physical map of this region. |
| 17796 | 8872171 | There was also a trend for higher TNF-alpha secretion by peripheral blood mononuclear cells from individuals homozygous for [HLA-B8, SC01, DR3] than from individuals homozygous for [HLA-B7, SC31, DR2]. |
| 17797 | 8872171 | There was also a trend for higher TNF-alpha secretion by peripheral blood mononuclear cells from individuals homozygous for [HLA-B8, SC01, DR3] than from individuals homozygous for [HLA-B7, SC31, DR2]. |
| 17798 | 8830831 | Primary nonfunction of islet grafts in autoimmune diabetic nonobese diabetic mice is prevented by treatment with interleukin-4 and interleukin-10. |
| 17799 | 8830831 | Treatment of the recipients with the Th2-associated cytokine interleukin (IL)-4 alone did not prevent primary nonfunction, whereas treatment of the recipients with a combination of IL-4 and IL-10 restored immediate function of the grafts. |
| 17800 | 8830831 | Histological analysis of the grafts revealed less severely infiltrated islets, with well preserved islet architecture, in only normoglycemic animals treated with IL-4 or with IL-4 and IL-10. |
| 17801 | 8830831 | Staining for lymphocytes, macrophages, and tumor necrosis factor (TNF)-alpha did not show differences between the groups, but IFN-gamma was markedly less expressed in IL-4- and IL-10-treated grafts. |
| 17802 | 8830831 | Concomitantly, analysis of animals treated for 8 days after injection of cyclophosphamide, with IL-4 and IL-10, revealed a reduction of IL-12 mRNA in the pancreas. |
| 17803 | 8830831 | We conclude from these data that primary nonfunction of islet grafts is prevented by treatment of the recipients with a combination of IL-4 and IL-10, via downregulation of Th1 cytokines. |
| 17804 | 8968689 | Dominant TCR alpha-chain clonotypes and interferon-gamma are expressed in the pancreas of patients with recent-onset insulin-dependent diabetes mellitus. |
| 17805 | 8968689 | In order to clarify the nature of T lymphocytes infiltrating the pancreatic islets of patients with insulin-dependent diabetes mellitus (IDDM), we analysed T cell receptor (TCR) gene transcripts expressed in pancreatic biopsy specimens of patients with recent-onset IDDM. |
| 17806 | 8968689 | We also investigated the expression of cytokines (interferon-gamma: IFN-gamma; tumour necrosis factor-alpha: TNF-alpha; interleukin-4: IL-4; interleukin-6: IL-6) in the same specimens. |
| 17807 | 8968689 | IFN-gamma mRNA was highly expressed in the pancreas of IDDM patients, while IL-4 mRNA was deficient. |
| 17808 | 8968689 | A lower level of expression of IL-6 mRNA was detected in the IDDM pancreas than in the control tissue. |
| 17809 | 8894488 | Furthermore, TNF alpha expression and secretion are increased in adipose tissue from obese subjects and correlates with insulin resistance roughly measured as elevated fasting plasma insulin in spite of normal fasting blood glucose. |
| 17810 | 8814255 | Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. |
| 17811 | 8814255 | Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. |
| 17812 | 8814255 | Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. |
| 17813 | 8814255 | Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. |
| 17814 | 8814255 | TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. |
| 17815 | 8814255 | TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. |
| 17816 | 8814255 | TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. |
| 17817 | 8814255 | TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. |
| 17818 | 8814255 | TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. |
| 17819 | 8814255 | TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. |
| 17820 | 8814255 | TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. |
| 17821 | 8814255 | TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. |
| 17822 | 8814255 | Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). |
| 17823 | 8814255 | Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). |
| 17824 | 8814255 | Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). |
| 17825 | 8814255 | Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). |
| 17826 | 8784069 | The cytokine combination of interleukin-1 beta (50 U/mL), tumor necrosis factor-alpha (10(3) U/mL), and interferon-gamma (10(3) U/mL) induced significant increases in MDA and nitrite and significant decreases in insulin and DNA in islets after 60-h incubation. |
| 17827 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17828 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17829 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17830 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17831 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17832 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17833 | 8781295 | Effect of tumor necrosis factor-alpha on basal and insulin-stimulated glucose transport in cultured muscle and fat cells. |
| 17834 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17835 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17836 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17837 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17838 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17839 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17840 | 8781295 | It has been reported that tumor necrosis factor-alpha (TNF-alpha) inhibits insulin action in adipocytes and plays an important role as mediator of insulin resistance in non-insulin-dependent diabetes. |
| 17841 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17842 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17843 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17844 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17845 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17846 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17847 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 17848 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17849 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17850 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17851 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17852 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17853 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17854 | 8781295 | TNF-alpha treatment for 5 days up to a concentration of 20 ng/mL or 8 days at 10 ng/mL did not inhibit the insulin-stimulated increase in deoxyglucose transport in L6 cells. |
| 17855 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17856 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17857 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17858 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17859 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17860 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17861 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 17862 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17863 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17864 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17865 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17866 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17867 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17868 | 8781295 | Cells cultured without insulin were more sensitive to inhibition of 14C-alanine incorporation into proteins by low concentrations of TNF-alpha compared with cells cultured with insulin. |
| 17869 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17870 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17871 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17872 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17873 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17874 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17875 | 8781295 | TNF-alpha appears to affect general cell metabolism, including glucose transport in adipocytes, and not specifically insulin-stimulated glucose transport. |
| 17876 | 8899294 | Inhibition of insulin receptor signaling by TNF: potential role in obesity and non-insulin-dependent diabetes mellitus. |
| 17877 | 8899294 | Inhibition of insulin receptor signaling by TNF: potential role in obesity and non-insulin-dependent diabetes mellitus. |
| 17878 | 8899294 | Inhibition of insulin receptor signaling by TNF: potential role in obesity and non-insulin-dependent diabetes mellitus. |
| 17879 | 8899294 | Inhibition of insulin receptor signaling by TNF: potential role in obesity and non-insulin-dependent diabetes mellitus. |
| 17880 | 8899294 | Inhibition of insulin receptor signaling by TNF: potential role in obesity and non-insulin-dependent diabetes mellitus. |
| 17881 | 8899294 | Tumor necrosis factor (TNF) is one of the proteins produced by adipocytes that has been shown to regulate adipocyte function. |
| 17882 | 8899294 | Tumor necrosis factor (TNF) is one of the proteins produced by adipocytes that has been shown to regulate adipocyte function. |
| 17883 | 8899294 | Tumor necrosis factor (TNF) is one of the proteins produced by adipocytes that has been shown to regulate adipocyte function. |
| 17884 | 8899294 | Tumor necrosis factor (TNF) is one of the proteins produced by adipocytes that has been shown to regulate adipocyte function. |
| 17885 | 8899294 | Tumor necrosis factor (TNF) is one of the proteins produced by adipocytes that has been shown to regulate adipocyte function. |
| 17886 | 8899294 | Interestingly, adipocyte expression of TNF increases with increasing adipocyte mass and expression of TNF is increased in adipocytes isolated from several genetic models of rodent obesity and from obese humans. |
| 17887 | 8899294 | Interestingly, adipocyte expression of TNF increases with increasing adipocyte mass and expression of TNF is increased in adipocytes isolated from several genetic models of rodent obesity and from obese humans. |
| 17888 | 8899294 | Interestingly, adipocyte expression of TNF increases with increasing adipocyte mass and expression of TNF is increased in adipocytes isolated from several genetic models of rodent obesity and from obese humans. |
| 17889 | 8899294 | Interestingly, adipocyte expression of TNF increases with increasing adipocyte mass and expression of TNF is increased in adipocytes isolated from several genetic models of rodent obesity and from obese humans. |
| 17890 | 8899294 | Interestingly, adipocyte expression of TNF increases with increasing adipocyte mass and expression of TNF is increased in adipocytes isolated from several genetic models of rodent obesity and from obese humans. |
| 17891 | 8899294 | Increased production of TNF by adipocytes, however, may contribute to insulin resistance in obesity and in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17892 | 8899294 | Increased production of TNF by adipocytes, however, may contribute to insulin resistance in obesity and in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17893 | 8899294 | Increased production of TNF by adipocytes, however, may contribute to insulin resistance in obesity and in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17894 | 8899294 | Increased production of TNF by adipocytes, however, may contribute to insulin resistance in obesity and in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17895 | 8899294 | Increased production of TNF by adipocytes, however, may contribute to insulin resistance in obesity and in non-insulin-dependent diabetes mellitus (NIDDM). |
| 17896 | 8899294 | TNF has been shown to inhibit insulin-simulated tyrosine phosphorylation of both the insulin receptor (IR) and insulin receptor substrate (IRS)-1 and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT4, in adipocytes. |
| 17897 | 8899294 | TNF has been shown to inhibit insulin-simulated tyrosine phosphorylation of both the insulin receptor (IR) and insulin receptor substrate (IRS)-1 and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT4, in adipocytes. |
| 17898 | 8899294 | TNF has been shown to inhibit insulin-simulated tyrosine phosphorylation of both the insulin receptor (IR) and insulin receptor substrate (IRS)-1 and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT4, in adipocytes. |
| 17899 | 8899294 | TNF has been shown to inhibit insulin-simulated tyrosine phosphorylation of both the insulin receptor (IR) and insulin receptor substrate (IRS)-1 and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT4, in adipocytes. |
| 17900 | 8899294 | TNF has been shown to inhibit insulin-simulated tyrosine phosphorylation of both the insulin receptor (IR) and insulin receptor substrate (IRS)-1 and to stimulate downregulation of the insulin-sensitive glucose transporter, GLUT4, in adipocytes. |
| 17901 | 8894440 | Citrulline (0.1-1.0 mM) or arginine (0.1-1.0 mM) led to a similar dose dependent nitric oxide (NO) production by rat islets exposed to interleukin 1 beta (IL-1 beta) or human islets exposed to IL-1 beta + tumour necrosis factor alpha (TNF-alpha) + interferon gamma (IFN-gamma). |
| 17902 | 8894440 | Studies of IL-1 beta exposed rat islets revealed both NO-dependent and NO-independent effects: (1) IL-1 beta inhibits glucose-induced insulin release even in the absence of NO synthesis, but this inhibition is more severe when the presence of citrulline or arginine enables NO production; (2) NO formation in the presence of arginine or citrulline is necessary for cytokine-induced inhibition of protein biosynthesis. |
| 17903 | 8760354 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation. |
| 17904 | 8760354 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation. |
| 17905 | 8760354 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation. |
| 17906 | 8760354 | A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). |
| 17907 | 8760354 | A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). |
| 17908 | 8760354 | A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). |
| 17909 | 8760354 | Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. |
| 17910 | 8760354 | Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. |
| 17911 | 8760354 | Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. |
| 17912 | 8760354 | Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. |
| 17913 | 8760354 | Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. |
| 17914 | 8760354 | Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. |
| 17915 | 8760354 | Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. |
| 17916 | 8760354 | Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. |
| 17917 | 8760354 | Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. |
| 17918 | 8760354 | Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). |
| 17919 | 8760354 | Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). |
| 17920 | 8760354 | Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). |
| 17921 | 8760354 | Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA. |
| 17922 | 8760354 | Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA. |
| 17923 | 8760354 | Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA. |
| 17924 | 8760354 | Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription. |
| 17925 | 8760354 | Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription. |
| 17926 | 8760354 | Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription. |
| 17927 | 8760354 | As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM. |
| 17928 | 8760354 | As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM. |
| 17929 | 8760354 | As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM. |
| 17930 | 8757935 | Signal transduction pathways constructed around a core module of three consecutive protein kinases, the most distal being a member of the extracellular signal-regulated kinase (ERK) family, are ubiquitous among eukaryotes. |
| 17931 | 8757935 | Recent work has defined two cascades activated preferentially by the inflammatory cytokines TNF-alpha and IL-1-beta, as well as by a wide variety of cellular stresses such as UV and ionizing radiation, hyperosmolarity, heat stress, oxidative stress, etc. |
| 17932 | 8757935 | One pathway converges on the ERK subfamily known as the "stress activated' protein kinases (SAPKs, also termed Jun N-terminal kinases, JNKs), whereas the second pathway recruits the p38 kinases. |
| 17933 | 8757935 | Upstream inputs are diverse, and include small GTPases (primarily Rac and Cdc42; secondarily Ras) acting through mammalian homologs of the yeast Ste20 kinase, other kinase subfamilies (e.g. |
| 17934 | 8674888 | The accumulation of CEs in macrophages exposed to LDL-ICs is unique to this type of IC and is associated with paradoxical overexpression of LDL receptor and with increased synthesis and release of interleukin 1 beta and tumor necrosis factor (TNF) alpha. |
| 17935 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17936 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17937 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17938 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17939 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17940 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17941 | 8666148 | Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. |
| 17942 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17943 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17944 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17945 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17946 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17947 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17948 | 8666148 | To clarify the mechanisms that cause elevation of plasma fibrinogen levels in diabetes, we first examined the effect of hyperglycemia on the production of interleukin 6 (IL-6) and tumor necrosis factor (TNF) by cultured human peripheral blood monocytes. |
| 17949 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17950 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17951 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17952 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17953 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17954 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17955 | 8666148 | After 6 h of incubation, IL-6 and TNF-alpha mRNA levels were analyzed by reverse transcription and polymerase chain reaction. |
| 17956 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17957 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17958 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17959 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17960 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17961 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17962 | 8666148 | In addition, after 24 h of incubation, IL-6 and TNF-alpha immunoreactivity in the culture medium was measured by enzyme-linked immunoassay. |
| 17963 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17964 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17965 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17966 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17967 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17968 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17969 | 8666148 | Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. |
| 17970 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17971 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17972 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17973 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17974 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17975 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17976 | 8666148 | The results of this study demonstrate that hyperglycemia stimulated IL-6 and TNF synthesis and secretion by human peripheral monocytes in vitro and that the IL-6 response to hyperglycemia may be mediated by TNF. |
| 17977 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17978 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17979 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17980 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17981 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17982 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17983 | 8666148 | These results suggest that hyperglycemia may cause hyperfibrinogenemia in diabetic patients through an IL-6-dependent and TNF-dependent mechanism. |
| 17984 | 8666137 | Effects of an engineered human anti-TNF-alpha antibody (CDP571) on insulin sensitivity and glycemic control in patients with NIDDM. |
| 17985 | 8666137 | Effects of an engineered human anti-TNF-alpha antibody (CDP571) on insulin sensitivity and glycemic control in patients with NIDDM. |
| 17986 | 8666137 | Effects of an engineered human anti-TNF-alpha antibody (CDP571) on insulin sensitivity and glycemic control in patients with NIDDM. |
| 17987 | 8666137 | Inhibition of tumor necrosis factor (TNF)-alpha action has recently been shown to reverse insulin resistance dramatically and to improve glycemic control in obese rodents. |
| 17988 | 8666137 | Inhibition of tumor necrosis factor (TNF)-alpha action has recently been shown to reverse insulin resistance dramatically and to improve glycemic control in obese rodents. |
| 17989 | 8666137 | Inhibition of tumor necrosis factor (TNF)-alpha action has recently been shown to reverse insulin resistance dramatically and to improve glycemic control in obese rodents. |
| 17990 | 8666137 | TNF-alpha neutralization over a period of 4 weeks had no effect on insulin sensitivity in obese NIDDM subjects. |
| 17991 | 8666137 | TNF-alpha neutralization over a period of 4 weeks had no effect on insulin sensitivity in obese NIDDM subjects. |
| 17992 | 8666137 | TNF-alpha neutralization over a period of 4 weeks had no effect on insulin sensitivity in obese NIDDM subjects. |
| 17993 | 8662965 | Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. |
| 17994 | 8662965 | Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. |
| 17995 | 8662965 | Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. |
| 17996 | 8662965 | Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. |
| 17997 | 8662965 | Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. |
| 17998 | 8662965 | Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. |
| 17999 | 8662965 | Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. |
| 18000 | 8662965 | Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. |
| 18001 | 8662965 | Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. |
| 18002 | 8662965 | Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. |
| 18003 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 18004 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 18005 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 18006 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 18007 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 18008 | 8662965 | These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. |
| 18009 | 8662965 | These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. |
| 18010 | 8662965 | These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. |
| 18011 | 8662965 | These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. |
| 18012 | 8662965 | These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. |
| 18013 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 18014 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 18015 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 18016 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 18017 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 18018 | 8764141 | TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells. |
| 18019 | 8764141 | TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells. |
| 18020 | 8764141 | TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells. |
| 18021 | 8764141 | Mannose receptor mRNA was induced in a dose- and time-dependent manner in mesangial cells by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. |
| 18022 | 8764141 | Mannose receptor mRNA was induced in a dose- and time-dependent manner in mesangial cells by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. |
| 18023 | 8764141 | Mannose receptor mRNA was induced in a dose- and time-dependent manner in mesangial cells by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. |
| 18024 | 8764141 | TNF-alpha and IL-1 alpha also induced apoptosis in mesangial cells. |
| 18025 | 8764141 | TNF-alpha and IL-1 alpha also induced apoptosis in mesangial cells. |
| 18026 | 8764141 | TNF-alpha and IL-1 alpha also induced apoptosis in mesangial cells. |
| 18027 | 8764139 | Tyrosine kinase inhibitors prevent cytokine-induced expression of iNOS and COX-2 by human islets. |
| 18028 | 8764139 | Tyrosine kinase inhibitors prevent cytokine-induced expression of iNOS and COX-2 by human islets. |
| 18029 | 8764139 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that is characterized by selective destruction of insulin-secreting beta-cells. |
| 18030 | 8764139 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that is characterized by selective destruction of insulin-secreting beta-cells. |
| 18031 | 8764139 | In this study, the effects of cytokines on the expression of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2) by human islets were examined. |
| 18032 | 8764139 | In this study, the effects of cytokines on the expression of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2) by human islets were examined. |
| 18033 | 8764139 | In combination, the cytokines, human recombinant interleukin-1 beta (IL-1 beta), human recombinant tumor necrosis factor-alpha (TNF-alpha), and human recombinant interferon-gamma (IFN-gamma), induce the time-dependent formation of nitrite and prostaglandin E2 (PGE2) by human islets. |
| 18034 | 8764139 | In combination, the cytokines, human recombinant interleukin-1 beta (IL-1 beta), human recombinant tumor necrosis factor-alpha (TNF-alpha), and human recombinant interferon-gamma (IFN-gamma), induce the time-dependent formation of nitrite and prostaglandin E2 (PGE2) by human islets. |
| 18035 | 8764139 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also induces the expression of iNOS mRNA by human islets as demonstrated by both reverse transcriptase-polymerase chain reaction and Northern blot analysis. |
| 18036 | 8764139 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also induces the expression of iNOS mRNA by human islets as demonstrated by both reverse transcriptase-polymerase chain reaction and Northern blot analysis. |
| 18037 | 8764139 | We further show that the tyrosine kinase inhibitors genistein and herbimycin A prevent IL-1 beta plus IFN-gamma-induced expression of COX-2 and iNOS and the production of PGE2 and nitric oxide by human islets. |
| 18038 | 8764139 | We further show that the tyrosine kinase inhibitors genistein and herbimycin A prevent IL-1 beta plus IFN-gamma-induced expression of COX-2 and iNOS and the production of PGE2 and nitric oxide by human islets. |
| 18039 | 8764139 | These results demonstrate that cytokines induce the expression of iNOS and COX-2 by human islets and that cytokine-induced expression of both COX-2 and iNOS by human islets appears to require the activation of a tyrosine kinase(s). |
| 18040 | 8764139 | These results demonstrate that cytokines induce the expression of iNOS and COX-2 by human islets and that cytokine-induced expression of both COX-2 and iNOS by human islets appears to require the activation of a tyrosine kinase(s). |
| 18041 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18042 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18043 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18044 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18045 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18046 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18047 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18048 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18049 | 8641197 | Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells. |
| 18050 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18051 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18052 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18053 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18054 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18055 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18056 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18057 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18058 | 8641197 | In this study, the acute effects of tumor necrosis factor (TNF)-alpha on insulin-stimulated glucose uptake, glycogen synthesis, and protein phosphatase-1 (PP-1) activation were examined in cultured rat skeletal muscle cell line, L6. |
| 18059 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18060 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18061 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18062 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18063 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18064 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18065 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18066 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18067 | 8641197 | Exposure of L6 cells to low concentrations of TNF-alpha (10 ng/ml for 60 min) inhibited basal and insulin stimulated 2-deoxyglucose uptake (40-50% decrease in basal and insulin stimulated glucose uptake respectively, when compared with controls, P < 0.05). |
| 18068 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18069 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18070 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18071 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18072 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18073 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18074 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18075 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18076 | 8641197 | TNF-alpha also blocked insulin activation of glycogen synthase (GS) and inhibited glycogen synthesis (measured as [14C]-glucose incorporated into glycogen). |
| 18077 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18078 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18079 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18080 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18081 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18082 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18083 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18084 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18085 | 8641197 | Because GS is activated by dephosphorylation via protein phosphatase-1 (PP-1), we examined the effect of TNF- alpha on PP-1 activation. |
| 18086 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18087 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18088 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18089 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18090 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18091 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18092 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18093 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18094 | 8641197 | Begum, J Biol Chem 269:16662-16667, 1994), insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in L6 cells. |
| 18095 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18096 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18097 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18098 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18099 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18100 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18101 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18102 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18103 | 8641197 | Pretreatment with TNF- alpha for 10-60 min blocked subsequent insulin-induced activation of PP-1. |
| 18104 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18105 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18106 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18107 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18108 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18109 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18110 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18111 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18112 | 8641197 | The impaired activation of PP-1 was accompanied by a reduction in insulin-stimulated phosphorylation of the regulatory subunit of PP-1. cAMP-Rp diastereomer, a cAMP antagonist failed to prevent the detrimental effects of TNF-alpha on PP-1. |
| 18113 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18114 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18115 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18116 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18117 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18118 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18119 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18120 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18121 | 8641197 | Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition. |
| 18122 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18123 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18124 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18125 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18126 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18127 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18128 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18129 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18130 | 8641197 | We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release. |
| 18131 | 8635653 | A possible role of transporter associated with antigen processing (TAP)-1 in the pathogenesis of IDDM has been investigated by examining the level of TAP-1 expression in the islets of IDDM pancreas and by studying in vitro the effect of interferon (IFN)-gamma, IFN-alpha, and tumor necrosis factor-alpha in TAP-1 expression by cultured islet cells. |
| 18132 | 8635653 | TAP-1 hyperexpression correlated clearly with HLA class I hyperexpression but only very partially with HLA class II ectopic expression. |
| 18133 | 8635653 | IFN-gamma and IFN-alpha, both cytokines putatively implicated in IDDM pathogenesis, were capable of inducing TAP-1 protein (as assessed by immunofluorescence flow cytometry) and message (by Northern blot analysis and reverse transcription polymerase chain reaction). |
| 18134 | 8635653 | These findings suggest that under the influence of cytokines (most probably IFN-alpha) beta-cells may express in their surface a high density of HLA class I-peptide complexes that may facilitate their recognition and lysis by low-affinity CD8+ T-cells. |
| 18135 | 8635648 | Tumor necrosis factor-alpha, IL-4, and IL-10 mRNA levels were not significantly different in islet leukocytes from the four groups of rats. |
| 18136 | 8635648 | These findings suggest that production of T-helper 1 (Th1)-type cytokines, IFN-gamma and IL-2, by islet-infiltrating cells in BB rats is associated with beta-cell destruction and IDDM development. |
| 18137 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18138 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18139 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18140 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18141 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18142 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18143 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18144 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18145 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18146 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18147 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18148 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18149 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18150 | 8665940 | Effect of tumor necrosis factor-alpha on insulin-stimulated mitogen-activated protein kinase cascade in cultured rat skeletal muscle cells. |
| 18151 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18152 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18153 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18154 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18155 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18156 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18157 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18158 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18159 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18160 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18161 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18162 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18163 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18164 | 8665940 | Tumor necrosis factor-alpha (TNF-alpha) is a proposed mediator of insulin resistance in obese/diabetic animals through its effects on tyrosine phosphorylation of the insulin receptor and its substrate, insulin receptor substrate-1. |
| 18165 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18166 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18167 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18168 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18169 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18170 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18171 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18172 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18173 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18174 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18175 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18176 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18177 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18178 | 8665940 | In this study, the acute effects of TNF-alpha on the mitogen-activated protein kinase (MAPK) signalling cascade were examined in cultured rat skeletal muscle cell line, L6. |
| 18179 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18180 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18181 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18182 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18183 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18184 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18185 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18186 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18187 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18188 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18189 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18190 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18191 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18192 | 8665940 | Insulin treatment of L6 cells resulted in a rapid increase in MAPK activity (> twofold in 5 min with 10 nM insulin). |
| 18193 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18194 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18195 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18196 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18197 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18198 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18199 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18200 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18201 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18202 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18203 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18204 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18205 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18206 | 8665940 | Prior treatment with TNF-alpha for 60 min blocked subsequent insulin-induced activation of MAPK in a dose- and time-dependent manner. |
| 18207 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18208 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18209 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18210 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18211 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18212 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18213 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18214 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18215 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18216 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18217 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18218 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18219 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18220 | 8665940 | Metabolic labelling studies with inorganic [32P]phosphate followed by immuno-precipitation of MAPK and its upstream activator, mitogen-activated protein kinase kinase, indicated decreased phosphorylation of MAPK and its kinase in response to insulin in cells exposed to TNF-alpha. |
| 18221 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18222 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18223 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18224 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18225 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18226 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18227 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18228 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18229 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18230 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18231 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18232 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18233 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18234 | 8665940 | This effect of TNF-alpha was not due to inhibition of insulin-stimulated p21ras-GTP loading or Raf-1 phosphorylation. |
| 18235 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18236 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18237 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18238 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18239 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18240 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18241 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18242 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18243 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18244 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18245 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18246 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18247 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18248 | 8665940 | Low concentrations (2 nM) of okadaic acid, a serine/threonine phosphatase inhibitor, prevented TNF-alpha-induced inhibition of MAPK and restored insulin's effect on MAPK activity, while orthovanadate (a tyrosine phosphatase inhibitor), inhibitor 2 (phosphatase-1 inhibitor) and FK506 (phosphatase-2B inhibitor) were ineffective. |
| 18249 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18250 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18251 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18252 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18253 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18254 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18255 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18256 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18257 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18258 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18259 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18260 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18261 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18262 | 8665940 | These results suggested an involvement of an okadaic-acid-sensitive serine/threonine phosphatase in TNF-alpha-induced blockade of insulin's effect on MAPK and/or its kinase. |
| 18263 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18264 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18265 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18266 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18267 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18268 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18269 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18270 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18271 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18272 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18273 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18274 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18275 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18276 | 8665940 | Therefore, we examined the effect of TNF-alpha on protein phosphatase-1 (PP-1) and protein phosphatase-2A (PP-2A) activities. |
| 18277 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18278 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18279 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18280 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18281 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18282 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18283 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18284 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18285 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18286 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18287 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18288 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18289 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18290 | 8665940 | As reported by us earlier, insulin rapidly stimulated PP-1 and concomitantly inhibited PP-2A activities in control cells. |
| 18291 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18292 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18293 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18294 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18295 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18296 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18297 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18298 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18299 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18300 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18301 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18302 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18303 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18304 | 8665940 | TNF-alpha treatment blocked insulin-induced activation of PP-1. |
| 18305 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18306 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18307 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18308 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18309 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18310 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18311 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18312 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18313 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18314 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18315 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18316 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18317 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18318 | 8665940 | In contrast to PP-1, TNF-alpha caused a 60% increase in PP-2A activity and insulin failed to prevent this TNF-alpha effect. |
| 18319 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18320 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18321 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18322 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18323 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18324 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18325 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18326 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18327 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18328 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18329 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18330 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18331 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18332 | 8665940 | The time course of PP-2A activation by TNF-alpha preceded the kinetics of inhibition of MAPK. |
| 18333 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18334 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18335 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18336 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18337 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18338 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18339 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18340 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18341 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18342 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18343 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18344 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18345 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18346 | 8665940 | Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation. |
| 18347 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18348 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18349 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18350 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18351 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18352 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18353 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18354 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18355 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18356 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18357 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18358 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18359 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18360 | 8665940 | We conclude that TNF-alpha abrogates the insulin effect on MAPK activation by increasing dephosphorylation of MAPK kinase via an activated phosphatase. |
| 18361 | 8671656 | Partially purified MLR-IA inhibits IL-2 production in a primary allo-MLR, and decreases IFN-gamma production during secondary allo-MLR and Con A activation, whereas it enhances IL-4 production in both primary and secondary Con A activation. |
| 18362 | 8671656 | MLR-IA is not neutralized by combination of antibodies specific for transforming growth factor-beta, IL-10, tumor necrosis factor-alpha/beta or IFN-gamma, suggestive of a novel activity. |
| 18363 | 8671656 | Our work suggests that a potentially novel immunoregulatory activity, capable of inhibiting T lymphocyte proliferation and IFN-gamma production, and stimulating IL-4 production, may regulate development of autoimmune diabetes in NOD mice. |
| 18364 | 8617981 | We have found that IL-2, IL-4, TNF-alpha, and IFN-gamma are expressed by the time the fourth dose of STZ is given. |
| 18365 | 8617981 | However, expression of IFN-gamma, but not IL-4, was limited to intrapancreatic lymphocytes and was not detectable at extrapancreatic lymphoid sites. |
| 18366 | 8617981 | Moreover, mAbs against IFN-gamma, but not against IL-4 or IL-2, prevent hyperglycemia and insulitis in MDSDM, suggesting that IFN-gamma regulates development of disease. |
| 18367 | 8617981 | Cells in the pancreases of nondiabetic mice treated with anti-IFN-gamma mAb and STZ show enhanced expression of IL-4, but the prevention of disease is due to blockade of the IFN-gamma itself, and not due to secretion of IL-4, because systemic administration of IL-4 does not prevent MDSDM. |
| 18368 | 8612552 | In this study, we used a semiquantitative PCR assay to measure levels of messenger RNA (mRNA) expression of the inflammatory cytokines, interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha, and interferon-gamma (IFN gamma), and of the inducible form of NO synthase (iNOS) in mononuclear leukocytes isolated from pancreatic islets of autoimmune diabetes-prone nonobese diabetic (NOD) female mice. |
| 18369 | 8612552 | We found that mRNA levels of iNOS, IL-1 alpha, and IFN gamma in islet mononuclear leukocytes increased from 5 weeks of age to onset of diabetes ( > 13 weeks of age). |
| 18370 | 8612552 | To determine whether increased iNOS, IL-1 alpha, and IFN gamma mRNA expressions were related to diabetes development, we compared mRNA levels of these molecules in mononuclear leukocytes from islets of 12 week-old diabetes-prone NOD female mice and three groups of 12-week-old mice with low diabetes risk: NOD female mice injected with complete Freund's adjuvant at 4 weeks of age, NOD male mice, and BALB/c female mice that do not develop diabetes. |
| 18371 | 8612552 | We found that iNOS, IL-1 alpha, and IFN gamma mRNA levels were higher in mononuclear leukocytes from islets of diabetes-prone NOD female mice than in those from mice correlated with IL-1 alpha and IFN gamma mRNA levels. |
| 18372 | 8612552 | These findings suggest that IL-1 alpha and IFN gamma may promote islet beta-cell destruction at least in part by up-regulating iNOS expression an No production by both macrophages and beta-cells in the islets of autoimmune diabetes-prone NOD mice. |
| 18373 | 8803477 | To further delineate the TNF-alpha signal transduction pathway mediating glucose metabolism, we utilized L6 rat myoblasts which contain the receptors for the insulin-like growth factor-I (IGF-I) and TNF-alpha, and the ability of both ligands to stimulate glucose uptake was compared. |
| 18374 | 8803477 | To further delineate the TNF-alpha signal transduction pathway mediating glucose metabolism, we utilized L6 rat myoblasts which contain the receptors for the insulin-like growth factor-I (IGF-I) and TNF-alpha, and the ability of both ligands to stimulate glucose uptake was compared. |
| 18375 | 8803477 | To further delineate the TNF-alpha signal transduction pathway mediating glucose metabolism, we utilized L6 rat myoblasts which contain the receptors for the insulin-like growth factor-I (IGF-I) and TNF-alpha, and the ability of both ligands to stimulate glucose uptake was compared. |
| 18376 | 8803477 | To further delineate the TNF-alpha signal transduction pathway mediating glucose metabolism, we utilized L6 rat myoblasts which contain the receptors for the insulin-like growth factor-I (IGF-I) and TNF-alpha, and the ability of both ligands to stimulate glucose uptake was compared. |
| 18377 | 8803477 | To further delineate the TNF-alpha signal transduction pathway mediating glucose metabolism, we utilized L6 rat myoblasts which contain the receptors for the insulin-like growth factor-I (IGF-I) and TNF-alpha, and the ability of both ligands to stimulate glucose uptake was compared. |
| 18378 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 18379 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 18380 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 18381 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 18382 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 18383 | 8803477 | IGF-I receptor beta-subunit, insulin receptor substrate-1 (IRS-1), and mitogen-activated protein (MAP) kinase were all phosphorylated in response to 6.5 nM IGF-I after 10 min incubation. |
| 18384 | 8803477 | IGF-I receptor beta-subunit, insulin receptor substrate-1 (IRS-1), and mitogen-activated protein (MAP) kinase were all phosphorylated in response to 6.5 nM IGF-I after 10 min incubation. |
| 18385 | 8803477 | IGF-I receptor beta-subunit, insulin receptor substrate-1 (IRS-1), and mitogen-activated protein (MAP) kinase were all phosphorylated in response to 6.5 nM IGF-I after 10 min incubation. |
| 18386 | 8803477 | IGF-I receptor beta-subunit, insulin receptor substrate-1 (IRS-1), and mitogen-activated protein (MAP) kinase were all phosphorylated in response to 6.5 nM IGF-I after 10 min incubation. |
| 18387 | 8803477 | IGF-I receptor beta-subunit, insulin receptor substrate-1 (IRS-1), and mitogen-activated protein (MAP) kinase were all phosphorylated in response to 6.5 nM IGF-I after 10 min incubation. |
| 18388 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 18389 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 18390 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 18391 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 18392 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 18393 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 18394 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 18395 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 18396 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 18397 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 18398 | 8803477 | The results indicate that MAP kinase phosphorylation is not sufficient for glucose uptake in L6 myoblasts. |
| 18399 | 8803477 | The results indicate that MAP kinase phosphorylation is not sufficient for glucose uptake in L6 myoblasts. |
| 18400 | 8803477 | The results indicate that MAP kinase phosphorylation is not sufficient for glucose uptake in L6 myoblasts. |
| 18401 | 8803477 | The results indicate that MAP kinase phosphorylation is not sufficient for glucose uptake in L6 myoblasts. |
| 18402 | 8803477 | The results indicate that MAP kinase phosphorylation is not sufficient for glucose uptake in L6 myoblasts. |
| 18403 | 8803477 | TNF-alpha-elicited signal transduction to glucose uptake may utilize a different pathway from that seen with IGF-I. |
| 18404 | 8803477 | TNF-alpha-elicited signal transduction to glucose uptake may utilize a different pathway from that seen with IGF-I. |
| 18405 | 8803477 | TNF-alpha-elicited signal transduction to glucose uptake may utilize a different pathway from that seen with IGF-I. |
| 18406 | 8803477 | TNF-alpha-elicited signal transduction to glucose uptake may utilize a different pathway from that seen with IGF-I. |
| 18407 | 8803477 | TNF-alpha-elicited signal transduction to glucose uptake may utilize a different pathway from that seen with IGF-I. |
| 18408 | 8737986 | The inducible nitric oxide synthase antisense lines showed up to 84% reduction of nitric oxide production in response to lipopolysaccharide stimulation and 66% reduction of nitric oxide production in response to interferon-gamma and a combination of interferon-gamma and lipopolysaccharide stimulation. |
| 18409 | 8737986 | The deficiency in inducible nitric oxide synthase expression had no impact on lipopolysaccharide induced tumor necrosis factor alpha and interleukin-1 secretion. |
| 18410 | 8613699 | For example, in the case of arthritis, TNF has been found to transmit its pathogenic effects entirely through interleukin-1, which may therefore represent an additional important target for therapeutic intervention in the human disease. |
| 18411 | 8608164 | Inflammatory cytokines may participate in the destruction of pancreatic islets during the pathogenesis of insulin-dependent diabetes mellitus, and the cytokine interleukin-1 (IL-1) strongly inhibits insulin secretion from rat pancreatic islets by a process which involves induction of expression of the inducible isoform of nitric oxide synthase and the overproduction of nitric oxide. |
| 18412 | 8608164 | The signaling events between IL-1 receptor occupancy and induction of nitric oxide synthase in rat islets involve activation of the transcriptional activator NFkappa B. |
| 18413 | 8608164 | Neither interleukin-1 nor tumor necrosis factor-alpha was found to induce hydrolysis of islet sphingomyelin species, and neither an exogenous, cell-permeant ceramide species (N-acetyl-D-sphingosine) nor exogenous sphingomyelinase mimicked or potentiated the effect of IL-1 to increase rat islet nitric oxide generation, as reflected by nitrite production. |
| 18414 | 9157089 | An association in non-insulin-dependent diabetes mellitus subjects between susceptibility to retinopathy and tumor necrosis factor polymorphism. |
| 18415 | 9157089 | However, these associations are complicated by a primary association between the MHC and IDDM. |
| 18416 | 8602469 | The authors earlier demonstrated that alginates enriched in mannuronic acid stimulate human monocytes to produce high levels of cytokines such as tumour necrosis factor (TNF), IL-1 IL-6. |
| 18417 | 8602469 | The authors earlier demonstrated that alginates enriched in mannuronic acid stimulate human monocytes to produce high levels of cytokines such as tumour necrosis factor (TNF), IL-1 IL-6. |
| 18418 | 8602469 | The authors earlier demonstrated that alginates enriched in mannuronic acid stimulate human monocytes to produce high levels of cytokines such as tumour necrosis factor (TNF), IL-1 IL-6. |
| 18419 | 8602469 | In this study the authors have measured the TNF production from peripheral blood mononuclear cells (PBMC) in different groups of insulin-dependent diabetes mellitus (IDDM) patients after stimulation with different alginates and lipopolysaccharide (LPS). |
| 18420 | 8602469 | In this study the authors have measured the TNF production from peripheral blood mononuclear cells (PBMC) in different groups of insulin-dependent diabetes mellitus (IDDM) patients after stimulation with different alginates and lipopolysaccharide (LPS). |
| 18421 | 8602469 | In this study the authors have measured the TNF production from peripheral blood mononuclear cells (PBMC) in different groups of insulin-dependent diabetes mellitus (IDDM) patients after stimulation with different alginates and lipopolysaccharide (LPS). |
| 18422 | 8602469 | The highest TNF response was found in newly diagnosed IDDM patients and the lowest was in the controls. |
| 18423 | 8602469 | The highest TNF response was found in newly diagnosed IDDM patients and the lowest was in the controls. |
| 18424 | 8602469 | The highest TNF response was found in newly diagnosed IDDM patients and the lowest was in the controls. |
| 18425 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18426 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18427 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18428 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18429 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18430 | 8613535 | TNFalpha is orverexpressed in the adipose tissue of obese rodents and humans, and is associated with insulin resistance. |
| 18431 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18432 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18433 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18434 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18435 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18436 | 8613535 | To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. |
| 18437 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18438 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18439 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18440 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18441 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18442 | 8613535 | Using competitive RT-PCR, TNF was quantitated in the muscle biopsy specimens from 15 subjects whose insulin sensitivity had been characterized using the glucose clamp. technique. |
| 18443 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18444 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18445 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18446 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18447 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18448 | 8613535 | TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). |
| 18449 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18450 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18451 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18452 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18453 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18454 | 8613535 | Thus, TNF is expressed in human muscle, and is expressed at a higher level in the muscle tissue and in the cultured muscle cells from insulin resistant and diabetic subjects. |
| 18455 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18456 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18457 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18458 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18459 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18460 | 8613535 | These data suggest another mechanism by which TNF may play an important role in human insulin resistance. |
| 18461 | 8571133 | IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. |
| 18462 | 8571133 | IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. |
| 18463 | 8571133 | IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. |
| 18464 | 8571133 | IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. |
| 18465 | 8571133 | IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. |
| 18466 | 8571133 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). |
| 18467 | 8571133 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). |
| 18468 | 8571133 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). |
| 18469 | 8571133 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). |
| 18470 | 8571133 | Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). |
| 18471 | 8571133 | Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. |
| 18472 | 8571133 | Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. |
| 18473 | 8571133 | Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. |
| 18474 | 8571133 | Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. |
| 18475 | 8571133 | Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. |
| 18476 | 8571133 | Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. |
| 18477 | 8571133 | Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. |
| 18478 | 8571133 | Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. |
| 18479 | 8571133 | Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. |
| 18480 | 8571133 | Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. |
| 18481 | 8571133 | These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling. |
| 18482 | 8571133 | These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling. |
| 18483 | 8571133 | These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling. |
| 18484 | 8571133 | These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling. |
| 18485 | 8571133 | These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling. |
| 18486 | 8882412 | No primary association between the 308 polymorphism in the tumor necrosis factor alpha promoter region and insulin-dependent diabetes mellitus. |
| 18487 | 8882412 | No primary association between the 308 polymorphism in the tumor necrosis factor alpha promoter region and insulin-dependent diabetes mellitus. |
| 18488 | 8882412 | No primary association between the 308 polymorphism in the tumor necrosis factor alpha promoter region and insulin-dependent diabetes mellitus. |
| 18489 | 8882412 | No primary association between the 308 polymorphism in the tumor necrosis factor alpha promoter region and insulin-dependent diabetes mellitus. |
| 18490 | 8882412 | Whereas TNF-alpha has been implicated in the pathogenesis of IDDM, its possible role as a primary genetic susceptibility factor has not been well investigated. |
| 18491 | 8882412 | Whereas TNF-alpha has been implicated in the pathogenesis of IDDM, its possible role as a primary genetic susceptibility factor has not been well investigated. |
| 18492 | 8882412 | Whereas TNF-alpha has been implicated in the pathogenesis of IDDM, its possible role as a primary genetic susceptibility factor has not been well investigated. |
| 18493 | 8882412 | Whereas TNF-alpha has been implicated in the pathogenesis of IDDM, its possible role as a primary genetic susceptibility factor has not been well investigated. |
| 18494 | 8882412 | In this study, we analyzed a biallelic polymorphism in the TNF-alpha promotor region in a large collection of IDDM patients and controls ascertained from two ethnic populations (U.S. |
| 18495 | 8882412 | In this study, we analyzed a biallelic polymorphism in the TNF-alpha promotor region in a large collection of IDDM patients and controls ascertained from two ethnic populations (U.S. |
| 18496 | 8882412 | In this study, we analyzed a biallelic polymorphism in the TNF-alpha promotor region in a large collection of IDDM patients and controls ascertained from two ethnic populations (U.S. |
| 18497 | 8882412 | In this study, we analyzed a biallelic polymorphism in the TNF-alpha promotor region in a large collection of IDDM patients and controls ascertained from two ethnic populations (U.S. |
| 18498 | 8882412 | Our analyses of extended haplotypes for the HLA region further substantiate the conclusion that no primary association exists between IDDM and the TNF-alpha promoter polymorphism. |
| 18499 | 8882412 | Our analyses of extended haplotypes for the HLA region further substantiate the conclusion that no primary association exists between IDDM and the TNF-alpha promoter polymorphism. |
| 18500 | 8882412 | Our analyses of extended haplotypes for the HLA region further substantiate the conclusion that no primary association exists between IDDM and the TNF-alpha promoter polymorphism. |
| 18501 | 8882412 | Our analyses of extended haplotypes for the HLA region further substantiate the conclusion that no primary association exists between IDDM and the TNF-alpha promoter polymorphism. |
| 18502 | 8834012 | Tumor necrosis factor-alpha (TNF alpha), interferon-gamma (IFN-gamma), and interleukin-1 (IL-1) stimulate adhesion receptor expression on lymphoid and nonlymphoid tissues. |
| 18503 | 8834012 | Although differences between specific autoimmune diseases exist, key interactions facilitating the development of autoimmune inflammation appear to include L-selectin/P-selectin/E-selectin, lymphocyte function-associated antigen-1 (LFA-1)/intercellular adhesion molecule-1 (ICAM-1), very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1), and alpha 4B7/MadCAM or VCAM-1 adhesion. |
| 18504 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18505 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18506 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18507 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18508 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18509 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18510 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 18511 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18512 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18513 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18514 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18515 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18516 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18517 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 18518 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18519 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18520 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18521 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18522 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18523 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18524 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 18525 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18526 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18527 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18528 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18529 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18530 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18531 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 18532 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18533 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18534 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18535 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18536 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18537 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18538 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 18539 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18540 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18541 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18542 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18543 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18544 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18545 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 18546 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18547 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18548 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18549 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18550 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18551 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18552 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 18553 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18554 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18555 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18556 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18557 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18558 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18559 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 18560 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18561 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18562 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18563 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18564 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18565 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18566 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18567 | 8549863 | Tumor necrosis factor-alpha and interferon-gamma inhibit insulin secretion and cause DNA damage in unweaned-rat islets. |
| 18568 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18569 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18570 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18571 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18572 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18573 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18574 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18575 | 8549863 | Nitric oxide has been implicated as one possible mediator of interleukin-1 beta (IL-1)-induced inhibition of insulin secretion and islet cell damage. |
| 18576 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18577 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18578 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18579 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18580 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18581 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18582 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18583 | 8549863 | The aim of this study was to define the effects of tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) on nitric oxide production, insulin secretion, and DNA damage in islets from unweaned rats. |
| 18584 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18585 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18586 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18587 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18588 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18589 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18590 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18591 | 8549863 | Treatment of islets with 0.5-500 U/ml of either TNF or IFN on their own inhibited glucose-stimulated insulin secretion in a dose-dependent manner (minimum effective dose 5 U/ml). |
| 18592 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18593 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18594 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18595 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18596 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18597 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18598 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18599 | 8549863 | Used alone or in combination, TNF and IFN significantly enhanced the activity of inducible nitric oxide synthase as determined by measuring the conversion of 14C-labeled arginine to 14C-labeled citrulline and nitric oxide. |
| 18600 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18601 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18602 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18603 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18604 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18605 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18606 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18607 | 8549863 | Use of arginine-free medium, without or with NG-monomethyl-L-arginine, resulted in inhibition of nitrite formation by 5-1,000 U/ml IFN+TNF and partial restoration of the insulin secretory response to glucose. |
| 18608 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18609 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18610 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18611 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18612 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18613 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18614 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18615 | 8549863 | Treatment of rat islets with increasing doses of TNF+IFN (5, 50, and 500 U/ml) resulted in a progressive increase in DNA damage, as shown by the comet assay, which detects DNA strand breaks in individual islet cells. |
| 18616 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18617 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18618 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18619 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18620 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18621 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18622 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18623 | 8549863 | The DNA damage caused by an intermediate concentration (50 U/ml) of TNF+IFN was comparable to that generated by IL-1 when used at 20 U/ml. |
| 18624 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18625 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18626 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18627 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18628 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18629 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18630 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18631 | 8549863 | We conclude that TNF and IFN induce nitric oxide formation, which partially inhibits glucose-induced insulin secretion and causes significant DNA strand breakage, but that as cytokine concentrations increase, non-nitric-oxide-mediated events predominate. |
| 18632 | 9012538 | Cytokine-inducers prevent insulin-dependent diabetes mellitus (IDDM) in animal models. |
| 18633 | 9012538 | We extend this therapy to non-insulin-dependent diabetes mellitus (NIDDM), because it was reported that diabetes of KK-Ay mice, a model for NIDDM, was recovered by allogenic bone-marrow transplantation that also prevented IDDM in animal models. |
| 18634 | 9012538 | Among various cytokines possibly induced by OK-432 and BCG, IL-1 alpha, TNF alpha and lymphotoxin significantly improved FBG and GTT in KK-Ay mice, whereas IL-2 and IFN gamma did not. |
| 18635 | 8772524 | Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and reactive oxygen species. |
| 18636 | 8772524 | Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and reactive oxygen species. |
| 18637 | 8772524 | TNF-alpha, IL-1 beta, and antioxidants (superoxide dismutase; catalase; and dimethyl sulfoxide) all induced RBC adhesion to BPAEC. |
| 18638 | 8772524 | TNF-alpha, IL-1 beta, and antioxidants (superoxide dismutase; catalase; and dimethyl sulfoxide) all induced RBC adhesion to BPAEC. |
| 18639 | 8568461 | Cytokines, particularly interleukin 1 (IL-1) and tumor necrosis factor, are known to induce hypoglycemia in normal rodents or different experimental models of type II diabetes. |
| 18640 | 8568461 | We investigated, at the pre-diabetic stage, the effect of short-term administration of murine recombinant interleukin-1 alpha (mrIL-1 alpha) on the levels of glucose, insulin and corticosterone in the non-obese diabetic (NOD) mouse, a spontaneous model of type I diabetes. |
| 18641 | 8568461 | With regard to the effect of IL-1 on NOD mouse glycemia, therefore, these results suggest that glucocorticoids and/or androgens, according to the animal's sex, may induce a state of insulin-resistance. |
| 18642 | 8536614 | These metabolic changes were accompanied by increased expression of tumor necrosis factor-alpha and decreased expression of GLUT4 and beta 3-adrenergic receptor messenger RNA levels in white adipose tissue of UCP-DTA transgenic mice receiving the Western diet compared to those in the other experimental groups. |
| 18643 | 8554587 | TGF-beta 1 overexpression in murine pancreas induces chronic pancreatitis and, together with TNF-alpha, triggers insulin-dependent diabetes. |
| 18644 | 8554587 | TGF-beta 1 overexpression in murine pancreas induces chronic pancreatitis and, together with TNF-alpha, triggers insulin-dependent diabetes. |
| 18645 | 8554587 | Backcrossing to transgenic mice overexpressing TNF-alpha in their islet beta cells (which also remain normoglycemic, (1)) yielded double transgenics, most of which became diabetic by the age of 4 months; histological analysis revealed a dramatic decrease in insulin-containing beta cells. |
| 18646 | 8554587 | Backcrossing to transgenic mice overexpressing TNF-alpha in their islet beta cells (which also remain normoglycemic, (1)) yielded double transgenics, most of which became diabetic by the age of 4 months; histological analysis revealed a dramatic decrease in insulin-containing beta cells. |
| 18647 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18648 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18649 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18650 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18651 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18652 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18653 | 8543058 | TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). |
| 18654 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18655 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18656 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18657 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18658 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18659 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18660 | 8543058 | Recent studies suggest that TNF-alpha affects various biochemical and physiological processes which may be linked to the etiology of non-insulin-dependent diabetes mellitus (NIDDM). |
| 18661 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18662 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18663 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18664 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18665 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18666 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18667 | 8543058 | For example, TNF-alpha interferes with the signaling of the insulin receptor and the metabolism of glucose transporters. |
| 18668 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18669 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18670 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18671 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18672 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18673 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18674 | 8543058 | The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). |
| 18675 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18676 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18677 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18678 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18679 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18680 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18681 | 8543058 | TNF-alpha did not affect glucose-induced acute insulin secretion (30 min). |
| 18682 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18683 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18684 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18685 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18686 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18687 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18688 | 8543058 | However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. |
| 18689 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18690 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18691 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18692 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18693 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18694 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18695 | 8543058 | In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. |
| 18696 | 8750759 | Rat islets cultured for 4 days in the presence of 5, 10, and 30 mmol/l glucose were exposed to interferon-gamma (IFN, 500 U/ml) and tumor necrosis factor-alpha (TNF, 250 U/ml) for the last 24 h. |
| 18697 | 8750759 | Rat islets cultured for 4 days in the presence of 5, 10, and 30 mmol/l glucose were exposed to interferon-gamma (IFN, 500 U/ml) and tumor necrosis factor-alpha (TNF, 250 U/ml) for the last 24 h. |
| 18698 | 8750759 | In conclusion, high beta cell activity increases islet susceptibility to TNF+IFN. |
| 18699 | 8750759 | In conclusion, high beta cell activity increases islet susceptibility to TNF+IFN. |
| 18700 | 8746558 | Likewise, the NOD-derived NIT-1 beta cell line did not express surface B7 or B7-1 mRNA either constitutively or following exposure to IFN-gamma and TNF-alpha, two cytokines known to be present in the insulitis lesion of NOD mice, or cAMP which can induce B7-1 expression on B cells. |
| 18701 | 8746558 | By immunohistochemistry and flow cytometry, it was determined that the phenotype of B7+ cells in the pancreas of NOD mice 9 days after cyclophosphamide included a mixture of macrophages and both CD4+ and CD8+ T cells. |
| 18702 | 8746558 | RIP-IL-2 transgenic mice, which have extensive islet infiltration but no autoimmune beta cell destruction, also had virtually no B7-1 expression and a minority of B7-2-expressing inflammatory cells. |
| 18703 | 8664448 | During the early phase of insulitis from 6 to 12 weeks of age, mainly the monokines IL-1 alpha, IL-6, and TNF were detected. |
| 18704 | 8664448 | During the early phase of insulitis from 6 to 12 weeks of age, mainly the monokines IL-1 alpha, IL-6, and TNF were detected. |
| 18705 | 8664448 | After stimulation, also IFN-gamma and low numbers of IL-10 and GM-CSF producing cells could be observed, but no IL-2 or IL-4 was seen. |
| 18706 | 8664448 | After stimulation, also IFN-gamma and low numbers of IL-10 and GM-CSF producing cells could be observed, but no IL-2 or IL-4 was seen. |
| 18707 | 8664448 | During a later phase, between 4 and 6 months, there is a characteristic TH1 cytokine profile with production of IL-2 and IFN-gamma occurring after stimulation, as well as lymphocytes producing TNF, supposedly TNF-beta. |
| 18708 | 8664448 | During a later phase, between 4 and 6 months, there is a characteristic TH1 cytokine profile with production of IL-2 and IFN-gamma occurring after stimulation, as well as lymphocytes producing TNF, supposedly TNF-beta. |
| 18709 | 8664448 | During this period IL-10 was very rarely observed, and no IL-4 production could be found throughout the study. |
| 18710 | 8664448 | During this period IL-10 was very rarely observed, and no IL-4 production could be found throughout the study. |
| 18711 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 18712 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 18713 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 18714 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 18715 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 18716 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 18717 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 18718 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 18719 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 18720 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 18721 | 7477268 | Activation of the SAPK pathway by the human STE20 homologue germinal centre kinase. |
| 18722 | 7477268 | Eukaryotic cells respond to different extracellular stimuli by recruiting homologous signalling pathways that use members of the MEKK, MEK and ERK families of protein kinases. |
| 18723 | 7477268 | The MEKK-->MEK-->ERK core pathways of Saccharomyces cerevisiae may themselves be regulated by members of the STE20 family of protein kinases. |
| 18724 | 7477268 | Here we report specific activation of the mammalian stress-activated protein kinase (SAPK) pathway by germinal centre kinase (GCK), a human STE20 homologue. |
| 18725 | 7477268 | SAPKs, members of the ERK family, are activated in situ by inflammatory stimuli, including tumour-necrosis factor (TNF) and interleukin-1, and phosphorylate and probably stimulate the transactivation function of c-Jun. |
| 18726 | 7477268 | Activation of the SAPK pathway by GCK illustrates further the striking conservation of eukaryotic signalling mechanisms and defines the first physiological function of a mammalian Ste20. |
| 18727 | 8847231 | Genetic polymorphism of the human tumor necrosis factor region in insulin-dependent diabetes mellitus. |
| 18728 | 8847231 | Genetic polymorphism of the human tumor necrosis factor region in insulin-dependent diabetes mellitus. |
| 18729 | 8847231 | Genetic polymorphism of the human tumor necrosis factor region in insulin-dependent diabetes mellitus. |
| 18730 | 8847231 | The TNF region within the MHC includes a number of immunologically important genes. |
| 18731 | 8847231 | The TNF region within the MHC includes a number of immunologically important genes. |
| 18732 | 8847231 | The TNF region within the MHC includes a number of immunologically important genes. |
| 18733 | 8847231 | Microsatellites TNFa and TNFb adjacent to TNF exhibit extensive polymorphism. |
| 18734 | 8847231 | Microsatellites TNFa and TNFb adjacent to TNF exhibit extensive polymorphism. |
| 18735 | 8847231 | Microsatellites TNFa and TNFb adjacent to TNF exhibit extensive polymorphism. |
| 18736 | 8847231 | Employing a PCR-based technique, we identified TNFab haplotypes and defined their distribution in 97 controls and 48 diabetics of Caucasoid origin in a search for other genes within the MHC potentially associated with IDDM. |
| 18737 | 8847231 | Employing a PCR-based technique, we identified TNFab haplotypes and defined their distribution in 97 controls and 48 diabetics of Caucasoid origin in a search for other genes within the MHC potentially associated with IDDM. |
| 18738 | 8847231 | Employing a PCR-based technique, we identified TNFab haplotypes and defined their distribution in 97 controls and 48 diabetics of Caucasoid origin in a search for other genes within the MHC potentially associated with IDDM. |
| 18739 | 7560085 | The coding sequences and splicing donor and acceptor sequences of the Tnfa gene, a candidate gene for Idd-16, were identical in the NOD, CTS, and BALB/c alleles, ruling out amino acid changes in the TNF molecule as a determinant of insulin-dependent diabetes mellitus susceptibility. |
| 18740 | 7647584 | Markers of cell-mediated immune activation were studied in 32 Chinese patients with recent-onset insulin-dependent diabetes mellitus (IDDM) as compared with 12 patients with recent-onset non-insulin-dependent diabetes mellitus (NIDDM) and 34 normal subjects. |
| 18741 | 7647584 | Sera were assessed for soluble markers of T-cell activation (sCD4, sCD8, sIL-2R); the cytokines (IL-1 beta, TNF-alpha, IL-2, IL-6), and T-cell subsets were also determined. |
| 18742 | 7647584 | Three IDDM patients had detectable IL-1 beta and this weakly so (< 3.5 pg/ml). |
| 18743 | 7647584 | However, the other cytokine data and the frequency of activated T-cells, CD4+, CD8+ T-cell subsets and CD4:CD8 ratio showed no significant differences among the IDDM, NIDDM and normal subjects. |
| 18744 | 7496336 | Its interaction with different cytokines [interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma)] is important for lymphocyte migration into inflammatory sites. |
| 18745 | 7652767 | Combined therapy with interleukin-4 and interleukin-10 inhibits autoimmune diabetes recurrence in syngeneic islet-transplanted nonobese diabetic mice. |
| 18746 | 7652767 | Combined therapy with interleukin-4 and interleukin-10 inhibits autoimmune diabetes recurrence in syngeneic islet-transplanted nonobese diabetic mice. |
| 18747 | 7652767 | IL-4 and IL-10 are cytokines that inhibit cell-mediated immunity. |
| 18748 | 7652767 | IL-4 and IL-10 are cytokines that inhibit cell-mediated immunity. |
| 18749 | 7652767 | In this study, we evaluated the effects of IL-4 and IL-10 on the survival of syngeneic pancreatic islets transplanted into diabetic NOD mice. |
| 18750 | 7652767 | In this study, we evaluated the effects of IL-4 and IL-10 on the survival of syngeneic pancreatic islets transplanted into diabetic NOD mice. |
| 18751 | 7652767 | Islet grafts survived beyond 18 days and normoglycemia was maintained in 67% (10 of 15) of mice treated with IL-4 plus IL-10, but in none (0 of 20) of vehicle-injected (control) mice. |
| 18752 | 7652767 | Islet grafts survived beyond 18 days and normoglycemia was maintained in 67% (10 of 15) of mice treated with IL-4 plus IL-10, but in none (0 of 20) of vehicle-injected (control) mice. |
| 18753 | 7652767 | Also, 40% (6 of 15) of the mice treated with IL-4 plus IL-10 were normoglycemic at 30 days after transplantation, compared with 14% (1 of 7) of the mice treated with IL-4 alone, 8% (1 of 13) of the mice treated with IL-10 alone, and none (0 of 20) of the control mice. |
| 18754 | 7652767 | Also, 40% (6 of 15) of the mice treated with IL-4 plus IL-10 were normoglycemic at 30 days after transplantation, compared with 14% (1 of 7) of the mice treated with IL-4 alone, 8% (1 of 13) of the mice treated with IL-10 alone, and none (0 of 20) of the control mice. |
| 18755 | 7652767 | Histological examination of grafts at 10 days after transplantation revealed peri-islet accumulations of mononuclear leukocytes and intact islet beta cells in grafts from IL-4 plus IL-10-treated mice, whereas islets were infiltrated by leukocytes and the beta cell mass was greatly reduced in grafts from control mice. |
| 18756 | 7652767 | Histological examination of grafts at 10 days after transplantation revealed peri-islet accumulations of mononuclear leukocytes and intact islet beta cells in grafts from IL-4 plus IL-10-treated mice, whereas islets were infiltrated by leukocytes and the beta cell mass was greatly reduced in grafts from control mice. |
| 18757 | 7652767 | Polymerase chain reaction (PCR) analysis of cytokine mRNA expression in the grafts revealed higher levels of IL-2, IFN gamma, and IL-10 mRNA in grafts of diabetic compared with normoglycemic control mice, whereas IFN gamma and TNF alpha mRNA levels were significantly decreased in grafts of IL-4 plus IL-10-treated mice compared with either normoglycemic or diabetic control mice. |
| 18758 | 7652767 | Polymerase chain reaction (PCR) analysis of cytokine mRNA expression in the grafts revealed higher levels of IL-2, IFN gamma, and IL-10 mRNA in grafts of diabetic compared with normoglycemic control mice, whereas IFN gamma and TNF alpha mRNA levels were significantly decreased in grafts of IL-4 plus IL-10-treated mice compared with either normoglycemic or diabetic control mice. |
| 18759 | 7652767 | These results suggest that T helper (Th)1 cells and their cytokine products (IL-2, IFN gamma, and TNF alpha) may promote islet beta cell destructive insulitis and autoimmune diabetes recurrence in syngeneic islet-transplanted NOD mice, and that administration of IL-4 plus IL-10 may inhibit diabetes recurrence by suppressing Th1 cytokine production in the islet grafts. |
| 18760 | 7652767 | These results suggest that T helper (Th)1 cells and their cytokine products (IL-2, IFN gamma, and TNF alpha) may promote islet beta cell destructive insulitis and autoimmune diabetes recurrence in syngeneic islet-transplanted NOD mice, and that administration of IL-4 plus IL-10 may inhibit diabetes recurrence by suppressing Th1 cytokine production in the islet grafts. |
| 18761 | 8529511 | Activation of protein kinase C probably leads to phosphorylation of the beta-subunit of the insulin receptor at serine residues. |
| 18762 | 8529511 | The hyperglycaemic effect can be antagonized in the isolated cell system both by protein kinase C inhibitors and so-called insulin sensitizers such as thiazolidindiones. |
| 18763 | 8529511 | As TNF alpha is probably increasingly expressed in obesity, the modulation of receptor kinase activity by TNF alpha could be an important factor for insulin resistance in obesity. |
| 18764 | 7628352 | Nitric oxide (NO) may be a mediator of beta-cell damage in insulin-dependent diabetes mellitus. beta-Cells express the inducible form of NO synthase (iNOS) and produce large amounts of NO upon exposure to cytokines. iNOS requires the amino acid arginine for NO formation. |
| 18765 | 7628352 | Nitric oxide (NO) may be a mediator of beta-cell damage in insulin-dependent diabetes mellitus. beta-Cells express the inducible form of NO synthase (iNOS) and produce large amounts of NO upon exposure to cytokines. iNOS requires the amino acid arginine for NO formation. |
| 18766 | 7628352 | It has been shown in other cell types that interferon-gamma (IFN gamma) and bacterial lipopolysaccharide induce the enzyme argininosuccinate synthetase (AS), enhancing the capacity of these cells to regenerate arginine from citrulline and maintain NO production in the presence of low arginine concentrations. |
| 18767 | 7628352 | It has been shown in other cell types that interferon-gamma (IFN gamma) and bacterial lipopolysaccharide induce the enzyme argininosuccinate synthetase (AS), enhancing the capacity of these cells to regenerate arginine from citrulline and maintain NO production in the presence of low arginine concentrations. |
| 18768 | 7628352 | To characterize the messenger RNA (mRNA) expression of AS in insulin-producing cells, RINm5F cells (RIN cells) were exposed to interleukin-1 beta (IL-1 beta) or to tumor necrosis factor-alpha plus IFN gamma. |
| 18769 | 7628352 | To characterize the messenger RNA (mRNA) expression of AS in insulin-producing cells, RINm5F cells (RIN cells) were exposed to interleukin-1 beta (IL-1 beta) or to tumor necrosis factor-alpha plus IFN gamma. |
| 18770 | 7628352 | IL-1 beta-induced AS and iNOS mRNA expression was prevented by an inhibitor of the activation factor NF-kappa B pyrrolidine diaminoguanidine, an inhibitor of gene transcription (actinomycin D), and a blocker of protein synthesis (cycloheximide), suggesting coregulation of AS and iNOS by cytokines. |
| 18771 | 7628352 | IL-1 beta-induced AS and iNOS mRNA expression was prevented by an inhibitor of the activation factor NF-kappa B pyrrolidine diaminoguanidine, an inhibitor of gene transcription (actinomycin D), and a blocker of protein synthesis (cycloheximide), suggesting coregulation of AS and iNOS by cytokines. |
| 18772 | 7628352 | Both adult rat islets exposed to IL-1 beta and human pancreatic islets cultured in the presence of IL-1 beta, tumor necrosis factor-alpha, and IFN gamma were able to use citrulline to regenerate arginine and produce NO. |
| 18773 | 7628352 | Both adult rat islets exposed to IL-1 beta and human pancreatic islets cultured in the presence of IL-1 beta, tumor necrosis factor-alpha, and IFN gamma were able to use citrulline to regenerate arginine and produce NO. |
| 18774 | 7621993 | We have previously reported that the mRNA levels of extracellular matrix (ECM) components including alpha 1(I), alpha 1(III), and alpha 1(IV) collagen chains, laminin B1 and B2 chains, and growth factors including tumor necrosis factor (TNF)-alpha, platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF)-beta, and basic fibroblast growth factor (FGF) all increase with age in diabetic glomeruli. |
| 18775 | 7621993 | We have previously reported that the mRNA levels of extracellular matrix (ECM) components including alpha 1(I), alpha 1(III), and alpha 1(IV) collagen chains, laminin B1 and B2 chains, and growth factors including tumor necrosis factor (TNF)-alpha, platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF)-beta, and basic fibroblast growth factor (FGF) all increase with age in diabetic glomeruli. |
| 18776 | 7621993 | FR139317 attenuated the increases in glomerular mRNA levels of alpha 1(I) (P < 0.01), alpha 1(III) (P < 0.01), and alpha 1(IV) (P < 0.01) collagen chains, laminin B1 (P < 0.01) and B2 (P < 0.01) chains, TNF-alpha (P < 0.01), PDGF-B (P < 0.01), TGF-beta (P < 0.001) and basic FGF (P < 0.01) in diabetic rats. |
| 18777 | 7621993 | FR139317 attenuated the increases in glomerular mRNA levels of alpha 1(I) (P < 0.01), alpha 1(III) (P < 0.01), and alpha 1(IV) (P < 0.01) collagen chains, laminin B1 (P < 0.01) and B2 (P < 0.01) chains, TNF-alpha (P < 0.01), PDGF-B (P < 0.01), TGF-beta (P < 0.001) and basic FGF (P < 0.01) in diabetic rats. |
| 18778 | 7789642 | Intercellular adhesion molecule 1 (ICAM-1) plays an important role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) by being involved in the extravasation of lymphocytes from the circulation into the inflamed pancreas. |
| 18779 | 7789642 | Immunohistochemical study under light microscopy demonstrated that all of the mononuclear cells infiltrating the islets strongly expressed ICAM-1 and leukocyte function-associated antigen 1 (LFA-1), a counterreceptor of ICAM-1, whereas ICAM-1 expression on islet cells was not apparent. |
| 18780 | 7789642 | Flow cytometric analysis showed that the ICAM-1 expression on NOD islet cells and NOD-derived insulinoma cells (MIN6N8a) was inducible by interferon (IFN)-gamma or tumor necrosis factor-alpha. |
| 18781 | 7789642 | Susceptibility of MIN6N8a cells to lysis by a NOD islet-derived CD8+ cytotoxic T-cell clone was greatly enhanced by IFN-gamma pretreatment, and this enhancement was abolished by anti-ICAM-1 and anti-LFA-1 mAbs. |
| 18782 | 7667243 | These responses were associated with a marked increase in splenocyte interleukin-4 (IL-4) production, a reduction in interferon-gamma production, and a down-regulation of CD45RB isoform expression. |
| 18783 | 7667243 | Macrophages in the EFAD group exerted a reduced suppressive effect on concanavalin A-induced splenocyte proliferation and were found to release increased amounts of tumor necrosis factor-alpha and IL-1 and reduced amounts of prostaglandin E2. |
| 18784 | 7556976 | Presence of 5 nmol/l TNF alpha for 24 h resulted in a complete loss of the stimulatory effect of insulin on 2-deoxy-glucose transport. |
| 18785 | 7556976 | Presence of 5 nmol/l TNF alpha for 24 h resulted in a complete loss of the stimulatory effect of insulin on 2-deoxy-glucose transport. |
| 18786 | 7556976 | Presence of 5 nmol/l TNF alpha for 24 h resulted in a complete loss of the stimulatory effect of insulin on 2-deoxy-glucose transport. |
| 18787 | 7556976 | Presence of 5 nmol/l TNF alpha for 24 h resulted in a complete loss of the stimulatory effect of insulin on 2-deoxy-glucose transport. |
| 18788 | 7556976 | The amount of cellular GLUT4 protein was reduced by 49 +/- 3% after a 24-h exposure and by 82 +/- 18% after a 72-h exposure to 5 nmol/l TNF alpha. |
| 18789 | 7556976 | The amount of cellular GLUT4 protein was reduced by 49 +/- 3% after a 24-h exposure and by 82 +/- 18% after a 72-h exposure to 5 nmol/l TNF alpha. |
| 18790 | 7556976 | The amount of cellular GLUT4 protein was reduced by 49 +/- 3% after a 24-h exposure and by 82 +/- 18% after a 72-h exposure to 5 nmol/l TNF alpha. |
| 18791 | 7556976 | The amount of cellular GLUT4 protein was reduced by 49 +/- 3% after a 24-h exposure and by 82 +/- 18% after a 72-h exposure to 5 nmol/l TNF alpha. |
| 18792 | 7556976 | GLUT4 mRNA was almost undetectable after a 24-h incubation with 5 nmol/l TNF alpha. |
| 18793 | 7556976 | GLUT4 mRNA was almost undetectable after a 24-h incubation with 5 nmol/l TNF alpha. |
| 18794 | 7556976 | GLUT4 mRNA was almost undetectable after a 24-h incubation with 5 nmol/l TNF alpha. |
| 18795 | 7556976 | GLUT4 mRNA was almost undetectable after a 24-h incubation with 5 nmol/l TNF alpha. |
| 18796 | 7556976 | In a similar time-dependent manner, TNF alpha dramatically reduced the lipoprotein lipase mRNA content of the cells. |
| 18797 | 7556976 | In a similar time-dependent manner, TNF alpha dramatically reduced the lipoprotein lipase mRNA content of the cells. |
| 18798 | 7556976 | In a similar time-dependent manner, TNF alpha dramatically reduced the lipoprotein lipase mRNA content of the cells. |
| 18799 | 7556976 | In a similar time-dependent manner, TNF alpha dramatically reduced the lipoprotein lipase mRNA content of the cells. |
| 18800 | 7540573 | An inducible nitric oxide (NO) synthase isoform (iNOS) is specifically induced in the beta-cells of interleukin (IL)-1 beta-exposed rat islets, suggesting a role for NO in the pathogenesis of type I diabetes. |
| 18801 | 7540573 | Addition of IL-1 beta alone or in combination with tumor necrosis factor-alpha induced a concentration- and time-dependent expression of the iNOS gene and associated NO production (measured as nitrite) from both islets and RIN cells. iNOS transcripts were cloned by reverse transcriptase-polymerase chain reaction from the cytokine-exposed rat islets and RIN cells, and DNA sequence analysis revealed a near 100% identity to the recently published iNOS cDNA cloned from cytokine-exposed rat hepatocytes and smooth muscle cells. |
| 18802 | 7540573 | In conclusion, the IL-1 beta-induced iNOS cloned and expressed from rat islets and RIN cells is encoded by the same transcript as the iNOS induced in other cell types. |
| 18803 | 7540572 | Furthermore, in the presence of tumor necrosis factor (TNF)-alpha, large amounts of NO were produced by IL-1 beta and DNA cleavage occurred more noticeably, although TNF-alpha alone did not generate NO. |
| 18804 | 7598712 | Recent evidence suggests that expression of tumor necrosis factor-alpha (TNF-alpha) by adipocytes is a molecular mediator of insulin resistance in obesity. |
| 18805 | 7598712 | Recent evidence suggests that expression of tumor necrosis factor-alpha (TNF-alpha) by adipocytes is a molecular mediator of insulin resistance in obesity. |
| 18806 | 7598712 | We have therefore tested the hypothesis that variations within the regulatory region of the TNF-alpha gene, which might cause increased adipocyte or generalized TNF-alpha synthesis, are associated with NIDDM, a state in which insulin resistance is routinely observed. |
| 18807 | 7598712 | We have therefore tested the hypothesis that variations within the regulatory region of the TNF-alpha gene, which might cause increased adipocyte or generalized TNF-alpha synthesis, are associated with NIDDM, a state in which insulin resistance is routinely observed. |
| 18808 | 7540571 | We detect a significant increase in the level of expression of interferon (IFN)-alpha in the pancreases of the diabetic patients as compared with the control pancreases. |
| 18809 | 7540571 | We detect a significant increase in the level of expression of interferon (IFN)-alpha in the pancreases of the diabetic patients as compared with the control pancreases. |
| 18810 | 7540571 | In contrast, IFN-beta was detected at comparable levels in both groups, while IFN-gamma was detected in three of four control pancreases and one of four pancreases from the diabetic individuals. |
| 18811 | 7540571 | In contrast, IFN-beta was detected at comparable levels in both groups, while IFN-gamma was detected in three of four control pancreases and one of four pancreases from the diabetic individuals. |
| 18812 | 7540571 | The IFN-alpha cDNAs generated by the RT-PCR were cloned and sequenced to determine which alpha-subtypes were being expressed. |
| 18813 | 7540571 | The IFN-alpha cDNAs generated by the RT-PCR were cloned and sequenced to determine which alpha-subtypes were being expressed. |
| 18814 | 7540571 | We also examined these pancreases for the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-2, IL-4, and IL-6. |
| 18815 | 7540571 | We also examined these pancreases for the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-2, IL-4, and IL-6. |
| 18816 | 7540571 | We found no detectable expression of TNF-alpha or IL-2 in any pancreases, and the expression of the other cytokines was variable, with no pattern emerging from the comparison of the diabetic and nondiabetic individuals. |
| 18817 | 7540571 | We found no detectable expression of TNF-alpha or IL-2 in any pancreases, and the expression of the other cytokines was variable, with no pattern emerging from the comparison of the diabetic and nondiabetic individuals. |
| 18818 | 7540571 | We conclude that, of the cytokines examined, only IFN-alpha was significantly increased in the diabetic patients, a result that is consistent with the possibility that this cytokine is directly involved in the development of type I diabetes. |
| 18819 | 7540571 | We conclude that, of the cytokines examined, only IFN-alpha was significantly increased in the diabetic patients, a result that is consistent with the possibility that this cytokine is directly involved in the development of type I diabetes. |
| 18820 | 7759509 | We found a large induction of VEGF expression upon treatment of quiescent cells with serum, epidermal growth factor, transforming growth factor-beta 1, keratinocyte growth factor, or the proinflammatory cytokine tumor necrosis factor alpha, respectively. |
| 18821 | 7738205 | Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. |
| 18822 | 7738205 | Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. |
| 18823 | 7738205 | Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. |
| 18824 | 7738205 | Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. |
| 18825 | 7738205 | Recent studies in animal models have indicated that TNF-alpha plays an important role in mediating the insulin resistance of obesity through its overexpression in fat tissue. |
| 18826 | 7738205 | Recent studies in animal models have indicated that TNF-alpha plays an important role in mediating the insulin resistance of obesity through its overexpression in fat tissue. |
| 18827 | 7738205 | Recent studies in animal models have indicated that TNF-alpha plays an important role in mediating the insulin resistance of obesity through its overexpression in fat tissue. |
| 18828 | 7738205 | Recent studies in animal models have indicated that TNF-alpha plays an important role in mediating the insulin resistance of obesity through its overexpression in fat tissue. |
| 18829 | 7738205 | A strong positive correlation was observed between TNF-alpha mRNA expression levels in fat tissue and the level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance. |
| 18830 | 7738205 | A strong positive correlation was observed between TNF-alpha mRNA expression levels in fat tissue and the level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance. |
| 18831 | 7738205 | A strong positive correlation was observed between TNF-alpha mRNA expression levels in fat tissue and the level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance. |
| 18832 | 7738205 | A strong positive correlation was observed between TNF-alpha mRNA expression levels in fat tissue and the level of hyperinsulinemia (P < 0.001), an indirect measure of insulin resistance. |
| 18833 | 7738205 | Finally, body weight reduction in obese subjects which resulted in improved insulin sensitivity was also associated with a decrease in TNF-alpha mRNA expression (45%, P < 0.001) in fat tissue. |
| 18834 | 7738205 | Finally, body weight reduction in obese subjects which resulted in improved insulin sensitivity was also associated with a decrease in TNF-alpha mRNA expression (45%, P < 0.001) in fat tissue. |
| 18835 | 7738205 | Finally, body weight reduction in obese subjects which resulted in improved insulin sensitivity was also associated with a decrease in TNF-alpha mRNA expression (45%, P < 0.001) in fat tissue. |
| 18836 | 7738205 | Finally, body weight reduction in obese subjects which resulted in improved insulin sensitivity was also associated with a decrease in TNF-alpha mRNA expression (45%, P < 0.001) in fat tissue. |
| 18837 | 7642180 | Hypothetical relationship between the presence of TNF alpha in the sera of insulin-dependent diabetes mellitus type I patients and control of the disease. |
| 18838 | 7602783 | The expression of the second isozyme, Mn-SOD localized at mitochondrial matrix, is regulated in a complex manner by many stimulants such as interleukin-1, -6, tumor necrosis factor, lipopolysaccharide, and tumor promoters phorbol ester (TPA) and okadaic acid. |
| 18839 | 7587921 | This study was undertaken to determine whether this reduced lymphocyte proliferation is mediated by a decreased production of cytokine or decreased expression of interleukin-2 receptor (IL-2R). |
| 18840 | 7587921 | However, the production of IL-1 beta, IL-2 and interferon-gamma, the percentages of pan T cells (CD3), T helper cells (CD4), T suppressor cells (CD8), the ratio of CD4/CD8 and the expression of CR1 and Fc receptors for immunoglobulin G (Fc gamma RII and Fc gamma RIII) were not significantly different between NIDDM patients and healthy subjects. |
| 18841 | 7587921 | These findings suggest that decreased expression of CR3 on monocytes, decreased lymphocyte proliferation and decreased IL-2R expression despite a higher production of TNF-alpha may explain the impaired cell-mediated immunity seen in NIDDM patients. |
| 18842 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18843 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18844 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18845 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18846 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18847 | 7895657 | Antidiabetic thiazolidinediones block the inhibitory effect of tumor necrosis factor-alpha on differentiation, insulin-stimulated glucose uptake, and gene expression in 3T3-L1 cells. |
| 18848 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18849 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18850 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18851 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18852 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18853 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 18854 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18855 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18856 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18857 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18858 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18859 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 18860 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18861 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18862 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18863 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18864 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18865 | 7895657 | Long term incubation of 3T3-L1 adipocytes with a low dose of TNF alpha (50 pM) significantly decreased the levels of the adipocyte/muscle-specific glucose transporter (GLUT4) and the CCAAT enhancer-binding protein mRNAs, but did not affect expression of the ubiquitously expressed glucose transporter (GLUT1) or lipoprotein lipase mRNAs. |
| 18866 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18867 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18868 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18869 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18870 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18871 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 18872 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18873 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18874 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18875 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18876 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18877 | 7895657 | These results implicate that the insulin-sensitizing agents may exert their antidiabetic activities by antagonizing the inhibitory effects of TNF alpha. |
| 18878 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 18879 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 18880 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 18881 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 18882 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 18883 | 7882592 | In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. |
| 18884 | 7882592 | In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. |
| 18885 | 7882592 | In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. |
| 18886 | 7882592 | In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. |
| 18887 | 7882592 | In particular, the TNF-alpha derived from adipose tissues might be involved in the induction of peripheral insulin resistance in rodent models of obesity. |
| 18888 | 7882592 | In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. |
| 18889 | 7882592 | In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. |
| 18890 | 7882592 | In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. |
| 18891 | 7882592 | In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. |
| 18892 | 7882592 | In obese (ob/ob) and obese diabetic (db/db) mice, both of which are known to have severe insulin resistance, unstimulated serum bioactivity of TNF-alpha was significantly higher than that in lean control mice. |
| 18893 | 7882592 | Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. |
| 18894 | 7882592 | Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. |
| 18895 | 7882592 | Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. |
| 18896 | 7882592 | Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. |
| 18897 | 7882592 | Spontaneous TNF-alpha mRNA expression in splenic macrophages was also enhanced in obese mice, but not in monosodium-L-glutamate (MST)-induced obese mice which have no insulin resistance. |
| 18898 | 7882592 | Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. |
| 18899 | 7882592 | Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. |
| 18900 | 7882592 | Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. |
| 18901 | 7882592 | Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. |
| 18902 | 7882592 | Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity. |
| 18903 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18904 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18905 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18906 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18907 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18908 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18909 | 7706477 | Tumor necrosis factor-alpha eliminates binding of NF-Y and an octamer-binding protein to the lipoprotein lipase promoter in 3T3-L1 adipocytes. |
| 18910 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18911 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18912 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18913 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18914 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18915 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18916 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 18917 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18918 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18919 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18920 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18921 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18922 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18923 | 7706477 | Regulation of LPL by TNF alpha occurs at the level of LPL gene transcription and posttranscriptionally. |
| 18924 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18925 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18926 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18927 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18928 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18929 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18930 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 18931 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18932 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18933 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18934 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18935 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18936 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18937 | 7706477 | Transient transfections using LPL promoter deletions fused to luciferase in differentiated 3T3-L1 cells with and without TNF alpha treatment indicated that a DNA region downstream of -180 bp confers the TNF alpha effect. |
| 18938 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18939 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18940 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18941 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18942 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18943 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18944 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 18945 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18946 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18947 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18948 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18949 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18950 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18951 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 18952 | 7698507 | Further, IL-1 beta-induced and tumor necrosis factor alpha-induced islet damage partly depends on the intracellular production of the nitric oxide (NO) radical. |
| 18953 | 7698507 | The demonstrated changes in protein expression caused by IL-1 beta +/- nicotinamide and L-arginine depletion may form the basis for identification of proteins with possible protective and deleterious roles in the initial beta-cell destruction in insulin-dependent diabetes mellitus. |
| 18954 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18955 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18956 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18957 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18958 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18959 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18960 | 7530759 | Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. |
| 18961 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18962 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18963 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18964 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18965 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18966 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18967 | 7530759 | In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. |
| 18968 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18969 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18970 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18971 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18972 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18973 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18974 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 18975 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18976 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18977 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18978 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18979 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18980 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18981 | 7530759 | Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). |
| 18982 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18983 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18984 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18985 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18986 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18987 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18988 | 7530759 | In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. |
| 18989 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18990 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18991 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18992 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18993 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18994 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18995 | 7530759 | Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. |
| 18996 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 18997 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 18998 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 18999 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 19000 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 19001 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 19002 | 7530759 | The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. |
| 19003 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19004 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19005 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19006 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19007 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19008 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19009 | 7530759 | Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. |
| 19010 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19011 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19012 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19013 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19014 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19015 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19016 | 7530759 | Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. |
| 19017 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19018 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19019 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19020 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19021 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19022 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19023 | 7530759 | These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes. |
| 19024 | 7695204 | To clarify the mechanism that causes elevation of plasma fibrinogen levels in diabetes, we examined the effect of high concentration of glucose and/or advanced glycosylation end products (AGEs) on the production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by human monocytes. |
| 19025 | 7695204 | To clarify the mechanism that causes elevation of plasma fibrinogen levels in diabetes, we examined the effect of high concentration of glucose and/or advanced glycosylation end products (AGEs) on the production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by human monocytes. |
| 19026 | 7695204 | To clarify the mechanism that causes elevation of plasma fibrinogen levels in diabetes, we examined the effect of high concentration of glucose and/or advanced glycosylation end products (AGEs) on the production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by human monocytes. |
| 19027 | 7695204 | To clarify the mechanism that causes elevation of plasma fibrinogen levels in diabetes, we examined the effect of high concentration of glucose and/or advanced glycosylation end products (AGEs) on the production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by human monocytes. |
| 19028 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants were measured by ELISA methods. |
| 19029 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants were measured by ELISA methods. |
| 19030 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants were measured by ELISA methods. |
| 19031 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants were measured by ELISA methods. |
| 19032 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. |
| 19033 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. |
| 19034 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. |
| 19035 | 7695204 | IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. |
| 19036 | 7695204 | In this study, we revealed the effect of glucose and AGEs on the production of IL-6 or TNF-alpha by human monocytes. |
| 19037 | 7695204 | In this study, we revealed the effect of glucose and AGEs on the production of IL-6 or TNF-alpha by human monocytes. |
| 19038 | 7695204 | In this study, we revealed the effect of glucose and AGEs on the production of IL-6 or TNF-alpha by human monocytes. |
| 19039 | 7695204 | In this study, we revealed the effect of glucose and AGEs on the production of IL-6 or TNF-alpha by human monocytes. |
| 19040 | 18475668 | IL-6-mediated MHC class II induction on RIN-5AH insulinoma cells by IFN-gamma occurs via the G-protein pathway. |
| 19041 | 18475668 | Major histocompatibility complex (MHC) class II antigen expression has been implicated in the pathogenesis of autoimmune type 1 diabetes. |
| 19042 | 18475668 | As in another study, the ability of IFN-gamma to amplify MHC class II antigen expression 4-fold is demonstrated. |
| 19043 | 18475668 | Signal transduction analysis reveals that IL-6-induced MHC class II expression is specifically mediated by the G-protein system (activation of p21(ras) by IL-6) since mevalonic acid lactone (a Gprotein inhibitor) abolishes the action of IL-6. |
| 19044 | 18475668 | In contrast, IFN-gamma, which does not activate p21(ras), is not inhibited by protein kinase C (PKC) inhibitors but by those of the G-protein pathway. |
| 19045 | 18475668 | This finding raises the possibility that IFN-gamma induces RIN cells to secrete IL-6 (as shown previously, as well as in this paper) which, in turn, increases class II antigen expression via the G-protein pathway. |
| 19046 | 18475668 | This action may be unique to IL-6 or in synergy with IFN-gamma. |
| 19047 | 18475668 | Other cytokines such as IL-1alpha and beta, and TNF-alpha induce a smaller increase in MHC class II antigens on RIN cells, and appear to activate both the G-protein and the PKC signal transduction pathways to varying degrees. |
| 19048 | 18475668 | Therefore, injury of pancreatic beta-cells and possible induction of autoimmune type 1 diabetes via various cytokines may be caused by IL-6 or IFN-gamma, or by their ability to induce MHC class II antigen upregulation. |
| 19049 | 8781713 | Since glutamic acid decarboxylase-65 (GAD-65) is a target autoantigen in IDDM, we investigated whether the cytokines IL-1 beta, TNF alpha IFN gamma altered islet cell expression of GAD-65 and whether the effect of cytokines on GAD-65 expression was similar to their effect on insulin secretion. |
| 19050 | 8781713 | Since glutamic acid decarboxylase-65 (GAD-65) is a target autoantigen in IDDM, we investigated whether the cytokines IL-1 beta, TNF alpha IFN gamma altered islet cell expression of GAD-65 and whether the effect of cytokines on GAD-65 expression was similar to their effect on insulin secretion. |
| 19051 | 8781713 | Since glutamic acid decarboxylase-65 (GAD-65) is a target autoantigen in IDDM, we investigated whether the cytokines IL-1 beta, TNF alpha IFN gamma altered islet cell expression of GAD-65 and whether the effect of cytokines on GAD-65 expression was similar to their effect on insulin secretion. |
| 19052 | 8781713 | We found that: 1) IL-1 beta at low dose (1 U/ml) which stimulated insulin secretion, had no effect on GAD-65 expression, whereas higher doses of IL-1 beta (10, 100, 1000 U/ml) which inhibited insulin secretion, decreased GAD-65 expression. 2) TNF alpha at doses of 10, 100, 1000 U/ml which stimulated insulin secretion had no effect on GAD-65 expression. 3) IFN gamma at doses of 10, 100, 1000 U/ml had no effect on insulin secretion or on GAD-65 expression. 4) In combination, IL-1 beta plus TNF alpha and IFN gamma showed a similar inhibitory effect on GAD-65 expression as IL-1 beta alone. |
| 19053 | 8781713 | We found that: 1) IL-1 beta at low dose (1 U/ml) which stimulated insulin secretion, had no effect on GAD-65 expression, whereas higher doses of IL-1 beta (10, 100, 1000 U/ml) which inhibited insulin secretion, decreased GAD-65 expression. 2) TNF alpha at doses of 10, 100, 1000 U/ml which stimulated insulin secretion had no effect on GAD-65 expression. 3) IFN gamma at doses of 10, 100, 1000 U/ml had no effect on insulin secretion or on GAD-65 expression. 4) In combination, IL-1 beta plus TNF alpha and IFN gamma showed a similar inhibitory effect on GAD-65 expression as IL-1 beta alone. |
| 19054 | 8781713 | We found that: 1) IL-1 beta at low dose (1 U/ml) which stimulated insulin secretion, had no effect on GAD-65 expression, whereas higher doses of IL-1 beta (10, 100, 1000 U/ml) which inhibited insulin secretion, decreased GAD-65 expression. 2) TNF alpha at doses of 10, 100, 1000 U/ml which stimulated insulin secretion had no effect on GAD-65 expression. 3) IFN gamma at doses of 10, 100, 1000 U/ml had no effect on insulin secretion or on GAD-65 expression. 4) In combination, IL-1 beta plus TNF alpha and IFN gamma showed a similar inhibitory effect on GAD-65 expression as IL-1 beta alone. |
| 19055 | 8781713 | In summary: 1) IL-1 beta dramatically inhibits GAD-65 expression. 2) TNF alpha and IFN gamma have no effect on GAD-65 expression. |
| 19056 | 8781713 | In summary: 1) IL-1 beta dramatically inhibits GAD-65 expression. 2) TNF alpha and IFN gamma have no effect on GAD-65 expression. |
| 19057 | 8781713 | In summary: 1) IL-1 beta dramatically inhibits GAD-65 expression. 2) TNF alpha and IFN gamma have no effect on GAD-65 expression. |
| 19058 | 8781713 | Of these three cytokines, IL-1 beta is the primary cytokine affecting GAD-65 expression. |
| 19059 | 8781713 | Of these three cytokines, IL-1 beta is the primary cytokine affecting GAD-65 expression. |
| 19060 | 8781713 | Of these three cytokines, IL-1 beta is the primary cytokine affecting GAD-65 expression. |
| 19061 | 8700808 | The role of free radicals as well as cytokines (IL-1, tumor necrosis factor alpha, interferon gamma) and nitric oxide in the immune-mediated processes leading to the beta-cell destruction during IDDM is described. |
| 19062 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19063 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19064 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19065 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19066 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19067 | 7813805 | Accelerated beta-cell destruction in adoptively transferred autoimmune diabetes correlates with an increased expression of the genes coding for TNF-alpha and granzyme A in the intra-islet infiltrates. |
| 19068 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19069 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19070 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19071 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19072 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19073 | 7813805 | Autoimmune destruction of beta-cells in nonobese diabetic (NOD) mice is greatly accelerated by adoptive cotransfer of syngeneic CD4+ and CD8+ T-cells from diabetic animals into newborn NOD mice. |
| 19074 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19075 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19076 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19077 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19078 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19079 | 7813805 | We followed, by in situ hybridization, the appearance of mRNA of the tumor necrosis factor (TNF)-alpha gene and, as a marker for activated cytotoxic T-cells, of the serine protease granzyme A gene in the cellular infiltrates generated by cell transfer at birth. |
| 19080 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19081 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19082 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19083 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19084 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19085 | 7813805 | Cells expressing the genes for granzyme A or TNF-alpha were seen in considerable numbers already on day 14, after adoptive transfer. |
| 19086 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19087 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19088 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19089 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19090 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19091 | 7813805 | Compared with our previous findings in NOD mice developing spontaneous insulin-dependent diabetes mellitus (IDDM) (Held W, MacDonald HR, Weissman IL, Hess MW, Mueller C: Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 19092 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19093 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19094 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19095 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19096 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19097 | 7813805 | Proc Natl Acad Sci USA 87:2239-2243, 1990), frequencies of cells with TNF-alpha and granzyme A mRNA were 2- and 12-fold higher, respectively, in transferred IDDM (trIDDM). |
| 19098 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19099 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19100 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19101 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19102 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19103 | 7813805 | TNF-alpha mRNA positive cells were predominantly found in the CD4+ T-cell subset of the pancreas-infiltrating cells, whereas granzyme A mRNA positive cells were mainly observed in the CD4- T-cell subset. |
| 19104 | 7782051 | Low serum levels of tumor necrosis factor-alpha in insulin-dependent diabetic children. |
| 19105 | 7782051 | Low serum levels of tumor necrosis factor-alpha in insulin-dependent diabetic children. |
| 19106 | 7782051 | Low serum levels of tumor necrosis factor-alpha in insulin-dependent diabetic children. |
| 19107 | 7782051 | Low serum levels of tumor necrosis factor-alpha in insulin-dependent diabetic children. |
| 19108 | 7782051 | We measured serum levels of tumor necrosis factor-alpha (TNF-alpha) in 48 children with insulin-dependent diabetes mellitus (IDDM), divided into two groups according to disease duration (group I < 6 months and group II > 3 years): group I 15 patients, aged 2.2-13.7 years, and group II 33 patients, aged 4.5-25.5 years. |
| 19109 | 7782051 | We measured serum levels of tumor necrosis factor-alpha (TNF-alpha) in 48 children with insulin-dependent diabetes mellitus (IDDM), divided into two groups according to disease duration (group I < 6 months and group II > 3 years): group I 15 patients, aged 2.2-13.7 years, and group II 33 patients, aged 4.5-25.5 years. |
| 19110 | 7782051 | We measured serum levels of tumor necrosis factor-alpha (TNF-alpha) in 48 children with insulin-dependent diabetes mellitus (IDDM), divided into two groups according to disease duration (group I < 6 months and group II > 3 years): group I 15 patients, aged 2.2-13.7 years, and group II 33 patients, aged 4.5-25.5 years. |
| 19111 | 7782051 | We measured serum levels of tumor necrosis factor-alpha (TNF-alpha) in 48 children with insulin-dependent diabetes mellitus (IDDM), divided into two groups according to disease duration (group I < 6 months and group II > 3 years): group I 15 patients, aged 2.2-13.7 years, and group II 33 patients, aged 4.5-25.5 years. |
| 19112 | 7782051 | We found that TNF-alpha levels were lower in all IDDM patients (29.65 +/- 3.83 pg/ml) than in controls (74.74 +/- 10.17 pg/ml) (p < 0.0001), as well as in group I (24.07 +/- 3.65 pg/ml) and group II (32.16 +/- 5.29 pg/ml) as compared to controls (p < 0.001). |
| 19113 | 7782051 | We found that TNF-alpha levels were lower in all IDDM patients (29.65 +/- 3.83 pg/ml) than in controls (74.74 +/- 10.17 pg/ml) (p < 0.0001), as well as in group I (24.07 +/- 3.65 pg/ml) and group II (32.16 +/- 5.29 pg/ml) as compared to controls (p < 0.001). |
| 19114 | 7782051 | We found that TNF-alpha levels were lower in all IDDM patients (29.65 +/- 3.83 pg/ml) than in controls (74.74 +/- 10.17 pg/ml) (p < 0.0001), as well as in group I (24.07 +/- 3.65 pg/ml) and group II (32.16 +/- 5.29 pg/ml) as compared to controls (p < 0.001). |
| 19115 | 7782051 | We found that TNF-alpha levels were lower in all IDDM patients (29.65 +/- 3.83 pg/ml) than in controls (74.74 +/- 10.17 pg/ml) (p < 0.0001), as well as in group I (24.07 +/- 3.65 pg/ml) and group II (32.16 +/- 5.29 pg/ml) as compared to controls (p < 0.001). |
| 19116 | 7782051 | No correlation was found between serum TNF-alpha and chronologic age, duration of disease, metabolic control, insulin requirement and HLA typing. |
| 19117 | 7782051 | No correlation was found between serum TNF-alpha and chronologic age, duration of disease, metabolic control, insulin requirement and HLA typing. |
| 19118 | 7782051 | No correlation was found between serum TNF-alpha and chronologic age, duration of disease, metabolic control, insulin requirement and HLA typing. |
| 19119 | 7782051 | No correlation was found between serum TNF-alpha and chronologic age, duration of disease, metabolic control, insulin requirement and HLA typing. |
| 19120 | 7650434 | We have assessed, in parallel, a profile of the cytokines involved in vascular phenomenons including TNF alpha, IL-1 beta et IL-6. |
| 19121 | 7578879 | Effects of prolonged exposure in vitro to interferon-gamma and tumour necrosis factor-alpha on nitric oxide and insulin production of rat pancreatic islets. |
| 19122 | 7578879 | Effects of prolonged exposure in vitro to interferon-gamma and tumour necrosis factor-alpha on nitric oxide and insulin production of rat pancreatic islets. |
| 19123 | 7578879 | For this purpose 5-7 days precultured (medium RPMI 1640 +/- 10% fetal calf serum) rat pancreatic islets were exposed for another 48 h to either culture medium alone or with addition of rat interferon-gamma (IFN-gamma; 1000 U/ml), or human tumor necrosis factor-alpha (TNF-alpha; 1000 U/ml) or a combination of the cytokines. |
| 19124 | 7578879 | For this purpose 5-7 days precultured (medium RPMI 1640 +/- 10% fetal calf serum) rat pancreatic islets were exposed for another 48 h to either culture medium alone or with addition of rat interferon-gamma (IFN-gamma; 1000 U/ml), or human tumor necrosis factor-alpha (TNF-alpha; 1000 U/ml) or a combination of the cytokines. |
| 19125 | 7578879 | The combination IFN-gamma + TNF-alpha caused a 5-fold increase in the medium nitrite accumulation, indicating induction of nitric oxide formation. |
| 19126 | 7578879 | The combination IFN-gamma + TNF-alpha caused a 5-fold increase in the medium nitrite accumulation, indicating induction of nitric oxide formation. |
| 19127 | 7578879 | It was found that IFN-gamma reduced medium insulin accumulation and basal insulin secretion at 1.7 mM glucose, without affecting the medium nitrite level. |
| 19128 | 7578879 | It was found that IFN-gamma reduced medium insulin accumulation and basal insulin secretion at 1.7 mM glucose, without affecting the medium nitrite level. |
| 19129 | 9098456 | The segregation of these alleles has been associated with levels of TNF alpha or TNF beta production in systemic lupus erythematosis (SLE), insulin-dependent diabetes mellitus (IDDM) and in healthy control individuals. |
| 19130 | 7853768 | Although the correlation between IIP and NIDDM is unclear, we noted recent reports that advanced glycation and products can stimulate macrophages to secrete tumor necrosis factor and interleukin-1 in vitro, and can stimulate free radical generation by early glycation products in vitro. |
| 19131 | 7756973 | Glucose-induced insulin secretion is inhibited by the cytokines interleukin-1 beta (IL-1 beta), interleukin-6 and tumour necrosis factor alpha (TNF) when combined with IL-1 beta in cultured rat islets, by IL-1 beta, TNF and interferon gamma in mouse islets, and by combined treatment of IL-1 beta, TNF and interferon gamma in human islets. |
| 19132 | 7756973 | Glucose-induced insulin secretion is inhibited by the cytokines interleukin-1 beta (IL-1 beta), interleukin-6 and tumour necrosis factor alpha (TNF) when combined with IL-1 beta in cultured rat islets, by IL-1 beta, TNF and interferon gamma in mouse islets, and by combined treatment of IL-1 beta, TNF and interferon gamma in human islets. |
| 19133 | 7756973 | A key factor in the inhibitory effect of IL-1 beta and TNF in rat islets is the generation of nitric oxide which inactivates enzymes such as aconitase and ribonucleotide reductase by formation of iron-nitrosyl complexes. |
| 19134 | 7756973 | A key factor in the inhibitory effect of IL-1 beta and TNF in rat islets is the generation of nitric oxide which inactivates enzymes such as aconitase and ribonucleotide reductase by formation of iron-nitrosyl complexes. |
| 19135 | 7756973 | Potentially important defence and repair responses induced by IL-1 beta treatment of rat islets are formation of heat shock protein, haem oxygenase, and superoxide dismutase. |
| 19136 | 7756973 | Potentially important defence and repair responses induced by IL-1 beta treatment of rat islets are formation of heat shock protein, haem oxygenase, and superoxide dismutase. |
| 19137 | 7534733 | Studies on the molecular regulation of the inducible form of nitric oxide synthase (iNOS) in insulin-producing cells. |
| 19138 | 7534733 | Nitric oxide, a radical generated by the enzyme nitric oxide synthase (iNOS), may be an important mediator of beta-cell damage in early insulin-dependent diabetes mellitus. |
| 19139 | 7534733 | We have investigated the molecular regulation of iNOS in insulin-producing RINm5F cells. |
| 19140 | 7534733 | The data obtained suggest that iNOS is maximally induced in these cells by a 6-h exposure to IL-1 beta or TNF-alpha + IFN-gamma, but not by endotoxin. iNOS mRNA degradation is rapid and it is not affected by IL-1 beta. |
| 19141 | 7956951 | Troglitazone prevents the inhibitory effects of inflammatory cytokines on insulin-induced adipocyte differentiation in 3T3-L1 cells. |
| 19142 | 7956951 | Troglitazone prevents the inhibitory effects of inflammatory cytokines on insulin-induced adipocyte differentiation in 3T3-L1 cells. |
| 19143 | 7956951 | Troglitazone prevents the inhibitory effects of inflammatory cytokines on insulin-induced adipocyte differentiation in 3T3-L1 cells. |
| 19144 | 7956951 | Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. |
| 19145 | 7956951 | Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. |
| 19146 | 7956951 | Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. |
| 19147 | 7956951 | TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. |
| 19148 | 7956951 | TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. |
| 19149 | 7956951 | TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. |
| 19150 | 7956951 | Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. |
| 19151 | 7956951 | Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. |
| 19152 | 7956951 | Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. |
| 19153 | 7956951 | Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. |
| 19154 | 7956951 | Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. |
| 19155 | 7956951 | Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. |
| 19156 | 7926300 | Recent data have suggested a key role for tumor necrosis factor (TNF)-alpha in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus (NIDDM). |
| 19157 | 7926300 | Recent data have suggested a key role for tumor necrosis factor (TNF)-alpha in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus (NIDDM). |
| 19158 | 7926300 | Recent data have suggested a key role for tumor necrosis factor (TNF)-alpha in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus (NIDDM). |
| 19159 | 7926300 | Recent data have suggested a key role for tumor necrosis factor (TNF)-alpha in the insulin resistance of obesity and non-insulin-dependent diabetes mellitus (NIDDM). |
| 19160 | 7926300 | Neutralization of TNF-alpha in one of these models improves insulin sensitivity by increasing the activity of the insulin receptor tyrosine kinase, specifically in muscle and fat tissues. |
| 19161 | 7926300 | Neutralization of TNF-alpha in one of these models improves insulin sensitivity by increasing the activity of the insulin receptor tyrosine kinase, specifically in muscle and fat tissues. |
| 19162 | 7926300 | Neutralization of TNF-alpha in one of these models improves insulin sensitivity by increasing the activity of the insulin receptor tyrosine kinase, specifically in muscle and fat tissues. |
| 19163 | 7926300 | Neutralization of TNF-alpha in one of these models improves insulin sensitivity by increasing the activity of the insulin receptor tyrosine kinase, specifically in muscle and fat tissues. |
| 19164 | 7926300 | On a cellular level, TNF-alpha is a potent inhibitor of the insulin-stimulated tyrosine phosphorylations on the beta-chain of the insulin receptor and insulin receptor substrate-1, suggesting a defect at or near the tyrosine kinase activity of the insulin receptor. |
| 19165 | 7926300 | On a cellular level, TNF-alpha is a potent inhibitor of the insulin-stimulated tyrosine phosphorylations on the beta-chain of the insulin receptor and insulin receptor substrate-1, suggesting a defect at or near the tyrosine kinase activity of the insulin receptor. |
| 19166 | 7926300 | On a cellular level, TNF-alpha is a potent inhibitor of the insulin-stimulated tyrosine phosphorylations on the beta-chain of the insulin receptor and insulin receptor substrate-1, suggesting a defect at or near the tyrosine kinase activity of the insulin receptor. |
| 19167 | 7926300 | On a cellular level, TNF-alpha is a potent inhibitor of the insulin-stimulated tyrosine phosphorylations on the beta-chain of the insulin receptor and insulin receptor substrate-1, suggesting a defect at or near the tyrosine kinase activity of the insulin receptor. |
| 19168 | 7926300 | Given the clear link between obesity, insulin resistance, and diabetes, these results strongly suggest that TNF-alpha may play a crucial role in the systemic insulin resistance of NIDDM. |
| 19169 | 7926300 | Given the clear link between obesity, insulin resistance, and diabetes, these results strongly suggest that TNF-alpha may play a crucial role in the systemic insulin resistance of NIDDM. |
| 19170 | 7926300 | Given the clear link between obesity, insulin resistance, and diabetes, these results strongly suggest that TNF-alpha may play a crucial role in the systemic insulin resistance of NIDDM. |
| 19171 | 7926300 | Given the clear link between obesity, insulin resistance, and diabetes, these results strongly suggest that TNF-alpha may play a crucial role in the systemic insulin resistance of NIDDM. |
| 19172 | 7926295 | Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) have been implicated as immune effector molecules in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19173 | 7926295 | Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) have been implicated as immune effector molecules in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19174 | 7926295 | Recently, an increased frequency of the A1/A1 genotype of an IL-1 receptor antagonist (IL-1Ra) gene polymorphism was observed in patients with IDDM. |
| 19175 | 7926295 | Recently, an increased frequency of the A1/A1 genotype of an IL-1 receptor antagonist (IL-1Ra) gene polymorphism was observed in patients with IDDM. |
| 19176 | 7926295 | Therefore, we investigated plasma IL-1Ra and soluble TNF p55 receptor (TNFsRp55) levels in 18 men with recent-onset IDDM, 10 men with long-standing IDDM, and 35 age-matched healthy men. |
| 19177 | 7926295 | Therefore, we investigated plasma IL-1Ra and soluble TNF p55 receptor (TNFsRp55) levels in 18 men with recent-onset IDDM, 10 men with long-standing IDDM, and 35 age-matched healthy men. |
| 19178 | 7926295 | However, when the plasma IL-1Ra levels in the subjects with IDDM and the control subjects were analyzed according to IL-1Ra genotypes, we found a 30% lower level of plasma IL-1Ra in subjects with IDDM carrying the A1/A1 genotype compared with the levels in those carrying the A1/A2 genotype (372 +/- 40 vs. 530 +/- 54 ng/l, respectively, P = 0.025). |
| 19179 | 7926295 | However, when the plasma IL-1Ra levels in the subjects with IDDM and the control subjects were analyzed according to IL-1Ra genotypes, we found a 30% lower level of plasma IL-1Ra in subjects with IDDM carrying the A1/A1 genotype compared with the levels in those carrying the A1/A2 genotype (372 +/- 40 vs. 530 +/- 54 ng/l, respectively, P = 0.025). |
| 19180 | 7523453 | We have previously demonstrated that tumor necrosis factor-alpha produced by adipose tissue is a key mediator of insulin resistance in animal models of obesity-diabetes. |
| 19181 | 7523453 | We have previously demonstrated that tumor necrosis factor-alpha produced by adipose tissue is a key mediator of insulin resistance in animal models of obesity-diabetes. |
| 19182 | 7523453 | We have previously demonstrated that tumor necrosis factor-alpha produced by adipose tissue is a key mediator of insulin resistance in animal models of obesity-diabetes. |
| 19183 | 7523453 | We have previously demonstrated that tumor necrosis factor-alpha produced by adipose tissue is a key mediator of insulin resistance in animal models of obesity-diabetes. |
| 19184 | 7523453 | However, the mechanism by which TNF-alpha interferes with insulin action is not known. |
| 19185 | 7523453 | However, the mechanism by which TNF-alpha interferes with insulin action is not known. |
| 19186 | 7523453 | However, the mechanism by which TNF-alpha interferes with insulin action is not known. |
| 19187 | 7523453 | However, the mechanism by which TNF-alpha interferes with insulin action is not known. |
| 19188 | 7523453 | Since a defective insulin receptor (IR) tyrosine kinase activity has been observed in obesity and NIDDM, we measured the IR tyrosine kinase activity in the Zucker (fa/fa) rat model of obesity and insulin resistance after neutralizing TNF-alpha with a soluble TNF receptor (TNFR)-lgG fusion protein. |
| 19189 | 7523453 | Since a defective insulin receptor (IR) tyrosine kinase activity has been observed in obesity and NIDDM, we measured the IR tyrosine kinase activity in the Zucker (fa/fa) rat model of obesity and insulin resistance after neutralizing TNF-alpha with a soluble TNF receptor (TNFR)-lgG fusion protein. |
| 19190 | 7523453 | Since a defective insulin receptor (IR) tyrosine kinase activity has been observed in obesity and NIDDM, we measured the IR tyrosine kinase activity in the Zucker (fa/fa) rat model of obesity and insulin resistance after neutralizing TNF-alpha with a soluble TNF receptor (TNFR)-lgG fusion protein. |
| 19191 | 7523453 | Since a defective insulin receptor (IR) tyrosine kinase activity has been observed in obesity and NIDDM, we measured the IR tyrosine kinase activity in the Zucker (fa/fa) rat model of obesity and insulin resistance after neutralizing TNF-alpha with a soluble TNF receptor (TNFR)-lgG fusion protein. |
| 19192 | 7523453 | This neutralization resulted in a marked increase in insulin-stimulated autophosphorylation of the IR, as well as phosphorylation of insulin receptor substrate 1 (IRS-1) in muscle and fat tissues of the fa/fa rats, restoring them to near control (lean) levels. |
| 19193 | 7523453 | This neutralization resulted in a marked increase in insulin-stimulated autophosphorylation of the IR, as well as phosphorylation of insulin receptor substrate 1 (IRS-1) in muscle and fat tissues of the fa/fa rats, restoring them to near control (lean) levels. |
| 19194 | 7523453 | This neutralization resulted in a marked increase in insulin-stimulated autophosphorylation of the IR, as well as phosphorylation of insulin receptor substrate 1 (IRS-1) in muscle and fat tissues of the fa/fa rats, restoring them to near control (lean) levels. |
| 19195 | 7523453 | This neutralization resulted in a marked increase in insulin-stimulated autophosphorylation of the IR, as well as phosphorylation of insulin receptor substrate 1 (IRS-1) in muscle and fat tissues of the fa/fa rats, restoring them to near control (lean) levels. |
| 19196 | 7523453 | In contrast, no significant changes were observed in insulin-stimulated tyrosine phosphorylations of IR and IRS-1 in liver. |
| 19197 | 7523453 | In contrast, no significant changes were observed in insulin-stimulated tyrosine phosphorylations of IR and IRS-1 in liver. |
| 19198 | 7523453 | In contrast, no significant changes were observed in insulin-stimulated tyrosine phosphorylations of IR and IRS-1 in liver. |
| 19199 | 7523453 | In contrast, no significant changes were observed in insulin-stimulated tyrosine phosphorylations of IR and IRS-1 in liver. |
| 19200 | 7523453 | These results demonstrate that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat. |
| 19201 | 7523453 | These results demonstrate that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat. |
| 19202 | 7523453 | These results demonstrate that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat. |
| 19203 | 7523453 | These results demonstrate that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat. |
| 19204 | 8064245 | Effect of tumor necrosis factor alpha on insulin-dependent diabetes mellitus in NOD mice. |
| 19205 | 8064245 | Effect of tumor necrosis factor alpha on insulin-dependent diabetes mellitus in NOD mice. |
| 19206 | 8064245 | To assess the potential role of this cytokine in the early development of autoimmunity, we investigated the effect of TNF on the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice, a spontaneous murine model for autoimmune, insulin-dependent type I diabetes. |
| 19207 | 8064245 | To assess the potential role of this cytokine in the early development of autoimmunity, we investigated the effect of TNF on the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice, a spontaneous murine model for autoimmune, insulin-dependent type I diabetes. |
| 19208 | 8015071 | Bladder wash fluid interleukin-6 and tumor necrosis factor were not detectable. |
| 19209 | 7895326 | Role of TNF-alpha in the development of autoimmunity and the pathogenesis of insulin-dependent diabetes mellitus in NOD mice. |
| 19210 | 7523746 | We reviewed the recent studies on the relation between IFN and diseases concerning; 1) the IFN-alpha and -gamma producing capacity in patients with cancers, liver cirrhosis, diabetes mellitus and rheumatoid arthritis, 2) endogenous IFN in sera and exudates or extracts of local lesions obtained from patients with immunological diseases such as SLE, sarcoidosis, rheumatoid arthritis, Behçet's disease, and psoriasis, 3) deletion of IFN-alpha and -beta genes in human lymphoblastoid cells lines and leukemia, and 4) the expression of IFN and other cytokine (interleukins and TNF) mRNA in normal organs under physiological conditions. |
| 19211 | 7958397 | Nuclear response of pancreatic islets to interleukin-1 beta. |
| 19212 | 7958397 | The mechanisms by which interleukin-1 (IL-1) exerts destructive action on the pancreatic islet beta-cells remain elusive. |
| 19213 | 7958397 | Under these conditions, the presence of IFN-alpha (24 U/ml) and TNF (120 U/ml) was necessary to induce a response to rIL-1 beta. |
| 19214 | 7958397 | The nuclear effects of IL-1 beta were modified by nicotinamide (10 mM), an inhibitor of poly(ADP-ribose) synthetase. |
| 19215 | 7958397 | It is thus conceivable that an increase in poly(ADP-ribose) synthetase activity together with DNA break is implicated in the beta cytotoxic effect of interleukin-1 beta. |
| 19216 | 7948748 | TNF-alpha and IFN-gamma potentiate the deleterious effects of IL-1 beta on mouse pancreatic islets mainly via generation of nitric oxide. |
| 19217 | 7948748 | TNF-alpha and IFN-gamma potentiate the deleterious effects of IL-1 beta on mouse pancreatic islets mainly via generation of nitric oxide. |
| 19218 | 7948748 | TNF-alpha and IFN-gamma potentiate the deleterious effects of IL-1 beta on mouse pancreatic islets mainly via generation of nitric oxide. |
| 19219 | 7948748 | TNF-alpha and IFN-gamma potentiate the deleterious effects of IL-1 beta on mouse pancreatic islets mainly via generation of nitric oxide. |
| 19220 | 7948748 | TNF-alpha and IFN-gamma potentiate the deleterious effects of IL-1 beta on mouse pancreatic islets mainly via generation of nitric oxide. |
| 19221 | 7948748 | In order to further characterize the mechanism(s) of action of cytokines on insulin-producing cells, mouse pancreatic islets were exposed for 48 h to IL-1 beta, IFN-gamma or TNF-alpha, alone or in combinations. |
| 19222 | 7948748 | In order to further characterize the mechanism(s) of action of cytokines on insulin-producing cells, mouse pancreatic islets were exposed for 48 h to IL-1 beta, IFN-gamma or TNF-alpha, alone or in combinations. |
| 19223 | 7948748 | In order to further characterize the mechanism(s) of action of cytokines on insulin-producing cells, mouse pancreatic islets were exposed for 48 h to IL-1 beta, IFN-gamma or TNF-alpha, alone or in combinations. |
| 19224 | 7948748 | In order to further characterize the mechanism(s) of action of cytokines on insulin-producing cells, mouse pancreatic islets were exposed for 48 h to IL-1 beta, IFN-gamma or TNF-alpha, alone or in combinations. |
| 19225 | 7948748 | In order to further characterize the mechanism(s) of action of cytokines on insulin-producing cells, mouse pancreatic islets were exposed for 48 h to IL-1 beta, IFN-gamma or TNF-alpha, alone or in combinations. |
| 19226 | 7948748 | In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. |
| 19227 | 7948748 | In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. |
| 19228 | 7948748 | In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. |
| 19229 | 7948748 | In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. |
| 19230 | 7948748 | In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. |
| 19231 | 7948748 | Both IL-1 beta and TNF-alpha, but not IFN-gamma, induced NO production and expression of the mRNA encoding for the inducible form of the enzyme NO synthase (iNOS). |
| 19232 | 7948748 | Both IL-1 beta and TNF-alpha, but not IFN-gamma, induced NO production and expression of the mRNA encoding for the inducible form of the enzyme NO synthase (iNOS). |
| 19233 | 7948748 | Both IL-1 beta and TNF-alpha, but not IFN-gamma, induced NO production and expression of the mRNA encoding for the inducible form of the enzyme NO synthase (iNOS). |
| 19234 | 7948748 | Both IL-1 beta and TNF-alpha, but not IFN-gamma, induced NO production and expression of the mRNA encoding for the inducible form of the enzyme NO synthase (iNOS). |
| 19235 | 7948748 | Both IL-1 beta and TNF-alpha, but not IFN-gamma, induced NO production and expression of the mRNA encoding for the inducible form of the enzyme NO synthase (iNOS). |
| 19236 | 7948748 | These effects were most pronounced when combinations of IL-1 beta+IFN-gamma or IL-1 beta+IFN-gamma+TNF-alpha were used. |
| 19237 | 7948748 | These effects were most pronounced when combinations of IL-1 beta+IFN-gamma or IL-1 beta+IFN-gamma+TNF-alpha were used. |
| 19238 | 7948748 | These effects were most pronounced when combinations of IL-1 beta+IFN-gamma or IL-1 beta+IFN-gamma+TNF-alpha were used. |
| 19239 | 7948748 | These effects were most pronounced when combinations of IL-1 beta+IFN-gamma or IL-1 beta+IFN-gamma+TNF-alpha were used. |
| 19240 | 7948748 | These effects were most pronounced when combinations of IL-1 beta+IFN-gamma or IL-1 beta+IFN-gamma+TNF-alpha were used. |
| 19241 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19242 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19243 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19244 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19245 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19246 | 8197147 | Tumor necrosis factor alpha inhibits signaling from the insulin receptor. |
| 19247 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19248 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19249 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19250 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19251 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19252 | 8197147 | We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. |
| 19253 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19254 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19255 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19256 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19257 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19258 | 8197147 | Here, we investigate how TNF-alpha interferes with insulin action. |
| 19259 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19260 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19261 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19262 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19263 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19264 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 19265 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19266 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19267 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19268 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19269 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19270 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 19271 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19272 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19273 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19274 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19275 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19276 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 19277 | 8177321 | The mitogen-activated protein (MAP) kinases Erk-1 and Erk-2 are proline-directed kinases that are themselves activated through concomitant phosphorylation of tyrosine and threonine residues. |
| 19278 | 8177321 | The mitogen-activated protein (MAP) kinases Erk-1 and Erk-2 are proline-directed kinases that are themselves activated through concomitant phosphorylation of tyrosine and threonine residues. |
| 19279 | 8177321 | The mitogen-activated protein (MAP) kinases Erk-1 and Erk-2 are proline-directed kinases that are themselves activated through concomitant phosphorylation of tyrosine and threonine residues. |
| 19280 | 8177321 | The kinase p54 (M(r) 54,000), which was first isolated from cycloheximide-treated rats, is proline-directed like Erks-1/2, and requires both Tyr and Ser/Thr phosphorylation for activity. p54 is, however, distinct from Erks-1/2 in its substrate specificity, being unable to phosphorylate pp90rsk but more active in phosphorylating the c-Jun transactivation domain. |
| 19281 | 8177321 | The kinase p54 (M(r) 54,000), which was first isolated from cycloheximide-treated rats, is proline-directed like Erks-1/2, and requires both Tyr and Ser/Thr phosphorylation for activity. p54 is, however, distinct from Erks-1/2 in its substrate specificity, being unable to phosphorylate pp90rsk but more active in phosphorylating the c-Jun transactivation domain. |
| 19282 | 8177321 | The kinase p54 (M(r) 54,000), which was first isolated from cycloheximide-treated rats, is proline-directed like Erks-1/2, and requires both Tyr and Ser/Thr phosphorylation for activity. p54 is, however, distinct from Erks-1/2 in its substrate specificity, being unable to phosphorylate pp90rsk but more active in phosphorylating the c-Jun transactivation domain. |
| 19283 | 8177321 | However, p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-alpha, hence they are designated stress-activated protein kinases, or SAPKs. |
| 19284 | 8177321 | However, p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-alpha, hence they are designated stress-activated protein kinases, or SAPKs. |
| 19285 | 8177321 | However, p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-alpha, hence they are designated stress-activated protein kinases, or SAPKs. |
| 19286 | 8177321 | SAPKs are also activated by sphingomyelinase, which elicits a subset of cellular responses to TNF-alpha (ref. 9). |
| 19287 | 8177321 | SAPKs are also activated by sphingomyelinase, which elicits a subset of cellular responses to TNF-alpha (ref. 9). |
| 19288 | 8177321 | SAPKs are also activated by sphingomyelinase, which elicits a subset of cellular responses to TNF-alpha (ref. 9). |
| 19289 | 8177321 | SAPKs therefore define a new TNF-alpha and stress-activated signalling pathway, possibly initiated by sphingomyelin-based second messengers, which regulates the activity of c-Jun. |
| 19290 | 8177321 | SAPKs therefore define a new TNF-alpha and stress-activated signalling pathway, possibly initiated by sphingomyelin-based second messengers, which regulates the activity of c-Jun. |
| 19291 | 8177321 | SAPKs therefore define a new TNF-alpha and stress-activated signalling pathway, possibly initiated by sphingomyelin-based second messengers, which regulates the activity of c-Jun. |
| 19292 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 19293 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 19294 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 19295 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 19296 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 19297 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 19298 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 19299 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 19300 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 19301 | 8056188 | Insulin-dependent diabetes mellitus (IDDM) is associated with class II molecules of the MHC on chromosome 6, in particular HLA-DR and -DQ alleles, but a pathogenic role for TNF-alpha in the class III region of the MHC has also been implied. |
| 19302 | 8056188 | Insulin-dependent diabetes mellitus (IDDM) is associated with class II molecules of the MHC on chromosome 6, in particular HLA-DR and -DQ alleles, but a pathogenic role for TNF-alpha in the class III region of the MHC has also been implied. |
| 19303 | 8056188 | Insulin-dependent diabetes mellitus (IDDM) is associated with class II molecules of the MHC on chromosome 6, in particular HLA-DR and -DQ alleles, but a pathogenic role for TNF-alpha in the class III region of the MHC has also been implied. |
| 19304 | 8056188 | We therefore tested whether there was any independent association between a biallelic TNF polymorphism and IDDM. |
| 19305 | 8056188 | We therefore tested whether there was any independent association between a biallelic TNF polymorphism and IDDM. |
| 19306 | 8056188 | We therefore tested whether there was any independent association between a biallelic TNF polymorphism and IDDM. |
| 19307 | 8056188 | The TNF2 allele was present in 61 of 114 (54%) IDDM patients compared to 101 of 253 (40%) control subjects (odds ratio 1.73; p < 0.02). |
| 19308 | 8056188 | The TNF2 allele was present in 61 of 114 (54%) IDDM patients compared to 101 of 253 (40%) control subjects (odds ratio 1.73; p < 0.02). |
| 19309 | 8056188 | The TNF2 allele was present in 61 of 114 (54%) IDDM patients compared to 101 of 253 (40%) control subjects (odds ratio 1.73; p < 0.02). |
| 19310 | 8022753 | Interleukin-1, tumor necrosis factor, and interleukin-6 inhibit insulin release and may be cytotoxic to isolated pancreatic islets. |
| 19311 | 8022753 | The present study was designed to investigate the effect of the above cytokines on insulin, glucagon, somatostatin, and thyrotropin-releasing hormone secretion by isolated human islets. |
| 19312 | 8022753 | All three cytokines studied, although not modifying insulin and somatostatin release to glucose 5 mmol/L, inhibited the response of both hormones to glucose 20 mmol/L. |
| 19313 | 7514190 | Islets from 30 human pancreata were exposed for 6-144 h to the following human recombinant cytokines, alone or in combination: IFN-gamma (1,000 U/ml), TNF-alpha (1,000 U/ml), IL-6 (25 U/ml), and IL-1 beta (50 U/ml). |
| 19314 | 7514190 | Islets from 30 human pancreata were exposed for 6-144 h to the following human recombinant cytokines, alone or in combination: IFN-gamma (1,000 U/ml), TNF-alpha (1,000 U/ml), IL-6 (25 U/ml), and IL-1 beta (50 U/ml). |
| 19315 | 7514190 | Islets from 30 human pancreata were exposed for 6-144 h to the following human recombinant cytokines, alone or in combination: IFN-gamma (1,000 U/ml), TNF-alpha (1,000 U/ml), IL-6 (25 U/ml), and IL-1 beta (50 U/ml). |
| 19316 | 7514190 | Islets from 30 human pancreata were exposed for 6-144 h to the following human recombinant cytokines, alone or in combination: IFN-gamma (1,000 U/ml), TNF-alpha (1,000 U/ml), IL-6 (25 U/ml), and IL-1 beta (50 U/ml). |
| 19317 | 7514190 | After 48 h, none of the cytokines alone increased islet nitrite production, but IFN-gamma induced a 20% decrease in glucose-induced insulin release. |
| 19318 | 7514190 | After 48 h, none of the cytokines alone increased islet nitrite production, but IFN-gamma induced a 20% decrease in glucose-induced insulin release. |
| 19319 | 7514190 | After 48 h, none of the cytokines alone increased islet nitrite production, but IFN-gamma induced a 20% decrease in glucose-induced insulin release. |
| 19320 | 7514190 | After 48 h, none of the cytokines alone increased islet nitrite production, but IFN-gamma induced a 20% decrease in glucose-induced insulin release. |
| 19321 | 7514190 | Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. |
| 19322 | 7514190 | Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. |
| 19323 | 7514190 | Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. |
| 19324 | 7514190 | Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. |
| 19325 | 7514190 | An exposure of 144 h to IL-1 beta plus IFN-gamma plus TNF-alpha increased NO production and decreased both glucose-induced insulin release and insulin content. |
| 19326 | 7514190 | An exposure of 144 h to IL-1 beta plus IFN-gamma plus TNF-alpha increased NO production and decreased both glucose-induced insulin release and insulin content. |
| 19327 | 7514190 | An exposure of 144 h to IL-1 beta plus IFN-gamma plus TNF-alpha increased NO production and decreased both glucose-induced insulin release and insulin content. |
| 19328 | 7514190 | An exposure of 144 h to IL-1 beta plus IFN-gamma plus TNF-alpha increased NO production and decreased both glucose-induced insulin release and insulin content. |
| 19329 | 7514190 | Inhibitors of NO generation, aminoguanidine or NG-nitro-L-arginine, blocked this cytokine-induced NO generation, but did not prevent the suppressive effect of IL-1 beta plus IFN-gamma plus TNF-alpha on insulin release and content. |
| 19330 | 7514190 | Inhibitors of NO generation, aminoguanidine or NG-nitro-L-arginine, blocked this cytokine-induced NO generation, but did not prevent the suppressive effect of IL-1 beta plus IFN-gamma plus TNF-alpha on insulin release and content. |
| 19331 | 7514190 | Inhibitors of NO generation, aminoguanidine or NG-nitro-L-arginine, blocked this cytokine-induced NO generation, but did not prevent the suppressive effect of IL-1 beta plus IFN-gamma plus TNF-alpha on insulin release and content. |
| 19332 | 7514190 | Inhibitors of NO generation, aminoguanidine or NG-nitro-L-arginine, blocked this cytokine-induced NO generation, but did not prevent the suppressive effect of IL-1 beta plus IFN-gamma plus TNF-alpha on insulin release and content. |
| 19333 | 8178347 | We have shown that, although tolerant in vivo, animals bearing long-term cultured islet allografts are donor-reactive in vitro as assessed by (1) CTL precursor frequency, (2) antidonor proliferative and cytotoxic responses, and (3) lymphokine production (IL-2, IL-3, TNF, and IFN-gamma). |
| 19334 | 8314014 | Insulin, carboxypeptidase-H (CP-H), and glutamate decarboxylase (GAD) have been identified as potential autoantigens in insulin-dependent diabetes mellitus (IDDM). |
| 19335 | 8314014 | In contrast, islet cells failed to reveal cell-surface staining for GAD65, another putative autoantigen in IDDM, under either basal or insulin stimulatory conditions or following exposure of islet cells to the cytokines interleukin-1 beta, tumor necrosis factor-alpha, and recombinant human interferon-gamma. |
| 19336 | 8119136 | The cytokine combination of interleukin-1 beta (IL-1 beta; 10 U/ml), tumor necrosis factor-alpha (10(3) U/ml), and interferon-gamma (10(3) U/ml) induced DNA fragmentation (first detected at 6 h), mitochondrial damage (by 12 h), and death (by 24 h) of RIN cells, whereas the individual cytokines did not have these destructive effects. |
| 19337 | 8119136 | The cytokine combination of interleukin-1 beta (IL-1 beta; 10 U/ml), tumor necrosis factor-alpha (10(3) U/ml), and interferon-gamma (10(3) U/ml) induced DNA fragmentation (first detected at 6 h), mitochondrial damage (by 12 h), and death (by 24 h) of RIN cells, whereas the individual cytokines did not have these destructive effects. |
| 19338 | 8119136 | Also, the cytokine combination of IL-1 beta, tumor necrosis factor-alpha, and interferon-gamma induced a 10-fold increase in NO production by RIN cells, and L-NG-monomethyl arginine, an inhibitor of NO synthase, produced a dose-dependent inhibition of cytokine-induced NO production, DNA fragmentation, and cell destruction. |
| 19339 | 8119136 | Also, the cytokine combination of IL-1 beta, tumor necrosis factor-alpha, and interferon-gamma induced a 10-fold increase in NO production by RIN cells, and L-NG-monomethyl arginine, an inhibitor of NO synthase, produced a dose-dependent inhibition of cytokine-induced NO production, DNA fragmentation, and cell destruction. |
| 19340 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19341 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19342 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19343 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19344 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19345 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19346 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19347 | 8130898 | Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. |
| 19348 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19349 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19350 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19351 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19352 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19353 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19354 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19355 | 8130898 | The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. |
| 19356 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19357 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19358 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19359 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19360 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19361 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19362 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19363 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 19364 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19365 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19366 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19367 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19368 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19369 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19370 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19371 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 19372 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19373 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19374 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19375 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19376 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19377 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19378 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19379 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 19380 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19381 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19382 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19383 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19384 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19385 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19386 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19387 | 8130898 | After 2 days of culture, increasing doses of IL-1-25, 50, 75 and 100 ng/l--caused progressively increased cytotoxicity and impaired insulin release. |
| 19388 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19389 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19390 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19391 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19392 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19393 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19394 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19395 | 8130898 | In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. |
| 19396 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19397 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19398 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19399 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19400 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19401 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19402 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19403 | 8130898 | Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 micrograms/l also was slightly cytotoxic but increased insulin release. |
| 19404 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19405 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19406 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19407 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19408 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19409 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19410 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19411 | 8130898 | The augmented insulin release declined progressively with increasing TNF dose. |
| 19412 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19413 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19414 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19415 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19416 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19417 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19418 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19419 | 8130898 | However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 micrograms/l) suppressed insulin release. |
| 19420 | 7516851 | The percentage of CD57+ cells was similar in IDDM patients and controls, while the percentage of CD16+ cells was lower in IDDM patients (P < 0.05) than in controls. |
| 19421 | 7516851 | The decreased NK cytotoxic activity observed in our patients, in particular in long-standing diabetics, with normal NK cell number, could be due to a qualitative defect of the NK cells, or to a deficient IL-2 and/or TNF-alpha production, or to a immunomodulatory or immunosuppressing effect of insulin. |
| 19422 | 8276864 | Arachidonic acid down-regulates the insulin-dependent glucose transporter gene (GLUT4) in 3T3-L1 adipocytes by inhibiting transcription and enhancing mRNA turnover. |
| 19423 | 8276864 | Chronic exposure of fully differentiated 3T3-L1 adipocytes to 50 microM arachidonic acid (AA) resulted in an inhibition (approximately 91%) in cellular GLUT4 mRNA content after a 48-h exposure, without similarly affecting the mRNA content of the ubiquitous glucose transporter, GLUT1. |
| 19424 | 8276864 | Western blot analysis revealed that AA was specifically reducing the insulin-responsive glucose transporter (GLUT4) in both plasma and intracellular membranes. |
| 19425 | 8276864 | Subsequently, AA was observed to alter the ability of the GLUT4 transporter to respond to insulin and mediate a significant enhancement of glucose uptake. |
| 19426 | 8276864 | The results presented in this study indicate that AA can partially mimic the effects of both tumor necrosis factor-alpha and insulin which, when chronically supplied to 3T3-L1 adipocytes, also down-regulate GLUT4 gene expression. |
| 19427 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19428 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19429 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19430 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19431 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19432 | 8275942 | Altered gene expression for tumor necrosis factor-alpha and its receptors during drug and dietary modulation of insulin resistance. |
| 19433 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19434 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19435 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19436 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19437 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19438 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 19439 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19440 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19441 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19442 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19443 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19444 | 8275942 | Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. |
| 19445 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19446 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19447 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19448 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19449 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19450 | 8275942 | In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. |
| 19451 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19452 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19453 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19454 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19455 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19456 | 8275942 | We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. |
| 19457 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19458 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19459 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19460 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19461 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19462 | 8275942 | These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. |
| 19463 | 8167386 | Effect of cyclosporine A on serum tumor necrosis factor alpha in new-onset type I (insulin-dependent) diabetes mellitus. |
| 19464 | 8167386 | Effect of cyclosporine A on serum tumor necrosis factor alpha in new-onset type I (insulin-dependent) diabetes mellitus. |
| 19465 | 8167386 | Because the etiology of insulin-dependent diabetes mellitus (IDDM) is thought to be autoimmune, several clinical trials have utilized immunosuppression to treat newly diagnosed diabetic patients. |
| 19466 | 8167386 | Because the etiology of insulin-dependent diabetes mellitus (IDDM) is thought to be autoimmune, several clinical trials have utilized immunosuppression to treat newly diagnosed diabetic patients. |
| 19467 | 8167386 | At time 0, tumor necrosis factor alpha (TNF alpha) levels were similar in the CyA (40.1 +/- 14.2 pg/mL) and placebo group (38.5 +/- 12.1 pg/mL) of IDDM subjects (normal 32.0 +/- 5.0 pg/mL). |
| 19468 | 8167386 | At time 0, tumor necrosis factor alpha (TNF alpha) levels were similar in the CyA (40.1 +/- 14.2 pg/mL) and placebo group (38.5 +/- 12.1 pg/mL) of IDDM subjects (normal 32.0 +/- 5.0 pg/mL). |
| 19469 | 8167386 | Soluble interleukin 2 receptor (IL-2R) levels in IDDM patients were significantly higher than in normal subjects at diagnosis of IDDM. |
| 19470 | 8167386 | Soluble interleukin 2 receptor (IL-2R) levels in IDDM patients were significantly higher than in normal subjects at diagnosis of IDDM. |
| 19471 | 8162294 | In vitro inhibition of insulin release by blood mononuclear cells from insulin-dependent diabetic and healthy subjects: synergistic action of IL-1 and TNF. |
| 19472 | 8162294 | In vitro inhibition of insulin release by blood mononuclear cells from insulin-dependent diabetic and healthy subjects: synergistic action of IL-1 and TNF. |
| 19473 | 8162294 | In vitro inhibition of insulin release by blood mononuclear cells from insulin-dependent diabetic and healthy subjects: synergistic action of IL-1 and TNF. |
| 19474 | 8162294 | In vitro inhibition of insulin release by blood mononuclear cells from insulin-dependent diabetic and healthy subjects: synergistic action of IL-1 and TNF. |
| 19475 | 8162294 | In vitro inhibition of insulin release by blood mononuclear cells from insulin-dependent diabetic and healthy subjects: synergistic action of IL-1 and TNF. |
| 19476 | 8162294 | To study whether this inhibition was due to soluble mediators we added supernatants of LPS-stimulated BMC or recombinant human interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) at concentrations comparable to those found in the supernatants to rat islet cells. |
| 19477 | 8162294 | To study whether this inhibition was due to soluble mediators we added supernatants of LPS-stimulated BMC or recombinant human interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) at concentrations comparable to those found in the supernatants to rat islet cells. |
| 19478 | 8162294 | To study whether this inhibition was due to soluble mediators we added supernatants of LPS-stimulated BMC or recombinant human interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) at concentrations comparable to those found in the supernatants to rat islet cells. |
| 19479 | 8162294 | To study whether this inhibition was due to soluble mediators we added supernatants of LPS-stimulated BMC or recombinant human interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) at concentrations comparable to those found in the supernatants to rat islet cells. |
| 19480 | 8162294 | To study whether this inhibition was due to soluble mediators we added supernatants of LPS-stimulated BMC or recombinant human interleukin-1 beta (IL-1) and tumor necrosis factor-alpha (TNF) at concentrations comparable to those found in the supernatants to rat islet cells. |
| 19481 | 8162294 | We found that neither IL-1 nor TNF alone inhibit IR from dispersed adult rat islet cells. |
| 19482 | 8162294 | We found that neither IL-1 nor TNF alone inhibit IR from dispersed adult rat islet cells. |
| 19483 | 8162294 | We found that neither IL-1 nor TNF alone inhibit IR from dispersed adult rat islet cells. |
| 19484 | 8162294 | We found that neither IL-1 nor TNF alone inhibit IR from dispersed adult rat islet cells. |
| 19485 | 8162294 | We found that neither IL-1 nor TNF alone inhibit IR from dispersed adult rat islet cells. |
| 19486 | 8162294 | However, the combination of IL-1 and TNF was highly effective. |
| 19487 | 8162294 | However, the combination of IL-1 and TNF was highly effective. |
| 19488 | 8162294 | However, the combination of IL-1 and TNF was highly effective. |
| 19489 | 8162294 | However, the combination of IL-1 and TNF was highly effective. |
| 19490 | 8162294 | However, the combination of IL-1 and TNF was highly effective. |
| 19491 | 8162294 | Ultrafiltration of supernatants of LPS-stimulated BMC through a PM-10 membrane (10 kDa cutoff) deprived the supernatants of the inhibitory activity indicating that only intact IL-1 and TNF (m.w. about 17 kDa), but not smaller IL-1 and TNF fragments, were responsible for the effects on islet cells. |
| 19492 | 8162294 | Ultrafiltration of supernatants of LPS-stimulated BMC through a PM-10 membrane (10 kDa cutoff) deprived the supernatants of the inhibitory activity indicating that only intact IL-1 and TNF (m.w. about 17 kDa), but not smaller IL-1 and TNF fragments, were responsible for the effects on islet cells. |
| 19493 | 8162294 | Ultrafiltration of supernatants of LPS-stimulated BMC through a PM-10 membrane (10 kDa cutoff) deprived the supernatants of the inhibitory activity indicating that only intact IL-1 and TNF (m.w. about 17 kDa), but not smaller IL-1 and TNF fragments, were responsible for the effects on islet cells. |
| 19494 | 8162294 | Ultrafiltration of supernatants of LPS-stimulated BMC through a PM-10 membrane (10 kDa cutoff) deprived the supernatants of the inhibitory activity indicating that only intact IL-1 and TNF (m.w. about 17 kDa), but not smaller IL-1 and TNF fragments, were responsible for the effects on islet cells. |
| 19495 | 8162294 | Ultrafiltration of supernatants of LPS-stimulated BMC through a PM-10 membrane (10 kDa cutoff) deprived the supernatants of the inhibitory activity indicating that only intact IL-1 and TNF (m.w. about 17 kDa), but not smaller IL-1 and TNF fragments, were responsible for the effects on islet cells. |
| 19496 | 8056134 | Since monocyte-derived factors have been proposed to be involved in endothelial cell growth regulations we have measured the effect of monocyte-conditioned medium (MO-CM) on endothelial cell proliferation and the production of Tumor necrosis factor alpha and interleukin 1-beta, cytokines known to alter endothelial cell functions. |
| 19497 | 8056134 | Since monocyte-derived factors have been proposed to be involved in endothelial cell growth regulations we have measured the effect of monocyte-conditioned medium (MO-CM) on endothelial cell proliferation and the production of Tumor necrosis factor alpha and interleukin 1-beta, cytokines known to alter endothelial cell functions. |
| 19498 | 8056134 | The increase in interleukin 1-beta and in tumor necrosis factor alpha production after lipopolysaccharide stimulation were similar in the 2 groups. |
| 19499 | 8056134 | The increase in interleukin 1-beta and in tumor necrosis factor alpha production after lipopolysaccharide stimulation were similar in the 2 groups. |
| 19500 | 7927538 | We have used genomic analysis to characterize a region of the central major histocompatibility complex (MHC) spanning approximately 300 kilobases (kb) between TNF and HLA-B. |
| 19501 | 7927538 | A genomic probe, JAB, containing putative coding sequences (PERB11) located 60 kb centromeric of HLA-B, was used for northern analysis of human tissues. |
| 19502 | 7927538 | Southern analysis of genomic DNA and overlapping YAC clones, covering the region from BAT1 to HLA-F, indicated that there are at least five copies of PERB11, four of which are located within this region of the MHC. |
| 19503 | 7927538 | The putative amino acid sequence of PERB11 shares approximately 30% identity to MHC class I molecules from various species, including reptiles, chickens, and frogs, as well as to other MHC class I-like molecules, such as the IgG FcR of the mouse and rat and the human Zn-alpha 2-glycoprotein. |
| 19504 | 7927538 | From direct comparison of amino acid sequences, it is concluded that PERB11 is a distinct molecule more closely related to nonmammalian than known mammalian MHC class I molecules. |
| 19505 | 7927538 | Genomic sequence analysis of PERB11 from five MHC ancestral haplotypes (AH) indicated that the gene is polymorphic at both DNA and protein level. |
| 19506 | 7870341 | In the present cross-sectional study urinary excretion of IL-1 beta, TNF-alpha, IL-6, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. |
| 19507 | 7870341 | In the present cross-sectional study urinary excretion of IL-1 beta, TNF-alpha, IL-6, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. |
| 19508 | 7870341 | In the present cross-sectional study urinary excretion of IL-1 beta, TNF-alpha, IL-6, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. |
| 19509 | 7870341 | No significant correlation with corresponding serum values was observed for urinary IL-6 or TNF-alpha excretion. |
| 19510 | 7870341 | No significant correlation with corresponding serum values was observed for urinary IL-6 or TNF-alpha excretion. |
| 19511 | 7870341 | No significant correlation with corresponding serum values was observed for urinary IL-6 or TNF-alpha excretion. |
| 19512 | 7870341 | Urinary IL-1 beta and TNF-alpha correlated with decreased renal function. |
| 19513 | 7870341 | Urinary IL-1 beta and TNF-alpha correlated with decreased renal function. |
| 19514 | 7870341 | Urinary IL-1 beta and TNF-alpha correlated with decreased renal function. |
| 19515 | 7858101 | Tumour necrosis factor (TNF) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19516 | 7858101 | Tumour necrosis factor (TNF) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19517 | 7858101 | Tumour necrosis factor (TNF) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19518 | 7858101 | Tumour necrosis factor (TNF) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19519 | 7858101 | Tumour necrosis factor (TNF) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19520 | 7858101 | To investigate a possible role for TNF in IDDM we compared endogenous TNF production in two lines of non-obese diabetic (NOD) mice, NOD/Lt and NOD/WEHI, that have a high and low incidence of diabetes, respectively. |
| 19521 | 7858101 | To investigate a possible role for TNF in IDDM we compared endogenous TNF production in two lines of non-obese diabetic (NOD) mice, NOD/Lt and NOD/WEHI, that have a high and low incidence of diabetes, respectively. |
| 19522 | 7858101 | To investigate a possible role for TNF in IDDM we compared endogenous TNF production in two lines of non-obese diabetic (NOD) mice, NOD/Lt and NOD/WEHI, that have a high and low incidence of diabetes, respectively. |
| 19523 | 7858101 | To investigate a possible role for TNF in IDDM we compared endogenous TNF production in two lines of non-obese diabetic (NOD) mice, NOD/Lt and NOD/WEHI, that have a high and low incidence of diabetes, respectively. |
| 19524 | 7858101 | To investigate a possible role for TNF in IDDM we compared endogenous TNF production in two lines of non-obese diabetic (NOD) mice, NOD/Lt and NOD/WEHI, that have a high and low incidence of diabetes, respectively. |
| 19525 | 7858101 | Plasma TNF-alpha was measured in 8 week-old female non-diabetic mice primed with 1000 units IV of murine interferon gamma (IFN-gamma) followed after 3 hours by 5 micrograms IV of lipopolysaccharide (LPS). |
| 19526 | 7858101 | Plasma TNF-alpha was measured in 8 week-old female non-diabetic mice primed with 1000 units IV of murine interferon gamma (IFN-gamma) followed after 3 hours by 5 micrograms IV of lipopolysaccharide (LPS). |
| 19527 | 7858101 | Plasma TNF-alpha was measured in 8 week-old female non-diabetic mice primed with 1000 units IV of murine interferon gamma (IFN-gamma) followed after 3 hours by 5 micrograms IV of lipopolysaccharide (LPS). |
| 19528 | 7858101 | Plasma TNF-alpha was measured in 8 week-old female non-diabetic mice primed with 1000 units IV of murine interferon gamma (IFN-gamma) followed after 3 hours by 5 micrograms IV of lipopolysaccharide (LPS). |
| 19529 | 7858101 | Plasma TNF-alpha was measured in 8 week-old female non-diabetic mice primed with 1000 units IV of murine interferon gamma (IFN-gamma) followed after 3 hours by 5 micrograms IV of lipopolysaccharide (LPS). |
| 19530 | 7858101 | A separate group of female NOD/Lt mice had IFN-gamma/LPS-stimulated plasma TNF-alpha measured at 10 weeks and were followed to age 30 weeks. |
| 19531 | 7858101 | A separate group of female NOD/Lt mice had IFN-gamma/LPS-stimulated plasma TNF-alpha measured at 10 weeks and were followed to age 30 weeks. |
| 19532 | 7858101 | A separate group of female NOD/Lt mice had IFN-gamma/LPS-stimulated plasma TNF-alpha measured at 10 weeks and were followed to age 30 weeks. |
| 19533 | 7858101 | A separate group of female NOD/Lt mice had IFN-gamma/LPS-stimulated plasma TNF-alpha measured at 10 weeks and were followed to age 30 weeks. |
| 19534 | 7858101 | A separate group of female NOD/Lt mice had IFN-gamma/LPS-stimulated plasma TNF-alpha measured at 10 weeks and were followed to age 30 weeks. |
| 19535 | 7858101 | These results suggest that endogenous TNF-alpha production may be a trait marker of IDDM susceptibility. |
| 19536 | 7858101 | These results suggest that endogenous TNF-alpha production may be a trait marker of IDDM susceptibility. |
| 19537 | 7858101 | These results suggest that endogenous TNF-alpha production may be a trait marker of IDDM susceptibility. |
| 19538 | 7858101 | These results suggest that endogenous TNF-alpha production may be a trait marker of IDDM susceptibility. |
| 19539 | 7858101 | These results suggest that endogenous TNF-alpha production may be a trait marker of IDDM susceptibility. |
| 19540 | 7605871 | It has been recently reported that human pancreatic islets in tissue culture produce nitric oxide (NO) and show a decreased function when exposed for 6 days to combinations of cytokines (interleukin-1 beta (IL-1 beta) + tumor necrosis factor-alpha (TNF-alpha) + interferon-gamma (IFN-gamma). |
| 19541 | 7605871 | It has been recently reported that human pancreatic islets in tissue culture produce nitric oxide (NO) and show a decreased function when exposed for 6 days to combinations of cytokines (interleukin-1 beta (IL-1 beta) + tumor necrosis factor-alpha (TNF-alpha) + interferon-gamma (IFN-gamma). |
| 19542 | 7605871 | Here we study the effects of nicotinamide (Nic; 10 or 20 mmol/l) on these deleterious effects of cytokines (50 U/ml IL-1 beta + 1000 U/ml TNF-alpha + 1000 U/ml IFN-gamma). |
| 19543 | 7605871 | Here we study the effects of nicotinamide (Nic; 10 or 20 mmol/l) on these deleterious effects of cytokines (50 U/ml IL-1 beta + 1000 U/ml TNF-alpha + 1000 U/ml IFN-gamma). |
| 19544 | 7605869 | The markers included MHC class I, II and III loci, the manganese superoxide dismutase (MnSOD) locus (chr. 6q), interleukin-1 beta (IL1B), the IL-1 receptor antagonist (IL1RN), and the IL-1 type 1 receptor (IL1RI) loci (each chr. 2q). |
| 19545 | 7605869 | No significant differences between familial and sporadic cases were found within the MHC region (including the following loci: HLA-DQ, -DR, heat shock protein (HSP) 70, tumour necrosis factor (TNF), HLA-B and -A). |
| 19546 | 7605869 | For the IL1B RFLP a trend for difference was observed between familial cases and control subjects (p = 0.046), whereas no differences between sporadic cases and control subjects could be demonstrated neither at the IL1B nor at the IL1RN loci. |
| 19547 | 7528151 | Angiogenesis is due to factors locally produced (as FGF, TGF and u-PA produced by anoxic tissues), systemic (IGF-1) or released by inflammatory reaction (IL1, TNF alpha and beta). |
| 19548 | 7516691 | The cytokine interleukin-1 (IL-1) turned out to be the ultimate inducer, whereas tumour necrosis factor-alpha (TNF) and unexpectedly the phorbol ester TPA (12-O-tetradecanoylphorbol-13-acetate; 10 nM) synergistically promoted nitrite accumulation. |
| 19549 | 7516691 | The cytokine interleukin-1 (IL-1) turned out to be the ultimate inducer, whereas tumour necrosis factor-alpha (TNF) and unexpectedly the phorbol ester TPA (12-O-tetradecanoylphorbol-13-acetate; 10 nM) synergistically promoted nitrite accumulation. |
| 19550 | 7516691 | Besides employing TPA directly, the synergistic effect of TNF could be traced back to protein kinase C activation since protein kinase C inhibitors (IC50 value for staurosporine: 4 nM) potently suppressed nitrite production in the case of IL-1/TNF administration. |
| 19551 | 7516691 | Besides employing TPA directly, the synergistic effect of TNF could be traced back to protein kinase C activation since protein kinase C inhibitors (IC50 value for staurosporine: 4 nM) potently suppressed nitrite production in the case of IL-1/TNF administration. |
| 19552 | 7516691 | Moreover, the nitric oxide synthase inductive IL-1 signal was antagonized by lipophilic cAMP analogues. |
| 19553 | 7516691 | Moreover, the nitric oxide synthase inductive IL-1 signal was antagonized by lipophilic cAMP analogues. |
| 19554 | 7516691 | Our results for nitrite accumulation in RINm5F cells point to activating protein kinase C and inhibitory protein kinase A signalling pathways. |
| 19555 | 7516691 | Our results for nitrite accumulation in RINm5F cells point to activating protein kinase C and inhibitory protein kinase A signalling pathways. |
| 19556 | 8242903 | We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). |
| 19557 | 8242903 | We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). |
| 19558 | 8242903 | We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). |
| 19559 | 8242903 | On the other hand, there was no difference between BB/Sendai and Wistar rats in the in vivo TNF/LT productivity induced with LPS or with IFN-gamma plus LPS, and the TNF/LT productivity of these rats was lower on stimulation with LPS alone, but higher with IFN-gamma plus LPS than the other normal rats. |
| 19560 | 8242903 | On the other hand, there was no difference between BB/Sendai and Wistar rats in the in vivo TNF/LT productivity induced with LPS or with IFN-gamma plus LPS, and the TNF/LT productivity of these rats was lower on stimulation with LPS alone, but higher with IFN-gamma plus LPS than the other normal rats. |
| 19561 | 8242903 | On the other hand, there was no difference between BB/Sendai and Wistar rats in the in vivo TNF/LT productivity induced with LPS or with IFN-gamma plus LPS, and the TNF/LT productivity of these rats was lower on stimulation with LPS alone, but higher with IFN-gamma plus LPS than the other normal rats. |
| 19562 | 8242903 | These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT. |
| 19563 | 8242903 | These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT. |
| 19564 | 8242903 | These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT. |
| 19565 | 7510100 | The stimulatory cytokines include interleukin-1 (IL-1), interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and migration inhibitory factor. |
| 19566 | 7510100 | A number of cytokines, including IL-4, IL-10 and transforming growth factor-beta, can down regulate the induction of NO synthase in macrophages. |
| 19567 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19568 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19569 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19570 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19571 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19572 | 8223882 | No independent association between a tumor necrosis factor-alpha promotor region polymorphism and insulin-dependent diabetes mellitus. |
| 19573 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19574 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19575 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19576 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19577 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19578 | 8223882 | Several studies have implicated tumor necrosis factor (TNF)-alpha in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19579 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19580 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19581 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19582 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19583 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19584 | 8223882 | In the present study we analyzed the first reported TNF-alpha gene polymorphism in relation to IDDM. |
| 19585 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19586 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19587 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19588 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19589 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19590 | 8223882 | However, a very strong association of the uncommon TNF2 allele was observed with the HLA-B8, -DR3 alleles. |
| 19591 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19592 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19593 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19594 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19595 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19596 | 8223882 | The relative risk (RR) of TNF2 was 2.2 compared to a RR of 3.1 for DR3. |
| 19597 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19598 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19599 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19600 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19601 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19602 | 8223882 | Thus, the IDDM-associated TNF2 allele had no DR3-independent value as a disease marker. |
| 19603 | 7901896 | Polymorphic analysis of the human MHC-linked heat shock protein 70 (HSP70-2) and HSP70-Hom genes in insulin-dependent diabetes mellitus (IDDM). |
| 19604 | 7901896 | Polymorphic analysis of the human MHC-linked heat shock protein 70 (HSP70-2) and HSP70-Hom genes in insulin-dependent diabetes mellitus (IDDM). |
| 19605 | 7901896 | In the present study we characterized the frequencies of two polymorphisms within the MHC-linked heat shock protein (HSP) 70 genes in patients with insulin-dependent diabetes mellitus (IDDM) (n = 114) and healthy control individuals (n = 110). |
| 19606 | 7901896 | In the present study we characterized the frequencies of two polymorphisms within the MHC-linked heat shock protein (HSP) 70 genes in patients with insulin-dependent diabetes mellitus (IDDM) (n = 114) and healthy control individuals (n = 110). |
| 19607 | 7901896 | However, for the HSP70-2 polymorphisms this was solely due to linkage disequilibrium with DR3. |
| 19608 | 7901896 | However, for the HSP70-2 polymorphisms this was solely due to linkage disequilibrium with DR3. |
| 19609 | 7901896 | The rate HSP70-Hom 2-allele was significantly more frequent in controls than in patients. |
| 19610 | 7901896 | The rate HSP70-Hom 2-allele was significantly more frequent in controls than in patients. |
| 19611 | 7901896 | It showed strong association with certain tumour necrosis factor (TNF) (class III) and HLA-B and -A (class I) alleles independent of HLA-DQ and -DR alleles. |
| 19612 | 7901896 | It showed strong association with certain tumour necrosis factor (TNF) (class III) and HLA-B and -A (class I) alleles independent of HLA-DQ and -DR alleles. |
| 19613 | 7901896 | By typing 257 individuals from 55 IDDM multiple-case families two extended MHC-haplotypes, including class II-, TNF- and class I-markers, carrying the rare HSP70-Hom allele were defined. |
| 19614 | 7901896 | By typing 257 individuals from 55 IDDM multiple-case families two extended MHC-haplotypes, including class II-, TNF- and class I-markers, carrying the rare HSP70-Hom allele were defined. |
| 19615 | 7901896 | The functional implication of the polymorphism in the heat shock-inducible HSP70-2 gene was analysed by studying HSP70-2 mRNA expression after heat shock in peripheral blood mononuclear cells from individuals with different HSP70-2 genotypes. |
| 19616 | 7901896 | The functional implication of the polymorphism in the heat shock-inducible HSP70-2 gene was analysed by studying HSP70-2 mRNA expression after heat shock in peripheral blood mononuclear cells from individuals with different HSP70-2 genotypes. |
| 19617 | 8415751 | CSF-1 stimulation of NOD marrow induced Møs to differentiate to the point that they secreted levels of tumor necrosis factor alpha equivalent to that of controls. |
| 19618 | 8415751 | However, CSF-1 failed to prime NOD M phi s to completely differentiate in response to gamma-interferon, as shown by their decreased lipopolysaccharide-stimulated interleukin 1 secretion. |
| 19619 | 8415751 | These defects, in turn, were associated with an inability of CSF-1 to up-regulate c-fms (CSF-1 receptor) and Ifgr (gamma-interferon receptor) expression. |
| 19620 | 8415751 | Even though the combination of CSF-1 and gamma-interferon up-regulated c-fms and Ifgr transcript levels in NOD M phi s to levels induced in control M phi s by CSF-1 alone, the protein kinase C activities coupled to these receptors remained 4-fold lower in NOD M phi s than in M phi s derived from the marrow of diabetes-resistant NON and SWR control mice. |
| 19621 | 8408455 | In vitro production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha in insulin-dependent diabetes mellitus. |
| 19622 | 8408455 | In vitro production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha in insulin-dependent diabetes mellitus. |
| 19623 | 8408455 | In vitro production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha in insulin-dependent diabetes mellitus. |
| 19624 | 8408455 | In vitro production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha in insulin-dependent diabetes mellitus. |
| 19625 | 8408455 | The in vitro production of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) by monocytes was examined in patients with insulin-dependent diabetes mellitus (IDDM), in those with noninsulin-dependent diabetes mellitus (NIDDM), and in healthy volunteers. |
| 19626 | 8408455 | The in vitro production of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) by monocytes was examined in patients with insulin-dependent diabetes mellitus (IDDM), in those with noninsulin-dependent diabetes mellitus (NIDDM), and in healthy volunteers. |
| 19627 | 8408455 | The in vitro production of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) by monocytes was examined in patients with insulin-dependent diabetes mellitus (IDDM), in those with noninsulin-dependent diabetes mellitus (NIDDM), and in healthy volunteers. |
| 19628 | 8408455 | The in vitro production of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) by monocytes was examined in patients with insulin-dependent diabetes mellitus (IDDM), in those with noninsulin-dependent diabetes mellitus (NIDDM), and in healthy volunteers. |
| 19629 | 8408455 | The production of IL-1 and IL-6 by monocytes was significantly lower in IDDM patients than in NIDDM patients and normal subjects whereas the TNF-alpha production by monocytes did not differ between IDDM patients and normal subjects. |
| 19630 | 8408455 | The production of IL-1 and IL-6 by monocytes was significantly lower in IDDM patients than in NIDDM patients and normal subjects whereas the TNF-alpha production by monocytes did not differ between IDDM patients and normal subjects. |
| 19631 | 8408455 | The production of IL-1 and IL-6 by monocytes was significantly lower in IDDM patients than in NIDDM patients and normal subjects whereas the TNF-alpha production by monocytes did not differ between IDDM patients and normal subjects. |
| 19632 | 8408455 | The production of IL-1 and IL-6 by monocytes was significantly lower in IDDM patients than in NIDDM patients and normal subjects whereas the TNF-alpha production by monocytes did not differ between IDDM patients and normal subjects. |
| 19633 | 8408455 | On the other hand, the TNF-alpha production was significantly higher in NIDDM patients than in IDDM patients and normal subjects. |
| 19634 | 8408455 | On the other hand, the TNF-alpha production was significantly higher in NIDDM patients than in IDDM patients and normal subjects. |
| 19635 | 8408455 | On the other hand, the TNF-alpha production was significantly higher in NIDDM patients than in IDDM patients and normal subjects. |
| 19636 | 8408455 | On the other hand, the TNF-alpha production was significantly higher in NIDDM patients than in IDDM patients and normal subjects. |
| 19637 | 8408455 | There was a significant correlation between IL-1 and IL-6 concentrations in culture supernatants of monocytes for IDDM patients but not for NIDDM patients and normal subjects. |
| 19638 | 8408455 | There was a significant correlation between IL-1 and IL-6 concentrations in culture supernatants of monocytes for IDDM patients but not for NIDDM patients and normal subjects. |
| 19639 | 8408455 | There was a significant correlation between IL-1 and IL-6 concentrations in culture supernatants of monocytes for IDDM patients but not for NIDDM patients and normal subjects. |
| 19640 | 8408455 | There was a significant correlation between IL-1 and IL-6 concentrations in culture supernatants of monocytes for IDDM patients but not for NIDDM patients and normal subjects. |
| 19641 | 8408455 | In the serial observation lasting 3-18 months, the monocyte production of IL-1 was found to be consistently reduced in IDDM patients unrelated to the control state of diabetes, suggesting that the reduction of the IL-1 and IL-6 production by monocytes in IDDM patients may be intrinsically affected by immunological defects. |
| 19642 | 8408455 | In the serial observation lasting 3-18 months, the monocyte production of IL-1 was found to be consistently reduced in IDDM patients unrelated to the control state of diabetes, suggesting that the reduction of the IL-1 and IL-6 production by monocytes in IDDM patients may be intrinsically affected by immunological defects. |
| 19643 | 8408455 | In the serial observation lasting 3-18 months, the monocyte production of IL-1 was found to be consistently reduced in IDDM patients unrelated to the control state of diabetes, suggesting that the reduction of the IL-1 and IL-6 production by monocytes in IDDM patients may be intrinsically affected by immunological defects. |
| 19644 | 8408455 | In the serial observation lasting 3-18 months, the monocyte production of IL-1 was found to be consistently reduced in IDDM patients unrelated to the control state of diabetes, suggesting that the reduction of the IL-1 and IL-6 production by monocytes in IDDM patients may be intrinsically affected by immunological defects. |
| 19645 | 8062134 | [Dysregulation of in vitro TNF-beta production in insulin-dependent diabetes mellitus]. |
| 19646 | 8062134 | The possible role of tumor necrosis factors (TNF) in autoimmunity led us to explore the relationship between TNF production, polymorphism of the TNF-beta gene and type one diabetes. |
| 19647 | 8307785 | In humans, susceptibility genes for MG and IDDM have been localized to the region between TNF and HLA-B. |
| 19648 | 8307783 | Recently identified genes within the MHC include PERB6, a large gene producing multiple transcripts located between HLA-B and TNF, and PERB1, a member of the protein tyrosine kinase-gene family. |
| 19649 | 8240789 | Changes in the plasma concentrations of interleukin-1 beta (IL-1 beta), tumour necrosis factor alpha (TNF alpha), interleukin 2 (IL-2), and lymphocyte subsets were investigated in 19 persons with newly diagnosed (type 1) insulin-dependent diabetes mellitus (IDDM) from admission to hospital prior to insulin treatment and following 1 week and 1 month of treatment. |
| 19650 | 8240789 | Changes in the plasma concentrations of interleukin-1 beta (IL-1 beta), tumour necrosis factor alpha (TNF alpha), interleukin 2 (IL-2), and lymphocyte subsets were investigated in 19 persons with newly diagnosed (type 1) insulin-dependent diabetes mellitus (IDDM) from admission to hospital prior to insulin treatment and following 1 week and 1 month of treatment. |
| 19651 | 8240789 | The lymphocyte subsets (CD5+, CD8+, CD4+, CD16+, CD20+, HLA-DR+) did not show any significant changes from admission to after the start of insulin treatment. |
| 19652 | 8240789 | The lymphocyte subsets (CD5+, CD8+, CD4+, CD16+, CD20+, HLA-DR+) did not show any significant changes from admission to after the start of insulin treatment. |
| 19653 | 8240789 | It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM. |
| 19654 | 8240789 | It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM. |
| 19655 | 8222374 | Although these disease associations can be explained by linkage disequilibrium with extended MHC haplotypes, a direct role of genetically determined TNF production in the etiology of these diseases remains to be excluded. |
| 19656 | 8218598 | The functional state of the beta cell modulates IL-1 and TNF-induced cytotoxicity. |
| 19657 | 8218598 | The functional state of the beta cell modulates IL-1 and TNF-induced cytotoxicity. |
| 19658 | 8218598 | The functional state of the beta cell modulates IL-1 and TNF-induced cytotoxicity. |
| 19659 | 8218598 | The functional state of the beta cell modulates IL-1 and TNF-induced cytotoxicity. |
| 19660 | 8218598 | Cytotoxicity of cultured rat islets was induced by IL-1 (100 pg/ml) and TNF (62.5 ng/ml) individually and in combination and beta cell activity was modulated by culturing the islets in media containing 3.3, 5.5, 11, and 20 mmol/liter glucose. |
| 19661 | 8218598 | Cytotoxicity of cultured rat islets was induced by IL-1 (100 pg/ml) and TNF (62.5 ng/ml) individually and in combination and beta cell activity was modulated by culturing the islets in media containing 3.3, 5.5, 11, and 20 mmol/liter glucose. |
| 19662 | 8218598 | Cytotoxicity of cultured rat islets was induced by IL-1 (100 pg/ml) and TNF (62.5 ng/ml) individually and in combination and beta cell activity was modulated by culturing the islets in media containing 3.3, 5.5, 11, and 20 mmol/liter glucose. |
| 19663 | 8218598 | Cytotoxicity of cultured rat islets was induced by IL-1 (100 pg/ml) and TNF (62.5 ng/ml) individually and in combination and beta cell activity was modulated by culturing the islets in media containing 3.3, 5.5, 11, and 20 mmol/liter glucose. |
| 19664 | 8218598 | Both IL-1 and TNF were cytotoxic when administered individually and the combination of IL-1 and TNF was more cytotoxic than either cytokine alone. |
| 19665 | 8218598 | Both IL-1 and TNF were cytotoxic when administered individually and the combination of IL-1 and TNF was more cytotoxic than either cytokine alone. |
| 19666 | 8218598 | Both IL-1 and TNF were cytotoxic when administered individually and the combination of IL-1 and TNF was more cytotoxic than either cytokine alone. |
| 19667 | 8218598 | Both IL-1 and TNF were cytotoxic when administered individually and the combination of IL-1 and TNF was more cytotoxic than either cytokine alone. |
| 19668 | 8218598 | These results firmly establish that islet cytotoxicity of IL-1 and TNF is highly dependent on the functional state of the beta cells. |
| 19669 | 8218598 | These results firmly establish that islet cytotoxicity of IL-1 and TNF is highly dependent on the functional state of the beta cells. |
| 19670 | 8218598 | These results firmly establish that islet cytotoxicity of IL-1 and TNF is highly dependent on the functional state of the beta cells. |
| 19671 | 8218598 | These results firmly establish that islet cytotoxicity of IL-1 and TNF is highly dependent on the functional state of the beta cells. |
| 19672 | 8333833 | Interleukin-1 induction of tumor necrosis factor-alpha mRNA and bioactive tumor necrosis factor-alpha in a pancreatic beta-cell line by a mechanism requiring no de novo protein synthesis. |
| 19673 | 8333833 | Interleukin-1 induction of tumor necrosis factor-alpha mRNA and bioactive tumor necrosis factor-alpha in a pancreatic beta-cell line by a mechanism requiring no de novo protein synthesis. |
| 19674 | 8333833 | Interleukin-1 induction of tumor necrosis factor-alpha mRNA and bioactive tumor necrosis factor-alpha in a pancreatic beta-cell line by a mechanism requiring no de novo protein synthesis. |
| 19675 | 8333833 | Interleukin-1 induction of tumor necrosis factor-alpha mRNA and bioactive tumor necrosis factor-alpha in a pancreatic beta-cell line by a mechanism requiring no de novo protein synthesis. |
| 19676 | 8333833 | Interleukin-1 (IL-1) has been implicated as an effector in insulitis of Type 1 (insulin-dependent) diabetes. |
| 19677 | 8333833 | Interleukin-1 (IL-1) has been implicated as an effector in insulitis of Type 1 (insulin-dependent) diabetes. |
| 19678 | 8333833 | Interleukin-1 (IL-1) has been implicated as an effector in insulitis of Type 1 (insulin-dependent) diabetes. |
| 19679 | 8333833 | Interleukin-1 (IL-1) has been implicated as an effector in insulitis of Type 1 (insulin-dependent) diabetes. |
| 19680 | 8333833 | Tumor necrosis factor-alpha (TNF-alpha) mRNA expression by beta TC1 cells was demonstrated 1-3 h after the addition of IL-1 beta. |
| 19681 | 8333833 | Tumor necrosis factor-alpha (TNF-alpha) mRNA expression by beta TC1 cells was demonstrated 1-3 h after the addition of IL-1 beta. |
| 19682 | 8333833 | Tumor necrosis factor-alpha (TNF-alpha) mRNA expression by beta TC1 cells was demonstrated 1-3 h after the addition of IL-1 beta. |
| 19683 | 8333833 | Tumor necrosis factor-alpha (TNF-alpha) mRNA expression by beta TC1 cells was demonstrated 1-3 h after the addition of IL-1 beta. |
| 19684 | 8333833 | TNF bioactivity was detected in homogenates of beta TC1 cells exposed to IL-1. |
| 19685 | 8333833 | TNF bioactivity was detected in homogenates of beta TC1 cells exposed to IL-1. |
| 19686 | 8333833 | TNF bioactivity was detected in homogenates of beta TC1 cells exposed to IL-1. |
| 19687 | 8333833 | TNF bioactivity was detected in homogenates of beta TC1 cells exposed to IL-1. |
| 19688 | 8333833 | The supplementation of cycloheximide (CHX) together with IL-1 beta resulted in the superinduction of TNF-alpha mRNA, suggesting that de novo protein synthesis is not required in IL-1-induced TNF-alpha mRNA expression. |
| 19689 | 8333833 | The supplementation of cycloheximide (CHX) together with IL-1 beta resulted in the superinduction of TNF-alpha mRNA, suggesting that de novo protein synthesis is not required in IL-1-induced TNF-alpha mRNA expression. |
| 19690 | 8333833 | The supplementation of cycloheximide (CHX) together with IL-1 beta resulted in the superinduction of TNF-alpha mRNA, suggesting that de novo protein synthesis is not required in IL-1-induced TNF-alpha mRNA expression. |
| 19691 | 8333833 | The supplementation of cycloheximide (CHX) together with IL-1 beta resulted in the superinduction of TNF-alpha mRNA, suggesting that de novo protein synthesis is not required in IL-1-induced TNF-alpha mRNA expression. |
| 19692 | 8099883 | Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1. |
| 19693 | 8099883 | Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1. |
| 19694 | 8099883 | Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1. |
| 19695 | 8099883 | Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1. |
| 19696 | 8099883 | We demonstrated in this study, using cell lines of transformed mouse beta-cells and alpha-cells, that only pancreatic beta-cells but not alpha-cells produced tumor necrosis factor-alpha when exposed to interleukin-1 beta. |
| 19697 | 8099883 | We demonstrated in this study, using cell lines of transformed mouse beta-cells and alpha-cells, that only pancreatic beta-cells but not alpha-cells produced tumor necrosis factor-alpha when exposed to interleukin-1 beta. |
| 19698 | 8099883 | We demonstrated in this study, using cell lines of transformed mouse beta-cells and alpha-cells, that only pancreatic beta-cells but not alpha-cells produced tumor necrosis factor-alpha when exposed to interleukin-1 beta. |
| 19699 | 8099883 | We demonstrated in this study, using cell lines of transformed mouse beta-cells and alpha-cells, that only pancreatic beta-cells but not alpha-cells produced tumor necrosis factor-alpha when exposed to interleukin-1 beta. |
| 19700 | 8099883 | Interleukin-1 beta also provoked tumor necrosis factor-alpha mRNA expression in vitro by normal mouse islet cells. |
| 19701 | 8099883 | Interleukin-1 beta also provoked tumor necrosis factor-alpha mRNA expression in vitro by normal mouse islet cells. |
| 19702 | 8099883 | Interleukin-1 beta also provoked tumor necrosis factor-alpha mRNA expression in vitro by normal mouse islet cells. |
| 19703 | 8099883 | Interleukin-1 beta also provoked tumor necrosis factor-alpha mRNA expression in vitro by normal mouse islet cells. |
| 19704 | 8099883 | Because tumor necrosis factor-alpha has been shown to potentiate beta-cell cytotoxicity of interleukin-1 and interferon-gamma, tumor necrosis factor-alpha produced in situ by beta-cells might be self-destructive. |
| 19705 | 8099883 | Because tumor necrosis factor-alpha has been shown to potentiate beta-cell cytotoxicity of interleukin-1 and interferon-gamma, tumor necrosis factor-alpha produced in situ by beta-cells might be self-destructive. |
| 19706 | 8099883 | Because tumor necrosis factor-alpha has been shown to potentiate beta-cell cytotoxicity of interleukin-1 and interferon-gamma, tumor necrosis factor-alpha produced in situ by beta-cells might be self-destructive. |
| 19707 | 8099883 | Because tumor necrosis factor-alpha has been shown to potentiate beta-cell cytotoxicity of interleukin-1 and interferon-gamma, tumor necrosis factor-alpha produced in situ by beta-cells might be self-destructive. |
| 19708 | 8099883 | In fact, a low dose of interleukin-1 beta in combination with a low dose of interferon-gamma preferentially injured beta-cells. |
| 19709 | 8099883 | In fact, a low dose of interleukin-1 beta in combination with a low dose of interferon-gamma preferentially injured beta-cells. |
| 19710 | 8099883 | In fact, a low dose of interleukin-1 beta in combination with a low dose of interferon-gamma preferentially injured beta-cells. |
| 19711 | 8099883 | In fact, a low dose of interleukin-1 beta in combination with a low dose of interferon-gamma preferentially injured beta-cells. |
| 19712 | 8496610 | To study self reactivity, a transgenic mouse model has been established in which the lymphocytic choriomeningitis virus (LCMV) glycoprotein (gp) is expressed in the beta-islet cells of the pancreas (rat insulin promoter (RIP)-gp). |
| 19713 | 8496610 | In this study, comparative analysis of H-2k RIP-gp-transgenic animals demonstrated that the haplotype influences the incidence and kinetics of diabetes and alters the requirement for the CD4+ T cell subset. |
| 19714 | 8496610 | Transgenic mice expressing both LCMV-gp and TNF-alpha under the control of the RIP were infected with vacc-gp, and 50% of RIP-gp/TNF-alpha-transgenic animals became hyperglycemic. |
| 19715 | 8278654 | TNF-alpha and insulin-dependent diabetes mellitus. |
| 19716 | 8354339 | Pancreatic beta-cell function and interleukin-1 beta in plasma during the acute phase response in patients with major burn injuries. |
| 19717 | 8354339 | Animal experiments demonstrate that interleukin-1 beta (IL-1 beta) is beta-cell cytotoxic in vitro and inhibits insulin secretion in vivo. |
| 19718 | 8354339 | Since IL-1 beta and other cytokines are main mediators of the acute phase response, the objectives of the present study were to examine beta-cell function in patients with major burn injuries, and to test if changes in beta-cell function correlated to systemic levels of IL-1 beta and tumour necrosis factor alpha (TNF alpha). |
| 19719 | 8354339 | However, we could not demonstrate any correlation between C-peptide, proinsulin, insulin or proinsulin/insulin ratio and plasma concentration of IL-1 beta. |
| 19720 | 8218929 | Involvement of interleukin 1 and interleukin 1 antagonist in pancreatic beta-cell destruction in insulin-dependent diabetes mellitus. |
| 19721 | 8218929 | In this review we propose that the balance between the action of interleukin 1 (IL-1) and its natural antagonist IL-1ra on the level of the insulin-producing pancreatic beta-cell may play a decisive role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). |
| 19722 | 8218929 | We argue that IL-1 potentiated by other cytokines (tumor necrosis factor alpha, interferon gamma) is an important effector molecule involved in both early and late events in the immune-mediated process that leads to beta-cell destruction and IDDM. |
| 19723 | 8218929 | We also point out that surprisingly high molar excesses of IL-1ra over IL-1 are necessary to block the action of IL-1 on islet beta-cells compared to islet alpha-cells in vitro and in animals. |
| 19724 | 8218929 | We suggest that the selectivity of beta-cell destruction in IDDM may be conferred on several levels: (1) homing of beta-cell antigen specific T cells, (2) targeted delivery of cytokines by lymphocytic and monocytic cells beta-cells, (3) high molar excesses of IL-1ra over IL-1 needed to prevent IL-1 mediated beta-cell toxicity, (4) increased beta-cell sensitivity to free nitric oxide and oxygen radical formation induced by IL-1 and (5) inadequate oxidative stress response by beta-cells to cytokines. |
| 19725 | 8218929 | Further studies are needed to establish the in vivo role of an imbalance between the amounts of IL-1 and IL-1ra produced relative to their action in the pathogenesis of IDDM. |
| 19726 | 8098044 | Sorted islet B cells and non-B cells were permanently labeled with two different fluorescent dyes (DiO and DiI), mixed, and allowed to form aggregates during a 5-d culture in the presence or absence of TNF-alpha (100 U/ml), a cytokine suggested to be implicated in the early physiological events leading to insulin-dependent diabetes mellitus. |
| 19727 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19728 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19729 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19730 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19731 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19732 | 7682590 | Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. |
| 19733 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19734 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19735 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19736 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19737 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19738 | 7682590 | To understand the role of TNF in the regulation of inflammation and the development of autoimmune diseases such as insulin-dependent diabetes mellitus, we produced transgenic mice in which the synthesis of murine TNF-alpha was directed by the rat insulin II promoter. |
| 19739 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19740 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19741 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19742 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19743 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19744 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 19745 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19746 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19747 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19748 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19749 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19750 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 19751 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19752 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19753 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19754 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19755 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19756 | 7682590 | Moreover, in contrast to the predominant peri-insulitis observed in TNF-beta transgenic mice, the majority of the infiltrate in the TNF-alpha transgenic mice was within the islet itself. |
| 19757 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19758 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19759 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19760 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19761 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19762 | 7682590 | Both TNF-alpha and TNF-beta transgenic mice show elevated expression of leukocyte adhesion molecules VCAM-1 and ICAM-1 in islet endothelia and increased expression of MHC class I on islet cells. |
| 19763 | 8097912 | Hsp70, Bat5, Tnfa and Tnfb loci were studied by microsatellite polymorphism analysis and/or restriction mapping. |
| 19764 | 8097912 | Hsp70, Bat5, Tnfa and Tnfb loci were studied by microsatellite polymorphism analysis and/or restriction mapping. |
| 19765 | 8097912 | The CTS mouse had the same allele as the NOD mouse at the Hsp70 locus, but different alleles at the Bat5, Tnfa and Tnfb loci from those of the NOD mouse. |
| 19766 | 8097912 | The CTS mouse had the same allele as the NOD mouse at the Hsp70 locus, but different alleles at the Bat5, Tnfa and Tnfb loci from those of the NOD mouse. |
| 19767 | 8097912 | Our previous studies indicated that in the CTS mouse, class II MHC was the same as that of the NOD mouse, but that class I MHC was different at both K and D loci, and that CTS MHC was diabetogenic in the presence of NOD background genes. |
| 19768 | 8097912 | Our previous studies indicated that in the CTS mouse, class II MHC was the same as that of the NOD mouse, but that class I MHC was different at both K and D loci, and that CTS MHC was diabetogenic in the presence of NOD background genes. |
| 19769 | 8097912 | Moreover, since the diabetogenic effect of the CTS MHC is weaker than that of the NOD MHC, these data suggest the presence of a second MHC-linked gene or gene complexes that modulate susceptibility to type 1 diabetes outside this segment. |
| 19770 | 8097912 | Moreover, since the diabetogenic effect of the CTS MHC is weaker than that of the NOD MHC, these data suggest the presence of a second MHC-linked gene or gene complexes that modulate susceptibility to type 1 diabetes outside this segment. |
| 19771 | 8445033 | Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. |
| 19772 | 8445033 | Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. |
| 19773 | 8445033 | Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. |
| 19774 | 8445033 | Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. |
| 19775 | 8445033 | Tumor necrosis factor-alpha prevents the differentiation of human adipocyte precursor cells and causes delipidation of newly developed fat cells. |
| 19776 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 19777 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 19778 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 19779 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 19780 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 19781 | 8445033 | Exposure of cultured preadipocytes to TNF alpha resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), an established marker of adipocyte differentiation. |
| 19782 | 8445033 | Exposure of cultured preadipocytes to TNF alpha resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), an established marker of adipocyte differentiation. |
| 19783 | 8445033 | Exposure of cultured preadipocytes to TNF alpha resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), an established marker of adipocyte differentiation. |
| 19784 | 8445033 | Exposure of cultured preadipocytes to TNF alpha resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), an established marker of adipocyte differentiation. |
| 19785 | 8445033 | Exposure of cultured preadipocytes to TNF alpha resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), an established marker of adipocyte differentiation. |
| 19786 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 19787 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 19788 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 19789 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 19790 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 19791 | 8445033 | These results clearly demonstrate that TNF alpha inhibits the differentiation of human adipocyte precursor cells and, in addition, promotes the delipidation of mature fat cells. |
| 19792 | 8445033 | These results clearly demonstrate that TNF alpha inhibits the differentiation of human adipocyte precursor cells and, in addition, promotes the delipidation of mature fat cells. |
| 19793 | 8445033 | These results clearly demonstrate that TNF alpha inhibits the differentiation of human adipocyte precursor cells and, in addition, promotes the delipidation of mature fat cells. |
| 19794 | 8445033 | These results clearly demonstrate that TNF alpha inhibits the differentiation of human adipocyte precursor cells and, in addition, promotes the delipidation of mature fat cells. |
| 19795 | 8445033 | These results clearly demonstrate that TNF alpha inhibits the differentiation of human adipocyte precursor cells and, in addition, promotes the delipidation of mature fat cells. |
| 19796 | 8432410 | We have reported previously that chronic and systemic administration of a streptococcal preparation (OK-432), an inducer of TNF, or of recombinant hTNF prevented the development of IDDM in the two animal models of IDDM-NOD mice and BB rats. |
| 19797 | 8383325 | In this report we demonstrate that the cytokine combination of human recombinant interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) induces the formation of nitric oxide by human islets. |
| 19798 | 8383325 | In this report we demonstrate that the cytokine combination of human recombinant interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) induces the formation of nitric oxide by human islets. |
| 19799 | 8383325 | In this report we demonstrate that the cytokine combination of human recombinant interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) induces the formation of nitric oxide by human islets. |
| 19800 | 8383325 | In this report we demonstrate that the cytokine combination of human recombinant interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) induces the formation of nitric oxide by human islets. |
| 19801 | 8383325 | In this report we demonstrate that the cytokine combination of human recombinant interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) induces the formation of nitric oxide by human islets. |
| 19802 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 19803 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 19804 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 19805 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 19806 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 19807 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 19808 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 19809 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 19810 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 19811 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 19812 | 8383325 | Pretreatment of human islets with low concentrations of this cytokine combination (IL-1 beta at 15 units/ml, 0.7 nM TNF-alpha, and IFN-gamma at 150 units/ml) appears to slightly stimulate insulin secretion. |
| 19813 | 8383325 | Pretreatment of human islets with low concentrations of this cytokine combination (IL-1 beta at 15 units/ml, 0.7 nM TNF-alpha, and IFN-gamma at 150 units/ml) appears to slightly stimulate insulin secretion. |
| 19814 | 8383325 | Pretreatment of human islets with low concentrations of this cytokine combination (IL-1 beta at 15 units/ml, 0.7 nM TNF-alpha, and IFN-gamma at 150 units/ml) appears to slightly stimulate insulin secretion. |
| 19815 | 8383325 | Pretreatment of human islets with low concentrations of this cytokine combination (IL-1 beta at 15 units/ml, 0.7 nM TNF-alpha, and IFN-gamma at 150 units/ml) appears to slightly stimulate insulin secretion. |
| 19816 | 8383325 | Pretreatment of human islets with low concentrations of this cytokine combination (IL-1 beta at 15 units/ml, 0.7 nM TNF-alpha, and IFN-gamma at 150 units/ml) appears to slightly stimulate insulin secretion. |
| 19817 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 19818 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 19819 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 19820 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 19821 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 19822 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 19823 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 19824 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 19825 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 19826 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 19827 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 19828 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 19829 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 19830 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 19831 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 19832 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 19833 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 19834 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 19835 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 19836 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 19837 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 19838 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 19839 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 19840 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 19841 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 19842 | 8093442 | Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus. |
| 19843 | 8093442 | Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus. |
| 19844 | 8093442 | Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus. |
| 19845 | 8093442 | Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus. |
| 19846 | 8093442 | Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus. |
| 19847 | 8093442 | We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals. |
| 19848 | 8093442 | We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals. |
| 19849 | 8093442 | We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals. |
| 19850 | 8093442 | We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals. |
| 19851 | 8093442 | We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals. |
| 19852 | 8093442 | Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified. |
| 19853 | 8093442 | Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified. |
| 19854 | 8093442 | Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified. |
| 19855 | 8093442 | Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified. |
| 19856 | 8093442 | Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified. |
| 19857 | 8093442 | In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals. |
| 19858 | 8093442 | In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals. |
| 19859 | 8093442 | In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals. |
| 19860 | 8093442 | In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals. |
| 19861 | 8093442 | In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals. |
| 19862 | 8093442 | In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype. |
| 19863 | 8093442 | In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype. |
| 19864 | 8093442 | In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype. |
| 19865 | 8093442 | In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype. |
| 19866 | 8093442 | In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype. |
| 19867 | 8093442 | This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response. |
| 19868 | 8093442 | This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response. |
| 19869 | 8093442 | This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response. |
| 19870 | 8093442 | This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response. |
| 19871 | 8093442 | This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response. |
| 19872 | 8093442 | These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM. |
| 19873 | 8093442 | These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM. |
| 19874 | 8093442 | These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM. |
| 19875 | 8093442 | These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM. |
| 19876 | 8093442 | These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM. |
| 19877 | 7678183 | Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. |
| 19878 | 7678183 | Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. |
| 19879 | 7678183 | These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity. |
| 19880 | 7678183 | These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity. |
| 19881 | 1463043 | Sixteen vitreous and paired serum samples from 13 patients with proliferative diabetic retinopathy, vitreous samples from seven cadaveric control subjects, and aqueous humor samples from 15 normal control subjects were assayed for the cytokines interleukin-1, tumor necrosis factor-alpha, interleukin-6, and interferon-gamma. |
| 19882 | 1463043 | Sixteen vitreous and paired serum samples from 13 patients with proliferative diabetic retinopathy, vitreous samples from seven cadaveric control subjects, and aqueous humor samples from 15 normal control subjects were assayed for the cytokines interleukin-1, tumor necrosis factor-alpha, interleukin-6, and interferon-gamma. |
| 19883 | 1463043 | Sixteen vitreous and paired serum samples from 13 patients with proliferative diabetic retinopathy, vitreous samples from seven cadaveric control subjects, and aqueous humor samples from 15 normal control subjects were assayed for the cytokines interleukin-1, tumor necrosis factor-alpha, interleukin-6, and interferon-gamma. |
| 19884 | 1463043 | Interleukin-1 was detected in seven of 16 vitreous samples (44%) and in four of ten aqueous humor samples (40%), whereas tumor necrosis factor-alpha and interferon-gamma were never detected in vitreous or aqueous fluid. |
| 19885 | 1463043 | Interleukin-1 was detected in seven of 16 vitreous samples (44%) and in four of ten aqueous humor samples (40%), whereas tumor necrosis factor-alpha and interferon-gamma were never detected in vitreous or aqueous fluid. |
| 19886 | 1463043 | Interleukin-1 was detected in seven of 16 vitreous samples (44%) and in four of ten aqueous humor samples (40%), whereas tumor necrosis factor-alpha and interferon-gamma were never detected in vitreous or aqueous fluid. |
| 19887 | 1463043 | Interleukin-1, tumor necrosis factor-alpha, and interferon-gamma were not found in any of the sera. |
| 19888 | 1463043 | Interleukin-1, tumor necrosis factor-alpha, and interferon-gamma were not found in any of the sera. |
| 19889 | 1463043 | Interleukin-1, tumor necrosis factor-alpha, and interferon-gamma were not found in any of the sera. |
| 19890 | 1466799 | Thus, cytokines, such as tumor necrosis factor-alpha, are implicated in the pathogenesis of rheumatoid arthritis based on in vitro studies on synovial tissue from patients with rheumatoid arthritis, which suggest that the effects of tumor necrosis factor-alpha are amplified by its potential to induce other pro-inflammatory cytokines, such as interleukin-1 and granulocyte-macrophage colony-stimulating factor. |
| 19891 | 1466799 | Interleukin-2 has also been identified by transgenic technology as a cytokine involved in the pathogenesis of insulin-dependent diabetes mellitus through the activation and stimulation of growth of autoreactive T cells. |
| 19892 | 1460428 | Mice bearing a tumor necrosis factor (TNF) alpha transgene controlled by an insulin promoter developed an increasingly severe lymphocytic insulitis, apparently resulting from the induction of endothelial changes with features similar to those observed in other places of intense lymphocytic traffic. |
| 19893 | 1446804 | In an attempt to establish whether the putative ICSA autoantigen is present in the surface of human islet cells in the diabetic pancreas, the insulitis microenvironment was emulated by exposing the islets to three types of stress: 1) cytokines (IFN-gamma and TNF-alpha); 2) heat shock; and 3) hyperglycemia. |
| 19894 | 1361076 | The genes located between class II and class I HLA genes including polymorphic tumour necrosis factor (TNF) genes may contribute to the disease susceptibility in IDDM. |
| 19895 | 1361076 | The genes located between class II and class I HLA genes including polymorphic tumour necrosis factor (TNF) genes may contribute to the disease susceptibility in IDDM. |
| 19896 | 1361076 | The genes located between class II and class I HLA genes including polymorphic tumour necrosis factor (TNF) genes may contribute to the disease susceptibility in IDDM. |
| 19897 | 1361076 | Restriction fragment polymorphisms of the TNF-beta gene have been found to be fixed in the major IDDM susceptibility haplotypes, the B62,DR4 haplotype being associated with the 10.5-kb fragment and the B8,DR3 haplotype with a 5.5-kb fragment. |
| 19898 | 1361076 | Restriction fragment polymorphisms of the TNF-beta gene have been found to be fixed in the major IDDM susceptibility haplotypes, the B62,DR4 haplotype being associated with the 10.5-kb fragment and the B8,DR3 haplotype with a 5.5-kb fragment. |
| 19899 | 1361076 | Restriction fragment polymorphisms of the TNF-beta gene have been found to be fixed in the major IDDM susceptibility haplotypes, the B62,DR4 haplotype being associated with the 10.5-kb fragment and the B8,DR3 haplotype with a 5.5-kb fragment. |
| 19900 | 1361076 | Among IDDM haplotypes the B62,DR4 haplotype was characterized by the 10.5-kb TNF fragment, whereas two other common Finnish IDDM-associated DR4 haplotypes--A24,B39,DR4 and A2,B56,DR4--had the 5.5-kb TNF fragment. |
| 19901 | 1361076 | Among IDDM haplotypes the B62,DR4 haplotype was characterized by the 10.5-kb TNF fragment, whereas two other common Finnish IDDM-associated DR4 haplotypes--A24,B39,DR4 and A2,B56,DR4--had the 5.5-kb TNF fragment. |
| 19902 | 1361076 | Among IDDM haplotypes the B62,DR4 haplotype was characterized by the 10.5-kb TNF fragment, whereas two other common Finnish IDDM-associated DR4 haplotypes--A24,B39,DR4 and A2,B56,DR4--had the 5.5-kb TNF fragment. |
| 19903 | 1361076 | Both IDDM-associated and non-associated DR3 positive haplotypes were linked to the 5.5-kb fragment. |
| 19904 | 1361076 | Both IDDM-associated and non-associated DR3 positive haplotypes were linked to the 5.5-kb fragment. |
| 19905 | 1361076 | Both IDDM-associated and non-associated DR3 positive haplotypes were linked to the 5.5-kb fragment. |
| 19906 | 1361076 | The distribution of various combinations of TNF alleles in IDDM probands (n = 63) did not differ from that expected according to the Hardy-Weinberg distribution. |
| 19907 | 1361076 | The distribution of various combinations of TNF alleles in IDDM probands (n = 63) did not differ from that expected according to the Hardy-Weinberg distribution. |
| 19908 | 1361076 | The distribution of various combinations of TNF alleles in IDDM probands (n = 63) did not differ from that expected according to the Hardy-Weinberg distribution. |
| 19909 | 1361076 | Our results indicate that the 10.5-kb allele of TNF-beta gene as such is not a risk factor contributing to DR4/DQ8-associated susceptibility. |
| 19910 | 1361076 | Our results indicate that the 10.5-kb allele of TNF-beta gene as such is not a risk factor contributing to DR4/DQ8-associated susceptibility. |
| 19911 | 1361076 | Our results indicate that the 10.5-kb allele of TNF-beta gene as such is not a risk factor contributing to DR4/DQ8-associated susceptibility. |
| 19912 | 1360342 | Insulin-dependent diabetes mellitus (IDDM) results from a T cell-dependent autoimmune destruction of insulin-producing pancreatic beta cells. |
| 19913 | 1360342 | Freshly isolated pancreatic beta cells from ob/ob mice did not express ICAM-1, but treatment of the cells with IL-1-beta, TNF-alpha, or INF-gamma strongly induced its expression as measured by immunofluorescence flow cytometry. |
| 19914 | 1360342 | Immunoprecipitation from IL-1-beta-treated beta cells demonstrated a cell-surface glycoprotein with an apparent molecular weight of 95 kDa. |
| 19915 | 1334599 | Effect of tumor necrosis factor alpha and of the soluble tumor necrosis factor receptor on insulin secretion of isolated islets of Langerhans. |
| 19916 | 1294780 | [Case study of interleukin-1 beta, tumor necrosis factor alpha and interleukin-6 production peripheral blood monocytes in patients with diabetes mellitus complicated by pulmonary tuberculosis]. |
| 19917 | 1294780 | [Case study of interleukin-1 beta, tumor necrosis factor alpha and interleukin-6 production peripheral blood monocytes in patients with diabetes mellitus complicated by pulmonary tuberculosis]. |
| 19918 | 1294780 | [Case study of interleukin-1 beta, tumor necrosis factor alpha and interleukin-6 production peripheral blood monocytes in patients with diabetes mellitus complicated by pulmonary tuberculosis]. |
| 19919 | 1294780 | This study measured the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) by the peripheral monocytes of patients diagnosed with pulmonary tuberculosis accompanied by DM (TB+DM) and patients without DM complications (TB) using age-matched, healthy control subjects for comparison. |
| 19920 | 1294780 | This study measured the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) by the peripheral monocytes of patients diagnosed with pulmonary tuberculosis accompanied by DM (TB+DM) and patients without DM complications (TB) using age-matched, healthy control subjects for comparison. |
| 19921 | 1294780 | This study measured the production of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) by the peripheral monocytes of patients diagnosed with pulmonary tuberculosis accompanied by DM (TB+DM) and patients without DM complications (TB) using age-matched, healthy control subjects for comparison. |
| 19922 | 1294780 | The results were as follows: (1) The production of IL-1 beta, TNF alpha and IL-6 in TB patients was significantly higher than that observed in the healthy control subjects. (2) The production of IL-1 beta, TNF alpha and IL-6 in TB+DM patients was significantly lower than that observed in the TB patients. (3) The production of IL-1 beta and TNF alpha in TB+DM patients with poor control was significantly lower than that observed in the patients with good control. (4) The TNF alpha production had a significant inverse correlation to HbA1c in the TB+DM patients. |
| 19923 | 1294780 | The results were as follows: (1) The production of IL-1 beta, TNF alpha and IL-6 in TB patients was significantly higher than that observed in the healthy control subjects. (2) The production of IL-1 beta, TNF alpha and IL-6 in TB+DM patients was significantly lower than that observed in the TB patients. (3) The production of IL-1 beta and TNF alpha in TB+DM patients with poor control was significantly lower than that observed in the patients with good control. (4) The TNF alpha production had a significant inverse correlation to HbA1c in the TB+DM patients. |
| 19924 | 1294780 | The results were as follows: (1) The production of IL-1 beta, TNF alpha and IL-6 in TB patients was significantly higher than that observed in the healthy control subjects. (2) The production of IL-1 beta, TNF alpha and IL-6 in TB+DM patients was significantly lower than that observed in the TB patients. (3) The production of IL-1 beta and TNF alpha in TB+DM patients with poor control was significantly lower than that observed in the patients with good control. (4) The TNF alpha production had a significant inverse correlation to HbA1c in the TB+DM patients. |
| 19925 | 1395129 | The Bio-Breeding (BB) rat develops spontaneous insulin-dependent diabetes mellitus (IDDM) and provides a useful animal model to study this human autoimmune disease. |
| 19926 | 1395129 | The Bio-Breeding (BB) rat develops spontaneous insulin-dependent diabetes mellitus (IDDM) and provides a useful animal model to study this human autoimmune disease. |
| 19927 | 1395129 | The Bio-Breeding (BB) rat develops spontaneous insulin-dependent diabetes mellitus (IDDM) and provides a useful animal model to study this human autoimmune disease. |
| 19928 | 1395129 | Treatment of BB rats with tumor necrosis factor (TNF) has been reported to prevent the development of IDDM. |
| 19929 | 1395129 | Treatment of BB rats with tumor necrosis factor (TNF) has been reported to prevent the development of IDDM. |
| 19930 | 1395129 | Treatment of BB rats with tumor necrosis factor (TNF) has been reported to prevent the development of IDDM. |
| 19931 | 1395129 | TNF production in short-term cultures of peritoneal macrophages from DP rats was significantly less than that from control DR rats, both in the basal state and after stimulation with either interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) in vivo and in vitro. |
| 19932 | 1395129 | TNF production in short-term cultures of peritoneal macrophages from DP rats was significantly less than that from control DR rats, both in the basal state and after stimulation with either interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) in vivo and in vitro. |
| 19933 | 1395129 | TNF production in short-term cultures of peritoneal macrophages from DP rats was significantly less than that from control DR rats, both in the basal state and after stimulation with either interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) in vivo and in vitro. |
| 19934 | 1395129 | In contrast, TNF production by macrophages from CFA-injected DP rats (basal and IFN-gamma or LPS-stimulated) was equal to or greater than that by macrophages from DP rats and similar to TNF production by macrophages from CFA-injected DR rats. |
| 19935 | 1395129 | In contrast, TNF production by macrophages from CFA-injected DP rats (basal and IFN-gamma or LPS-stimulated) was equal to or greater than that by macrophages from DP rats and similar to TNF production by macrophages from CFA-injected DR rats. |
| 19936 | 1395129 | In contrast, TNF production by macrophages from CFA-injected DP rats (basal and IFN-gamma or LPS-stimulated) was equal to or greater than that by macrophages from DP rats and similar to TNF production by macrophages from CFA-injected DR rats. |
| 19937 | 1526345 | Although in vitro studies showed that TNF decreases adipose tissue lipoprotein lipase activity, recent studies with intact animals demonstrated that TNF increases serum triglyceride levels by stimulating hepatic lipid secretion, not by affecting clearance. |
| 19938 | 1526345 | Other cytokines including IL-1, IL-6, and alpha-interferon increase hepatic de novo fatty acid synthesis. |
| 19939 | 1526343 | In addition, macrophages are activated when ingesting LDL-IC and release IL-1 beta and TNF-alpha, which can contribute to the initiation and progression of an atheromatous lesion by several mechanisms. |
| 19940 | 1333964 | Pro-inflammatory cytokines such as IL-1, IL-6 and TNF alpha play a role in mediating these interactions. |
| 19941 | 1333964 | Pro-inflammatory cytokines such as IL-1, IL-6 and TNF alpha play a role in mediating these interactions. |
| 19942 | 1333964 | The data reported here show that IL-1 plays a crucial rôle in the mediation of the hypoglycaemia induced by LPS, since other cytokines released following inoculation of endotoxin, such as TNF alpha and IL-6, have only marginal effects or do not induce hypoglycaemia when administered in doses similar to those of IL-1. |
| 19943 | 1333964 | The data reported here show that IL-1 plays a crucial rôle in the mediation of the hypoglycaemia induced by LPS, since other cytokines released following inoculation of endotoxin, such as TNF alpha and IL-6, have only marginal effects or do not induce hypoglycaemia when administered in doses similar to those of IL-1. |
| 19944 | 1326453 | A macrophage-monocyte receptor system for AGE moieties is shown to mediate the uptake of AGE-modified proteins by a process that also induces cachectin-TNF, IL-1, IGF-I, and PDGF secretion. |
| 19945 | 1326453 | Fibroblast AGE receptors may influence cellular proliferation by EGF and EGF-receptor regulation. |
| 19946 | 1477295 | Experimental data suggest that cytokines, e.g. interleukin 1 and tumor necrosis factor, could play a fundamental role. |
| 19947 | 1503874 | One animal study examined the induction of acute synovitis by the intra-articular injection of bacterial endotoxin and the cytokines tumor necrosis factor-alpha, and interleukin-1 beta; and the other studied the effects of early and delayed synovectomy in the management of septic arthritis. |
| 19948 | 1638523 | Interleukin 6 reduces lipoprotein lipase activity in adipose tissue of mice in vivo and in 3T3-L1 adipocytes: a possible role for interleukin 6 in cancer cachexia. |
| 19949 | 1638523 | Interleukin 6 reduces lipoprotein lipase activity in adipose tissue of mice in vivo and in 3T3-L1 adipocytes: a possible role for interleukin 6 in cancer cachexia. |
| 19950 | 1638523 | Interleukin 6 reduces lipoprotein lipase activity in adipose tissue of mice in vivo and in 3T3-L1 adipocytes: a possible role for interleukin 6 in cancer cachexia. |
| 19951 | 1638523 | To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. |
| 19952 | 1638523 | To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. |
| 19953 | 1638523 | To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. |
| 19954 | 1638523 | Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. |
| 19955 | 1638523 | Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. |
| 19956 | 1638523 | Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. |
| 19957 | 1638523 | Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. |
| 19958 | 1638523 | Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. |
| 19959 | 1638523 | Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. |
| 19960 | 1638523 | Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. |
| 19961 | 1638523 | Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. |
| 19962 | 1638523 | Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. |
| 19963 | 1638523 | Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. |
| 19964 | 1638523 | Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. |
| 19965 | 1638523 | Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. |
| 19966 | 1638523 | Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6. |
| 19967 | 1638523 | Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6. |
| 19968 | 1638523 | Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6. |
| 19969 | 1378415 | NMMA and NAME, both inhibitors of nitric oxide synthase, completely protect islets from the deleterious effects of IL-1 beta. |
| 19970 | 1378415 | In vivo administration of TNF IL-1 has been shown to induce anti-diabetogenic effects in the NOD mouse. |
| 19971 | 1322036 | To this end, fetal rat pancreatic islets containing a high fraction of beta-cells were exposed in culture for 1-3 days to interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interferon-alpha (IFN-alpha), and interleukin-6 (IL-6) at different concentrations. |
| 19972 | 1322036 | In contrast, basal as well as glucose- and GH-stimulated insulin secretion was consistently suppressed by IL-1 beta from days 1-3. |
| 19973 | 1322036 | However, addition of the stimulatory cAMP analogue Sp-diastereomer of adenosine 3',5'-cyclic monophosphothioate or pertussis toxin, which themselves enhanced DNA synthesis and insulin secretion, failed to prevent the inhibitory actions of IL-1 beta on these parameters, making it unlikely that a decrease in cAMP is an important event in transduction of the inhibitory effects of the cytokine. |
| 19974 | 1627786 | Tumor necrosis factor and interferon gamma: relevance for immune regulation and genetic predisposition to autoimmune disease. |
| 19975 | 1627786 | Tumor necrosis factor and interferon gamma: relevance for immune regulation and genetic predisposition to autoimmune disease. |
| 19976 | 1627786 | The role of TNF-alpha and IFN-gamma in various models of autoimmune disease were analyzed. |
| 19977 | 1627786 | The role of TNF-alpha and IFN-gamma in various models of autoimmune disease were analyzed. |
| 19978 | 1320950 | Interleukin-1 and tumor necrosis factor: effector cytokines in autoimmune diseases. |
| 19979 | 1320950 | Interleukin-1 and tumor necrosis factor: effector cytokines in autoimmune diseases. |
| 19980 | 1320950 | Although the immune response is responsible for the initiation of autoimmune diseases, the effectors of the disease process likely involves cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). |
| 19981 | 1320950 | Although the immune response is responsible for the initiation of autoimmune diseases, the effectors of the disease process likely involves cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). |
| 19982 | 1320950 | Blocking IL-1 with its naturally occurring receptor antagonist, the IL-1 receptor antagonist reduces the severity of disease in animal models of inflammation and autoimmune processes. |
| 19983 | 1320950 | Blocking IL-1 with its naturally occurring receptor antagonist, the IL-1 receptor antagonist reduces the severity of disease in animal models of inflammation and autoimmune processes. |
| 19984 | 1320950 | Clinical studies with the IL-1 receptor antagonist will define the role for this cytokine in the pathogenesis of autoimmune diseases such as arthritis, inflammatory bowel disease, type I diabetes and vasculitis. |
| 19985 | 1320950 | Clinical studies with the IL-1 receptor antagonist will define the role for this cytokine in the pathogenesis of autoimmune diseases such as arthritis, inflammatory bowel disease, type I diabetes and vasculitis. |
| 19986 | 1503634 | Of the different cytokines which are present in the synovial fluid or produced by cells in the synovial tissue, most are presumed to have originated in macrophages/monocytes such as IL-1, IL-6, IL-8, TNF-alpha and TGF-beta. |
| 19987 | 1541051 | We have recently reported that chronic and systemic administration of tumor necrosis factor alpha (TNF) inhibits development of autoimmune diabetes in NOD mice and BB rats, animal models of insulin-dependent diabetes mellitus (IDDM). |
| 19988 | 1541051 | We have recently reported that chronic and systemic administration of tumor necrosis factor alpha (TNF) inhibits development of autoimmune diabetes in NOD mice and BB rats, animal models of insulin-dependent diabetes mellitus (IDDM). |
| 19989 | 1541051 | The in vivo TNF productivity in the diabetic rats, including the short-term- and long-term-diabetic rats, was correlated positively with the level of fructosamine/albumin (P less than 0.05) and negatively with the level of serum albumin (P less than 0.05), but not with levels of blood glucose. |
| 19990 | 1541051 | The in vivo TNF productivity in the diabetic rats, including the short-term- and long-term-diabetic rats, was correlated positively with the level of fructosamine/albumin (P less than 0.05) and negatively with the level of serum albumin (P less than 0.05), but not with levels of blood glucose. |
| 19991 | 1563985 | Haplospecific polymorphism between HLA B and tumor necrosis factor. |
| 19992 | 1563985 | Haplospecific polymorphism between HLA B and tumor necrosis factor. |
| 19993 | 1563985 | Haplospecific polymorphism between HLA B and tumor necrosis factor. |
| 19994 | 1563985 | Polymorphisms were sought between HLA B and tumor necrosis factor (TNF) using three genomic probes. |
| 19995 | 1563985 | Polymorphisms were sought between HLA B and tumor necrosis factor (TNF) using three genomic probes. |
| 19996 | 1563985 | Polymorphisms were sought between HLA B and tumor necrosis factor (TNF) using three genomic probes. |
| 19997 | 1563985 | Four were shared by more than one AH, but in these instances there were extensive similarities in other regions within the major histocompatibility complex (MHC), for example, the Japanese 46.2 (HLA Bw46-DRw8) and the Chinese 46.1 (Bw46-DR9) share all alleles between HLA C and C4 and differ only in class II, suggesting their relatively recent divergence by recombination between C4 and DR. |
| 19998 | 1563985 | Four were shared by more than one AH, but in these instances there were extensive similarities in other regions within the major histocompatibility complex (MHC), for example, the Japanese 46.2 (HLA Bw46-DRw8) and the Chinese 46.1 (Bw46-DR9) share all alleles between HLA C and C4 and differ only in class II, suggesting their relatively recent divergence by recombination between C4 and DR. |
| 19999 | 1563985 | Four were shared by more than one AH, but in these instances there were extensive similarities in other regions within the major histocompatibility complex (MHC), for example, the Japanese 46.2 (HLA Bw46-DRw8) and the Chinese 46.1 (Bw46-DR9) share all alleles between HLA C and C4 and differ only in class II, suggesting their relatively recent divergence by recombination between C4 and DR. |
| 20000 | 1563985 | Surprisingly, two insulin-dependent diabetes mellitus (IDDM)-resistant but race-specific AHs 52.1 (Bw52-DRB1*1502, Japanese) and 7.1 (B7-DRB1*1501, Caucasoid) carry the same Y-X-V haplotype, suggesting the possibility of localizing gene(s) relevant to IDDM. |
| 20001 | 1563985 | Surprisingly, two insulin-dependent diabetes mellitus (IDDM)-resistant but race-specific AHs 52.1 (Bw52-DRB1*1502, Japanese) and 7.1 (B7-DRB1*1501, Caucasoid) carry the same Y-X-V haplotype, suggesting the possibility of localizing gene(s) relevant to IDDM. |
| 20002 | 1563985 | Surprisingly, two insulin-dependent diabetes mellitus (IDDM)-resistant but race-specific AHs 52.1 (Bw52-DRB1*1502, Japanese) and 7.1 (B7-DRB1*1501, Caucasoid) carry the same Y-X-V haplotype, suggesting the possibility of localizing gene(s) relevant to IDDM. |
| 20003 | 1563985 | The present study confirms that MHC AHs have been conserved en bloc, including the region between HLA B and TNF. |
| 20004 | 1563985 | The present study confirms that MHC AHs have been conserved en bloc, including the region between HLA B and TNF. |
| 20005 | 1563985 | The present study confirms that MHC AHs have been conserved en bloc, including the region between HLA B and TNF. |
| 20006 | 1286540 | Prediction of insulin dependent diabetes mellitus in non-obese diabetic mice by the endogeneous tumor necrosis factor-alpha level. |
| 20007 | 1737960 | To investigate further the role of cytokines in the pathogenesis of type I insulin-dependent diabetes mellitus, the effects of interleukin-1 beta (IL-1), tumour necrosis factor-alpha (TNF) and gamma-interferon (IFN) were tested on rat insulinoma INS-1 cells. |
| 20008 | 1737960 | To investigate further the role of cytokines in the pathogenesis of type I insulin-dependent diabetes mellitus, the effects of interleukin-1 beta (IL-1), tumour necrosis factor-alpha (TNF) and gamma-interferon (IFN) were tested on rat insulinoma INS-1 cells. |
| 20009 | 1737960 | To investigate further the role of cytokines in the pathogenesis of type I insulin-dependent diabetes mellitus, the effects of interleukin-1 beta (IL-1), tumour necrosis factor-alpha (TNF) and gamma-interferon (IFN) were tested on rat insulinoma INS-1 cells. |
| 20010 | 1737960 | To investigate further the role of cytokines in the pathogenesis of type I insulin-dependent diabetes mellitus, the effects of interleukin-1 beta (IL-1), tumour necrosis factor-alpha (TNF) and gamma-interferon (IFN) were tested on rat insulinoma INS-1 cells. |
| 20011 | 1737960 | Whereas TNF and IFN had, respectively, a minor or no effect on insulin production, IL-1 caused a time- and dose-dependent decrease in insulin release and lowered the insulin content as well as the preproinsulin mRNA content of INS-1 cells. |
| 20012 | 1737960 | Whereas TNF and IFN had, respectively, a minor or no effect on insulin production, IL-1 caused a time- and dose-dependent decrease in insulin release and lowered the insulin content as well as the preproinsulin mRNA content of INS-1 cells. |
| 20013 | 1737960 | Whereas TNF and IFN had, respectively, a minor or no effect on insulin production, IL-1 caused a time- and dose-dependent decrease in insulin release and lowered the insulin content as well as the preproinsulin mRNA content of INS-1 cells. |
| 20014 | 1737960 | Whereas TNF and IFN had, respectively, a minor or no effect on insulin production, IL-1 caused a time- and dose-dependent decrease in insulin release and lowered the insulin content as well as the preproinsulin mRNA content of INS-1 cells. |
| 20015 | 1737960 | Both IL-1 and TNF exerted a cytostatic effect, estimated by a decrease in [3H]thymidine incorporation, while only IL-1 decreased cell viability as measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. |
| 20016 | 1737960 | Both IL-1 and TNF exerted a cytostatic effect, estimated by a decrease in [3H]thymidine incorporation, while only IL-1 decreased cell viability as measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. |
| 20017 | 1737960 | Both IL-1 and TNF exerted a cytostatic effect, estimated by a decrease in [3H]thymidine incorporation, while only IL-1 decreased cell viability as measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. |
| 20018 | 1737960 | Both IL-1 and TNF exerted a cytostatic effect, estimated by a decrease in [3H]thymidine incorporation, while only IL-1 decreased cell viability as measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. |
| 20019 | 1737960 | The glutathione content of INS-1 cells was shown to be modulated by the presence of 2-mercaptoethanol in the culture medium, but was not affected by IL-1 or TNF. |
| 20020 | 1737960 | The glutathione content of INS-1 cells was shown to be modulated by the presence of 2-mercaptoethanol in the culture medium, but was not affected by IL-1 or TNF. |
| 20021 | 1737960 | The glutathione content of INS-1 cells was shown to be modulated by the presence of 2-mercaptoethanol in the culture medium, but was not affected by IL-1 or TNF. |
| 20022 | 1737960 | The glutathione content of INS-1 cells was shown to be modulated by the presence of 2-mercaptoethanol in the culture medium, but was not affected by IL-1 or TNF. |
| 20023 | 1424744 | The presence of interleukin 6 (IL-6), interleukin 1 (IL-1), interleukin 2 (IL-2) and tumour necrosis factor (TNF) was investigated in vitreous and aqueous aspirates from eyes undergoing vitrectomy for the treatment of different inflammatory conditions. |
| 20024 | 1424744 | The present observations suggest that cytokines, particularly IL-6 and IL-1, may act as local amplification signals in pathological processes associated with chronic eye inflammation. |
| 20025 | 1399323 | Interleukin-1 (IL-1) is a 17-kDa pro-inflammatory cytokine synthesized from a variety of cell types primarily in association with disease states or during host perturbation such as immune responses. |
| 20026 | 1399323 | Organ failure, capillary leak and death occur in animals after a combination of tumour necrosis factor (TNF) and IL-1 which is more effective in inducing these changes than either cytokine alone. |
| 20027 | 1399323 | IL-1 is also a potent inducer of endothelial cell adhesion molecules, IL-6, and IL-8, a neutrophil chemotactic and activating factor. |
| 20028 | 1399323 | A naturally occurring IL-1-specific receptor antagonist (IL-1ra), which shares 40% conserved amino-acid homology with IL-1 beta, binds to IL-1 surface receptors with the same affinity as IL-1 but does not possess agonist activity and acts as a competitive inhibitor of IL-1. |
| 20029 | 1399323 | Studies using the IL-1ra to block endogenous IL-1 in a variety of animal disease models suggest that IL-1 plays a key role in triggering the cascade of inflammatory responses. |
| 20030 | 1356098 | The major histocompatibility complex (MHC) contains multiple and diverse genes which may be relevant to the induction and regulation of autoimmune responses in insulin dependent diabetes mellitus (IDDM). |
| 20031 | 1356098 | In addition to HLA class I and II, the possible candidates include TNF, C4, and several other poorly defined polymorphic genes in the central MHC region. |
| 20032 | 1356098 | This study describes two approaches which take advantage of the fact that the relevant genes are carried by highly conserved ancestral haplotypes such as 8.1 (HLA-B8, TNFS, C4AQ0, C4B1, DR3, DQ2). |
| 20033 | 1356098 | Third, using haplotypic polymorphisms such as the one in BAT3, we have shown that all the patients carrying recombinants of the 8.1 ancestral haplotype share the central region adjacent to HLA-B. |
| 20034 | 1356098 | These findings suggest that both HLA and non-HLA genes are involved in conferring susceptibility to IDDM, and that the region between HLA-B and BAT3 contains some of the relevant genes. |
| 20035 | 1341919 | Serum levels of tumor necrosis factor in insulin-dependent diabetic patients. |
| 20036 | 1341919 | Serum levels of tumor necrosis factor in insulin-dependent diabetic patients. |
| 20037 | 1341919 | We determined the serum concentrations of tumor necrosis factor (TNF) in 15 nondiabetic healthy subjects and in 36 insulin-dependent (type I) diabetic outpatients. |
| 20038 | 1341919 | We determined the serum concentrations of tumor necrosis factor (TNF) in 15 nondiabetic healthy subjects and in 36 insulin-dependent (type I) diabetic outpatients. |
| 20039 | 1340530 | The blood monocytes adhere to endothelial cells unstimulated and after stimulation by interleukin-1, tumor necrosis factor or other mediators. |
| 20040 | 1340530 | E-Selectin (ELAM-1), P-Selectin (GMP-140) and receptors of the immunoglobulin superfamily (ICAM-1, ICAM-2 and VCAM-1) are expressed on endothelial cells in basal conditions and after activation. |
| 20041 | 1340530 | As estimated by flow cytometry CD11b/CD18 expression on diabetic monocytes was increased. |
| 20042 | 1340530 | Pentoxifylline reduced CD11b/CD18 expression on normal and diabetic monocytes. |
| 20043 | 1319488 | Immunomodulating functions of tumor necrosis factor and interleukin 1 inhibitors. |
| 20044 | 1319488 | Immunomodulating functions of tumor necrosis factor and interleukin 1 inhibitors. |
| 20045 | 1319488 | Inhibitors to interleukin 1 and tumor necrosis factor may have therapeutic potential in conditions such as inflammatory arthritis, diabetes mellitus, disseminated intravascular coagulopathy and septic shock. |
| 20046 | 1319488 | Inhibitors to interleukin 1 and tumor necrosis factor may have therapeutic potential in conditions such as inflammatory arthritis, diabetes mellitus, disseminated intravascular coagulopathy and septic shock. |
| 20047 | 1762301 | Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. |
| 20048 | 1762301 | Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. |
| 20049 | 1762301 | Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. |
| 20050 | 1762301 | Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. |
| 20051 | 1762301 | Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. |
| 20052 | 1762301 | The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. |
| 20053 | 1762301 | The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. |
| 20054 | 1762301 | The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. |
| 20055 | 1762301 | The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. |
| 20056 | 1762301 | The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. |
| 20057 | 1762301 | When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. |
| 20058 | 1762301 | When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. |
| 20059 | 1762301 | When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. |
| 20060 | 1762301 | When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. |
| 20061 | 1762301 | When thioglycollate-elicited peritoneal macrophages (M phi) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. |
| 20062 | 1762301 | The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. |
| 20063 | 1762301 | The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. |
| 20064 | 1762301 | The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. |
| 20065 | 1762301 | The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. |
| 20066 | 1762301 | The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. |
| 20067 | 1762301 | These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. |
| 20068 | 1762301 | These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. |
| 20069 | 1762301 | These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. |
| 20070 | 1762301 | These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. |
| 20071 | 1762301 | These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi. |
| 20072 | 1747949 | We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. |
| 20073 | 1747949 | We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. |
| 20074 | 1747949 | We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. |
| 20075 | 1747949 | We have recently reported that systemic and chronic administration of recombinant tumour necrosis factor alpha (TNF-alpha), as well as streptococcal preparation (OK-432), inhibits development of insulin-dependent diabetes mellitus (IDDM) in NOD mice and BB rats, models of IDDM. |
| 20076 | 1747949 | In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. |
| 20077 | 1747949 | In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. |
| 20078 | 1747949 | In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. |
| 20079 | 1747949 | In this study we examined whether serum containing endogenous TNF induced by OK-432 injection could inhibit IDDM in NOD mice. |
| 20080 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 20081 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 20082 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 20083 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 20084 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 20085 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 20086 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 20087 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 20088 | 1939517 | Role of tumor necrosis factor-alpha and interferon-gamma as growth factors to the human fetal beta-cell. |
| 20089 | 1939517 | Role of tumor necrosis factor-alpha and interferon-gamma as growth factors to the human fetal beta-cell. |
| 20090 | 1939517 | Role of tumor necrosis factor-alpha and interferon-gamma as growth factors to the human fetal beta-cell. |
| 20091 | 1939517 | The effects of the cytokines tumor necrosis factor-alpha and interferon-gamma on the adult beta-cell have been well described: a reduction of insulin secretion and content and death of the cell. |
| 20092 | 1939517 | The effects of the cytokines tumor necrosis factor-alpha and interferon-gamma on the adult beta-cell have been well described: a reduction of insulin secretion and content and death of the cell. |
| 20093 | 1939517 | The effects of the cytokines tumor necrosis factor-alpha and interferon-gamma on the adult beta-cell have been well described: a reduction of insulin secretion and content and death of the cell. |
| 20094 | 1939517 | It is hypothesized that the functional immaturity and lack of normal (adult) metabolic activity of the human fetal beta-cell somehow confers protection on these cells from the cytotoxic effects of tumor necrosis factor-alpha and interferon-gamma. |
| 20095 | 1939517 | It is hypothesized that the functional immaturity and lack of normal (adult) metabolic activity of the human fetal beta-cell somehow confers protection on these cells from the cytotoxic effects of tumor necrosis factor-alpha and interferon-gamma. |
| 20096 | 1939517 | It is hypothesized that the functional immaturity and lack of normal (adult) metabolic activity of the human fetal beta-cell somehow confers protection on these cells from the cytotoxic effects of tumor necrosis factor-alpha and interferon-gamma. |
| 20097 | 1934594 | Cytokines are known to play an important role in autoimmunity and have been suggested to be involved in the pathogenesis of insulin-dependent diabetes (IDDM). |
| 20098 | 1934594 | Cytokines are known to play an important role in autoimmunity and have been suggested to be involved in the pathogenesis of insulin-dependent diabetes (IDDM). |
| 20099 | 1934594 | In the present study we have measured IL-1, IL-2, IL-4, IL-6, interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) (using both immunoassays and bioassays) in sera from 50 patients affected by IDDM at the time of clinical diagnosis and 51 age and sex matched controls. |
| 20100 | 1934594 | In the present study we have measured IL-1, IL-2, IL-4, IL-6, interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) (using both immunoassays and bioassays) in sera from 50 patients affected by IDDM at the time of clinical diagnosis and 51 age and sex matched controls. |
| 20101 | 1934594 | Detectable levels of IL-1, IL-2, IL-6 and IFN-gamma were found in the serum of a small percentage of subjects and were not significantly different between patients and controls. |
| 20102 | 1934594 | Detectable levels of IL-1, IL-2, IL-6 and IFN-gamma were found in the serum of a small percentage of subjects and were not significantly different between patients and controls. |
| 20103 | 1934594 | IL-4 was detectable in a higher number of both patients and controls and circulating TNF-alpha (greater than 1 U/ml) was found in a percentage of patients (24%) significantly higher than controls (P less than 0.01). |
| 20104 | 1934594 | IL-4 was detectable in a higher number of both patients and controls and circulating TNF-alpha (greater than 1 U/ml) was found in a percentage of patients (24%) significantly higher than controls (P less than 0.01). |
| 20105 | 1718801 | De novo induction of ICAM-1 but not LFA-3. |
| 20106 | 1718801 | De novo induction of ICAM-1 but not LFA-3. |
| 20107 | 1718801 | T-lymphocyte recognition of surface antigens also involves adhesion accessory molecules: intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-associated antigen 3 (LFA-3). |
| 20108 | 1718801 | T-lymphocyte recognition of surface antigens also involves adhesion accessory molecules: intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-associated antigen 3 (LFA-3). |
| 20109 | 1718801 | Levels of ICAM-1 and LFA-3 expression in normal human islet cells and regulation of their expression by cytokines interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6 have been studied by two-color immunofluorescence staining of pancreatic cryostat sections and fluorescence-activated cell sorter analysis. |
| 20110 | 1718801 | Levels of ICAM-1 and LFA-3 expression in normal human islet cells and regulation of their expression by cytokines interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6 have been studied by two-color immunofluorescence staining of pancreatic cryostat sections and fluorescence-activated cell sorter analysis. |
| 20111 | 1718801 | Neither ICAM-1 nor LFA-3 could be demonstrated in sections or in fresh cell preparations, but after 18 h of culture, beta-, alpha-, and delta-cells expressed spontaneously moderate levels of ICAM-1 (but not LFA-3). |
| 20112 | 1718801 | Neither ICAM-1 nor LFA-3 could be demonstrated in sections or in fresh cell preparations, but after 18 h of culture, beta-, alpha-, and delta-cells expressed spontaneously moderate levels of ICAM-1 (but not LFA-3). |
| 20113 | 1718801 | IFN-gamma and TNF-alpha alone or in combination strongly enhanced this spontaneous expression of ICAM-1 in a time- and/or dose-dependent and additive manner but had no effect on LFA-3. |
| 20114 | 1718801 | IFN-gamma and TNF-alpha alone or in combination strongly enhanced this spontaneous expression of ICAM-1 in a time- and/or dose-dependent and additive manner but had no effect on LFA-3. |
| 20115 | 1718801 | An SV40-transformed islet cell line showed high basal levels of both ICAM-1 and LFA-3, but the response to cytokines followed the same pattern as primary cultures. |
| 20116 | 1718801 | An SV40-transformed islet cell line showed high basal levels of both ICAM-1 and LFA-3, but the response to cytokines followed the same pattern as primary cultures. |
| 20117 | 1768735 | The objective of this study was to determine whether transforming growth factor beta (TGF-beta) can inhibit the destruction of islet cells by either spleen cells from acutely diabetic BB/Wor rats, or by the cytokines tumor necrosis factor (TNF) and interferon gamma (IFN-gamma). |
| 20118 | 1768735 | The objective of this study was to determine whether transforming growth factor beta (TGF-beta) can inhibit the destruction of islet cells by either spleen cells from acutely diabetic BB/Wor rats, or by the cytokines tumor necrosis factor (TNF) and interferon gamma (IFN-gamma). |
| 20119 | 1768735 | The objective of this study was to determine whether transforming growth factor beta (TGF-beta) can inhibit the destruction of islet cells by either spleen cells from acutely diabetic BB/Wor rats, or by the cytokines tumor necrosis factor (TNF) and interferon gamma (IFN-gamma). |
| 20120 | 1768735 | Similarly, TNF and IFN-gamma have been shown to act synergistically to destroy islet cell monolayers. |
| 20121 | 1768735 | Similarly, TNF and IFN-gamma have been shown to act synergistically to destroy islet cell monolayers. |
| 20122 | 1768735 | Similarly, TNF and IFN-gamma have been shown to act synergistically to destroy islet cell monolayers. |
| 20123 | 1768735 | TGF-beta (10 ng/ml) was also shown to significantly inhibit the TNF and IFN-gamma-induced lysis of islet cell monolayers. |
| 20124 | 1768735 | TGF-beta (10 ng/ml) was also shown to significantly inhibit the TNF and IFN-gamma-induced lysis of islet cell monolayers. |
| 20125 | 1768735 | TGF-beta (10 ng/ml) was also shown to significantly inhibit the TNF and IFN-gamma-induced lysis of islet cell monolayers. |
| 20126 | 1656517 | Dietary supplementation with omega-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1 beta content but not monokine secretion in healthy and insulin-dependent diabetic individuals. |
| 20127 | 1656517 | Dietary supplementation with omega-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1 beta content but not monokine secretion in healthy and insulin-dependent diabetic individuals. |
| 20128 | 1656517 | Dietary supplementation with omega-3-polyunsaturated fatty acids decreases mononuclear cell proliferation and interleukin-1 beta content but not monokine secretion in healthy and insulin-dependent diabetic individuals. |
| 20129 | 1656517 | The effects of dietary supplementation with omega-3-polyunsaturated fatty acids (omega-3-PUFA) on the proliferative response of PBMC and on the secretion of monokines and arachidonic acid metabolites from PBMC and monocytes (Mo) from healthy subjects and patients with recent-onset insulin-dependent diabetes mellitus (IDDM) were examined. |
| 20130 | 1656517 | The effects of dietary supplementation with omega-3-polyunsaturated fatty acids (omega-3-PUFA) on the proliferative response of PBMC and on the secretion of monokines and arachidonic acid metabolites from PBMC and monocytes (Mo) from healthy subjects and patients with recent-onset insulin-dependent diabetes mellitus (IDDM) were examined. |
| 20131 | 1656517 | The effects of dietary supplementation with omega-3-polyunsaturated fatty acids (omega-3-PUFA) on the proliferative response of PBMC and on the secretion of monokines and arachidonic acid metabolites from PBMC and monocytes (Mo) from healthy subjects and patients with recent-onset insulin-dependent diabetes mellitus (IDDM) were examined. |
| 20132 | 1656517 | IL-1 beta production and TNF-alpha secretion was determined before and after 7 weeks of treatment, and 10 weeks after withdrawal of treatment. |
| 20133 | 1656517 | IL-1 beta production and TNF-alpha secretion was determined before and after 7 weeks of treatment, and 10 weeks after withdrawal of treatment. |
| 20134 | 1656517 | IL-1 beta production and TNF-alpha secretion was determined before and after 7 weeks of treatment, and 10 weeks after withdrawal of treatment. |
| 20135 | 1656517 | Significant increases in platelet and PBMC membrane eicosapentaenoic acid was found in omega-3-PUFA-treated individuals. omega-3-PUFA treatment significantly reduced the content of IL-1 beta in lysates of PBMC, but did not affect PBMC or Mo secretion of IL-1 beta, TNF-alpha or prostaglandin E2 (PGE2) or PBMC leukotriene B4 (LTB4) secretion in healthy subjects or in IDDM patients. |
| 20136 | 1656517 | Significant increases in platelet and PBMC membrane eicosapentaenoic acid was found in omega-3-PUFA-treated individuals. omega-3-PUFA treatment significantly reduced the content of IL-1 beta in lysates of PBMC, but did not affect PBMC or Mo secretion of IL-1 beta, TNF-alpha or prostaglandin E2 (PGE2) or PBMC leukotriene B4 (LTB4) secretion in healthy subjects or in IDDM patients. |
| 20137 | 1656517 | Significant increases in platelet and PBMC membrane eicosapentaenoic acid was found in omega-3-PUFA-treated individuals. omega-3-PUFA treatment significantly reduced the content of IL-1 beta in lysates of PBMC, but did not affect PBMC or Mo secretion of IL-1 beta, TNF-alpha or prostaglandin E2 (PGE2) or PBMC leukotriene B4 (LTB4) secretion in healthy subjects or in IDDM patients. |
| 20138 | 1656517 | No correlation was found between PHA-stimulated PBMC proliferation and PBMC secretion of TNF-alpha and IL-1 beta. |
| 20139 | 1656517 | No correlation was found between PHA-stimulated PBMC proliferation and PBMC secretion of TNF-alpha and IL-1 beta. |
| 20140 | 1656517 | No correlation was found between PHA-stimulated PBMC proliferation and PBMC secretion of TNF-alpha and IL-1 beta. |
| 20141 | 1656517 | There were no significant differences in the spontaneous or the PPD- or PHA-stimulated proliferative responses of PBMC between diabetic and healthy individuals at entry. |
| 20142 | 1656517 | There were no significant differences in the spontaneous or the PPD- or PHA-stimulated proliferative responses of PBMC between diabetic and healthy individuals at entry. |
| 20143 | 1656517 | There were no significant differences in the spontaneous or the PPD- or PHA-stimulated proliferative responses of PBMC between diabetic and healthy individuals at entry. |
| 20144 | 1656517 | We conclude that although dietary supplementation with 4.0 g/day of omega-3-PUFA inhibits the proliferation of PBMC and reduces IL-1 beta immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects. |
| 20145 | 1656517 | We conclude that although dietary supplementation with 4.0 g/day of omega-3-PUFA inhibits the proliferation of PBMC and reduces IL-1 beta immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects. |
| 20146 | 1656517 | We conclude that although dietary supplementation with 4.0 g/day of omega-3-PUFA inhibits the proliferation of PBMC and reduces IL-1 beta immunoreactivity in PBMC and Mo, it does not alter monokine, PGE2 or LTB4, secretion in healthy or IDDM subjects. |
| 20147 | 1959944 | For this purpose RINm5F cells were exposed in culture for 1-2 days to interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma) and interferon alpha (IFN-alpha) at different concentrations. |
| 20148 | 1959944 | For this purpose RINm5F cells were exposed in culture for 1-2 days to interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma) and interferon alpha (IFN-alpha) at different concentrations. |
| 20149 | 1959944 | It was found that IL-1 beta markedly decreased the cellular content of insulin and secretion of the hormone into the culture medium, while causing a very slight inhibition of RINm5F cell proliferation. |
| 20150 | 1959944 | It was found that IL-1 beta markedly decreased the cellular content of insulin and secretion of the hormone into the culture medium, while causing a very slight inhibition of RINm5F cell proliferation. |
| 20151 | 1959944 | On the other hand, IFN-gamma and IFN-alpha both elicited marked decreases in proliferation and insulin content and secretion by the insulinoma cells. |
| 20152 | 1959944 | On the other hand, IFN-gamma and IFN-alpha both elicited marked decreases in proliferation and insulin content and secretion by the insulinoma cells. |
| 20153 | 1959944 | IL-6 and TNF-alpha were found not to affect these parameters. |
| 20154 | 1959944 | IL-6 and TNF-alpha were found not to affect these parameters. |
| 20155 | 1959944 | There was no protection against the cytotoxicity of IL-1 beta, IFN-gamma or IFN-alpha by pre-treatment with pertussis toxin. |
| 20156 | 1959944 | There was no protection against the cytotoxicity of IL-1 beta, IFN-gamma or IFN-alpha by pre-treatment with pertussis toxin. |
| 20157 | 1959944 | From these findings it is concluded that the cytokines IL-1 beta, IFN-gamma and IFN-alpha act in a non-synergistic fashion in suppressing RINm5F cell proliferation and hormone secretion. |
| 20158 | 1959944 | From these findings it is concluded that the cytokines IL-1 beta, IFN-gamma and IFN-alpha act in a non-synergistic fashion in suppressing RINm5F cell proliferation and hormone secretion. |
| 20159 | 1958051 | Fasting blood samples were collected from 83 patients with histologically proven breast cancer and analysed for plasma glucagon, serum immunoreactive tumour necrosis factor (TNF alpha), insulin, glucose, growth hormone, cortisol and TSH. |
| 20160 | 1680332 | The presence of Neuron Specific Enolase, Protein Gene Product 9.5, cytokeratin, microvilli, cytoplasmic electrodense granules and the secretion of insulin, glucagon and somatostatin supports the neuroendocrine origin of this cell line. |
| 20161 | 1680332 | Flow cytometric analysis showed that HLA expression in this cell line is readily induced by IFN-gamma and modulated by TNF-alpha. |
| 20162 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 20163 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 20164 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 20165 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 20166 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 20167 | 2016534 | In this study, we utilized in situ hybridization to determine the expression of the IL-1, TNF, and IL-6 genes within the pancreas of the acute diabetic Biobreeding Worcester rat. |
| 20168 | 2016534 | In this study, we utilized in situ hybridization to determine the expression of the IL-1, TNF, and IL-6 genes within the pancreas of the acute diabetic Biobreeding Worcester rat. |
| 20169 | 2016534 | In this study, we utilized in situ hybridization to determine the expression of the IL-1, TNF, and IL-6 genes within the pancreas of the acute diabetic Biobreeding Worcester rat. |
| 20170 | 2016534 | In this study, we utilized in situ hybridization to determine the expression of the IL-1, TNF, and IL-6 genes within the pancreas of the acute diabetic Biobreeding Worcester rat. |
| 20171 | 2016534 | In this study, we utilized in situ hybridization to determine the expression of the IL-1, TNF, and IL-6 genes within the pancreas of the acute diabetic Biobreeding Worcester rat. |
| 20172 | 2016534 | These studies showed that cells expressing IL-1, TNF, and IL-6 were present within the islets and in the exocrine pancreas surrounding islets, ducts, and vessels and in an interstitial location. |
| 20173 | 2016534 | These studies showed that cells expressing IL-1, TNF, and IL-6 were present within the islets and in the exocrine pancreas surrounding islets, ducts, and vessels and in an interstitial location. |
| 20174 | 2016534 | These studies showed that cells expressing IL-1, TNF, and IL-6 were present within the islets and in the exocrine pancreas surrounding islets, ducts, and vessels and in an interstitial location. |
| 20175 | 2016534 | These studies showed that cells expressing IL-1, TNF, and IL-6 were present within the islets and in the exocrine pancreas surrounding islets, ducts, and vessels and in an interstitial location. |
| 20176 | 2016534 | These studies showed that cells expressing IL-1, TNF, and IL-6 were present within the islets and in the exocrine pancreas surrounding islets, ducts, and vessels and in an interstitial location. |
| 20177 | 2016534 | Cells expressing TNF and IL-1 mRNA were present in about 20% of the islets, whereas cells expressing IL-6 were present in about 4% of the islets. |
| 20178 | 2016534 | Cells expressing TNF and IL-1 mRNA were present in about 20% of the islets, whereas cells expressing IL-6 were present in about 4% of the islets. |
| 20179 | 2016534 | Cells expressing TNF and IL-1 mRNA were present in about 20% of the islets, whereas cells expressing IL-6 were present in about 4% of the islets. |
| 20180 | 2016534 | Cells expressing TNF and IL-1 mRNA were present in about 20% of the islets, whereas cells expressing IL-6 were present in about 4% of the islets. |
| 20181 | 2016534 | Cells expressing TNF and IL-1 mRNA were present in about 20% of the islets, whereas cells expressing IL-6 were present in about 4% of the islets. |
| 20182 | 2016534 | Islets containing TNF- or IL-1-positive cells contained about three positive cells per islet whereas only about one IL-6-positive cell was present per islet. |
| 20183 | 2016534 | Islets containing TNF- or IL-1-positive cells contained about three positive cells per islet whereas only about one IL-6-positive cell was present per islet. |
| 20184 | 2016534 | Islets containing TNF- or IL-1-positive cells contained about three positive cells per islet whereas only about one IL-6-positive cell was present per islet. |
| 20185 | 2016534 | Islets containing TNF- or IL-1-positive cells contained about three positive cells per islet whereas only about one IL-6-positive cell was present per islet. |
| 20186 | 2016534 | Islets containing TNF- or IL-1-positive cells contained about three positive cells per islet whereas only about one IL-6-positive cell was present per islet. |
| 20187 | 2016534 | Peri-insular IL-1 positive cells were seen in 14% of the islets and 8% showed peri-insular IL-6 positive cells. |
| 20188 | 2016534 | Peri-insular IL-1 positive cells were seen in 14% of the islets and 8% showed peri-insular IL-6 positive cells. |
| 20189 | 2016534 | Peri-insular IL-1 positive cells were seen in 14% of the islets and 8% showed peri-insular IL-6 positive cells. |
| 20190 | 2016534 | Peri-insular IL-1 positive cells were seen in 14% of the islets and 8% showed peri-insular IL-6 positive cells. |
| 20191 | 2016534 | Peri-insular IL-1 positive cells were seen in 14% of the islets and 8% showed peri-insular IL-6 positive cells. |
| 20192 | 2020184 | This study examines leukocyte infiltration and the appearance of tumor necrosis factor-alpha (TNF) and IL-6 in wound chambers implanted in normal and streptozotocin-induced diabetic mice. |
| 20193 | 2020184 | This study examines leukocyte infiltration and the appearance of tumor necrosis factor-alpha (TNF) and IL-6 in wound chambers implanted in normal and streptozotocin-induced diabetic mice. |
| 20194 | 2020184 | Wound fluid aspirated from the chambers 1, 3, and 7 days following implantation was analyzed for the total number of leukocytes and TNF and IL-6 levels. |
| 20195 | 2020184 | Wound fluid aspirated from the chambers 1, 3, and 7 days following implantation was analyzed for the total number of leukocytes and TNF and IL-6 levels. |
| 20196 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20197 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20198 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20199 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20200 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20201 | 1909136 | Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse. |
| 20202 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20203 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20204 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20205 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20206 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20207 | 1909136 | In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. |
| 20208 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20209 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20210 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20211 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20212 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20213 | 1909136 | In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. |
| 20214 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20215 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20216 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20217 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20218 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20219 | 1909136 | Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. |
| 20220 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20221 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20222 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20223 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20224 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20225 | 1909136 | The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. |
| 20226 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20227 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20228 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20229 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20230 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20231 | 1909136 | Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. |
| 20232 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20233 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20234 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20235 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20236 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20237 | 1909136 | We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model. |
| 20238 | 1893147 | Then TNF content of the medium and basal and stimulated insulin release were determined. |
| 20239 | 1893147 | Then TNF content of the medium and basal and stimulated insulin release were determined. |
| 20240 | 1893147 | Then TNF content of the medium and basal and stimulated insulin release were determined. |
| 20241 | 1893147 | Mononuclear cells from both healthy donors and diabetic patients could inhibit the insulin release with no correlation to TNF content. |
| 20242 | 1893147 | Mononuclear cells from both healthy donors and diabetic patients could inhibit the insulin release with no correlation to TNF content. |
| 20243 | 1893147 | Mononuclear cells from both healthy donors and diabetic patients could inhibit the insulin release with no correlation to TNF content. |
| 20244 | 1893147 | Addition of lipopolysaccharide resulted in a 5-7 times increase of TNF content of the medium followed by a more pronounced inhibition of insulin release. |
| 20245 | 1893147 | Addition of lipopolysaccharide resulted in a 5-7 times increase of TNF content of the medium followed by a more pronounced inhibition of insulin release. |
| 20246 | 1893147 | Addition of lipopolysaccharide resulted in a 5-7 times increase of TNF content of the medium followed by a more pronounced inhibition of insulin release. |
| 20247 | 2025250 | IL-1 and TNF alpha are assumed to be major mediators of islet cell destruction during the pathogenesis of type 1 diabetes. |
| 20248 | 2025250 | IL-1 and TNF alpha are assumed to be major mediators of islet cell destruction during the pathogenesis of type 1 diabetes. |
| 20249 | 2025250 | Here we show by neutralization of the two cytokines with excess antibody that IL-1 and TNF alpha do not contribute to the cytotoxic activity of activated macrophages towards isolated islet cells. |
| 20250 | 2025250 | Here we show by neutralization of the two cytokines with excess antibody that IL-1 and TNF alpha do not contribute to the cytotoxic activity of activated macrophages towards isolated islet cells. |
| 20251 | 1888882 | Monoclonal anti-interleukin-1 (IL-1) influences on direct and indirect IL-1-mediated islet effects. |
| 20252 | 1888882 | Suppression of both human and rat islet insulin secretion resulted from co-culture with recombinant interleukin-1 alpha (rIL-1 alpha) or interleukin-1 beta (rIL-1 beta); however, direct rIL-1 alpha and rIL-1 beta cytotoxicity was seen with rat islets but not with human islets. |
| 20253 | 1888882 | Human islet insulin secretion was also suppressed during co-culture with recombinant tumor necrosis factor (rTNF) or interferon (rIFN), but not with lymphotoxin (rLT) or rIL-6; rat islet insulin secretion was not suppressed by any of these cytokines. |
| 20254 | 1847937 | Ca2+ responses to interleukin 1 and tumor necrosis factor in cultured human skin fibroblasts. |
| 20255 | 1847937 | Ca2+ responses to interleukin 1 and tumor necrosis factor in cultured human skin fibroblasts. |
| 20256 | 1847937 | Ca2+ responses to interleukin 1 and tumor necrosis factor in cultured human skin fibroblasts. |
| 20257 | 1847937 | Ca2+ responses to interleukin 1 and tumor necrosis factor in cultured human skin fibroblasts. |
| 20258 | 1847937 | Ca2+ responses to interleukin 1 and tumor necrosis factor in cultured human skin fibroblasts. |
| 20259 | 1847937 | To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS. |
| 20260 | 1847937 | To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS. |
| 20261 | 1847937 | To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS. |
| 20262 | 1847937 | To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS. |
| 20263 | 1847937 | To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS. |
| 20264 | 1847937 | IL-1 and TNF caused rapid, transient, and concentration-dependent increases in cytosolic free Ca2+. |
| 20265 | 1847937 | IL-1 and TNF caused rapid, transient, and concentration-dependent increases in cytosolic free Ca2+. |
| 20266 | 1847937 | IL-1 and TNF caused rapid, transient, and concentration-dependent increases in cytosolic free Ca2+. |
| 20267 | 1847937 | IL-1 and TNF caused rapid, transient, and concentration-dependent increases in cytosolic free Ca2+. |
| 20268 | 1847937 | IL-1 and TNF caused rapid, transient, and concentration-dependent increases in cytosolic free Ca2+. |
| 20269 | 1847937 | The peak cytosolic free Ca2+ was greater and occurred at higher concentrations of IL-1 and TNF in patient cells than in cells from age-matched controls. |
| 20270 | 1847937 | The peak cytosolic free Ca2+ was greater and occurred at higher concentrations of IL-1 and TNF in patient cells than in cells from age-matched controls. |
| 20271 | 1847937 | The peak cytosolic free Ca2+ was greater and occurred at higher concentrations of IL-1 and TNF in patient cells than in cells from age-matched controls. |
| 20272 | 1847937 | The peak cytosolic free Ca2+ was greater and occurred at higher concentrations of IL-1 and TNF in patient cells than in cells from age-matched controls. |
| 20273 | 1847937 | The peak cytosolic free Ca2+ was greater and occurred at higher concentrations of IL-1 and TNF in patient cells than in cells from age-matched controls. |
| 20274 | 1847937 | In control cells, the Ca2+ transient diminished sharply with increasing amounts of IL-1 or TNF above the maximum stimulatory concentration. |
| 20275 | 1847937 | In control cells, the Ca2+ transient diminished sharply with increasing amounts of IL-1 or TNF above the maximum stimulatory concentration. |
| 20276 | 1847937 | In control cells, the Ca2+ transient diminished sharply with increasing amounts of IL-1 or TNF above the maximum stimulatory concentration. |
| 20277 | 1847937 | In control cells, the Ca2+ transient diminished sharply with increasing amounts of IL-1 or TNF above the maximum stimulatory concentration. |
| 20278 | 1847937 | In control cells, the Ca2+ transient diminished sharply with increasing amounts of IL-1 or TNF above the maximum stimulatory concentration. |
| 20279 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 20280 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 20281 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 20282 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 20283 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 20284 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 20285 | 2060425 | Tumor necrosis factor suppresses the endothelial anticoagulant cofactor thrombomodulin and induces expression of the procoagulant cofactor tissue factor. |
| 20286 | 1676685 | HLA-DQA1*1 contributes to resistance and A1*3 confers susceptibility to type 1 (insulin-dependent) diabetes mellitus in Japanese subjects. |
| 20287 | 1676685 | In this study HLA-DQA1 and TNF genes in addition to HLA-DQB1 gene were investigated at DNA level for elucidation of the genetic backgrounds of Type 1 (insulin-dependent) diabetes mellitus in Japanese subjects. |
| 20288 | 1996407 | HLA-class III region genes may be associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). |
| 20289 | 1996407 | HLA-class III region genes may be associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). |
| 20290 | 1996407 | HLA-class III region genes may be associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). |
| 20291 | 1996407 | HLA-class III region genes may be associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). |
| 20292 | 1996407 | In this study an NcoI polymorphism of the tumour necrosis factor beta (TNF-beta) gene, which is positioned next to the tumour necrosis factor alpha (TNF-alpha) gene in the HLA class III region, was detected by restriction fragment length polymorphism (RFLP). |
| 20293 | 1996407 | In this study an NcoI polymorphism of the tumour necrosis factor beta (TNF-beta) gene, which is positioned next to the tumour necrosis factor alpha (TNF-alpha) gene in the HLA class III region, was detected by restriction fragment length polymorphism (RFLP). |
| 20294 | 1996407 | In this study an NcoI polymorphism of the tumour necrosis factor beta (TNF-beta) gene, which is positioned next to the tumour necrosis factor alpha (TNF-alpha) gene in the HLA class III region, was detected by restriction fragment length polymorphism (RFLP). |
| 20295 | 1996407 | In this study an NcoI polymorphism of the tumour necrosis factor beta (TNF-beta) gene, which is positioned next to the tumour necrosis factor alpha (TNF-alpha) gene in the HLA class III region, was detected by restriction fragment length polymorphism (RFLP). |
| 20296 | 1996407 | In all groups there was a haplotype assignment of the TNF-beta 5.5-kb allele to B8,DR3 haplotypes, and of the TNF-beta 10.5-kb allele to B15,DR4-positive haplotypes. |
| 20297 | 1996407 | In all groups there was a haplotype assignment of the TNF-beta 5.5-kb allele to B8,DR3 haplotypes, and of the TNF-beta 10.5-kb allele to B15,DR4-positive haplotypes. |
| 20298 | 1996407 | In all groups there was a haplotype assignment of the TNF-beta 5.5-kb allele to B8,DR3 haplotypes, and of the TNF-beta 10.5-kb allele to B15,DR4-positive haplotypes. |
| 20299 | 1996407 | In all groups there was a haplotype assignment of the TNF-beta 5.5-kb allele to B8,DR3 haplotypes, and of the TNF-beta 10.5-kb allele to B15,DR4-positive haplotypes. |
| 20300 | 1996407 | The allelic and genotypic frequencies differed between DR3,4 IDDM patients and DR3,4 controls, and the DR3,4 control group differed significantly from the randomly selected control group (P less than 0.0079). |
| 20301 | 1996407 | The allelic and genotypic frequencies differed between DR3,4 IDDM patients and DR3,4 controls, and the DR3,4 control group differed significantly from the randomly selected control group (P less than 0.0079). |
| 20302 | 1996407 | The allelic and genotypic frequencies differed between DR3,4 IDDM patients and DR3,4 controls, and the DR3,4 control group differed significantly from the randomly selected control group (P less than 0.0079). |
| 20303 | 1996407 | The allelic and genotypic frequencies differed between DR3,4 IDDM patients and DR3,4 controls, and the DR3,4 control group differed significantly from the randomly selected control group (P less than 0.0079). |
| 20304 | 1996407 | In HLA-DR3,4- and DQw8-positive persons, the DR3 haplotypes carried the 10.5-kb allele three times more frequently in IDDM patients than in controls, suggesting that the 10.5-kb allele when present on DR3 haplotypes may contribute to susceptibility to IDDM in DR3,4 heterozygous individuals. |
| 20305 | 1996407 | In HLA-DR3,4- and DQw8-positive persons, the DR3 haplotypes carried the 10.5-kb allele three times more frequently in IDDM patients than in controls, suggesting that the 10.5-kb allele when present on DR3 haplotypes may contribute to susceptibility to IDDM in DR3,4 heterozygous individuals. |
| 20306 | 1996407 | In HLA-DR3,4- and DQw8-positive persons, the DR3 haplotypes carried the 10.5-kb allele three times more frequently in IDDM patients than in controls, suggesting that the 10.5-kb allele when present on DR3 haplotypes may contribute to susceptibility to IDDM in DR3,4 heterozygous individuals. |
| 20307 | 1996407 | In HLA-DR3,4- and DQw8-positive persons, the DR3 haplotypes carried the 10.5-kb allele three times more frequently in IDDM patients than in controls, suggesting that the 10.5-kb allele when present on DR3 haplotypes may contribute to susceptibility to IDDM in DR3,4 heterozygous individuals. |
| 20308 | 1996407 | A contributory role of the 10.5-kb allele in genetic IDDM susceptibility was supported by the sibpair analysis, in which all were TNF-beta identical. |
| 20309 | 1996407 | A contributory role of the 10.5-kb allele in genetic IDDM susceptibility was supported by the sibpair analysis, in which all were TNF-beta identical. |
| 20310 | 1996407 | A contributory role of the 10.5-kb allele in genetic IDDM susceptibility was supported by the sibpair analysis, in which all were TNF-beta identical. |
| 20311 | 1996407 | A contributory role of the 10.5-kb allele in genetic IDDM susceptibility was supported by the sibpair analysis, in which all were TNF-beta identical. |
| 20312 | 1996407 | Twenty-five healthy and eight newly diagnosed IDDM patients were randomly selected to study the Escherichia coli lipopolysaccharides (LPS)-purified protein derivate (tuberculin) (PPD)-, and phytohaemagglutinin (PHA)-stimulated monocyte (Mo) secretions of interleukin 1 beta (IL-1 beta) and TNF-alpha in relation to the NcoI TNF-beta gene polymorphism. |
| 20313 | 1996407 | Twenty-five healthy and eight newly diagnosed IDDM patients were randomly selected to study the Escherichia coli lipopolysaccharides (LPS)-purified protein derivate (tuberculin) (PPD)-, and phytohaemagglutinin (PHA)-stimulated monocyte (Mo) secretions of interleukin 1 beta (IL-1 beta) and TNF-alpha in relation to the NcoI TNF-beta gene polymorphism. |
| 20314 | 1996407 | Twenty-five healthy and eight newly diagnosed IDDM patients were randomly selected to study the Escherichia coli lipopolysaccharides (LPS)-purified protein derivate (tuberculin) (PPD)-, and phytohaemagglutinin (PHA)-stimulated monocyte (Mo) secretions of interleukin 1 beta (IL-1 beta) and TNF-alpha in relation to the NcoI TNF-beta gene polymorphism. |
| 20315 | 1996407 | Twenty-five healthy and eight newly diagnosed IDDM patients were randomly selected to study the Escherichia coli lipopolysaccharides (LPS)-purified protein derivate (tuberculin) (PPD)-, and phytohaemagglutinin (PHA)-stimulated monocyte (Mo) secretions of interleukin 1 beta (IL-1 beta) and TNF-alpha in relation to the NcoI TNF-beta gene polymorphism. |
| 20316 | 1996407 | The LPS- and PHA-stimulated Mo IL-1 beta and TNF-alpha secretions were significantly lower for the TNF-beta 5.5/10.5 kb heterozygous individuals than for TNF-beta 10.5 kb homozygous individuals. |
| 20317 | 1996407 | The LPS- and PHA-stimulated Mo IL-1 beta and TNF-alpha secretions were significantly lower for the TNF-beta 5.5/10.5 kb heterozygous individuals than for TNF-beta 10.5 kb homozygous individuals. |
| 20318 | 1996407 | The LPS- and PHA-stimulated Mo IL-1 beta and TNF-alpha secretions were significantly lower for the TNF-beta 5.5/10.5 kb heterozygous individuals than for TNF-beta 10.5 kb homozygous individuals. |
| 20319 | 1996407 | The LPS- and PHA-stimulated Mo IL-1 beta and TNF-alpha secretions were significantly lower for the TNF-beta 5.5/10.5 kb heterozygous individuals than for TNF-beta 10.5 kb homozygous individuals. |
| 20320 | 1996407 | Furthermore, the Mo IL-1 beta and TNF-alpha secretions of IDDM patients were significantly higher than the Mo secretions of TNF-beta genotype-matched healthy controls. |
| 20321 | 1996407 | Furthermore, the Mo IL-1 beta and TNF-alpha secretions of IDDM patients were significantly higher than the Mo secretions of TNF-beta genotype-matched healthy controls. |
| 20322 | 1996407 | Furthermore, the Mo IL-1 beta and TNF-alpha secretions of IDDM patients were significantly higher than the Mo secretions of TNF-beta genotype-matched healthy controls. |
| 20323 | 1996407 | Furthermore, the Mo IL-1 beta and TNF-alpha secretions of IDDM patients were significantly higher than the Mo secretions of TNF-beta genotype-matched healthy controls. |
| 20324 | 1996407 | This study suggests an association between the 10.5 kb TNF-beta allele and IDDM, and demonstrates an association between monokine responses and TNF-beta genotypes. |
| 20325 | 1996407 | This study suggests an association between the 10.5 kb TNF-beta allele and IDDM, and demonstrates an association between monokine responses and TNF-beta genotypes. |
| 20326 | 1996407 | This study suggests an association between the 10.5 kb TNF-beta allele and IDDM, and demonstrates an association between monokine responses and TNF-beta genotypes. |
| 20327 | 1996407 | This study suggests an association between the 10.5 kb TNF-beta allele and IDDM, and demonstrates an association between monokine responses and TNF-beta genotypes. |
| 20328 | 1991438 | Serum levels of tumor necrosis factor and IL-1 alpha and IL-1 beta in diabetic patients. |
| 20329 | 1684890 | [Immunogenetic markers (BF, C2, C4, 21-OH, TNF alpha, TCR beta, Ig) and insulin-dependent diabetes in the Tunisian population: serological and molecular study]. |
| 20330 | 1684890 | [Immunogenetic markers (BF, C2, C4, 21-OH, TNF alpha, TCR beta, Ig) and insulin-dependent diabetes in the Tunisian population: serological and molecular study]. |
| 20331 | 1684890 | 48 Tunisian people suffering from the IDDM auto-immune disease were compared to 35 control healthy persons for the polymorphisms of the complement BF, C2 and C4 proteins and genes, of the IgG (Gm allotypes) as well as of the TNF alpha and TCR C beta genes. |
| 20332 | 1684890 | 48 Tunisian people suffering from the IDDM auto-immune disease were compared to 35 control healthy persons for the polymorphisms of the complement BF, C2 and C4 proteins and genes, of the IgG (Gm allotypes) as well as of the TNF alpha and TCR C beta genes. |
| 20333 | 2125364 | Tumour necrosis factors alpha and beta (TNF-alpha and TNF-beta) and gamma interferon (IFN-gamma) were measured by ELISA in the supernatants of phytohaemagglutinin (PHA)-activated peripheral blood mononuclear cells (PBMNC) from 98 individuals (60 controls and 38 patients with insulin-dependent diabetes mellitus [IDDM]). |
| 20334 | 2125364 | Tumour necrosis factors alpha and beta (TNF-alpha and TNF-beta) and gamma interferon (IFN-gamma) were measured by ELISA in the supernatants of phytohaemagglutinin (PHA)-activated peripheral blood mononuclear cells (PBMNC) from 98 individuals (60 controls and 38 patients with insulin-dependent diabetes mellitus [IDDM]). |
| 20335 | 2125364 | Tumour necrosis factors alpha and beta (TNF-alpha and TNF-beta) and gamma interferon (IFN-gamma) were measured by ELISA in the supernatants of phytohaemagglutinin (PHA)-activated peripheral blood mononuclear cells (PBMNC) from 98 individuals (60 controls and 38 patients with insulin-dependent diabetes mellitus [IDDM]). |
| 20336 | 2125364 | In our population study we observed a correlation between the levels of secretion of TNF-alpha and IFN-gamma but not TNF-beta. |
| 20337 | 2125364 | In our population study we observed a correlation between the levels of secretion of TNF-alpha and IFN-gamma but not TNF-beta. |
| 20338 | 2125364 | In our population study we observed a correlation between the levels of secretion of TNF-alpha and IFN-gamma but not TNF-beta. |
| 20339 | 2125364 | Reduced levels of TNF-beta, but not TNF-alpha or IFN-gamma, secretion were found in IDDM patients stimulated with 1 and 5 micrograms/ml of PHA (P = 0.001 and 0.02 respectively). |
| 20340 | 2125364 | Reduced levels of TNF-beta, but not TNF-alpha or IFN-gamma, secretion were found in IDDM patients stimulated with 1 and 5 micrograms/ml of PHA (P = 0.001 and 0.02 respectively). |
| 20341 | 2125364 | Reduced levels of TNF-beta, but not TNF-alpha or IFN-gamma, secretion were found in IDDM patients stimulated with 1 and 5 micrograms/ml of PHA (P = 0.001 and 0.02 respectively). |
| 20342 | 2125364 | Analysis of the natural log-transformed data indicated that only for the TNF-beta levels (at 5 micrograms/ml PHA) could subjects be divided into high and low secretors, which also did not correlate with a particular HLA-B or -DR antigen. |
| 20343 | 2125364 | Analysis of the natural log-transformed data indicated that only for the TNF-beta levels (at 5 micrograms/ml PHA) could subjects be divided into high and low secretors, which also did not correlate with a particular HLA-B or -DR antigen. |
| 20344 | 2125364 | Analysis of the natural log-transformed data indicated that only for the TNF-beta levels (at 5 micrograms/ml PHA) could subjects be divided into high and low secretors, which also did not correlate with a particular HLA-B or -DR antigen. |
| 20345 | 1978829 | Previous studies demonstrated that administration of tumor necrosis factor (TNF) to diabetic rats rapidly increases serum triglyceride levels and stimulates hepatic lipogenesis without affecting the activity of adipose tissue lipoprotein lipase or serum insulin levels. |
| 20346 | 2261839 | Coupling of AGE proteins to their AGE receptors results in their degradation and removal and, simultaneously, in synthesis and secretion of pluripotential cytokines such as tumor necrosis factor and interleukin 1. |
| 20347 | 2384663 | We previously reported that streptococcal preparation (OK-432), which is a TNF inducer, inhibits insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and Bio-Breeding (BB) rats, as animal models of insulin-dependent diabetes mellitus. |
| 20348 | 2143488 | Class I expression was dose-dependently augmented by incubation with interferon-gamma (IFN-gamma) or tumor necrosis factor (TNF). |
| 20349 | 2143488 | Class I expression was dose-dependently augmented by incubation with interferon-gamma (IFN-gamma) or tumor necrosis factor (TNF). |
| 20350 | 2143488 | Class I expression was dose-dependently augmented by incubation with interferon-gamma (IFN-gamma) or tumor necrosis factor (TNF). |
| 20351 | 2143488 | Although neither IFN-gamma nor TNF alone induce class II molecules on islet cells, synergistic interaction of IFN-gamma (200 U/ml) and TNF (200 U/ml) may induce class II expression on approximately 50% of islet cells. |
| 20352 | 2143488 | Although neither IFN-gamma nor TNF alone induce class II molecules on islet cells, synergistic interaction of IFN-gamma (200 U/ml) and TNF (200 U/ml) may induce class II expression on approximately 50% of islet cells. |
| 20353 | 2143488 | Although neither IFN-gamma nor TNF alone induce class II molecules on islet cells, synergistic interaction of IFN-gamma (200 U/ml) and TNF (200 U/ml) may induce class II expression on approximately 50% of islet cells. |
| 20354 | 2143488 | Niacinamide and 3-aminobenzamide, both inhibitors of ADP ribosylation and scavengers of free radicals, attenuated the class II expression induced by IFN-gamma and TNF. |
| 20355 | 2143488 | Niacinamide and 3-aminobenzamide, both inhibitors of ADP ribosylation and scavengers of free radicals, attenuated the class II expression induced by IFN-gamma and TNF. |
| 20356 | 2143488 | Niacinamide and 3-aminobenzamide, both inhibitors of ADP ribosylation and scavengers of free radicals, attenuated the class II expression induced by IFN-gamma and TNF. |
| 20357 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20358 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20359 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20360 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20361 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20362 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20363 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20364 | 1698309 | Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region. |
| 20365 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20366 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20367 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20368 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20369 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20370 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20371 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20372 | 1698309 | Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4). |
| 20373 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20374 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20375 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20376 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20377 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20378 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20379 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20380 | 1698309 | Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS). |
| 20381 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20382 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20383 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20384 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20385 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20386 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20387 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20388 | 1698309 | In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM. |
| 20389 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20390 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20391 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20392 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20393 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20394 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20395 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20396 | 1698309 | We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes. |
| 20397 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20398 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20399 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20400 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20401 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20402 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20403 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20404 | 1698309 | IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied. |
| 20405 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20406 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20407 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20408 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20409 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20410 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20411 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20412 | 1698309 | LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated. |
| 20413 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20414 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20415 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20416 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20417 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20418 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20419 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20420 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 20421 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20422 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20423 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20424 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20425 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20426 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20427 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20428 | 1698309 | IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity. |
| 20429 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20430 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20431 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20432 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20433 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20434 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20435 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20436 | 1698309 | We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM. |
| 20437 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20438 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20439 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20440 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20441 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20442 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20443 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 20444 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20445 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20446 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20447 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20448 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20449 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20450 | 2115042 | In this study we examined the effects of IL-1, TNF, and IFN gamma on the viability and hormone secretion of islets isolated from adult human pancreas and maintained in monolayer culture. |
| 20451 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20452 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20453 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20454 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20455 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20456 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20457 | 2115042 | IL-1 and TNF were cytotoxic to the islet cells (20-30% cell lysis) in a 51Cr release cytotoxicity assay, and IFN gamma had only small effects (less than 10% lysis). |
| 20458 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20459 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20460 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20461 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20462 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20463 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20464 | 2115042 | Combination of maximally cytotoxic concentrations of IL-1 (10 U/mL) and TNF (10(3) U/mL) produced an additive cytotoxic effect. |
| 20465 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20466 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20467 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20468 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20469 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20470 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20471 | 2115042 | IFN gamma (10(3) U/mL) acted synergistically with IL-1 and TNF, and the three cytokines added together produced maximal islet cell lysis (46.4 +/- 4.3%). |
| 20472 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20473 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20474 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20475 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20476 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20477 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20478 | 2115042 | Assay of insulin and glucagon in the islet monolayers revealed that IL-1, TNF, and IFN gamma inhibited both B- and A-cell secretory functions; however, only IL-1 and TNF produced permanent decreases in insulin and glucagon contents in the islet cultures. |
| 20479 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20480 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20481 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20482 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20483 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20484 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20485 | 2115042 | These findings indicate that IL-1 and TNF, as single agents, are cytotoxic to human islet cells, and that this cytotoxicity can be amplified by combining the cytokines and/or adding IFN gamma. |
| 20486 | 1975742 | The inbred non-obese diabetic (NOD) mouse is a spontaneous model for insulin-dependent diabetes mellitus (IDDM). |
| 20487 | 1975742 | To facilitate the identification of Idd-1 we have further analysed the MHC region for restriction fragment length polymorphisms and we find that the NOD mouse has a distinct haplotype: H-2K1nod Kd A beta nod A alpha d E beta nod TNF-alpha beta. |
| 20488 | 1975742 | In contrast, the sister strain, the non-obese normal (NON) mouse, derived from the same cataract-prone line of mice as the NOD mouse, has an MHC Class I region indistinguishable from the b-haplotype, but the MHC Class II region is distinct from the NOD mouse as well as the b-, d- and k-haplotype. |
| 20489 | 2111138 | We used a modified 51Cr release cytotoxicity assay to define the interactive cytotoxic effects of interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) on rat islet cells in monolayer culture. |
| 20490 | 2111138 | We used a modified 51Cr release cytotoxicity assay to define the interactive cytotoxic effects of interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) on rat islet cells in monolayer culture. |
| 20491 | 2111138 | We used a modified 51Cr release cytotoxicity assay to define the interactive cytotoxic effects of interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) on rat islet cells in monolayer culture. |
| 20492 | 2111138 | We here demonstrate that (a) IFN-gamma, but not IL-1 or TNF, can sensitize islet cells to subsequent cytolysis by other cytokines (IL-1 or TNF); (b) the cytolytic effect of sequential addition of IFN-gamma, then IL-1 or TNF (approximately 35-40% 51Cr release) is similar to that produced by the concurrent addition of IFN-gamma plus IL-1 or TNF; (c) the priming effect of IFN-gamma persists for 3 to 6 or more days after its removal; and (d) islet cells preincubated with IFN-gamma are also more sensitive to cytolysis by splenic mononuclear cells from diabetes-prone BB/Wor rats. |
| 20493 | 2111138 | We here demonstrate that (a) IFN-gamma, but not IL-1 or TNF, can sensitize islet cells to subsequent cytolysis by other cytokines (IL-1 or TNF); (b) the cytolytic effect of sequential addition of IFN-gamma, then IL-1 or TNF (approximately 35-40% 51Cr release) is similar to that produced by the concurrent addition of IFN-gamma plus IL-1 or TNF; (c) the priming effect of IFN-gamma persists for 3 to 6 or more days after its removal; and (d) islet cells preincubated with IFN-gamma are also more sensitive to cytolysis by splenic mononuclear cells from diabetes-prone BB/Wor rats. |
| 20494 | 2111138 | We here demonstrate that (a) IFN-gamma, but not IL-1 or TNF, can sensitize islet cells to subsequent cytolysis by other cytokines (IL-1 or TNF); (b) the cytolytic effect of sequential addition of IFN-gamma, then IL-1 or TNF (approximately 35-40% 51Cr release) is similar to that produced by the concurrent addition of IFN-gamma plus IL-1 or TNF; (c) the priming effect of IFN-gamma persists for 3 to 6 or more days after its removal; and (d) islet cells preincubated with IFN-gamma are also more sensitive to cytolysis by splenic mononuclear cells from diabetes-prone BB/Wor rats. |
| 20495 | 2111138 | These findings suggest that IFN-gamma produced by activated T lymphocytes and monocytic cells infiltrating islets in Type 1 diabetes may play a direct and important role in sensitizing beta cells to damage by other cytokines (IL-1, TNF) and cytotoxic cells in the immune/inflammatory infiltrate. |
| 20496 | 2111138 | These findings suggest that IFN-gamma produced by activated T lymphocytes and monocytic cells infiltrating islets in Type 1 diabetes may play a direct and important role in sensitizing beta cells to damage by other cytokines (IL-1, TNF) and cytotoxic cells in the immune/inflammatory infiltrate. |
| 20497 | 2111138 | These findings suggest that IFN-gamma produced by activated T lymphocytes and monocytic cells infiltrating islets in Type 1 diabetes may play a direct and important role in sensitizing beta cells to damage by other cytokines (IL-1, TNF) and cytotoxic cells in the immune/inflammatory infiltrate. |
| 20498 | 2179951 | Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 20499 | 2179951 | Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 20500 | 2179951 | Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 20501 | 2179951 | Genes encoding tumor necrosis factor alpha and granzyme A are expressed during development of autoimmune diabetes. |
| 20502 | 2179951 | We show that the genes for tumor necrosis factor alpha and granzyme A, a serine protease associated with cytoplasmic granules of cytotoxic cells, are expressed during the development of spontaneous diabetes mellitus in the nonobese diabetic mouse. |
| 20503 | 2179951 | We show that the genes for tumor necrosis factor alpha and granzyme A, a serine protease associated with cytoplasmic granules of cytotoxic cells, are expressed during the development of spontaneous diabetes mellitus in the nonobese diabetic mouse. |
| 20504 | 2179951 | We show that the genes for tumor necrosis factor alpha and granzyme A, a serine protease associated with cytoplasmic granules of cytotoxic cells, are expressed during the development of spontaneous diabetes mellitus in the nonobese diabetic mouse. |
| 20505 | 2179951 | We show that the genes for tumor necrosis factor alpha and granzyme A, a serine protease associated with cytoplasmic granules of cytotoxic cells, are expressed during the development of spontaneous diabetes mellitus in the nonobese diabetic mouse. |
| 20506 | 2179951 | Tumor necrosis factor alpha expression is exclusively observed in the intra-islet infiltrate, predominantly in lymphocytes adjacent to insulin-producing beta cells, the targets of the autoimmune destruction, implying that tumor necrosis factor alpha expression is induced locally--i.e., in the islet. |
| 20507 | 2179951 | Tumor necrosis factor alpha expression is exclusively observed in the intra-islet infiltrate, predominantly in lymphocytes adjacent to insulin-producing beta cells, the targets of the autoimmune destruction, implying that tumor necrosis factor alpha expression is induced locally--i.e., in the islet. |
| 20508 | 2179951 | Tumor necrosis factor alpha expression is exclusively observed in the intra-islet infiltrate, predominantly in lymphocytes adjacent to insulin-producing beta cells, the targets of the autoimmune destruction, implying that tumor necrosis factor alpha expression is induced locally--i.e., in the islet. |
| 20509 | 2179951 | Tumor necrosis factor alpha expression is exclusively observed in the intra-islet infiltrate, predominantly in lymphocytes adjacent to insulin-producing beta cells, the targets of the autoimmune destruction, implying that tumor necrosis factor alpha expression is induced locally--i.e., in the islet. |
| 20510 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 20511 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 20512 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 20513 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 20514 | 1969186 | The L3 clone produces gamma-interferon and tumor necrosis factor but not IL-2 and IL-3. |
| 20515 | 2405400 | Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): similarities between TNF-alpha and interleukin 1. |
| 20516 | 2405400 | Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): similarities between TNF-alpha and interleukin 1. |
| 20517 | 2405400 | Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): similarities between TNF-alpha and interleukin 1. |
| 20518 | 2405400 | Treatment with TNF-alpha caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. |
| 20519 | 2405400 | Treatment with TNF-alpha caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. |
| 20520 | 2405400 | Treatment with TNF-alpha caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. |
| 20521 | 2405400 | These activities of TNF-alpha were shared by interleukin 1 alpha in this system. |
| 20522 | 2405400 | These activities of TNF-alpha were shared by interleukin 1 alpha in this system. |
| 20523 | 2405400 | These activities of TNF-alpha were shared by interleukin 1 alpha in this system. |
| 20524 | 2151129 | Mouse islet cell monolayers were damaged when cultured for five days in a medium containing 200 U/ml of recombinant murine interferon-gamma (IFN-gamma) and 300 U/ml of recombinant tumor necrosis factor (TNF). |
| 20525 | 2151129 | Mouse islet cell monolayers were damaged when cultured for five days in a medium containing 200 U/ml of recombinant murine interferon-gamma (IFN-gamma) and 300 U/ml of recombinant tumor necrosis factor (TNF). |
| 20526 | 2151129 | Mouse islet cell monolayers were damaged when cultured for five days in a medium containing 200 U/ml of recombinant murine interferon-gamma (IFN-gamma) and 300 U/ml of recombinant tumor necrosis factor (TNF). |
| 20527 | 2151129 | Mouse islet cell monolayers were damaged when cultured for five days in a medium containing 200 U/ml of recombinant murine interferon-gamma (IFN-gamma) and 300 U/ml of recombinant tumor necrosis factor (TNF). |
| 20528 | 2151129 | When 20 mM of nicotinamide or 5 mM of 3-aminobenzamide was supplemented to the medium, islet cell monolayers remained in the presence of the cytokines. 51Cr release studies showed that specific 51Cr release during five-day incubation with 200 U/ml of IFN-gamma and 300 U/ml of TNF was 30 +/- 4% (mean +/- SE). |
| 20529 | 2151129 | When 20 mM of nicotinamide or 5 mM of 3-aminobenzamide was supplemented to the medium, islet cell monolayers remained in the presence of the cytokines. 51Cr release studies showed that specific 51Cr release during five-day incubation with 200 U/ml of IFN-gamma and 300 U/ml of TNF was 30 +/- 4% (mean +/- SE). |
| 20530 | 2151129 | When 20 mM of nicotinamide or 5 mM of 3-aminobenzamide was supplemented to the medium, islet cell monolayers remained in the presence of the cytokines. 51Cr release studies showed that specific 51Cr release during five-day incubation with 200 U/ml of IFN-gamma and 300 U/ml of TNF was 30 +/- 4% (mean +/- SE). |
| 20531 | 2151129 | When 20 mM of nicotinamide or 5 mM of 3-aminobenzamide was supplemented to the medium, islet cell monolayers remained in the presence of the cytokines. 51Cr release studies showed that specific 51Cr release during five-day incubation with 200 U/ml of IFN-gamma and 300 U/ml of TNF was 30 +/- 4% (mean +/- SE). |
| 20532 | 2151129 | In a medium containing 20 mM of nicotinamide, together with IFN-gamma and TNF, specific 51Cr release was significantly reduced (12 +/- 3%, p less than 0.01). 3-aminobenzamide was effective at the level of 5 mM; specific 51Cr release was 2 +/- 5% (p less than 0.01). |
| 20533 | 2151129 | In a medium containing 20 mM of nicotinamide, together with IFN-gamma and TNF, specific 51Cr release was significantly reduced (12 +/- 3%, p less than 0.01). 3-aminobenzamide was effective at the level of 5 mM; specific 51Cr release was 2 +/- 5% (p less than 0.01). |
| 20534 | 2151129 | In a medium containing 20 mM of nicotinamide, together with IFN-gamma and TNF, specific 51Cr release was significantly reduced (12 +/- 3%, p less than 0.01). 3-aminobenzamide was effective at the level of 5 mM; specific 51Cr release was 2 +/- 5% (p less than 0.01). |
| 20535 | 2151129 | In a medium containing 20 mM of nicotinamide, together with IFN-gamma and TNF, specific 51Cr release was significantly reduced (12 +/- 3%, p less than 0.01). 3-aminobenzamide was effective at the level of 5 mM; specific 51Cr release was 2 +/- 5% (p less than 0.01). |
| 20536 | 2151129 | These results suggest that the mechanism by which IFN-gamma and TNF damage islet cells may be similar to that of streptozotocin and/or alloxan. |
| 20537 | 2151129 | These results suggest that the mechanism by which IFN-gamma and TNF damage islet cells may be similar to that of streptozotocin and/or alloxan. |
| 20538 | 2151129 | These results suggest that the mechanism by which IFN-gamma and TNF damage islet cells may be similar to that of streptozotocin and/or alloxan. |
| 20539 | 2151129 | These results suggest that the mechanism by which IFN-gamma and TNF damage islet cells may be similar to that of streptozotocin and/or alloxan. |
| 20540 | 2105545 | Cultured neonatal rat (F344, RT1(1v1)) islets that were devoid of MHC class II (OX6) antigen and antigen-presenting cells were treated with recombinant murine interferon (IFN-gamma) and/or recombinant murine tumor necrosis factor (TNF-alpha) in vitro. |
| 20541 | 2105545 | Cultured neonatal rat (F344, RT1(1v1)) islets that were devoid of MHC class II (OX6) antigen and antigen-presenting cells were treated with recombinant murine interferon (IFN-gamma) and/or recombinant murine tumor necrosis factor (TNF-alpha) in vitro. |
| 20542 | 2105545 | Cultured neonatal rat (F344, RT1(1v1)) islets that were devoid of MHC class II (OX6) antigen and antigen-presenting cells were treated with recombinant murine interferon (IFN-gamma) and/or recombinant murine tumor necrosis factor (TNF-alpha) in vitro. |
| 20543 | 2105545 | Cultured neonatal rat (F344, RT1(1v1)) islets that were devoid of MHC class II (OX6) antigen and antigen-presenting cells were treated with recombinant murine interferon (IFN-gamma) and/or recombinant murine tumor necrosis factor (TNF-alpha) in vitro. |
| 20544 | 2105545 | The IFN-gamma and TNF-alpha resulted in some disruption of the integrity of the islets by 7 days of culture, but the combination resulted in disaggregation of the islets within 7-8 days. |
| 20545 | 2105545 | The IFN-gamma and TNF-alpha resulted in some disruption of the integrity of the islets by 7 days of culture, but the combination resulted in disaggregation of the islets within 7-8 days. |
| 20546 | 2105545 | The IFN-gamma and TNF-alpha resulted in some disruption of the integrity of the islets by 7 days of culture, but the combination resulted in disaggregation of the islets within 7-8 days. |
| 20547 | 2105545 | The IFN-gamma and TNF-alpha resulted in some disruption of the integrity of the islets by 7 days of culture, but the combination resulted in disaggregation of the islets within 7-8 days. |
| 20548 | 2105545 | This effect of IFN-gamma was potentiated by TNF-alpha resulting in 27% of the cells expressing class II antigen. |
| 20549 | 2105545 | This effect of IFN-gamma was potentiated by TNF-alpha resulting in 27% of the cells expressing class II antigen. |
| 20550 | 2105545 | This effect of IFN-gamma was potentiated by TNF-alpha resulting in 27% of the cells expressing class II antigen. |
| 20551 | 2105545 | This effect of IFN-gamma was potentiated by TNF-alpha resulting in 27% of the cells expressing class II antigen. |
| 20552 | 2105545 | Islets treated with IFN-gamma and TNF-alpha alone or in combination were not rejected in a subsequent transplant underneath the kidney capsule of WF rats (RT1u). |
| 20553 | 2105545 | Islets treated with IFN-gamma and TNF-alpha alone or in combination were not rejected in a subsequent transplant underneath the kidney capsule of WF rats (RT1u). |
| 20554 | 2105545 | Islets treated with IFN-gamma and TNF-alpha alone or in combination were not rejected in a subsequent transplant underneath the kidney capsule of WF rats (RT1u). |
| 20555 | 2105545 | Islets treated with IFN-gamma and TNF-alpha alone or in combination were not rejected in a subsequent transplant underneath the kidney capsule of WF rats (RT1u). |
| 20556 | 2104593 | In this study, we tested inhibitors of arachidonate metabolism for possible protection against the toxic effects of the cytokine combination of tumor necrosis factor (TNF, 100 U/ml) and interferon-gamma (IFN-gamma, 100 U/ml) in rat islet cell monolayer cultures, using a 51Cr release cytotoxicity assay to measure islet cell lysis (% 51Cr release). |
| 20557 | 2104593 | In this study, we tested inhibitors of arachidonate metabolism for possible protection against the toxic effects of the cytokine combination of tumor necrosis factor (TNF, 100 U/ml) and interferon-gamma (IFN-gamma, 100 U/ml) in rat islet cell monolayer cultures, using a 51Cr release cytotoxicity assay to measure islet cell lysis (% 51Cr release). |
| 20558 | 2104593 | In this study, we tested inhibitors of arachidonate metabolism for possible protection against the toxic effects of the cytokine combination of tumor necrosis factor (TNF, 100 U/ml) and interferon-gamma (IFN-gamma, 100 U/ml) in rat islet cell monolayer cultures, using a 51Cr release cytotoxicity assay to measure islet cell lysis (% 51Cr release). |
| 20559 | 2104593 | In this study, we tested inhibitors of arachidonate metabolism for possible protection against the toxic effects of the cytokine combination of tumor necrosis factor (TNF, 100 U/ml) and interferon-gamma (IFN-gamma, 100 U/ml) in rat islet cell monolayer cultures, using a 51Cr release cytotoxicity assay to measure islet cell lysis (% 51Cr release). |
| 20560 | 2104593 | In this study, we tested inhibitors of arachidonate metabolism for possible protection against the toxic effects of the cytokine combination of tumor necrosis factor (TNF, 100 U/ml) and interferon-gamma (IFN-gamma, 100 U/ml) in rat islet cell monolayer cultures, using a 51Cr release cytotoxicity assay to measure islet cell lysis (% 51Cr release). |
| 20561 | 2104593 | The toxic effect of TNF/IFN-gamma (26.6 +/- 3.7%) was inhibited partially by both a cyclooxygenase inhibitor, indomethacin and a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), and combination of maximally effective concentrations of Indo and NDGA (30 microM) produced further protection against TNF/IFN-gamma-induced lysis (3.5 +/- 0.9%). |
| 20562 | 2104593 | The toxic effect of TNF/IFN-gamma (26.6 +/- 3.7%) was inhibited partially by both a cyclooxygenase inhibitor, indomethacin and a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), and combination of maximally effective concentrations of Indo and NDGA (30 microM) produced further protection against TNF/IFN-gamma-induced lysis (3.5 +/- 0.9%). |
| 20563 | 2104593 | The toxic effect of TNF/IFN-gamma (26.6 +/- 3.7%) was inhibited partially by both a cyclooxygenase inhibitor, indomethacin and a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), and combination of maximally effective concentrations of Indo and NDGA (30 microM) produced further protection against TNF/IFN-gamma-induced lysis (3.5 +/- 0.9%). |
| 20564 | 2104593 | The toxic effect of TNF/IFN-gamma (26.6 +/- 3.7%) was inhibited partially by both a cyclooxygenase inhibitor, indomethacin and a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), and combination of maximally effective concentrations of Indo and NDGA (30 microM) produced further protection against TNF/IFN-gamma-induced lysis (3.5 +/- 0.9%). |
| 20565 | 2104593 | The toxic effect of TNF/IFN-gamma (26.6 +/- 3.7%) was inhibited partially by both a cyclooxygenase inhibitor, indomethacin and a lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), and combination of maximally effective concentrations of Indo and NDGA (30 microM) produced further protection against TNF/IFN-gamma-induced lysis (3.5 +/- 0.9%). |
| 20566 | 2104593 | Also, the combined cyclo/lipoxygenase inhibitors, oxyphenbutazone and eicosa 5,8,11,14 tetrynoic acid, as well as the phospholipase A2 inhibitor, bromophenacyl bromide, significantly inhibited the cytotoxic effect of TNF/IFN-gamma. |
| 20567 | 2104593 | Also, the combined cyclo/lipoxygenase inhibitors, oxyphenbutazone and eicosa 5,8,11,14 tetrynoic acid, as well as the phospholipase A2 inhibitor, bromophenacyl bromide, significantly inhibited the cytotoxic effect of TNF/IFN-gamma. |
| 20568 | 2104593 | Also, the combined cyclo/lipoxygenase inhibitors, oxyphenbutazone and eicosa 5,8,11,14 tetrynoic acid, as well as the phospholipase A2 inhibitor, bromophenacyl bromide, significantly inhibited the cytotoxic effect of TNF/IFN-gamma. |
| 20569 | 2104593 | Also, the combined cyclo/lipoxygenase inhibitors, oxyphenbutazone and eicosa 5,8,11,14 tetrynoic acid, as well as the phospholipase A2 inhibitor, bromophenacyl bromide, significantly inhibited the cytotoxic effect of TNF/IFN-gamma. |
| 20570 | 2104593 | Also, the combined cyclo/lipoxygenase inhibitors, oxyphenbutazone and eicosa 5,8,11,14 tetrynoic acid, as well as the phospholipase A2 inhibitor, bromophenacyl bromide, significantly inhibited the cytotoxic effect of TNF/IFN-gamma. |
| 20571 | 2104593 | Whereas indomethacin and NDGA did not prevent TNF/IFN-gamma-induced inhibition of insulin release, this recovered after cytokine removal from cultures protected by the cyclo/lipoxygenase inhibitors. |
| 20572 | 2104593 | Whereas indomethacin and NDGA did not prevent TNF/IFN-gamma-induced inhibition of insulin release, this recovered after cytokine removal from cultures protected by the cyclo/lipoxygenase inhibitors. |
| 20573 | 2104593 | Whereas indomethacin and NDGA did not prevent TNF/IFN-gamma-induced inhibition of insulin release, this recovered after cytokine removal from cultures protected by the cyclo/lipoxygenase inhibitors. |
| 20574 | 2104593 | Whereas indomethacin and NDGA did not prevent TNF/IFN-gamma-induced inhibition of insulin release, this recovered after cytokine removal from cultures protected by the cyclo/lipoxygenase inhibitors. |
| 20575 | 2104593 | Whereas indomethacin and NDGA did not prevent TNF/IFN-gamma-induced inhibition of insulin release, this recovered after cytokine removal from cultures protected by the cyclo/lipoxygenase inhibitors. |
| 20576 | 2104593 | These results suggest that arachidonate metabolites may be involved in mediating the cytotoxic and not the functional inhibitory effects of TNF and IFN-gamma in islet cells. |
| 20577 | 2104593 | These results suggest that arachidonate metabolites may be involved in mediating the cytotoxic and not the functional inhibitory effects of TNF and IFN-gamma in islet cells. |
| 20578 | 2104593 | These results suggest that arachidonate metabolites may be involved in mediating the cytotoxic and not the functional inhibitory effects of TNF and IFN-gamma in islet cells. |
| 20579 | 2104593 | These results suggest that arachidonate metabolites may be involved in mediating the cytotoxic and not the functional inhibitory effects of TNF and IFN-gamma in islet cells. |
| 20580 | 2104593 | These results suggest that arachidonate metabolites may be involved in mediating the cytotoxic and not the functional inhibitory effects of TNF and IFN-gamma in islet cells. |
| 20581 | 1964791 | Coupling of AGE proteins to their AGE receptor results in TNF and IL-1 synthesis and secretion. |
| 20582 | 2577113 | TNF-alpha gene polymorphisms: association with type I (insulin-dependent) diabetes mellitus. |
| 20583 | 2577113 | TNF-alpha gene polymorphisms: association with type I (insulin-dependent) diabetes mellitus. |
| 20584 | 2577113 | TNF-alpha gene polymorphisms: association with type I (insulin-dependent) diabetes mellitus. |
| 20585 | 2577113 | TNF-alpha gene polymorphisms: association with type I (insulin-dependent) diabetes mellitus. |
| 20586 | 2577113 | The localization of TNF genes on the short arm of chromosome 6 between HLA B and the complement genes focused attention to that genetic region which harbors many immunologically relevant genes and is also thought to hold susceptibility genes for a variety of autoimmune diseases that are linked to specific alleles of particular loci in the HLA D region. |
| 20587 | 2577113 | The localization of TNF genes on the short arm of chromosome 6 between HLA B and the complement genes focused attention to that genetic region which harbors many immunologically relevant genes and is also thought to hold susceptibility genes for a variety of autoimmune diseases that are linked to specific alleles of particular loci in the HLA D region. |
| 20588 | 2577113 | The localization of TNF genes on the short arm of chromosome 6 between HLA B and the complement genes focused attention to that genetic region which harbors many immunologically relevant genes and is also thought to hold susceptibility genes for a variety of autoimmune diseases that are linked to specific alleles of particular loci in the HLA D region. |
| 20589 | 2577113 | The localization of TNF genes on the short arm of chromosome 6 between HLA B and the complement genes focused attention to that genetic region which harbors many immunologically relevant genes and is also thought to hold susceptibility genes for a variety of autoimmune diseases that are linked to specific alleles of particular loci in the HLA D region. |
| 20590 | 2577113 | Since the recently established HLA-DR-DQ variation accounts only for part of the genetic susceptibility to insulin-dependent diabetes mellitus (IDDM) we searched for genomic variation of the tumour necrosis factor (TNF) alpha. |
| 20591 | 2577113 | Since the recently established HLA-DR-DQ variation accounts only for part of the genetic susceptibility to insulin-dependent diabetes mellitus (IDDM) we searched for genomic variation of the tumour necrosis factor (TNF) alpha. |
| 20592 | 2577113 | Since the recently established HLA-DR-DQ variation accounts only for part of the genetic susceptibility to insulin-dependent diabetes mellitus (IDDM) we searched for genomic variation of the tumour necrosis factor (TNF) alpha. |
| 20593 | 2577113 | Since the recently established HLA-DR-DQ variation accounts only for part of the genetic susceptibility to insulin-dependent diabetes mellitus (IDDM) we searched for genomic variation of the tumour necrosis factor (TNF) alpha. |
| 20594 | 2577113 | This tight linkage of TNF-alpha alleles with extended haplotypes and the significant increase of heterozygotes in patients could lead to some explanation of the DR3 association with a variety of autoimmune diseases particularly IDDM. |
| 20595 | 2577113 | This tight linkage of TNF-alpha alleles with extended haplotypes and the significant increase of heterozygotes in patients could lead to some explanation of the DR3 association with a variety of autoimmune diseases particularly IDDM. |
| 20596 | 2577113 | This tight linkage of TNF-alpha alleles with extended haplotypes and the significant increase of heterozygotes in patients could lead to some explanation of the DR3 association with a variety of autoimmune diseases particularly IDDM. |
| 20597 | 2577113 | This tight linkage of TNF-alpha alleles with extended haplotypes and the significant increase of heterozygotes in patients could lead to some explanation of the DR3 association with a variety of autoimmune diseases particularly IDDM. |
| 20598 | 2556447 | A macrophage/monocyte receptor for AGE moieties mediates the uptake of AGE-modified proteins by a process that also induces cachectin/tumor necrosis factor (TNF) and IL-1 secretion. |
| 20599 | 2556447 | A macrophage/monocyte receptor for AGE moieties mediates the uptake of AGE-modified proteins by a process that also induces cachectin/tumor necrosis factor (TNF) and IL-1 secretion. |
| 20600 | 2556447 | A macrophage/monocyte receptor for AGE moieties mediates the uptake of AGE-modified proteins by a process that also induces cachectin/tumor necrosis factor (TNF) and IL-1 secretion. |
| 20601 | 2556447 | Reasoning that cytokines might regulate this AGE-receptor system, we have evaluated the effect of cachectin/TNF, IL-1, and IFN-gamma on AGE-protein processing. |
| 20602 | 2556447 | Reasoning that cytokines might regulate this AGE-receptor system, we have evaluated the effect of cachectin/TNF, IL-1, and IFN-gamma on AGE-protein processing. |
| 20603 | 2556447 | Reasoning that cytokines might regulate this AGE-receptor system, we have evaluated the effect of cachectin/TNF, IL-1, and IFN-gamma on AGE-protein processing. |
| 20604 | 2556447 | IL-1 and IFN-gamma alone did not increase AGE processing, but IFN-gamma consistently enhanced cachectin/TNF-induced changes in AGE-receptor kinetics. |
| 20605 | 2556447 | IL-1 and IFN-gamma alone did not increase AGE processing, but IFN-gamma consistently enhanced cachectin/TNF-induced changes in AGE-receptor kinetics. |
| 20606 | 2556447 | IL-1 and IFN-gamma alone did not increase AGE processing, but IFN-gamma consistently enhanced cachectin/TNF-induced changes in AGE-receptor kinetics. |
| 20607 | 2794065 | Among recombinant mouse IFN gamma, human IL1 alpha, human IL2, mouse granulocyte-macrophage colony-stimulating factor and human TNF alpha, only human TNF alpha suppressed insulitis and significantly (P less than 0.001) inhibited development of diabetes. |
| 20608 | 2794065 | Among recombinant mouse IFN gamma, human IL1 alpha, human IL2, mouse granulocyte-macrophage colony-stimulating factor and human TNF alpha, only human TNF alpha suppressed insulitis and significantly (P less than 0.001) inhibited development of diabetes. |
| 20609 | 2794065 | NOD mice were the lowest producers of the mRNA of TNF and serum TNF on stimulation with OK-432 or with IFN gamma plus LPS, compared with C57BL/6, C3H/He, and Balb/c mice. |
| 20610 | 2794065 | NOD mice were the lowest producers of the mRNA of TNF and serum TNF on stimulation with OK-432 or with IFN gamma plus LPS, compared with C57BL/6, C3H/He, and Balb/c mice. |
| 20611 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20612 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20613 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20614 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20615 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20616 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20617 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20618 | 2501390 | IFN-gamma and TNF-alpha injure the pancreatic beta-cell and may be involved in the pathogenesis of autoimmune type 1 diabetes. |
| 20619 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20620 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20621 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20622 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20623 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20624 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20625 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20626 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 20627 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20628 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20629 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20630 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20631 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20632 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20633 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20634 | 2501390 | Islet culture supernatants contained detectable IL-6 activity which was increased 6-fold when islets were exposed to IFN-gamma and 40- and 115-fold when islets were exposed to TNF-alpha and TNF-alpha + IFN-gamma, respectively. |
| 20635 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20636 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20637 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20638 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20639 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20640 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20641 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20642 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 20643 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20644 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20645 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20646 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20647 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20648 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20649 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20650 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 20651 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20652 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20653 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20654 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20655 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20656 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20657 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20658 | 2501390 | Northern blot hybridization analysis of islet total cytoplasmic RNA with a cDNA probe to murine IL-6 revealed a band at 1.3 kb, the intensity of which increased in islets exposed to IFN-gamma + TNF-alpha. |
| 20659 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20660 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20661 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20662 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20663 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20664 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20665 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20666 | 2501390 | IL-6 activity was also detected in culture supernatants from RIN-m5F cells exposed to TNF-alpha + IFN-gamma. |
| 20667 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20668 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20669 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20670 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20671 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20672 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20673 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20674 | 2501390 | Pancreatic islet cells, in all probability beta-cells, produce IL-6, the expression of which is up-regulated by IFN-gamma and/or TNF-alpha. |
| 20675 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20676 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20677 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20678 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20679 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20680 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20681 | 2787351 | Involvement of class II MHC molecules in the LPS-induction of IL-1/TNF secretions by human monocytes. |
| 20682 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20683 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20684 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20685 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20686 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20687 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20688 | 2787351 | Anti-class II ag mAb (DR and DQ) inhibited, in a dose-dependent manner, LPS-induced IL-1 and TNF secretions from human monocytes (34 to 95% inhibition). |
| 20689 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20690 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20691 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20692 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20693 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20694 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20695 | 2787351 | The potentiating effect of IFN-gamma on LPS-induced TNF secretion (15.3 +/- 0.7 to 44 +/- 0.6 ng/ml) was also blocked by anti-class II ag mAb (44 +/- 0.6 to 0.3 +/- 0.03 ng/ml). |
| 20696 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20697 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20698 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20699 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20700 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20701 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20702 | 2787351 | We also report a relationship between interindividual differences in monocyte IL-1 and TNF secretions and the HLA-D-encoded genetic polymorphism. |
| 20703 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20704 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20705 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20706 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20707 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20708 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20709 | 2787351 | Analysis of these secretions in heterozygotes demonstrated a differential effect of certain haplotype combinations (i.e., DR2-DR4 vs DR2-DR3) that could be arbitrarily characterized as being "low" or "high" secretors (6,230 +/- 2,950 vs 13,029 +/- 6,541 cpm for IL-1, and 12 +/- 10 vs 25 +/- 15 ng/ml for TNF, p = 0.006 and 0.048). |
| 20710 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20711 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20712 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20713 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20714 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20715 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20716 | 2787351 | DR-associated Dw subtypes appeared to account for differences within certain haplotype combinations (Dw18 vs Dw19 in DRw13/DR4) (11,227 +/- 3,648 vs 17,166 +/- 3,176 cpm for IL-1, and 13 +/- 9 vs 25 +/- 10 ng/ml for TNF, p = 0.02 and 0.047). |
| 20717 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20718 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20719 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20720 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20721 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20722 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20723 | 2787351 | Thus, we conclude that, a) LPS-induced IL-1 and TNF secretions are, at least in part, regulated by class II MHC molecules, b) that HLA-D region-encoded genetic polymorphism accounts for interindividual differences in these secretions, and c) that the HLA-associated risk to develop IDD is not explained by these cytokine secretory differences as previously proposed. |
| 20724 | 2502459 | Neither class I nor class II major histocompatibility complex (MHC) antigens are routinely expressed at the cell surface; however, MHC class I--but not class II--encoded gene products are detected after treatment with recombinant interferon-gamma (IFN-gamma) alone or in combination with tumor necrosis factor. |
| 20725 | 2677685 | In addition, macrophages synthesize a great number of substances involved in host defense and inflammation i.e. complement components, prostaglandins, IL-1, tumor necrosis factor-alpha and others. |
| 20726 | 2677685 | Monocyte-macrophage dysfunctions have been described in various disorders: defective chemotaxis (corticosteroids, drug induced immunosuppression, AIDS, diabetes), defective phagocytosis (lupus erythematosus, deficiency of a membrane glycoprotein), microbicidal defect (chronic granulomatous disease), decreased cytotoxicity (Wiskott-Aldrich-Syndrome), deficiencies in the clearance of physiologic substrates in lysosomal diseases. |
| 20727 | 2572498 | TNF-alpha gene polymorphisms in type 1 (insulin-dependent) diabetes mellitus. |
| 20728 | 2572498 | TNF-alpha gene polymorphisms in type 1 (insulin-dependent) diabetes mellitus. |
| 20729 | 2572498 | TNF-alpha gene polymorphisms in type 1 (insulin-dependent) diabetes mellitus. |
| 20730 | 2572498 | The localisation of tumour necrosis factor genes on the short arm of chromosome 6 between HLA-B and the complement genes (Class III) prompted us to investigate a possible polymorphism of TNF-alpha at the genomic level in relation to Type 1 diabetes susceptibility. |
| 20731 | 2572498 | The localisation of tumour necrosis factor genes on the short arm of chromosome 6 between HLA-B and the complement genes (Class III) prompted us to investigate a possible polymorphism of TNF-alpha at the genomic level in relation to Type 1 diabetes susceptibility. |
| 20732 | 2572498 | The localisation of tumour necrosis factor genes on the short arm of chromosome 6 between HLA-B and the complement genes (Class III) prompted us to investigate a possible polymorphism of TNF-alpha at the genomic level in relation to Type 1 diabetes susceptibility. |
| 20733 | 2572498 | All affected sibling pairs in 11 multiplex affected families were identical for TNF-alpha alleles, even if they were only haploidentical for HLA-B-DR haplotypes. |
| 20734 | 2572498 | All affected sibling pairs in 11 multiplex affected families were identical for TNF-alpha alleles, even if they were only haploidentical for HLA-B-DR haplotypes. |
| 20735 | 2572498 | All affected sibling pairs in 11 multiplex affected families were identical for TNF-alpha alleles, even if they were only haploidentical for HLA-B-DR haplotypes. |
| 20736 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 20737 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 20738 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 20739 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 20740 | 2498883 | IFN-gamma was 50% more potent than TNF-alpha; together, their effects were additive. |
| 20741 | 2498883 | IFN-gamma was 50% more potent than TNF-alpha; together, their effects were additive. |
| 20742 | 2498883 | IFN-gamma was 50% more potent than TNF-alpha; together, their effects were additive. |
| 20743 | 2498883 | IFN-gamma was 50% more potent than TNF-alpha; together, their effects were additive. |
| 20744 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 20745 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 20746 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 20747 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 20748 | 2498883 | In contrast, infection with reovirus type 3 did not induce ICAM-1 on islet cells, although it stimulated the expression of class I MHC proteins. |
| 20749 | 2498883 | In contrast, infection with reovirus type 3 did not induce ICAM-1 on islet cells, although it stimulated the expression of class I MHC proteins. |
| 20750 | 2498883 | In contrast, infection with reovirus type 3 did not induce ICAM-1 on islet cells, although it stimulated the expression of class I MHC proteins. |
| 20751 | 2498883 | In contrast, infection with reovirus type 3 did not induce ICAM-1 on islet cells, although it stimulated the expression of class I MHC proteins. |
| 20752 | 2498883 | By double-label indirect immunofluorescence microscopy, ICAM-1 expression was identified on both beta (insulin-secreting) and delta (somatostatin-secreting) islet cells. |
| 20753 | 2498883 | By double-label indirect immunofluorescence microscopy, ICAM-1 expression was identified on both beta (insulin-secreting) and delta (somatostatin-secreting) islet cells. |
| 20754 | 2498883 | By double-label indirect immunofluorescence microscopy, ICAM-1 expression was identified on both beta (insulin-secreting) and delta (somatostatin-secreting) islet cells. |
| 20755 | 2498883 | By double-label indirect immunofluorescence microscopy, ICAM-1 expression was identified on both beta (insulin-secreting) and delta (somatostatin-secreting) islet cells. |
| 20756 | 2498883 | Monoclonal antibody to ICAM-1 precipitated protein of Mr 97,000 from [35S]methionine-labeled islets exposed to IFN-gamma and TNF-alpha, but not from control islets. |
| 20757 | 2498883 | Monoclonal antibody to ICAM-1 precipitated protein of Mr 97,000 from [35S]methionine-labeled islets exposed to IFN-gamma and TNF-alpha, but not from control islets. |
| 20758 | 2498883 | Monoclonal antibody to ICAM-1 precipitated protein of Mr 97,000 from [35S]methionine-labeled islets exposed to IFN-gamma and TNF-alpha, but not from control islets. |
| 20759 | 2498883 | Monoclonal antibody to ICAM-1 precipitated protein of Mr 97,000 from [35S]methionine-labeled islets exposed to IFN-gamma and TNF-alpha, but not from control islets. |
| 20760 | 2545735 | Insulin-dependent (type 1) diabetes mellitus (IDDM) is due to the selective autoimmune-mediated destruction of pancreatic beta cells possibly initiated by viruses. |
| 20761 | 2545735 | Insulin-dependent (type 1) diabetes mellitus (IDDM) is due to the selective autoimmune-mediated destruction of pancreatic beta cells possibly initiated by viruses. |
| 20762 | 2545735 | Insulin-dependent (type 1) diabetes mellitus (IDDM) is due to the selective autoimmune-mediated destruction of pancreatic beta cells possibly initiated by viruses. |
| 20763 | 2545735 | To elucidate the possible role of viruses and cytokines in the pathogenesis of IDDM, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) on beta cell function in vitro. |
| 20764 | 2545735 | To elucidate the possible role of viruses and cytokines in the pathogenesis of IDDM, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) on beta cell function in vitro. |
| 20765 | 2545735 | To elucidate the possible role of viruses and cytokines in the pathogenesis of IDDM, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) on beta cell function in vitro. |
| 20766 | 2545735 | Murine islets cultured for 3 days with IFN-gamma and/or TNF-alpha had a significantly reduced insulin response to glucose, which was more marked with a combination of the cytokines. |
| 20767 | 2545735 | Murine islets cultured for 3 days with IFN-gamma and/or TNF-alpha had a significantly reduced insulin response to glucose, which was more marked with a combination of the cytokines. |
| 20768 | 2545735 | Murine islets cultured for 3 days with IFN-gamma and/or TNF-alpha had a significantly reduced insulin response to glucose, which was more marked with a combination of the cytokines. |
| 20769 | 2545735 | During 6 days of culture in IFN-gamma plus TNF-alpha islets underwent noticeable degeneration associated with an 80% reduction in insulin content. |
| 20770 | 2545735 | During 6 days of culture in IFN-gamma plus TNF-alpha islets underwent noticeable degeneration associated with an 80% reduction in insulin content. |
| 20771 | 2545735 | During 6 days of culture in IFN-gamma plus TNF-alpha islets underwent noticeable degeneration associated with an 80% reduction in insulin content. |
| 20772 | 2703526 | Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia. |
| 20773 | 2703526 | Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia. |
| 20774 | 2703526 | Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia. |
| 20775 | 2703526 | Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia. |
| 20776 | 2703526 | Evidence that inhibition of adipose tissue lipoprotein lipase activity is not required for TNF-induced hyperlipidemia. |
| 20777 | 2703526 | Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. |
| 20778 | 2703526 | Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. |
| 20779 | 2703526 | Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. |
| 20780 | 2703526 | Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. |
| 20781 | 2703526 | Tumor necrosis factor (TNF) administration produces an increase in plasma triglycerides that may be due to inhibition of adipose lipoprotein lipase activity and/or a stimulation of hepatic lipogenesis. |
| 20782 | 2703526 | Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. |
| 20783 | 2703526 | Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. |
| 20784 | 2703526 | Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. |
| 20785 | 2703526 | Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. |
| 20786 | 2703526 | Adipose tissue lipoprotein lipase activity was markedly decreased in diabetic animals compared with controls and was not further inhibited by TNF. |
| 20787 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 20788 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 20789 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 20790 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 20791 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 20792 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 20793 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 20794 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 20795 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 20796 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 20797 | 2518361 | When tested as single agents or added together at very low concentrations, interleukin 1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) inhibited insulin release from rat islet cell monolayer cultures during 4 day incubations; however, this secretory function improved after the cytokines were removed. |
| 20798 | 2518361 | When tested as single agents or added together at very low concentrations, interleukin 1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) inhibited insulin release from rat islet cell monolayer cultures during 4 day incubations; however, this secretory function improved after the cytokines were removed. |
| 20799 | 2518361 | When tested as single agents or added together at very low concentrations, interleukin 1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) inhibited insulin release from rat islet cell monolayer cultures during 4 day incubations; however, this secretory function improved after the cytokines were removed. |
| 20800 | 2518361 | In contrast, combinations of slightly higher concentrations of IL-1, TNF, and IFN-gamma produced irreversible inhibition of insulin release, as well as decreased cell insulin content and proportional increase in cell lysis, measured as release of 51Cr from labeled islet cell cultures. |
| 20801 | 2518361 | In contrast, combinations of slightly higher concentrations of IL-1, TNF, and IFN-gamma produced irreversible inhibition of insulin release, as well as decreased cell insulin content and proportional increase in cell lysis, measured as release of 51Cr from labeled islet cell cultures. |
| 20802 | 2518361 | In contrast, combinations of slightly higher concentrations of IL-1, TNF, and IFN-gamma produced irreversible inhibition of insulin release, as well as decreased cell insulin content and proportional increase in cell lysis, measured as release of 51Cr from labeled islet cell cultures. |
| 20803 | 2518361 | These findings suggest that cytokine products of T lymphocytes (IFN-gamma) and macrophage/monocytic cells (IL-1, TNF) infiltrating pancreatic islets in "autoimmune" diabetes may interact synergistically to produce functional inhibition or lethal cytocidal effects on islet beta-cells, possibly accounting for reversible and irreversible stages of insulin-dependent diabetes. |
| 20804 | 2518361 | These findings suggest that cytokine products of T lymphocytes (IFN-gamma) and macrophage/monocytic cells (IL-1, TNF) infiltrating pancreatic islets in "autoimmune" diabetes may interact synergistically to produce functional inhibition or lethal cytocidal effects on islet beta-cells, possibly accounting for reversible and irreversible stages of insulin-dependent diabetes. |
| 20805 | 2518361 | These findings suggest that cytokine products of T lymphocytes (IFN-gamma) and macrophage/monocytic cells (IL-1, TNF) infiltrating pancreatic islets in "autoimmune" diabetes may interact synergistically to produce functional inhibition or lethal cytocidal effects on islet beta-cells, possibly accounting for reversible and irreversible stages of insulin-dependent diabetes. |
| 20806 | 2537014 | Ia antigen expression was induced on isolated B10.BR murine islet parenchymal cells by culturing them for 5 days with lymphokine supernatants containing interferon-gamma (IFN-gamma) or with recombinant murine IFN-gamma + recombinant tumor necrosis factor. |
| 20807 | 2713885 | On some examples he demonstrates the importance of endocrinology for other medical disciplines: the interrelationship of stress and infectious reactions via interleukin 1, the discovery of a series of new growth and immune factors; the participation TNF (cachectin, tumour necrosis factor) in pathological processes (tumours, atherosclerosis); vasoactive peptides EDRF (endothelium derived relaxation factor), endothelin (vasoconstriction), GM-CSF (granulocyte-macrophage colony stimulating factor) in treatment of radiation sickness and adjuvans in chemotherapy; interleukins. |
| 20808 | 2674559 | Possible role of IL-1, TNF-alpha, and IL-6 in insulin-dependent diabetes mellitus and autoimmune thyroid disease. |
| 20809 | 2674559 | Possible role of IL-1, TNF-alpha, and IL-6 in insulin-dependent diabetes mellitus and autoimmune thyroid disease. |
| 20810 | 2674559 | Possible role of IL-1, TNF-alpha, and IL-6 in insulin-dependent diabetes mellitus and autoimmune thyroid disease. |
| 20811 | 2674559 | Possible role of IL-1, TNF-alpha, and IL-6 in insulin-dependent diabetes mellitus and autoimmune thyroid disease. |
| 20812 | 2674559 | Recent experiments indicate a central role of macrophages (M phi), and natural killer (NK) cells, and their products IL-1, IL-6 and TNF alpha in autoimmune endocrine diseases. |
| 20813 | 2674559 | Recent experiments indicate a central role of macrophages (M phi), and natural killer (NK) cells, and their products IL-1, IL-6 and TNF alpha in autoimmune endocrine diseases. |
| 20814 | 2674559 | Recent experiments indicate a central role of macrophages (M phi), and natural killer (NK) cells, and their products IL-1, IL-6 and TNF alpha in autoimmune endocrine diseases. |
| 20815 | 2674559 | Recent experiments indicate a central role of macrophages (M phi), and natural killer (NK) cells, and their products IL-1, IL-6 and TNF alpha in autoimmune endocrine diseases. |
| 20816 | 2674559 | Intermediate levels of IL-1 alpha/beta inhibit the function of pancreatic beta-cells and thyrocytes, an effect potentiated by TNF alpha. |
| 20817 | 2674559 | Intermediate levels of IL-1 alpha/beta inhibit the function of pancreatic beta-cells and thyrocytes, an effect potentiated by TNF alpha. |
| 20818 | 2674559 | Intermediate levels of IL-1 alpha/beta inhibit the function of pancreatic beta-cells and thyrocytes, an effect potentiated by TNF alpha. |
| 20819 | 2674559 | Intermediate levels of IL-1 alpha/beta inhibit the function of pancreatic beta-cells and thyrocytes, an effect potentiated by TNF alpha. |
| 20820 | 2674559 | In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. |
| 20821 | 2674559 | In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. |
| 20822 | 2674559 | In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. |
| 20823 | 2674559 | In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. |
| 20824 | 2674559 | Intermediate and high levels of IL-1 and IL-6 are cytotoxic to normal beta-cells. |
| 20825 | 2674559 | Intermediate and high levels of IL-1 and IL-6 are cytotoxic to normal beta-cells. |
| 20826 | 2674559 | Intermediate and high levels of IL-1 and IL-6 are cytotoxic to normal beta-cells. |
| 20827 | 2674559 | Intermediate and high levels of IL-1 and IL-6 are cytotoxic to normal beta-cells. |
| 20828 | 2674559 | IL-1 induces IL-6 in isolated islets and in thyrocytes. |
| 20829 | 2674559 | IL-1 induces IL-6 in isolated islets and in thyrocytes. |
| 20830 | 2674559 | IL-1 induces IL-6 in isolated islets and in thyrocytes. |
| 20831 | 2674559 | IL-1 induces IL-6 in isolated islets and in thyrocytes. |
| 20832 | 2674559 | The genes for TNF alpha and -beta, both located in the MHC region, and IL-6 are polymorphic, and specific alleles may control the amount of cytokine produced. |
| 20833 | 2674559 | The genes for TNF alpha and -beta, both located in the MHC region, and IL-6 are polymorphic, and specific alleles may control the amount of cytokine produced. |
| 20834 | 2674559 | The genes for TNF alpha and -beta, both located in the MHC region, and IL-6 are polymorphic, and specific alleles may control the amount of cytokine produced. |
| 20835 | 2674559 | The genes for TNF alpha and -beta, both located in the MHC region, and IL-6 are polymorphic, and specific alleles may control the amount of cytokine produced. |
| 20836 | 2550952 | Insulin appears to be a potent suppressor of this macrophage AGE removal activity, while TNF acts as a stimulant. |
| 20837 | 2550952 | Insulin appears to be a potent suppressor of this macrophage AGE removal activity, while TNF acts as a stimulant. |
| 20838 | 2550952 | Coupling of AGE-proteins to their AGE-receptor results in TNF and IL-1 synthesis and secretion. |
| 20839 | 2550952 | Coupling of AGE-proteins to their AGE-receptor results in TNF and IL-1 synthesis and secretion. |
| 20840 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20841 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20842 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20843 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20844 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20845 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20846 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20847 | 2491807 | Inhibitory effects of tumor necrosis factor-alpha and interferon-gamma on deoxyribonucleic acid and collagen synthesis by rat osteosarcoma cells (ROS 17/2.8). |
| 20848 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20849 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20850 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20851 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20852 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20853 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20854 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20855 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 20856 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20857 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20858 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20859 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20860 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20861 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20862 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20863 | 2491807 | Since the effects of TNF alpha and IFN gamma may result from interaction with multiple cell types, we studied the effects of these cytokines on the synthesis of DNA and collagen in one cell type with osteoblast phenotype, cloned rat osteosarcoma cells (ROS 17/2.8). |
| 20864 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20865 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20866 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20867 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20868 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20869 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20870 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20871 | 2491807 | Coincubation with TNF alpha and IFN gamma inhibited DNA synthesis more than maximal doses of either cytokine alone. |
| 20872 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20873 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20874 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20875 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20876 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20877 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20878 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20879 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 20880 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20881 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20882 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20883 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20884 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20885 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20886 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20887 | 2491807 | Preexposure to TNF alpha for 24 h, followed by IFN gamma alone, did not increase the inhibition of DNA synthesis. |
| 20888 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20889 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20890 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20891 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20892 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20893 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20894 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20895 | 2491807 | Incubation with either IFN gamma (5-500 U/ml) or TNF alpha (10(-10)-10(-6) M) inhibited the incorporation of [3H]proline into collagen. |
| 20896 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20897 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20898 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20899 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20900 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20901 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20902 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20903 | 2491807 | The results indicate that 1) IFN gamma and TNF alpha have direct actions on osteoblast-like cells in vitro; 2) IFN gamma modulates the DNA response to TNF alpha; and 3) the greater responses to combined cytokines than to high doses of either alone suggest that these cytokines act, at least in part, through different pathways. |
| 20904 | 3069387 | The pathogenetic mechanisms leading to beta-cell destruction and insulin-dependent diabetes mellitus (IDDM) are major histocompatibility complex (MHC) nonrestricted and are MHC associated and beta-cell specific. |
| 20905 | 3069387 | The pathogenetic mechanisms leading to beta-cell destruction and insulin-dependent diabetes mellitus (IDDM) are major histocompatibility complex (MHC) nonrestricted and are MHC associated and beta-cell specific. |
| 20906 | 3069387 | The macrophage peptide hormone interleukin 1 (IL-1) may be the primary MHC-nonrestricted beta-cell-destructive molecule. |
| 20907 | 3069387 | The macrophage peptide hormone interleukin 1 (IL-1) may be the primary MHC-nonrestricted beta-cell-destructive molecule. |
| 20908 | 3069387 | The potentiation of IL-1 effects on beta-cells by tumor necrosis factor alpha (TNF), another macrophage hormone controlled by a gene in the HLA region on chromosome 6, may account for the MHC association of IDDM. |
| 20909 | 3069387 | The potentiation of IL-1 effects on beta-cells by tumor necrosis factor alpha (TNF), another macrophage hormone controlled by a gene in the HLA region on chromosome 6, may account for the MHC association of IDDM. |
| 20910 | 3069387 | In the experimental model of IDDM etiopathogenesis described, release of beta-cell antigen, processed and presented by macrophages to helper T-lymphocytes, initiates a self-perpetuating and self-limiting circuit of cytokine production of which IL-1 is beta-cell cytotoxic. |
| 20911 | 3069387 | In the experimental model of IDDM etiopathogenesis described, release of beta-cell antigen, processed and presented by macrophages to helper T-lymphocytes, initiates a self-perpetuating and self-limiting circuit of cytokine production of which IL-1 is beta-cell cytotoxic. |
| 20912 | 3069387 | As postulated, the IL-1 effect is potentiated by TNF, whereas IL-1 and/or TNF production is controlled in a quantitative way by HLA-D genes. |
| 20913 | 3069387 | As postulated, the IL-1 effect is potentiated by TNF, whereas IL-1 and/or TNF production is controlled in a quantitative way by HLA-D genes. |
| 20914 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20915 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20916 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20917 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20918 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20919 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20920 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20921 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20922 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20923 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20924 | 3139756 | IFN-gamma and tumor necrosis factor-alpha. |
| 20925 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20926 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20927 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20928 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20929 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20930 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20931 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20932 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20933 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20934 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20935 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 20936 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20937 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20938 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20939 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20940 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20941 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20942 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20943 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20944 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20945 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20946 | 3139756 | IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. |
| 20947 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20948 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20949 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20950 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20951 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20952 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20953 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20954 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20955 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20956 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20957 | 3139756 | The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. |
| 20958 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20959 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20960 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20961 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20962 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20963 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20964 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20965 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20966 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20967 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20968 | 3139756 | Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. |
| 20969 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20970 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20971 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20972 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20973 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20974 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20975 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20976 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20977 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20978 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20979 | 3139756 | In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. |
| 20980 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20981 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20982 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20983 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20984 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20985 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20986 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20987 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20988 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20989 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20990 | 3139756 | In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. |
| 20991 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20992 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20993 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20994 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20995 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20996 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20997 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20998 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 20999 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 21000 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 21001 | 3139756 | The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. |
| 21002 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21003 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21004 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21005 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21006 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21007 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21008 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21009 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21010 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21011 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21012 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 21013 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21014 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21015 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21016 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21017 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21018 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21019 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21020 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21021 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21022 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21023 | 3139756 | The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. |
| 21024 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21025 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21026 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21027 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21028 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21029 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21030 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21031 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21032 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21033 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21034 | 3139756 | The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes. |
| 21035 | 2836251 | These findings suggest that 1) in addition to direct cytopathic effects, reovirus infection may contribute to beta-cell destruction by increasing expression of class I MHC proteins and therefore reactivity with cytotoxic T-lymphocytes; and 2) some viruses may increase MHC protein expression independent of and before the action of cytokines (e.g., interferon-gamma and tumor necrosis factor) released by immunoinflammatory cells. |
| 21036 | 3327310 | Study of two diseases with autoimmune characteristics (IDDM and SLE) has demonstrated that alleles carried in the MHC can confer disease susceptibility. |
| 21037 | 3327310 | The MHC alleles most strongly associated with the development of IDDM are encoded within the class II region (HLA-DR or -DQ). |
| 21038 | 3327310 | Recent studies indicating that the class III gene products TNF alpha and beta may play a critical role in the initiation of the autoimmune attack on the pancreatic beta-cells have suggested the possibility that the class III region may also contribute to genetic susceptibility in IDDM. |
| 21039 | 3121415 | Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1. |
| 21040 | 3121415 | Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1. |
| 21041 | 3121415 | Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1. |
| 21042 | 3121415 | Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1. |
| 21043 | 3121415 | When tested alone, murine (rat and mouse) interferon-gamma (mIFN-gamma) produced a small dose-dependent lysis of islet cells; human IFN-gamma, mouse IFN-alpha/beta, interleukins 1 and 2 (IL-1 and IL-2), tumor necrosis factor (TNF), and lymphotoxin (LT) were inactive. |
| 21044 | 3121415 | When tested alone, murine (rat and mouse) interferon-gamma (mIFN-gamma) produced a small dose-dependent lysis of islet cells; human IFN-gamma, mouse IFN-alpha/beta, interleukins 1 and 2 (IL-1 and IL-2), tumor necrosis factor (TNF), and lymphotoxin (LT) were inactive. |
| 21045 | 3121415 | When tested alone, murine (rat and mouse) interferon-gamma (mIFN-gamma) produced a small dose-dependent lysis of islet cells; human IFN-gamma, mouse IFN-alpha/beta, interleukins 1 and 2 (IL-1 and IL-2), tumor necrosis factor (TNF), and lymphotoxin (LT) were inactive. |
| 21046 | 3121415 | When tested alone, murine (rat and mouse) interferon-gamma (mIFN-gamma) produced a small dose-dependent lysis of islet cells; human IFN-gamma, mouse IFN-alpha/beta, interleukins 1 and 2 (IL-1 and IL-2), tumor necrosis factor (TNF), and lymphotoxin (LT) were inactive. |
| 21047 | 3121415 | When added together, the following combinations of cytokines showed synergistic cytotoxic effects: TNF (or LT) plus IL-1, TNF (or LT) plus mIFN-gamma, and IL-1 plus mIFN-gamma. |
| 21048 | 3121415 | When added together, the following combinations of cytokines showed synergistic cytotoxic effects: TNF (or LT) plus IL-1, TNF (or LT) plus mIFN-gamma, and IL-1 plus mIFN-gamma. |
| 21049 | 3121415 | When added together, the following combinations of cytokines showed synergistic cytotoxic effects: TNF (or LT) plus IL-1, TNF (or LT) plus mIFN-gamma, and IL-1 plus mIFN-gamma. |
| 21050 | 3121415 | When added together, the following combinations of cytokines showed synergistic cytotoxic effects: TNF (or LT) plus IL-1, TNF (or LT) plus mIFN-gamma, and IL-1 plus mIFN-gamma. |
| 21051 | 3121415 | These results indicate that the cytokine products of mononuclear cells of the immune system, IFN-gamma, TNF, LT, and IL-1 have strong synergistic cytotoxic effects on islet cells and therefore may act as direct chemical mediators of islet beta-cell destruction in type I (insulin-dependent) diabetes. |
| 21052 | 3121415 | These results indicate that the cytokine products of mononuclear cells of the immune system, IFN-gamma, TNF, LT, and IL-1 have strong synergistic cytotoxic effects on islet cells and therefore may act as direct chemical mediators of islet beta-cell destruction in type I (insulin-dependent) diabetes. |
| 21053 | 3121415 | These results indicate that the cytokine products of mononuclear cells of the immune system, IFN-gamma, TNF, LT, and IL-1 have strong synergistic cytotoxic effects on islet cells and therefore may act as direct chemical mediators of islet beta-cell destruction in type I (insulin-dependent) diabetes. |
| 21054 | 3121415 | These results indicate that the cytokine products of mononuclear cells of the immune system, IFN-gamma, TNF, LT, and IL-1 have strong synergistic cytotoxic effects on islet cells and therefore may act as direct chemical mediators of islet beta-cell destruction in type I (insulin-dependent) diabetes. |
| 21055 | 3320203 | Human tumor necrosis factor potentiates human interleukin 1-mediated rat pancreatic beta-cell cytotoxicity. |
| 21056 | 3320203 | Human tumor necrosis factor potentiates human interleukin 1-mediated rat pancreatic beta-cell cytotoxicity. |
| 21057 | 3320203 | Previous studies have established that the cytokine interleukin 1 (IL-1) is selectively cytotoxic for isolated human and rat pancreatic beta-cells. |
| 21058 | 3320203 | Previous studies have established that the cytokine interleukin 1 (IL-1) is selectively cytotoxic for isolated human and rat pancreatic beta-cells. |
| 21059 | 3320203 | This observation raises the possibility that insulin-dependent diabetes mellitus is in part due to immunologically mediated mechanisms involving IL-1. |
| 21060 | 3320203 | This observation raises the possibility that insulin-dependent diabetes mellitus is in part due to immunologically mediated mechanisms involving IL-1. |
| 21061 | 3320203 | To study possible modulatory effects of other cytokines on IL-1-mediated beta-cell cytotoxicity, we added human recombinant IL-1 alpha and beta (rIL-1 alpha, rIL-1 beta), tumor necrosis factor (rTNF), lymphotoxin (rLT), and interferon-gamma (rIFN-gamma) separately or in combinations to the culture medium of isolated rat islets of Langerhans. |
| 21062 | 3320203 | To study possible modulatory effects of other cytokines on IL-1-mediated beta-cell cytotoxicity, we added human recombinant IL-1 alpha and beta (rIL-1 alpha, rIL-1 beta), tumor necrosis factor (rTNF), lymphotoxin (rLT), and interferon-gamma (rIFN-gamma) separately or in combinations to the culture medium of isolated rat islets of Langerhans. |
| 21063 | 3308437 | Inhibitory effects of interleukin 1 on insulin secretion, insulin biosynthesis, and oxidative metabolism of isolated rat pancreatic islets. |
| 21064 | 3308437 | Inhibitory effects of interleukin 1 on insulin secretion, insulin biosynthesis, and oxidative metabolism of isolated rat pancreatic islets. |
| 21065 | 3308437 | Inhibitory effects of interleukin 1 on insulin secretion, insulin biosynthesis, and oxidative metabolism of isolated rat pancreatic islets. |
| 21066 | 3308437 | Recent observations suggest a role for interleukin 1 (IL-1), a macrophage-derived cytokine, in the autoimmune B cell destruction, which is observed in type 1 diabetes. |
| 21067 | 3308437 | Recent observations suggest a role for interleukin 1 (IL-1), a macrophage-derived cytokine, in the autoimmune B cell destruction, which is observed in type 1 diabetes. |
| 21068 | 3308437 | Recent observations suggest a role for interleukin 1 (IL-1), a macrophage-derived cytokine, in the autoimmune B cell destruction, which is observed in type 1 diabetes. |
| 21069 | 3308437 | In the present study we have investigated the effects of IL-1 and two other cytokines, namely tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma) on the pancreatic B cell paying particular attention to insulin production and glucose metabolism. |
| 21070 | 3308437 | In the present study we have investigated the effects of IL-1 and two other cytokines, namely tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma) on the pancreatic B cell paying particular attention to insulin production and glucose metabolism. |
| 21071 | 3308437 | In the present study we have investigated the effects of IL-1 and two other cytokines, namely tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma) on the pancreatic B cell paying particular attention to insulin production and glucose metabolism. |
| 21072 | 3308437 | The islets were subsequently transferred to media containing medium RPMI 1640 plus 0.5% human serum with or without additions of human recombinant preparations of either IL-1 (25 U/ml), TNF (1000 U/ml), or IFN-gamma (500 U/ml), and cultured for another 48 h. |
| 21073 | 3308437 | The islets were subsequently transferred to media containing medium RPMI 1640 plus 0.5% human serum with or without additions of human recombinant preparations of either IL-1 (25 U/ml), TNF (1000 U/ml), or IFN-gamma (500 U/ml), and cultured for another 48 h. |
| 21074 | 3308437 | The islets were subsequently transferred to media containing medium RPMI 1640 plus 0.5% human serum with or without additions of human recombinant preparations of either IL-1 (25 U/ml), TNF (1000 U/ml), or IFN-gamma (500 U/ml), and cultured for another 48 h. |
| 21075 | 3308437 | IL-1 was found to reduce insulin release in culture and totally inhibit glucose-stimulated insulin release in short-term incubations. |
| 21076 | 3308437 | IL-1 was found to reduce insulin release in culture and totally inhibit glucose-stimulated insulin release in short-term incubations. |
| 21077 | 3308437 | IL-1 was found to reduce insulin release in culture and totally inhibit glucose-stimulated insulin release in short-term incubations. |
| 21078 | 3308437 | Islet (pro)insulin biosynthesis, glucose oxidation, and oxygen uptake at 16.7 mM glucose were partially inhibited by IL-1. |
| 21079 | 3308437 | Islet (pro)insulin biosynthesis, glucose oxidation, and oxygen uptake at 16.7 mM glucose were partially inhibited by IL-1. |
| 21080 | 3308437 | Islet (pro)insulin biosynthesis, glucose oxidation, and oxygen uptake at 16.7 mM glucose were partially inhibited by IL-1. |
| 21081 | 3308437 | TNF and IFN-gamma were essentially without effect on islet morphology or function. |
| 21082 | 3308437 | TNF and IFN-gamma were essentially without effect on islet morphology or function. |
| 21083 | 3308437 | TNF and IFN-gamma were essentially without effect on islet morphology or function. |
| 21084 | 3102976 | The cytotoxins tumour necrosis factor (TNF) and lymphotoxin (LT) synergize with IFN-gamma in a number of activities. |
| 21085 | 3102976 | The cytotoxins tumour necrosis factor (TNF) and lymphotoxin (LT) synergize with IFN-gamma in a number of activities. |
| 21086 | 3102976 | We report here that IFN-gamma in combination with either TNF or LT induces islet cell class II expression. |
| 21087 | 3102976 | We report here that IFN-gamma in combination with either TNF or LT induces islet cell class II expression. |
| 21088 | 3497511 | A variety of factors may contribute to the regulation of Class II expression by thyrocytes: this is induced by interferon (IFN-gamma), and is enhanced by thyroid stimulating hormone (TSH) and by tumour necrosis factor (TNF). |