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PMID |
Sentence |
1 |
1303251
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Based on genetic analysis of several crosses, we show that development of diabetes involves at least three genes: Lyp, which is tightly linked to the neuropeptide Y (Npy) gene on chromosome 4, a gene linked to the major histocompatibility complex (MHC) on chromosome 20, and a third unmapped gene for which the Fischer rat strain carries an allele conferring resistance.
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2 |
8734569
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T cells from BB-DP rats show a unique cytokine mRNA profile associated with the IDDM1 susceptibility gene, Lyp.
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3 |
8734569
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One of the most pronounced abnormalities in these animals is a marked T cell lymphopenia which is evident in both CD4+ and CD8+ peripheral T cell subsets.
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4 |
9243099
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Lyp controls the number of peripheral lymphocytes by reducing T cells of the RT6+ phenotype by almost 90%.
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5 |
9243099
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The frequency of IFN gamma and interleukin (IL)-10 mRNA expressing cells in isolated thymocytes determined by quantitative image analysis, demonstrated an increased IFN gamma: IL-10 ratio in thymocytes from lyp/lyp homozygotes compared to lyp/+ and +/+ rats.
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6 |
9243099
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Recombinant human glutamic acid decarboxylase (GAD65) increased the number of IFN gamma and IL-10 mRNA expressing thymocytes after in vitro culture.
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7 |
10051319
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Secondly, caspase-2 maps close to Tcrb on mouse Chromosome (Chr) 6, while Lyp is closely linked to Tcrb on the homologous rat Chr 4.
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8 |
10051319
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Since Lyp maps distally to D4Mit5, between markers D4Rat75 and Npy, we exclude caspase-2 as a candidate gene for Lyp.
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9 |
10051319
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Secondly, caspase-2 maps close to Tcrb on mouse Chromosome (Chr) 6, while Lyp is closely linked to Tcrb on the homologous rat Chr 4.
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10 |
10051319
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Since Lyp maps distally to D4Mit5, between markers D4Rat75 and Npy, we exclude caspase-2 as a candidate gene for Lyp.
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11 |
10777670
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Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
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12 |
10777670
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In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
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13 |
10777670
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This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
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14 |
10777670
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We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
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15 |
10777670
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Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
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16 |
10777670
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In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
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17 |
10777670
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This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
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18 |
10777670
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We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
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19 |
10777670
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Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
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20 |
10777670
|
In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
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21 |
10777670
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This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
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22 |
10777670
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We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
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23 |
10830965
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Engagement of RAGE by a ligand triggers activation of key cell signalling pathways, such as p21ras, MAP kinases, NF-kappaB and cdc42/rac, thereby reprogramming cellular properties.
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24 |
10830965
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Inhibition of the RAGE-amphoterin interaction suppressed activation of p44/p42, p38 and SAP/JNK MAP kinases; molecular effector mechanisms importantly linked to tumour proliferation, invasion and expression of matrix metalloproteinases.
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25 |
11453032
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Troglitazone (TRO) and rosiglitazone (RSG) belong to the thiazolidinedione class (insulin-sensitizing agents) and exert many of their metabolic effects as peroxisome proliferator-activated receptor gamma (PPARgamma) ligands.
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26 |
11453032
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TRO and RSG had no effect on the LDL-induced stimulation of the MAP kinases ERK1/2, p38 and SAP/JNK.
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27 |
14747305
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Haplotype tag single nucleotide polymorphism analysis of the human orthologues of the rat type 1 diabetes genes Ian4 (Lyp/Iddm1) and Cblb.
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28 |
14747305
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Recently, a frameshift deletion in Ian4, a member of the immune-associated nucleotide (Ian)-related gene family, has been shown to map to BB rat Iddm1.
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29 |
14747305
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Evaluation of disease association by a multilocus transmission/disequilibrium test (TDT) gave a P value of 0.484 for IAN4L1 and 0.692 for CBLB, suggesting that neither gene influences susceptibility to common alleles of human type 1 diabetes in these populations.
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30 |
18260110
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Disease-causing mutations have been detected in the SH2 domains of cytoplasmic signaling proteins Bruton tyrosine kinase (BTK), SH2D1A, Ras GTPase activating protein (RasGAP), ZAP-70, SHP-2, STAT1, STAT5B, and the p85alpha subunit of the PIP3.
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31 |
18260110
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Mutations in the BTK, SH2D1A, ZAP70, STAT1, and STAT5B genes have been shown to cause diverse immunodeficiencies, whereas the mutations in RASA1 and PIK3R1 genes lead to basal carcinoma and diabetes, respectively.
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32 |
18260110
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Disease-causing mutations have been detected in the SH2 domains of cytoplasmic signaling proteins Bruton tyrosine kinase (BTK), SH2D1A, Ras GTPase activating protein (RasGAP), ZAP-70, SHP-2, STAT1, STAT5B, and the p85alpha subunit of the PIP3.
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33 |
18260110
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Mutations in the BTK, SH2D1A, ZAP70, STAT1, and STAT5B genes have been shown to cause diverse immunodeficiencies, whereas the mutations in RASA1 and PIK3R1 genes lead to basal carcinoma and diabetes, respectively.
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34 |
19050296
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Elimination of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease chronic inflammatory demyelinating polyneuropathy (CIDP).
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35 |
19050296
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In this study, we examined the immunopathogenic mechanisms in this model, including identification of SAP Ags.
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36 |
19050296
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There was an increase in IL-17 and a decrease in IL-10 transcript levels at 4 mo (preclinical phase), whereas IFN-gamma expression peaked at 8 mo (clinical phase).
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37 |
19050296
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There was also an increase in transcript levels of Th1 cytokines, CXCL10, and RANTES in sciatic nerves of mice that developed SAP.
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38 |
19050296
|
Elimination of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease chronic inflammatory demyelinating polyneuropathy (CIDP).
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39 |
19050296
|
In this study, we examined the immunopathogenic mechanisms in this model, including identification of SAP Ags.
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40 |
19050296
|
There was an increase in IL-17 and a decrease in IL-10 transcript levels at 4 mo (preclinical phase), whereas IFN-gamma expression peaked at 8 mo (clinical phase).
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41 |
19050296
|
There was also an increase in transcript levels of Th1 cytokines, CXCL10, and RANTES in sciatic nerves of mice that developed SAP.
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42 |
19050296
|
Elimination of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease chronic inflammatory demyelinating polyneuropathy (CIDP).
|
43 |
19050296
|
In this study, we examined the immunopathogenic mechanisms in this model, including identification of SAP Ags.
|
44 |
19050296
|
There was an increase in IL-17 and a decrease in IL-10 transcript levels at 4 mo (preclinical phase), whereas IFN-gamma expression peaked at 8 mo (clinical phase).
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45 |
19050296
|
There was also an increase in transcript levels of Th1 cytokines, CXCL10, and RANTES in sciatic nerves of mice that developed SAP.
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46 |
20383745
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However, it is unclear whether this polymorphism correlates with plasma levels of inflammatory markers including visfatin, hs-CRP, IL-6 and TNF-α in CAD patients.
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47 |
20383745
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The present study was to investigate the potential association of the -1535C>T polymorphism with plasma levels of visfatin, IL-6, C reactive protein (hs-CRP) and TNF-α in patients with CAD.
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48 |
20383745
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We conducted a hospital based study with 171 CAD patients to examine the association between the -1535C>T polymorphism and plasma levels of visfatin, hs-CRP, IL-6 and TNF-α.
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49 |
20383745
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Plasma visfatin levels were markedly different between patients with stable angina pectoris (SAP, 11.91 ± 0.70 ng/l) and those with unstable angina pectoris (UAP, 17.49 ± 0.20 ng/l) or acute myocardial infarction (AMI, 16.63 ± 0.22 ng/l; SAP versus UAP or AMI, P < 0.05).
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50 |
20383745
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Compared with the CC genotype, variant genotypes CT and TT correlated with significantly lower levels of visfatin, hs-CRP, IL-6 and TNF-α in the SAP group (P < 0.05), with lower levels of hs-CRP and IL-6 in the UAP group (P < 0.05), and with lower levels of visfatin in the AMI group (P < 0.05) after adjustment for age, gender, smoking, hypertension, diabetes, dyslipidemia and medication.
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