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Gene Information
Gene symbol: SERPINA1
Gene name: serpin peptidase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 1
HGNC ID: 8941
Synonyms: AAT, A1A, PI1, alpha-1-antitrypsin, A1AT, alpha1AT
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 88025 | [Behavior of alpha 2-macroglobulin and alpha 1-antitrypsin in mature diabetics]. |
| 2 | 94976 | Inhibitors studied included 1) fast (immediate) antiplasmin, 2) slow (progressive) antiplasmin, 3) alpha-2-macroglobulin, and 4) alpha-1-antitrypsin. |
| 3 | 94976 | Alpha-2-macroglobulin was significantly higher and alpha-1-antitrypsin significantly lower in diabetic women than in controls. |
| 4 | 94976 | Inhibitors studied included 1) fast (immediate) antiplasmin, 2) slow (progressive) antiplasmin, 3) alpha-2-macroglobulin, and 4) alpha-1-antitrypsin. |
| 5 | 94976 | Alpha-2-macroglobulin was significantly higher and alpha-1-antitrypsin significantly lower in diabetic women than in controls. |
| 6 | 115206 | In humans with diabetes mellitus and in baboons with pancreatectomy induced diabetes mellitus there were significant increases in Hbs A1, A1c, and A1a +A1b. |
| 7 | 488538 | To determine whether the carbohydrate content of serum proteins is related to overall glycemic control, we studied serum protein-bound hexose and glycosylated hemoglobin [HbA1(a+b+c)] in 37 ambulant diabetic patients and 32 nondiabetic controls. |
| 8 | 488538 | In nine of the diabetic patients, mean protein-bound hexose and HbA1(a+b+c) were significantly reduced during a period of intensive outpatient care, while two major serum glycoproteins, haptoglobins and alpha-1-antitrypsin, were unchanged. |
| 9 | 498507 | Quantitation of hemoglobin A1a+b and hemoglobin A1c by automated "high-performance" liquid chromatography. |
| 10 | 511582 | Hemoglobin A1a + b + c levels measured by a commercial column in 35 non-diabetic controls and in 56 diabetics showed good correlation (R = 0.91) with hemoglobin A1a + b + c levels determined by the homemade column. |
| 11 | 511582 | The commercial column is valid for the measurement of the combined glycosylated hemoglobin A1a + b + c fraction and may be used in the routine clinical laboratory to assess diabetic control. |
| 12 | 511582 | Hemoglobin A1a + b + c levels measured by a commercial column in 35 non-diabetic controls and in 56 diabetics showed good correlation (R = 0.91) with hemoglobin A1a + b + c levels determined by the homemade column. |
| 13 | 511582 | The commercial column is valid for the measurement of the combined glycosylated hemoglobin A1a + b + c fraction and may be used in the routine clinical laboratory to assess diabetic control. |
| 14 | 1280191 | The plasma concentration of trypsin-like activity and two of the most important plasma serine proteinase inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, were determined in 95 type 1 diabetic and 67 control subjects. |
| 15 | 1280191 | The plasma concentration of alpha 1 antitrypsin was found to be markedly decreased (P < 0.001), whereas plasma alpha 2-macroglobulin and trypsin-like activity were increased in diabetics compared to controls (P = 0.009 and < 0.001, respectively). |
| 16 | 1280191 | The plasma concentration of trypsin-like activity and two of the most important plasma serine proteinase inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, were determined in 95 type 1 diabetic and 67 control subjects. |
| 17 | 1280191 | The plasma concentration of alpha 1 antitrypsin was found to be markedly decreased (P < 0.001), whereas plasma alpha 2-macroglobulin and trypsin-like activity were increased in diabetics compared to controls (P = 0.009 and < 0.001, respectively). |
| 18 | 1319211 | Purification of proteinase-like and Na+/K(+)-ATPase stimulating substance from plasma of insulin-dependent diabetics and its identification as alpha 1-antitrypsin. |
| 19 | 1323058 | Effects of interleukin-6 on the expression of thyroid hormone-binding protein genes in cultured human hepatoblastoma-derived (Hep G2) cells. |
| 20 | 1323058 | T4-binding globulin (TBG) shares a high degree of homology with two serpin antiproteases, alpha 1-antichymotrypsin (ACT) and alpha 1-antitrypsin (AT), whose synthesis is increased during the acute phase phenomenon, which accompanies trauma, infections, and neoplasms. |
| 21 | 1323058 | When evaluated in human hepatoblastoma-derived (Hep G2) cells exposed to different doses of the recombinant human cytokine for variable time intervals, IL-6 caused a dose- and time-dependent decrease in the secretion of [35S]methionine-labeled TBG, transthyretin (TTR), and albumin. |
| 22 | 1323058 | IL-6 did, however, cause a decrease in the steady state levels of mRNA for TTR, TBG, and albumin and an increase in ACT and AT mRNAs. |
| 23 | 1323058 | In addition, nuclear run-off assay demonstrated a decrease in the transcription of TTR, TBG, and albumin genes and an increased transcription of the ACT gene. |
| 24 | 1323058 | Quantitation of the results showed that changes in the secretion of proteins, in steady state mRNA levels, and in gene transcription were superimposable for each protein, indicating that IL-6 exerts its effect on thyroid hormone-binding proteins mostly at the transcriptional level and that TTR is the thyroid hormone-binding protein showing the most pronounced negative regulation by IL-6. |
| 25 | 1323058 | The opposite effect of IL-6 on TBG and the antiproteases, despite their structural homology, underscores gene divergence among these proteins. |
| 26 | 1794787 | The major proteins included: albumin, transferrin, alpha-1-antitrypsin, and immunoglobulin G. |
| 27 | 1862849 | An immunochemistry analyser has been used in testing a series of specific proteins (complement components C3 and C4, properdin, factor B, immunoglobulins G, M and A, alpha 1-antitrypsin, alpha 1-acid protein and alpha 2-macroglobulin) in biological fluids of normal and diabetic women in third-trimester pregnancy. |
| 28 | 1916449 | Specific proteins such as haptoglobin, alpha 2 macroglobulin, alpha 1 antitrypsin, alpha 1 acid glycoprotein, properdin factor B, ceruloplasmin were determined on the Immunochemistry Analyzer. |
| 29 | 2044983 | Using enzyme-linked immunosorbent analysis (ELISA), we established mean values and 95% confidence intervals for six proteins of physiologic human vitreous: albumin (293 +/- 18 mg/l), transferrin (73.7 +/- 6.6 mg/l), immunoglobulin G (IgG), (33.5 +/- 3 mg/l), alpha 1-antitrypsin (14.1 +/- 2.9 mg/l), alpha 1-acid glycoprotein (4 +/- 0.7 mg/l), and lactoferrin (less than 50 micrograms/l). |
| 30 | 2044983 | We observed differences in transferrin between controls and proliferative diabetic retinopathy (PDR), and differences in alpha 1-acid glycoprotein between controls and both types of proliferative vitreoretinopathy (PVR). |
| 31 | 2376377 | Physiological levels of the individual proteins were determined as follows: albumin 293 +/- 18 mg/l, IgG 34 +/- 3 mg/l, transferrin 74 +/- 7 mg/l, alpha 1-antitrypsin 14 +/- 3 mg/l, alpha 1-acid glycoprotein 4 +/- 0.7 mg/l. |
| 32 | 2376377 | Significant differences were found for total vitreal protein and alpha 1-antitrypsin between the control groups and the three vitreoretinal disorders, between the PDR and control group for transferrin, and between both types of PVR and controls for alpha 1-acid glycoprotein. |
| 33 | 2376377 | Physiological levels of the individual proteins were determined as follows: albumin 293 +/- 18 mg/l, IgG 34 +/- 3 mg/l, transferrin 74 +/- 7 mg/l, alpha 1-antitrypsin 14 +/- 3 mg/l, alpha 1-acid glycoprotein 4 +/- 0.7 mg/l. |
| 34 | 2376377 | Significant differences were found for total vitreal protein and alpha 1-antitrypsin between the control groups and the three vitreoretinal disorders, between the PDR and control group for transferrin, and between both types of PVR and controls for alpha 1-acid glycoprotein. |
| 35 | 2433883 | They also had significantly elevated anti-thrombin III, alpha 2 macroglobulin, alpha 1 antitrypsin, C1 inhibitor, fibrinogen, FDP concentrations and prolongation of euglobulin lysis time. |
| 36 | 2458216 | Serum levels of six acute phase proteins (APP)--C-reactive protein (CRP), serum amyloid A (SAA), alpha 1-antitrypsin, haptoglobin and complement fractions C3 and C4--were serially studied in 24 patients with poorly controlled diabetes mellitus, ten of whom had unequivocal evidence of an underlying infection. |
| 37 | 2458216 | No correlation between the presence of infection, and fever, leukocytosis, a raised erythrocyte sedimentation rate, or serum levels of alpha 1-antitrypsin, haptoglobin or complement was apparent in these patients. |
| 38 | 2458216 | However, serum CRP and SAA were initially increased 10-100 times above normal in diabetic patients with an underlying infection (P less than 0.01); during the following week circulating levels of CRP and SAA decreased steadily in response to the infection being brought under control. |
| 39 | 2458216 | We conclude that serial measurement of CRP and/or SAA is a sensitive, albeit non-specific, parameter to detect and monitor the activity of infection in patients with diabetes. |
| 40 | 2458216 | Serum levels of six acute phase proteins (APP)--C-reactive protein (CRP), serum amyloid A (SAA), alpha 1-antitrypsin, haptoglobin and complement fractions C3 and C4--were serially studied in 24 patients with poorly controlled diabetes mellitus, ten of whom had unequivocal evidence of an underlying infection. |
| 41 | 2458216 | No correlation between the presence of infection, and fever, leukocytosis, a raised erythrocyte sedimentation rate, or serum levels of alpha 1-antitrypsin, haptoglobin or complement was apparent in these patients. |
| 42 | 2458216 | However, serum CRP and SAA were initially increased 10-100 times above normal in diabetic patients with an underlying infection (P less than 0.01); during the following week circulating levels of CRP and SAA decreased steadily in response to the infection being brought under control. |
| 43 | 2458216 | We conclude that serial measurement of CRP and/or SAA is a sensitive, albeit non-specific, parameter to detect and monitor the activity of infection in patients with diabetes. |
| 44 | 2466854 | The levels of alpha 1-antitrypsin (alpha 1-AT), alpha 1-acid glycoprotein (alpha 1-AG) or alpha 2-macroglobulin (alpha 2-MG) were measured by laser nephelometry. |
| 45 | 2472500 | The levels of immunoglobulins, complement components and APR proteins including alpha 1-antitrypsin (alpha 1-AT), alpha 1-acid glycoprotein (alpha 1-AG), alpha 2-macroglobulin (alpha 2-MG) and haptoglobin (Hpt) in the sera, as well as glycosylated or nonglycosylated protein fractions of these proteins in the sera, were examined by laser nephelometry in 49 patients with diabetes mellitus. |
| 46 | 2478861 | In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured. |
| 47 | 2478861 | Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally. |
| 48 | 2478861 | When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae. |
| 49 | 2478861 | In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured. |
| 50 | 2478861 | Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally. |
| 51 | 2478861 | When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae. |
| 52 | 2669494 | Total percent glycosylated hemoglobin (A1a + b + c) was measured before 16 weeks' gestation in 105 insulin-treated diabetic women enrolled for prenatal care at Parkland Memorial Hospital. |
| 53 | 3004244 | Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. |
| 54 | 3004244 | The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. |
| 55 | 3784285 | Endogenous marker substances of a defined MW (beta 2-microglobulin, myoglobin, RBP, alpha 1-microglobulin, acid alpha 1-glycoprotein, alpha 1-antitrypsin, prealbumin, and albumin were measured by laser nephelometry or radioimmune assay; sieving coefficients (SC) and protein eliminations were calculated for each low MW protein. |
| 56 | 4166389 | Serum concentration of alpha-2-macroglobulin, haptoglobin and alpha-1-antitrypsin in diabetes mellitus. |
| 57 | 4205523 | Associated with increased [eta] was a decline in albumin: globulin ratio and elevation of the acute phase reactant proteins, alpha(1)-acid glycoprotein, alpha(1)-antitrypsin, haptoglobin, and ceruloplasmin. |
| 58 | 6083539 | [Blood levels of alpha 1-antitrypsin and alpha 2-macroglobulin in children with diabetes mellitus]. |
| 59 | 6085525 | The sections were stained with FITC-labeled heavy chain specific anti-human IgG, alpha 1-antitrypsin, haptoglobin and beta-lipoprotein antisera, and then examined with a fluorescent microscope. |
| 60 | 6085653 | [Antithrombin III, alpha 2-macroglobulin, alpha 1-antitrypsin and plasminogen in childhood diabetes]. |
| 61 | 6162208 | Fibrinogen levels, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin and plasminogen were significantly increased in DM. |
| 62 | 6191995 | Concentrations of alpha 2 macroglobulin and alpha 1 antitrypsin were highest in diabetics with proliferative retinopathy (0.1 greater than P greater than 0.05, trend test) but mean prothrombin and activated partial thromboplastin times and mean concentrations of alpha 2 antiplasmin, plasminogen activator and antithrombin III were similar in all groups. |
| 63 | 6196185 | Although plasma inactive renin was not significantly correlated with serum alpha 1-antitrypsin, there was a significant correlation between plasma inactive renin and serum alpha 2-macroglobulin (r = 0.61, p less than 0.01). |
| 64 | 6375393 | Other plasma proteins of low isoelectric point were detected in basement membranes: albumin (pI 4.9), alpha-1-acid glycoprotein (pI 2.7), amyloid P (pI 3.9-4.8), and alpha-1-antitrypsin (pI 4.5). |
| 65 | 6552201 | Heating of blood plasma acidified to pH 3.0 for 15-20 min at 61 degrees C allows for the conditions under which the kallikrein inhibitors (alpha 1-antitrypsin, alpha 2-macroglobulin) are destroyed whereas kallikrein, prekallikrein, low- and high-molecular kininogens (HMK) are preserved, thus constituting a complex of proteins making the kininogenase reaction feasible. |
| 66 | 6780328 | The levels of hemoglobin A1a+b (HbA1a+b) and HbA1c and the sum of HbA1a+b and HbA1c (HbA1a+b+HbA1c) in normal subjects averaged 2.3 +/- 0.4 (SD)%, 5.3 +/- 0.8% and 7.6 +/- 1.0%, respectively. |
| 67 | 6788617 | Using a high resolution automated chromatographic method, the levels of the different minor haemoglobins Hb A1a, A1b, and A1c were measured in 20 healthy controls, in 20 patients with chronic renal failure, in 20 uraemic patients on intermittent haemodialysis, and in 20 insulin-dependent diabetic patients. |
| 68 | 6970536 | [Pulmonary emphysema, hepatic lesions, and insulin-dependent diabetes in a patient with alpha-1-antitrypsin (Pi ZZ) deficiency (author's transl)]. |
| 69 | 6970536 | A 47-year-old patient with panlobular emphysema and insulin-dependent diabetes had an alpha-1-antitrypsin phenotype Pi ZZ deficiency. |
| 70 | 6970536 | [Pulmonary emphysema, hepatic lesions, and insulin-dependent diabetes in a patient with alpha-1-antitrypsin (Pi ZZ) deficiency (author's transl)]. |
| 71 | 6970536 | A 47-year-old patient with panlobular emphysema and insulin-dependent diabetes had an alpha-1-antitrypsin phenotype Pi ZZ deficiency. |
| 72 | 6999400 | Minor components of adult hemoglobin (A1a,b, and c) are known to increase in the presence of sustained elevations of maternal blood glucose. |
| 73 | 7615300 | The gene frequencies of nine different genetic polymorphic markers [ABO, MNS and P blood groups; haptoglobin, transferrin, Gc protein, complement (C3), properdin factor B and alpha 1-antitrypsin] were determined in 94 Mexican-Americans residing in the Los Angeles, California area. |
| 74 | 7615300 | However, data from the current study demonstrated significant differences in ABO and haptoglobin allele frequencies compared to published non-Hispanic Caucasian data. |
| 75 | 7849428 | In normal vitreous, the protein content consisted mainly of albumin, transferrin, alpha 1-antitrypsin, IgG, and prealbumin as confirmed by the comparison with protein standards. |
| 76 | 7849428 | Compared to vitreous controls, all PDR samples were shown to have lower amounts of transferrin, alpha 1-antitrypsin, and prealbumin. |
| 77 | 7849428 | In normal vitreous, the protein content consisted mainly of albumin, transferrin, alpha 1-antitrypsin, IgG, and prealbumin as confirmed by the comparison with protein standards. |
| 78 | 7849428 | Compared to vitreous controls, all PDR samples were shown to have lower amounts of transferrin, alpha 1-antitrypsin, and prealbumin. |
| 79 | 8043910 | The cultures were exposed to modified human proteins: alpha-1-antitrypsin cleaved with papain, fibrinogen degradation products (fraction D) purified from plasmin digest, and non-enzymatically glycosylated (glycated) serum albumin. |
| 80 | 8048795 | Laboratory tests for fecal alpha 1-antitrypsin and an indium III-labeled plasma transferrin nuclear scan revealed a protein-losing enteropathy. |
| 81 | 8403400 | Mean analytical recovery of added human proinsulin (hPI) (2, 5, and 10 pmol/L) to serum was 84% (range 68-128%, n = 9). |
| 82 | 8543320 | Immunohistochemical study of the foamy cells in the lesion showed positive reaction to anti-Kp-1, anti-S-100 alpha, beta, anti-neuron-specific enolase (NSE), anti-alpha-1-antichymotrypsin, anti-alpha-1-antitrypsin, and anti-lysozyme antibodies. |
| 83 | 8569028 | Various hemostatic abnormalities have been reported and excess activation of coagulation factors, such as prothrombin, factor VII, factor IX, and factor XI, have been detected in thrombotic diseases states by various assay systems. |
| 84 | 8569028 | We recently developed the enzyme-linked differential immunoassay for activated factor XI-alpha 1 antitrypsin complex (FXIa-alpha 1 AT) and applied it with other assays for activated factors such as thrombin-antithrombin III complex (TAT) to detect the hypercoagulable state in clinical samples. |
| 85 | 8649928 | [Alpha-1-antitrypsin, albumin and whole protein in meconium and stools during the first days of life in the neonate]. |
| 86 | 8649928 | The variability and diagnostic value of determining alpha-1-antitrypsin (AAT), albumin and total protein in these samples was analyzed. |
| 87 | 8649928 | No correlation was found between the AAT and albumin concentrations in the studied material. |
| 88 | 8649928 | The concomitant determination of AAT, albumin and total protein in stool makes it possible to discriminate between these groups of neonates with a 91.7% accuracy. |
| 89 | 8649928 | [Alpha-1-antitrypsin, albumin and whole protein in meconium and stools during the first days of life in the neonate]. |
| 90 | 8649928 | The variability and diagnostic value of determining alpha-1-antitrypsin (AAT), albumin and total protein in these samples was analyzed. |
| 91 | 8649928 | No correlation was found between the AAT and albumin concentrations in the studied material. |
| 92 | 8649928 | The concomitant determination of AAT, albumin and total protein in stool makes it possible to discriminate between these groups of neonates with a 91.7% accuracy. |
| 93 | 8649928 | [Alpha-1-antitrypsin, albumin and whole protein in meconium and stools during the first days of life in the neonate]. |
| 94 | 8649928 | The variability and diagnostic value of determining alpha-1-antitrypsin (AAT), albumin and total protein in these samples was analyzed. |
| 95 | 8649928 | No correlation was found between the AAT and albumin concentrations in the studied material. |
| 96 | 8649928 | The concomitant determination of AAT, albumin and total protein in stool makes it possible to discriminate between these groups of neonates with a 91.7% accuracy. |
| 97 | 8649928 | [Alpha-1-antitrypsin, albumin and whole protein in meconium and stools during the first days of life in the neonate]. |
| 98 | 8649928 | The variability and diagnostic value of determining alpha-1-antitrypsin (AAT), albumin and total protein in these samples was analyzed. |
| 99 | 8649928 | No correlation was found between the AAT and albumin concentrations in the studied material. |
| 100 | 8649928 | The concomitant determination of AAT, albumin and total protein in stool makes it possible to discriminate between these groups of neonates with a 91.7% accuracy. |
| 101 | 8862946 | Levels of von Willebrand factor, insulin resistance syndrome, and a common vWF gene polymorphism in non-insulin-dependent (type 2) diabetes mellitus. |
| 102 | 8862946 | To examine the association between von Willebrand Factor (vWF) concentrations and features of the insulin resistance syndrome, 208 patients with Type 2 (non-insulin-dependent) diabetes (NIDDM) and 80 healthy controls were studied. |
| 103 | 8862946 | A restriction fragment length polymorphism in exon 12 of the vWF gene, detected by Aat II endonuclease, was also examined. vWF concentrations were elevated in the patient group (patients 1.28 IU ml-1 vs controls 1.12 IU ml-1, p = 0.003). |
| 104 | 8862946 | In a linear regression model, age and insulin remained as independent predictors of vWF levels, explaining 16% of inter-individual variance in the patient group. |
| 105 | 8862946 | In conclusion, these findings show vWF concentrations are elevated in NIDDM and are weakly related to features of the insulin resistance syndrome. |
| 106 | 8916594 | The levels of serum albumin, alpha-1 acid glycoprotein, alpha-1 antitrypsin and caeruloplasmin were not significantly different between the patients with retinopathy and controls. |
| 107 | 8934703 | Postmortem diagnosis of diabetic metabolic derangement: elevated alpha 1-antitrypsin and haptoglobin glycosylation levels as an index of antemortem hyperglycemia. |
| 108 | 8934703 | In the search for other, more reliable, indices of immediately antemortem blood glucose levels, we investigated the value of glycosylation levels of serum proteins with very brief biologic half-lives: a) In vitro studies were performed on the glycosylation course of the short-lived serum proteins alpha 1-antitrypsin (alpha 1-AT) and haptoglobin (HP). b) Glycosylation levels were measured after purification of alpha 1-AT and HP from sera of living and deceased non-diabetics and diabetics. c) The resistance of alpha 1-AT and HP glycosylation levels to autolysis was investigated. |
| 109 | 8934703 | Our studies revealed the following: 1) alpha 1-AT and HP glycosylate considerably more rapidly than either albumin or hemoglobin. |
| 110 | 8934703 | Postmortem diagnosis of diabetic metabolic derangement: elevated alpha 1-antitrypsin and haptoglobin glycosylation levels as an index of antemortem hyperglycemia. |
| 111 | 8934703 | In the search for other, more reliable, indices of immediately antemortem blood glucose levels, we investigated the value of glycosylation levels of serum proteins with very brief biologic half-lives: a) In vitro studies were performed on the glycosylation course of the short-lived serum proteins alpha 1-antitrypsin (alpha 1-AT) and haptoglobin (HP). b) Glycosylation levels were measured after purification of alpha 1-AT and HP from sera of living and deceased non-diabetics and diabetics. c) The resistance of alpha 1-AT and HP glycosylation levels to autolysis was investigated. |
| 112 | 8934703 | Our studies revealed the following: 1) alpha 1-AT and HP glycosylate considerably more rapidly than either albumin or hemoglobin. |
| 113 | 9096763 | Serum alpha-1 antitrypsin level was 224 (normal 85-213) mg/dL and PI phenotype was M1. |
| 114 | 10665286 | Metabolic disorders in patients with proliferative diabetic retinopathy with hemophthalmia are characterized by a notable increase in the activities of trypsin-like enzymes and alpha 2-macroglobulin level and normal activity of alpha 1-antitrypsin and shifted lipid metabolism parameters characteristic of types IIb and IV hyperlipoproteinemia. |
| 115 | 11013303 | The upregulated expression of well-characterized lipid metabolic enzymes, such as lipoprotein lipase, phosphoenolpyruvate carboxykinase, and cholesterol esterase, were observed in VAT of OLETF rats. |
| 116 | 11013303 | The C-terminal partial amino acid sequence of OL-64 revealed that it showed approximately 40% homology with alpha(1)-antitrypsin and it seemed to be a new member of the serine proteinase inhibitor (SERPIN) gene family. |
| 117 | 11230779 | A total of 29 type 2 diabetic patients (age, 55.2 +/- 1.8 years, glycosylated hemoglobin [HbA(1c)] 8.9% +/- 0.2%, body mass index [BMI] 30.9 +/- 0.8 kg/m(2), duration 5.9 +/- 1.3 years) participated in the study. |
| 118 | 11230779 | Basal C-reactive protein (CRP) level was related to acylation-stimulating protein (ASP) concentration (r =.55, P <.01), and many acute phase serum protein concentrations were associated with each other. |
| 119 | 11230779 | Glibenclamide treatment was associated with a reduction in alpha-1-antitrypsin (P <.05), ceruloplasmin (P <.01), and complement C3 protein (C3) (P <.05). |
| 120 | 12497307 | [Serum alpha-1 antitrypsin levels in patients with Cuban epidemic neuropathy]. |
| 121 | 12911121 | The conference "Stem Cell Therapies in Reparative Medicine," held aboard the cruise vessel Majesty of the Seas (Miami, USA-Nassau, Bahamas, April 19-22, 2002), focused on the analysis of these problems from different perspectives, including developmental biology (cell proliferation, fate determination, and enrichment), immunology (allorejection and prevention of autoimmunity recurrence), and clinical therapy, emphasizing the impact of stem cell technologies on the emerging field of tissue engineering and the treatment of alpha-1 antitrypsin deficiency. |
| 122 | 14712302 | Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice. |
| 123 | 14712302 | To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice. |
| 124 | 14712302 | Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u. |
| 125 | 14712302 | This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively. |
| 126 | 14712302 | Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice. |
| 127 | 14712302 | To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice. |
| 128 | 14712302 | Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u. |
| 129 | 14712302 | This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively. |
| 130 | 14712302 | Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice. |
| 131 | 14712302 | To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice. |
| 132 | 14712302 | Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u. |
| 133 | 14712302 | This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively. |
| 134 | 14712302 | Recombinant adeno-associated virus-mediated alpha-1 antitrypsin gene therapy prevents type I diabetes in NOD mice. |
| 135 | 14712302 | To test the ability of AAT to modulate the development of type I diabetes, we performed a series of investigations involving recombinant adeno-associated virus vector (rAAV)-mediated gene delivery of human alpha-1 antitrypsin (hAAT) to nonobese diabetic (NOD) mice. |
| 136 | 14712302 | Recombinant AAV-expressing hAAT (rAAV2-CB-AT) was administered intramuscularly to 4-week-old female NOD mice (1 x 10(10) i.u. |
| 137 | 14712302 | This study suggests a potential therapeutic role for AAT in preventing type I diabetes as well as the ability of AAV gene therapy-based approaches to ameliorate disease effectively. |
| 138 | 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. |
| 139 | 16093309 | In vitro, several islet responses to IL-1beta/IFNgamma stimulation were examined. |
| 140 | 16093309 | In the presence of AAT, islets displayed enhanced viability and inducible insulin secretion. |
| 141 | 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. |
| 142 | 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. |
| 143 | 16093309 | In vitro, several islet responses to IL-1beta/IFNgamma stimulation were examined. |
| 144 | 16093309 | In the presence of AAT, islets displayed enhanced viability and inducible insulin secretion. |
| 145 | 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. |
| 146 | 16776571 | Studies have demonstrated that two serine proteinase inhibitors, alpha1-antitrypsin (AAT) and elafin, act as potent antiinflammatory agents. |
| 147 | 16776571 | AAT gene therapy, contrary to elafin and saline, was remarkably effective in preventing type 1 diabetes. |
| 148 | 16776571 | Studies have demonstrated that two serine proteinase inhibitors, alpha1-antitrypsin (AAT) and elafin, act as potent antiinflammatory agents. |
| 149 | 16776571 | AAT gene therapy, contrary to elafin and saline, was remarkably effective in preventing type 1 diabetes. |
| 150 | 17211556 | The aim of the study was the assessment of the concentrations and establishment of mutual relationships between three main protease inhibitors: alpha-1-antitrypsin (AAT), alpha-2-macroglobulin (alpha-2-M) and antithrombin-III (AT-III), and of the total trypsin inhibitory capacity (TIC) in the serum of diabetic and non-diabetic children during adolescence. |
| 151 | 17211556 | The concentrations of AAT, alpha-2-M and AT-III were determined by the radial immunodiffusion method on NOR-Partigen plates (Dade-Behring), while TIC was determined by the method using BAPNA as substrate. |
| 152 | 17211556 | Hyperglycaemia and the duration of diabetes were found to have a significant association with alpha-2-M and AT-III concentrations, but not with AAT serum concentrations. |
| 153 | 17211556 | The aim of the study was the assessment of the concentrations and establishment of mutual relationships between three main protease inhibitors: alpha-1-antitrypsin (AAT), alpha-2-macroglobulin (alpha-2-M) and antithrombin-III (AT-III), and of the total trypsin inhibitory capacity (TIC) in the serum of diabetic and non-diabetic children during adolescence. |
| 154 | 17211556 | The concentrations of AAT, alpha-2-M and AT-III were determined by the radial immunodiffusion method on NOR-Partigen plates (Dade-Behring), while TIC was determined by the method using BAPNA as substrate. |
| 155 | 17211556 | Hyperglycaemia and the duration of diabetes were found to have a significant association with alpha-2-M and AT-III concentrations, but not with AAT serum concentrations. |
| 156 | 17211556 | The aim of the study was the assessment of the concentrations and establishment of mutual relationships between three main protease inhibitors: alpha-1-antitrypsin (AAT), alpha-2-macroglobulin (alpha-2-M) and antithrombin-III (AT-III), and of the total trypsin inhibitory capacity (TIC) in the serum of diabetic and non-diabetic children during adolescence. |
| 157 | 17211556 | The concentrations of AAT, alpha-2-M and AT-III were determined by the radial immunodiffusion method on NOR-Partigen plates (Dade-Behring), while TIC was determined by the method using BAPNA as substrate. |
| 158 | 17211556 | Hyperglycaemia and the duration of diabetes were found to have a significant association with alpha-2-M and AT-III concentrations, but not with AAT serum concentrations. |
| 159 | 17301191 | The spots were cut from the gel, and 20 were identified by mass spectrometry as charge forms of 11 plasma proteins: Orosomucoid, transferrin, alpha-1 microglobulin, zinc alpha-2 glycoprotein, alpha-1 antitrypsin, complement factor B, haptoglobin, transthyretin, plasma retinol binding protein, albumin, and hemopexin. |
| 160 | 17360983 | Specifically, strong antiapoptotic activities for AAT (Prolastin, human) were observed when murine insulinoma cells (MIN6) were exposed to tumor necrosis factor-alpha. |
| 161 | 17360983 | Importantly, in both model systems, treatment with AAT completely abolished induced caspase-3 activity. |
| 162 | 17360983 | Specifically, strong antiapoptotic activities for AAT (Prolastin, human) were observed when murine insulinoma cells (MIN6) were exposed to tumor necrosis factor-alpha. |
| 163 | 17360983 | Importantly, in both model systems, treatment with AAT completely abolished induced caspase-3 activity. |
| 164 | 18374100 | Alpha-1 antitrypsin treatment of spontaneously diabetic nonobese diabetic mice receiving islet allografts. |
| 165 | 18374100 | Alpha-1 antitrypsin (AAT) is a serine protease inhibitor able to prevent diabetes onset in nonobese diabetic (NOD) mice and to prolong islet allograft survival in a nonautoimmune murine model. |
| 166 | 18374100 | Alpha-1 antitrypsin treatment of spontaneously diabetic nonobese diabetic mice receiving islet allografts. |
| 167 | 18374100 | Alpha-1 antitrypsin (AAT) is a serine protease inhibitor able to prevent diabetes onset in nonobese diabetic (NOD) mice and to prolong islet allograft survival in a nonautoimmune murine model. |
| 168 | 18374099 | Prolonged islet allograft survival by alpha-1 antitrypsin: the role of humoral immunity. |
| 169 | 18374099 | Immunomodulatory properties have been recognized for human alpha-1 antitrypsin (hAAT). |
| 170 | 18374099 | Prolonged islet allograft survival by alpha-1 antitrypsin: the role of humoral immunity. |
| 171 | 18374099 | Immunomodulatory properties have been recognized for human alpha-1 antitrypsin (hAAT). |
| 172 | 18433156 | Comparison of noDR and PDR groups revealed increased levels of angiotensinogen and decreased levels of calsyntenin-1, interphotoreceptor retinoid-binding protein, and neuroserpin in PDR vitreous. |
| 173 | 18433156 | Five of them (complement C3, complement factor I, prothrombin, alpha-1-antitrypsin, and antithrombin III) were increased in PDR vitreous compared with NDM vitreous. |
| 174 | 18433156 | PDR vitreous also had increased levels of peroxiredoxin-1 and decreased levels of extracellular superoxide dismutase, compared with noDR or NDM vitreous. |
| 175 | 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. |
| 176 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 177 | 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. |
| 178 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 179 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 180 | 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. |
| 181 | 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. |
| 182 | 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. |
| 183 | 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. |
| 184 | 18772236 | This decrease in unprocessed TNF-alpha was prevented by the aldose reductase (AR) inhibitor sorbinil and AR small interference RNA. |
| 185 | 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. |
| 186 | 18772236 | HG-induced TACE phosphorylation and TNF-alpha processing were also prevented by TNF-alpha protease inhibitor-1, an inhibitor of TACE. |
| 187 | 18772236 | Inhibition of protein kinase C (PKC)-delta by rottlerin prevented HG-induced TACE activation and the accumulation of unprocessed TNF-alpha. |
| 188 | 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. |
| 189 | 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. |
| 190 | 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. |
| 191 | 20692406 | Culture of impure human islet fractions in the presence of alpha-1 antitrypsin prevents insulin cleavage and improves islet recovery. |
| 192 | 21099312 | INS-1E cells or primary rat pancreatic islets were used to study the effect of AAT on insulin secretion after glucose, glucagon-like peptide-1 (GLP-1) and forskolin stimulation and on cytokine-mediated apoptosis. |
| 193 | 21099312 | We found that AAT increases insulin secretion in a glucose-dependent manner, potentiates the effect of GLP-1 and forskolin and neutralizes the inhibitory effect of clonidine on insulin secretion. |
| 194 | 21099312 | The effect of AAT on insulin secretion was accompanied by an increase in cAMP levels. |
| 195 | 21099312 | Our findings show that AAT stimulates insulin secretion and protects β-cells against cytokine-induced apoptosis, and these effects of AAT seem to be mediated through the cAMP pathway. |
| 196 | 21099312 | In view of these novel findings we suggest that AAT may represent a novel anti-inflammatory compound to protect β-cells under the immunological attack in T1D but also therapeutic strategy to potentiate insulin secretion in type 2 diabetes (T2D). |
| 197 | 21099312 | INS-1E cells or primary rat pancreatic islets were used to study the effect of AAT on insulin secretion after glucose, glucagon-like peptide-1 (GLP-1) and forskolin stimulation and on cytokine-mediated apoptosis. |
| 198 | 21099312 | We found that AAT increases insulin secretion in a glucose-dependent manner, potentiates the effect of GLP-1 and forskolin and neutralizes the inhibitory effect of clonidine on insulin secretion. |
| 199 | 21099312 | The effect of AAT on insulin secretion was accompanied by an increase in cAMP levels. |
| 200 | 21099312 | Our findings show that AAT stimulates insulin secretion and protects β-cells against cytokine-induced apoptosis, and these effects of AAT seem to be mediated through the cAMP pathway. |
| 201 | 21099312 | In view of these novel findings we suggest that AAT may represent a novel anti-inflammatory compound to protect β-cells under the immunological attack in T1D but also therapeutic strategy to potentiate insulin secretion in type 2 diabetes (T2D). |
| 202 | 21099312 | INS-1E cells or primary rat pancreatic islets were used to study the effect of AAT on insulin secretion after glucose, glucagon-like peptide-1 (GLP-1) and forskolin stimulation and on cytokine-mediated apoptosis. |
| 203 | 21099312 | We found that AAT increases insulin secretion in a glucose-dependent manner, potentiates the effect of GLP-1 and forskolin and neutralizes the inhibitory effect of clonidine on insulin secretion. |
| 204 | 21099312 | The effect of AAT on insulin secretion was accompanied by an increase in cAMP levels. |
| 205 | 21099312 | Our findings show that AAT stimulates insulin secretion and protects β-cells against cytokine-induced apoptosis, and these effects of AAT seem to be mediated through the cAMP pathway. |
| 206 | 21099312 | In view of these novel findings we suggest that AAT may represent a novel anti-inflammatory compound to protect β-cells under the immunological attack in T1D but also therapeutic strategy to potentiate insulin secretion in type 2 diabetes (T2D). |
| 207 | 21099312 | INS-1E cells or primary rat pancreatic islets were used to study the effect of AAT on insulin secretion after glucose, glucagon-like peptide-1 (GLP-1) and forskolin stimulation and on cytokine-mediated apoptosis. |
| 208 | 21099312 | We found that AAT increases insulin secretion in a glucose-dependent manner, potentiates the effect of GLP-1 and forskolin and neutralizes the inhibitory effect of clonidine on insulin secretion. |
| 209 | 21099312 | The effect of AAT on insulin secretion was accompanied by an increase in cAMP levels. |
| 210 | 21099312 | Our findings show that AAT stimulates insulin secretion and protects β-cells against cytokine-induced apoptosis, and these effects of AAT seem to be mediated through the cAMP pathway. |
| 211 | 21099312 | In view of these novel findings we suggest that AAT may represent a novel anti-inflammatory compound to protect β-cells under the immunological attack in T1D but also therapeutic strategy to potentiate insulin secretion in type 2 diabetes (T2D). |
| 212 | 21099312 | INS-1E cells or primary rat pancreatic islets were used to study the effect of AAT on insulin secretion after glucose, glucagon-like peptide-1 (GLP-1) and forskolin stimulation and on cytokine-mediated apoptosis. |
| 213 | 21099312 | We found that AAT increases insulin secretion in a glucose-dependent manner, potentiates the effect of GLP-1 and forskolin and neutralizes the inhibitory effect of clonidine on insulin secretion. |
| 214 | 21099312 | The effect of AAT on insulin secretion was accompanied by an increase in cAMP levels. |
| 215 | 21099312 | Our findings show that AAT stimulates insulin secretion and protects β-cells against cytokine-induced apoptosis, and these effects of AAT seem to be mediated through the cAMP pathway. |
| 216 | 21099312 | In view of these novel findings we suggest that AAT may represent a novel anti-inflammatory compound to protect β-cells under the immunological attack in T1D but also therapeutic strategy to potentiate insulin secretion in type 2 diabetes (T2D). |
| 217 | 21698349 | This study sought to examine the relationship between proximal aortic dilatation and matrix metalloproteinase-9 (MMP-9) and alpha 1-antitrypsin (α1AT) levels in patients with BAV. |
| 218 | 22536212 | Specifically, some differentially expressed proteins were verified by MRM in urine from normoalbuminuric and microalbuminuric patients with type 2 diabetes, wherein alpha-1-antitrypsin, alpha-1-acid glycoprotein 1, and prostate stem cell antigen had excellent AUC values (0.849, 0.873, and 0.825, resp.). |
| 219 | 22634722 | An increasing amount of evidence appears to suggest that AAT possesses not only the ability to inhibit serine proteases, such as elastase and proteinase-3 (PR-3), but also to exert antiinflammatory and tissue-protective effects independent of protease inhibition. |
| 220 | 22634722 | AAT modifies dendritic cell maturation and promotes T regulatory cell differentiation, induces interleukin (IL)-1 receptor antagonist and IL-10 release, protects various cell types from cell death, inhibits caspases-1 and -3 activity and inhibits IL-1 production and activity. |
| 221 | 22634722 | An increasing amount of evidence appears to suggest that AAT possesses not only the ability to inhibit serine proteases, such as elastase and proteinase-3 (PR-3), but also to exert antiinflammatory and tissue-protective effects independent of protease inhibition. |
| 222 | 22634722 | AAT modifies dendritic cell maturation and promotes T regulatory cell differentiation, induces interleukin (IL)-1 receptor antagonist and IL-10 release, protects various cell types from cell death, inhibits caspases-1 and -3 activity and inhibits IL-1 production and activity. |
| 223 | 23541501 | In this study, we hypothesize that this control may be achieved via a promoter derived from the heat shock multigene family, Hsp70 A1A, which is inducible at 42°C. |
| 224 | 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. |
| 225 | 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. |
| 226 | 23562077 | NE null (Ela2(-/-)) mice and A1AT transgenic mice were resistant to high-fat diet (HFD)-induced body weight gain, insulin resistance, inflammation, and fatty liver. |
| 227 | 23562077 | Ela2(-/-) mice also augmented circulating high molecular weight (HMW) adiponectin levels, phosphorylation of AMP-activated protein kinase (AMPK), and fatty acid oxidation (FAO) in the liver and brown adipose tissue (BAT) and uncoupling protein (UCP1) levels in the BAT. |
| 228 | 23562077 | The imbalance between A1AT and NE contributes to the development of obesity and related inflammation, insulin resistance, and liver steatosis. |
| 229 | 23562077 | NE null (Ela2(-/-)) mice and A1AT transgenic mice were resistant to high-fat diet (HFD)-induced body weight gain, insulin resistance, inflammation, and fatty liver. |
| 230 | 23562077 | Ela2(-/-) mice also augmented circulating high molecular weight (HMW) adiponectin levels, phosphorylation of AMP-activated protein kinase (AMPK), and fatty acid oxidation (FAO) in the liver and brown adipose tissue (BAT) and uncoupling protein (UCP1) levels in the BAT. |
| 231 | 23562077 | The imbalance between A1AT and NE contributes to the development of obesity and related inflammation, insulin resistance, and liver steatosis. |
| 232 | 23709000 | GDM was associated with an up-regulation of four proteins: collagen alpha-2(VI) chain (CO6A2 (COL6A2)), fibrinogen beta chain (FIBB (FGB)), lumican (LUM) and S100A9. |
| 233 | 23709000 | These were alpha-1-antitrypsin (AIAT (SERPINA 1)), annexin A5 (ANXA5), fatty acid-binding protein, adipocyte (FABP4), glutathione S-transferase P (GSTP (GSTP1)), heat-shock protein beta-1 (HSP27 (HSPB1)), lactate dehydrogenase B chain (LDHB), perilipin-1 (PLIN1), peroxiredoxin-6 (PRX6 (PRDX6)), selenium-binding protein 1 (SBP1) and vinculin (VINC (VCL)). |
| 234 | 23717456 | Pancreatic islet xenograft survival in mice is extended by a combination of alpha-1-antitrypsin and single-dose anti-CD4/CD8 therapy. |
| 235 | 23717456 | Rat-to-mouse islet transplantation was examined in the following groups: untreated (n = 6), hAAT (n = 6, 60-240 mg/kg every 3 days from day -10), low-dose co-stimulation blockade (anti-CD154/LFA-1) and single-dose anti-CD4/CD8 (n = 5-7), either as mono- or combination therapies. |
| 236 | 23717456 | According to our results hAAT monotherapy and hAAT/anti-CD154/LFA-1 combined therapy, did not delay rejection day (11-24 days untreated vs. 10-22 day treated). |
| 237 | 23717456 | Pancreatic islet xenograft survival in mice is extended by a combination of alpha-1-antitrypsin and single-dose anti-CD4/CD8 therapy. |
| 238 | 23717456 | Rat-to-mouse islet transplantation was examined in the following groups: untreated (n = 6), hAAT (n = 6, 60-240 mg/kg every 3 days from day -10), low-dose co-stimulation blockade (anti-CD154/LFA-1) and single-dose anti-CD4/CD8 (n = 5-7), either as mono- or combination therapies. |
| 239 | 23717456 | According to our results hAAT monotherapy and hAAT/anti-CD154/LFA-1 combined therapy, did not delay rejection day (11-24 days untreated vs. 10-22 day treated). |
| 240 | 23717456 | Pancreatic islet xenograft survival in mice is extended by a combination of alpha-1-antitrypsin and single-dose anti-CD4/CD8 therapy. |
| 241 | 23717456 | Rat-to-mouse islet transplantation was examined in the following groups: untreated (n = 6), hAAT (n = 6, 60-240 mg/kg every 3 days from day -10), low-dose co-stimulation blockade (anti-CD154/LFA-1) and single-dose anti-CD4/CD8 (n = 5-7), either as mono- or combination therapies. |
| 242 | 23717456 | According to our results hAAT monotherapy and hAAT/anti-CD154/LFA-1 combined therapy, did not delay rejection day (11-24 days untreated vs. 10-22 day treated). |