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Gene Information
Gene symbol: F2
Gene name: coagulation factor II (thrombin)
HGNC ID: 3535
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 505501 | The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. |
| 2 | 1152862 | In five subjects, a four-hour infusion of somatostatin (500 micrograms per hour) had no definite effect on platelet count, leukocyte count, hematocrit, platelet adhesiveness and aggregation, bleeding time, partial thromboplastin time, prothrombin time, and fibrinogen levels. |
| 3 | 1248150 | The values of L-xylulose excretion in cirrhosis were correlated with the values of serum total bilirubin, albumin, albumin/globulin ratio, lactate dehydrogenase and prothrombin time. |
| 4 | 1332212 | To study factor VII (F VII) hyperactivity in chronic dialysis patients, we measured the plasma levels of F VII activity (F VII c) and antigen (F VII Ag), prothrombin activation fragments 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and thrombomodulin in 28 patients on hemodialysis. |
| 5 | 1332212 | Plasma TAT levels were significantly correlated with plasma thrombomodulin levels, suggesting that thrombin generation in blood as a result of hemodialysis could induce systemic endothelial cell injury. |
| 6 | 1332212 | To study factor VII (F VII) hyperactivity in chronic dialysis patients, we measured the plasma levels of F VII activity (F VII c) and antigen (F VII Ag), prothrombin activation fragments 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and thrombomodulin in 28 patients on hemodialysis. |
| 7 | 1332212 | Plasma TAT levels were significantly correlated with plasma thrombomodulin levels, suggesting that thrombin generation in blood as a result of hemodialysis could induce systemic endothelial cell injury. |
| 8 | 1333301 | 15-Hydroxyeicosatetraenoic acid-mediated potentiation of thrombin-induced platelet functions occurs via enhanced production of phosphoinositide-derived second messengers--sn-1,2-diacylglycerol and inositol-1,4,5-trisphosphate. |
| 9 | 1333301 | To understand the mechanism of the HETE modulation of platelet functions, we studied the effect of 10 and 100 nmol/L 15-HETE on the production of sn-1,2-diacylglycerol (DAG) and inositol-1,4,5-trisphosphate (1,4,5-IP3). 15-HETE enhanced thrombin-induced production of DAG and 1,4,5-IP3 in a time- and concentration-dependent manner. 15-HETE also potentiated agonist-induced phosphorylation of the 47-Kd platelet protein. |
| 10 | 1333301 | 15-Hydroxyeicosatetraenoic acid-mediated potentiation of thrombin-induced platelet functions occurs via enhanced production of phosphoinositide-derived second messengers--sn-1,2-diacylglycerol and inositol-1,4,5-trisphosphate. |
| 11 | 1333301 | To understand the mechanism of the HETE modulation of platelet functions, we studied the effect of 10 and 100 nmol/L 15-HETE on the production of sn-1,2-diacylglycerol (DAG) and inositol-1,4,5-trisphosphate (1,4,5-IP3). 15-HETE enhanced thrombin-induced production of DAG and 1,4,5-IP3 in a time- and concentration-dependent manner. 15-HETE also potentiated agonist-induced phosphorylation of the 47-Kd platelet protein. |
| 12 | 1386533 | Apolipoprotein(a), together with apo B-100 the apolipoprotein of Lp(a), is homologeous to plasminogen but lacks fibrinolytic capacity and appeared to interfere with fibrinolysis in in vitro and ex vivo experiments. |
| 13 | 1386533 | We determined the correlations between Lp(a) and other blood lipids (serum cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), coagulation parameters (fibrinogen, factor VII, factor VIII:C fibrin monomers, thrombin-antithrombin III) and fibrinolysis parameters (tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and D-dimer) in 54 patients with essential hypertension, in 65 non-insulin-dependent diabetic patients and in 116 insulin-regulated diabetic patients. |
| 14 | 1397782 | Generation of thrombin activity in relation to factor VIII:C concentrations and vascular complications in type 1 (insulin-dependent) diabetes mellitus. |
| 15 | 1418832 | The intracellular Ca-dependent protein kinase C and myosin light chain kinase activities on the phosphorylation of endogenous p47 and p20 proteins studied after 2 min of thrombin addition decreased only 10 to 25% in the presence of 5 to 10 mmol/L Mg. |
| 16 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 17 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 18 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 19 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 20 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 21 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 22 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 23 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 24 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 25 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 26 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 27 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 28 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 29 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 30 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 31 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 32 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 33 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 34 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 35 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 36 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 37 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 38 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 39 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 40 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 41 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 42 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 43 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 44 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 45 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 46 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. |
| 47 | 1440530 | Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. |
| 48 | 1440530 | Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). |
| 49 | 1440530 | Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). |
| 50 | 1440530 | Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. |
| 51 | 1440530 | Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). |
| 52 | 1451816 | This is accomplished by heparin in concert with antithrombin III (AT), but vessel wall glycosaminoglycans may act as substitutes for heparin and catalyse thrombin inhibition. |
| 53 | 1451816 | Preoperatively and during surgery the patients had elevated levels of fibrinogen, fibrinopeptide A (FPA) and thrombin-antithrombin (T-AT) complexes. |
| 54 | 1451816 | This is accomplished by heparin in concert with antithrombin III (AT), but vessel wall glycosaminoglycans may act as substitutes for heparin and catalyse thrombin inhibition. |
| 55 | 1451816 | Preoperatively and during surgery the patients had elevated levels of fibrinogen, fibrinopeptide A (FPA) and thrombin-antithrombin (T-AT) complexes. |
| 56 | 1476075 | Fibrinopeptide A (FPA), fibrinopeptide B beta 15-42 (FPB beta 15-42) and other coagulation factors (anti-thrombin III, thrombin-antithrombin complex, alpha 2-macroglobulin, plasmin inhibitor complex) were measured in the plasma of 101 patients with diabetes mellitus (DM). |
| 57 | 1562762 | Thrombin-antithrombin III complexes in type II diabetes mellitus. |
| 58 | 1562762 | Therefore determination of thrombin-antithrombin complex (TAT) could represent a sensitive parameter for specific detection of a latent activation of the clotting system. |
| 59 | 1562762 | Thrombin-antithrombin III complexes in type II diabetes mellitus. |
| 60 | 1562762 | Therefore determination of thrombin-antithrombin complex (TAT) could represent a sensitive parameter for specific detection of a latent activation of the clotting system. |
| 61 | 1579896 | Tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor (PAI) antigen and activity, thrombin-antithrombin III (TAT) complexes were determined in blood samples. |
| 62 | 1579896 | Diabetic CAD patients showed higher TAT levels with clearly increased PAI levels whereas t-PA levels levels were similar in patients and controls. |
| 63 | 1579896 | Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of PAI antigen and activity. |
| 64 | 1581696 | [Thrombin-antithrombin III complex. |
| 65 | 1581696 | We investigated the functional state of the coagulation system in 16 patients, 7 with a nonischemic and 9 with an ischemic retinal vein occlusion, with an enzyme-linked immunosorbent assay for the determination of thrombin-antithrombin III complex (TAT). |
| 66 | 1581696 | [Thrombin-antithrombin III complex. |
| 67 | 1581696 | We investigated the functional state of the coagulation system in 16 patients, 7 with a nonischemic and 9 with an ischemic retinal vein occlusion, with an enzyme-linked immunosorbent assay for the determination of thrombin-antithrombin III complex (TAT). |
| 68 | 1651430 | Plasma levels of thrombomodulin (TM), fibrinogen, antithrombin III (ATIII) and thrombin ATIII complex (TAT) were studied in healthy young subjects (group A), healthy elderly subjects (group B) and patients with level of TM in group B tended to be higher than that in group A. |
| 69 | 1655398 | We have examined thrombin-induced metabolism of phosphoinositides in the platelets from fifteen NIDDM (non-insulin-dependent diabetes mellitus) patients and fifteen healthy subjects (control). |
| 70 | 1660805 | We evaluated thrombin-induced inositol phosphate accumulation in [3H]inositol-labeled platelets prepared from patients with non-insulin-dependent diabetes mellitus. |
| 71 | 1693451 | The aim of this study was to evaluate the balance between thrombin and plasmin activity in a group of 79 diabetic patients (IDDM and NIDDM). |
| 72 | 1693451 | Moreover we investigated the behaviour of antithrombin III and alpha 2 antiplasmin, important inhibitors of blood coagulation and fibrinolysis. |
| 73 | 1693451 | Antithrombin III levels were not different from the controls and no correlation was found with Hb A1c. alpha 2 antiplasmin was found to be higher in IDDM when compared both with NIDDM and controls. |
| 74 | 1696196 | Here, we demonstrate the kinetic increase in specific binding of monoclonal antibodies to thrombospondin (P10) and to platelet membrane activation markers CD63 (GP53, a 53 kD lysosomal protein) and CD62 (GMP140, a 140 kD alpha granule protein) by using a flow-cytometric bio-assay and the related change in the actin status by using the DNase-I inhibition assay after stimulation of normal human platelets with 0.2 U/ml thrombin. |
| 75 | 1696196 | Simultaneously, the percentage of P10, CD63, and CD62 positive platelets was elevated from 5.4%, 24.4%, and 9.1% to 67.4%, 80.2%, and 82.3% respectively. |
| 76 | 1696196 | The mean number of P10, CD63, and CD62 antibody binding sites increased from 3,300, 1,715, and 2,146 to 6,400, 6,800, and 9,016 per platelet. |
| 77 | 1703110 | Thrombin/antithrombin III complex in patients with peripheral occlusive arterial disease. |
| 78 | 1703110 | Determinations of thrombin/antithrombin III complex (TAT) in human plasma with the new enzyme immunoassay (Enzygnost-TAT) were performed. |
| 79 | 1703110 | Thrombin/antithrombin III complex in patients with peripheral occlusive arterial disease. |
| 80 | 1703110 | Determinations of thrombin/antithrombin III complex (TAT) in human plasma with the new enzyme immunoassay (Enzygnost-TAT) were performed. |
| 81 | 1720765 | Plasma levels of fibronectin (FN), vitronectin (VN), thrombin-antithrombin III complex (TAT), and alpha 2-plasmin inhibitor-plasmin complex (PIC) were measured in 23 subjects who showed no evidence of vibration-induced white finger [VWF(-) group] and in 24 patients who presented with VWF [VWF(+) group]. |
| 82 | 1772997 | PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. |
| 83 | 1772997 | Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. |
| 84 | 1779452 | On the whole, D dimer values were positively correlated with plasmin-alpha 2-plasmin inhibitor complex and thrombin-antithrombin III complex. |
| 85 | 1851235 | It was revealed by experiments using cultured HUVEC in vitro that TM is released from endothelial cell membrane not with monensin, thrombin, fibroblast growth factor, interleukin-1 or endotoxin, but with H2O2 or endotoxin-treated granulocytes. |
| 86 | 1914539 | Serum (S-) transaminase was elevated in 92%, S-alkaline phosphatase in 47% and S-bilirubin in 23%, while plasma prothrombin time was below normal in 34%. |
| 87 | 2140088 | The role of hyperglycaemia-induced alterations of antithrombin III and factor X activation in the thrombin hyperactivity of diabetes mellitus. |
| 88 | 2140088 | The ratio of factor X activation to antithrombin III anti-factor Xa activity was increased in the diabetic patients (1.10 +/- 0.01 vs 1.01 +/- 0.02, p less than 0.01). |
| 89 | 2144055 | Platelet function (as production of thromboxane B2 by platelets stimulated with collagen, and plasma beta-thromboglobulin) and thrombin activity (as plasma fibrinopeptide A) were investigated in eight young (mean age 27 +/- 3 SE years) male patients in which type 1 diabetes mellitus had been diagnosed 2 to 6 months previously. |
| 90 | 2148199 | The aim of the present study was to evaluate whether coagulation-fibrinolytic system in patients with diabetic nephropathy were significantly correlated with the development of this disease using new parameters of plasma thrombin antithrombin III complex (TAT) and plasmin alpha 2 plasmin inhibitor complex (alpha 2PIC). |
| 91 | 2162303 | Platelet intracellular Ca2+ concentration ([Ca2+]i) and its response to stimuli (ADP and thrombin) were studied in 15 insulin-dependent and 22 non-insulin-dependent diabetes mellitus patients with the fluorescent probe Fura 2. |
| 92 | 2165005 | Thrombomodulin (TM) is a membrane protein in the vascular endothelium, and it plays an important role as a cofactor in the thrombin-catalyzed activation of protein C. |
| 93 | 2167823 | The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). |
| 94 | 2167823 | Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. |
| 95 | 2167823 | Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. |
| 96 | 2167823 | The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). |
| 97 | 2167823 | Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. |
| 98 | 2167823 | Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. |
| 99 | 2167823 | The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). |
| 100 | 2167823 | Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. |
| 101 | 2167823 | Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. |
| 102 | 2184068 | Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans. |
| 103 | 2184068 | In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. |
| 104 | 2184068 | Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. |
| 105 | 2184068 | In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. |
| 106 | 2184068 | These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus. |
| 107 | 2184068 | Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans. |
| 108 | 2184068 | In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. |
| 109 | 2184068 | Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. |
| 110 | 2184068 | In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. |
| 111 | 2184068 | These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus. |
| 112 | 2184068 | Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans. |
| 113 | 2184068 | In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. |
| 114 | 2184068 | Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. |
| 115 | 2184068 | In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. |
| 116 | 2184068 | These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus. |
| 117 | 2184068 | Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans. |
| 118 | 2184068 | In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. |
| 119 | 2184068 | Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. |
| 120 | 2184068 | In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. |
| 121 | 2184068 | These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus. |
| 122 | 2184068 | Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans. |
| 123 | 2184068 | In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. |
| 124 | 2184068 | Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. |
| 125 | 2184068 | In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. |
| 126 | 2184068 | These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus. |
| 127 | 2289707 | For the investigation of coagulation activation we determined activated partial thromboplastin time, thrombin time, and fibrinogen besides fibrin monomers and thrombin-antithrombin III complexes (TAT-III). |
| 128 | 2347433 | Non-enzymatic glycation reduces heparin cofactor II anti-thrombin activity. |
| 129 | 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. |
| 130 | 2474820 | We have found that ACBs inhibit only thrombin-induced platelet secretion, not secretion induced by ADP, collagen, or A23187. |
| 131 | 2528845 | Activation of blood coagulation and fibrinolysis in diabetes mellitus: evaluation by plasma levels of thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex. |
| 132 | 2528845 | In order to assess the actual degree of activation of the coagulation and fibrinolytic systems in diabetics, plasma levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PAP) were measured together with tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) in 18 patients with DM (three patients with type I DM and 15 with type II DM). |
| 133 | 2528845 | Plasma antigen concentration of t-PA but not of PAI-1 was also elevated. |
| 134 | 2528845 | Activation of blood coagulation and fibrinolysis in diabetes mellitus: evaluation by plasma levels of thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex. |
| 135 | 2528845 | In order to assess the actual degree of activation of the coagulation and fibrinolytic systems in diabetics, plasma levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PAP) were measured together with tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) in 18 patients with DM (three patients with type I DM and 15 with type II DM). |
| 136 | 2528845 | Plasma antigen concentration of t-PA but not of PAI-1 was also elevated. |
| 137 | 2597694 | Nonenzymatic glycation of antithrombin III has been reported to cause the reduction of heparin-catalyzed thrombin-inhibiting activity in diabetes. |
| 138 | 2736879 | Endogenous noradrenaline release from washed platelets incubated under resting conditions and in the presence of thrombin was examined in 14 normal subjects and 10 subjects with type 1 (insulin-dependent) diabetes. 2. |
| 139 | 2783675 | Modification of tissue-factor mRNA and protein response to thrombin and interleukin 1 by high glucose in cultured human endothelial cells. |
| 140 | 2783675 | The reciprocal effects of high glucose on the tissue-factor response to thrombin and interleukin 1 points to different pathways of tissue-factor stimulation by the two agents and suggests functional consequences pertinent to the increased thrombin activity and compromised host-defense mechanisms observed in diabetes. |
| 141 | 2783675 | Modification of tissue-factor mRNA and protein response to thrombin and interleukin 1 by high glucose in cultured human endothelial cells. |
| 142 | 2783675 | The reciprocal effects of high glucose on the tissue-factor response to thrombin and interleukin 1 points to different pathways of tissue-factor stimulation by the two agents and suggests functional consequences pertinent to the increased thrombin activity and compromised host-defense mechanisms observed in diabetes. |
| 143 | 2910581 | Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. |
| 144 | 2910581 | We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. |
| 145 | 2910581 | Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. |
| 146 | 2910581 | Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. |
| 147 | 2910581 | Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. |
| 148 | 2910581 | These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. |
| 149 | 2910581 | Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. |
| 150 | 2910581 | We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. |
| 151 | 2910581 | Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. |
| 152 | 2910581 | Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. |
| 153 | 2910581 | Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. |
| 154 | 2910581 | These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. |
| 155 | 2910581 | Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. |
| 156 | 2910581 | We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. |
| 157 | 2910581 | Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. |
| 158 | 2910581 | Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. |
| 159 | 2910581 | Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. |
| 160 | 2910581 | These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. |
| 161 | 2910581 | Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. |
| 162 | 2910581 | We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. |
| 163 | 2910581 | Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. |
| 164 | 2910581 | Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. |
| 165 | 2910581 | Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. |
| 166 | 2910581 | These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. |
| 167 | 2910581 | Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. |
| 168 | 2910581 | We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. |
| 169 | 2910581 | Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. |
| 170 | 2910581 | Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. |
| 171 | 2910581 | Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. |
| 172 | 2910581 | These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. |
| 173 | 2920976 | The low antithrombin III concentration (0.44 +/- 0.13 mg/dl) in protein-poor dialysate seems to be sufficient to inhibit the thrombin activity after acceleration by heparin. |
| 174 | 2935351 | To determine the relationship between thrombin generation and platelet secretion in vivo in diabetes mellitus, we measured simultaneous plasma beta-thromboglobulin (BTG) and fibrinopeptide A (FPA) in 40 insulin-dependent patients without renal disease, and 20 control subjects of similar age. |
| 175 | 2941327 | Sixteen healthy male subjects received a 60-min intravenous infusion of human regular insulin at the rate of 64 mU . m-2 . min-1: throughout 150 min, we serially measured plasma concentrations of glucose, insulin, and counterregulatory hormones; platelet sensitivity to ADP, thrombin and platelet-activating factor; plasma concentrations of platelet markers for specific proteins of in vivo release reaction (beta-thromboglobulin and platelet factor 4). |
| 176 | 2947762 | Soluble immune complexes, platelet factor IV (PF4), beta-thromboglobulin, fibrinogen, factor VIII related antigen and anti-thrombin III were significantly increased in Type 1 diabetic patients with retinopathy as compared to non-diabetic controls. |
| 177 | 2947762 | A significant correlation was found between positive values of soluble immune complexes and increased levels of PF4 and beta-thromboglobulin in diabetic patients with retinopathy. |
| 178 | 2970690 | Plasma concentrations of beta-thromboglobulin (index of platelet activation) and of fibrinopeptide A (index of thrombin formation) were measured before and 15 minutes after forearm immersion in melting ice. |
| 179 | 3010580 | It was found that pre-treatment with aspirin reduced collagen or thrombin-induced binding to platelets from non-retinopathic diabetics to the values seen in controls. |
| 180 | 3010580 | The combination of aspirin with apyrase (an ADP scavenger) almost completely inhibited binding and aggregation of platelets from normal controls or non-retinopathic diabetics exposed to collagen or thrombin, whereas it only partially affected binding and aggregation of platelets from retinopathics. |
| 181 | 3010580 | It was found that pre-treatment with aspirin reduced collagen or thrombin-induced binding to platelets from non-retinopathic diabetics to the values seen in controls. |
| 182 | 3010580 | The combination of aspirin with apyrase (an ADP scavenger) almost completely inhibited binding and aggregation of platelets from normal controls or non-retinopathic diabetics exposed to collagen or thrombin, whereas it only partially affected binding and aggregation of platelets from retinopathics. |
| 183 | 3080538 | We have examined the relative importance of these pathways in the responses to adenosine diphosphate (ADP), thrombin, or collagen of washed platelets from rats with diabetes induced by streptozocin. |
| 184 | 3080539 | The responses of washed platelets to adenosine diphosphate (ADP), thrombin, or collagen have been compared with platelets from spontaneously diabetic rats (these rats were hyperglycemic), their nondiabetic littermates (normoglycemic), and control rats from the same colony. |
| 185 | 3192039 | In this study, we observed that LDL isolated from patients with insulin-dependent diabetes mellitus (IDDM) enhanced thrombin-induced platelet aggregation to a greater extent than LDL isolated from matched controls (P less than .01). |
| 186 | 3192039 | LDL glycosylated in vitro enhanced thrombin-, collagen-, and adenosine 5'-diphosphate-induced platelet aggregation to a greater extent than control LDL (P less than .01). |
| 187 | 3192039 | In this study, we observed that LDL isolated from patients with insulin-dependent diabetes mellitus (IDDM) enhanced thrombin-induced platelet aggregation to a greater extent than LDL isolated from matched controls (P less than .01). |
| 188 | 3192039 | LDL glycosylated in vitro enhanced thrombin-, collagen-, and adenosine 5'-diphosphate-induced platelet aggregation to a greater extent than control LDL (P less than .01). |
| 189 | 3304967 | Studies in animals and man have demonstrated that ticlopidine is a potent inhibitor of platelet aggregation induced by adenosine diphosphate (ADP), and variably inhibits aggregation due to collagen, adrenaline (epinephrine), arachidonic acid, thrombin, and platelet activating factor. |
| 190 | 3304967 | Ticlopidine also inhibits the release reaction of platelets, prolongs bleeding time, reduces plasma levels of platelet factor 4 and beta-thromboglobulin in patients in whom these proteins are elevated, and may also inhibit platelet adhesion, increase red cell filtrability and decrease whole blood viscosity. |
| 191 | 3319468 | Plasma fibrinopeptide A (FPA) concentration, as a measure of thrombin activity, was determined during an insulin tolerance test in 17 non-obese diabetics. |
| 192 | 3319468 | These results indicate that insulin-induced hypoglycemia or a rapid fall in plasma glucose is associated with enhanced thrombin generation and fibrin formation, which may be considered as a contributory factor to the development of diabetic microangiopathy through a hypercoagulable state. |
| 193 | 3319468 | Plasma fibrinopeptide A (FPA) concentration, as a measure of thrombin activity, was determined during an insulin tolerance test in 17 non-obese diabetics. |
| 194 | 3319468 | These results indicate that insulin-induced hypoglycemia or a rapid fall in plasma glucose is associated with enhanced thrombin generation and fibrin formation, which may be considered as a contributory factor to the development of diabetic microangiopathy through a hypercoagulable state. |
| 195 | 3391345 | A detailed evaluation of the kinetics of inhibition of thrombin by glycosylated antithrombin III revealed that the second-order rate constant is three times smaller than that of normal antithrombin III. |
| 196 | 3696697 | The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, alpha 2-antiplasmin and alpha 2-macroglobulin. |
| 197 | 3924690 | Platelets from diabetic subjects synthesized significantly greater quantities of 12-HETE than did platelets from control subjects when 12-HETE synthesis was induced by thrombin or collagen, either in the presence or absence of indomethacin. |
| 198 | 3924690 | Thrombin- and collagen-induced platelet 12-HETE synthesis demonstrated a significant negative linear correlation with platelet vitamin E content when measurements from both diabetic and control groups were combined. |
| 199 | 3924690 | Platelets from diabetic subjects synthesized significantly greater quantities of 12-HETE than did platelets from control subjects when 12-HETE synthesis was induced by thrombin or collagen, either in the presence or absence of indomethacin. |
| 200 | 3924690 | Thrombin- and collagen-induced platelet 12-HETE synthesis demonstrated a significant negative linear correlation with platelet vitamin E content when measurements from both diabetic and control groups were combined. |
| 201 | 3928783 | Effect of insulin treatment in streptozocin-induced diabetic rats on in vitro platelet function and plasma von Willebrand factor activity and factor VIII-related antigen. |
| 202 | 3928783 | Insulin therapy returned ADP-induced, but not thrombin-induced, responses to normal. |
| 203 | 3933340 | Thromboxane B2 formation was normal in response to arachidonic acid (0.2 to 1 mM), whereas it was decreased by 30 to 50 percent in response to thrombin (0.5 to 10 units/ml), collagen (0.5 to 10 micrograms/ml), and the combination of collagen with adenosine diphosphate or epinephrine. |
| 204 | 3943666 | No differences in the amount of fibrinogen bound to platelets (stimulated by collagen or thrombin) were found when data from nonretinopathic and retinopathic patients were compared. |
| 205 | 6084321 | In diabetics without complications factor VIII functions, fibrinogen and thrombin time are related to age whereas there is a negative correlation for the fibrinolytic activity and antithrombin III. |
| 206 | 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. |
| 207 | 6235479 | Information on platelet functions was obtained by beta-thromboglobulin determination, and of heparin-thrombin coagulation time, platelet aggregation in vivo, and on the condition of the vessel walls by estimation of factor VIII-protein (VIIIR:Ag). |
| 208 | 6356254 | Platelets from diabetic rats receiving insulin (one unit protamine-zinc insulin/100 g BW) were consistently more responsive to aggregating agents (ADP, thrombin) than platelets from control rats (with or without insulin administration). |
| 209 | 6415193 | Platelet aggregation and the platelet release reaction in response to ADP, thrombin, and collagen were measured in suspensions of washed platelets prepared from rats 3, 7, 14, or 28 days after induction of diabetes and in control animals. |
| 210 | 6419383 | TXB2 formation in PRP after thrombin or arachidonic acid stimulation was determined in 23 young compensated insulin-dependent diabetic patients, and in 10 control subjects of equivalent age. |
| 211 | 6698315 | Platelets, but not plasma, from diabetic subjects contained significantly lower vitamin E levels and synthesized significantly greater amounts of TxA2 when challenged with collagen or thrombin than platelets from control subjects. |
| 212 | 6698315 | Platelet vitamin E content from control and diabetic groups combined exhibited a significant negative linear correlation with collagen- and thrombin-induced TxA2 production. |
| 213 | 6698315 | Platelets, but not plasma, from diabetic subjects contained significantly lower vitamin E levels and synthesized significantly greater amounts of TxA2 when challenged with collagen or thrombin than platelets from control subjects. |
| 214 | 6698315 | Platelet vitamin E content from control and diabetic groups combined exhibited a significant negative linear correlation with collagen- and thrombin-induced TxA2 production. |
| 215 | 6724150 | The effect of nonenzymatic glycosylation on the biologic function of human antithrombin III was evaluated using a chromogenic thrombin substrate assay in the presence of catalytic amounts of heparin. |
| 216 | 6724150 | Experimental conditions that increased the rate of nonenzymatic protein glycosylation were associated with decreases in the thrombin-inhibiting activity of antithrombin III. |
| 217 | 6724150 | The effect of nonenzymatic glycosylation on the biologic function of human antithrombin III was evaluated using a chromogenic thrombin substrate assay in the presence of catalytic amounts of heparin. |
| 218 | 6724150 | Experimental conditions that increased the rate of nonenzymatic protein glycosylation were associated with decreases in the thrombin-inhibiting activity of antithrombin III. |
| 219 | 6761893 | TxB2 formation in PRP after thrombin stimulus, serum TxB2 and platelet sensitivity to prostacyclin and the correlation with ambient fasting plasma glucose and lipoproteins were determined in 20 insulin-independent diabetics (IID) with macroangiopathy, 10 insulin-dependent diabetics (IDD) with microangiopathy and 30 matched controls. |
| 220 | 6766119 | Although the biological antithrombin III activity was clearly reduced in individual subjects, there was only a slight nonsignificant reduction in the mean anti-thrombin III activity values as compared to normal subjects. |
| 221 | 6804992 | Thrombin induced thromboxane A2 and prostaglandin E2 production were significantly increased in platelets of streptozotocin induced diabetic rats as compared to non-diabetic control rats, while collagen induced thromboxane A2 production was decreased. |
| 222 | 6816718 | The cultured arterial endothelial cells released prostacyclin in response to challenge with thrombin and protamine sulfate but not in response to bradykinin or the platelet-derived growth factor. |
| 223 | 7449596 | Plasma antithrombin III and thrombin generation time: correlation with hemoglobin A1 and fasting serum glucose in young diabetic women. |
| 224 | 7449596 | Three parameters of coagulability--thrombin generation time (TGT), antithrombin III (AT III), and activated partial thromboplastin time (ATPP)--and two parameters of diabetic control--serial measurements of fasting serum glucose (FG) and hemoglobin A1(HbA1)--were used to study the relationship between diabetic control and hypercoagulability. |
| 225 | 7449596 | Plasma antithrombin III and thrombin generation time: correlation with hemoglobin A1 and fasting serum glucose in young diabetic women. |
| 226 | 7449596 | Three parameters of coagulability--thrombin generation time (TGT), antithrombin III (AT III), and activated partial thromboplastin time (ATPP)--and two parameters of diabetic control--serial measurements of fasting serum glucose (FG) and hemoglobin A1(HbA1)--were used to study the relationship between diabetic control and hypercoagulability. |
| 227 | 7486814 | Using fluorescent dyes 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and Fura-2 AM, changes was evaluated in the concentration of baseline and thrombin-stimulated increases in intracellular ionized calcium (Ca2+i) relative to hydrogen ions in the platelets from control, insulin-treated, and non-treated diabetic rats. |
| 228 | 7486814 | Upon stimulation with thrombin, the mean peak [Ca2+]i for the insulin-treated (309 +/- 97 nmol/L) and untreated (339 +/- 135 nmol/L) diabetic rats was significantly higher than the concentration for the normal rats (213 +/- 101 nmol/L). |
| 229 | 7486814 | Using fluorescent dyes 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and Fura-2 AM, changes was evaluated in the concentration of baseline and thrombin-stimulated increases in intracellular ionized calcium (Ca2+i) relative to hydrogen ions in the platelets from control, insulin-treated, and non-treated diabetic rats. |
| 230 | 7486814 | Upon stimulation with thrombin, the mean peak [Ca2+]i for the insulin-treated (309 +/- 97 nmol/L) and untreated (339 +/- 135 nmol/L) diabetic rats was significantly higher than the concentration for the normal rats (213 +/- 101 nmol/L). |
| 231 | 7495061 | The levels of thrombin antithrombin III complex (p < 0.05), D-dimer (p < 0.05), tissue plasminogen activator (p < 0.005) and PA inhibitor 1 (p < 0.01) were significantly increased, while the level of thrombomodulin (p < 0.005) in the fasting plasma was significantly decreased in the WS cases compared with N. |
| 232 | 7495104 | Platelet rich (PRP) clots were formed by addition of thrombin, and lysis was induced by tissue-plasminogen-activator. |
| 233 | 7565477 | A variety of proinflammatory and vasoactive agents including thrombin, transforming growth factor beta, angiotensin II as well as mechanical forces enhance the renal synthesis of ET. |
| 234 | 7565477 | Two receptor subtypes, ETA and ETB, are widely expressed in the kidney, coupled to multiple intracellular signal transduction pathways that mediate distinct activities. |
| 235 | 7627704 | We studied the relationships between albuminuria, tissue factor-induced coagulation, and endothelial cell dysfunction in 67 patients with non-insulin-dependent diabetes mellitus (NIDDM) who were divided into three groups on the basis of their urinary albumin excretion rate (AER). |
| 236 | 7627704 | As markers of endothelial cell dysfunction, levels of von Willebrand factor (vWF), tissue-type plasminogen activator-plasminogen activator inhibitor-1 (TPA-PAI-1) complex, PAI-1, and tissue factor pathway inhibitor (TFPI) were measured. |
| 237 | 7627704 | This FVIIa increase was accompanied by an increase in thrombin-antithrombin III complex (TAT) levels, indicating increased activation of coagulation even in normoalbuminuric patients. |
| 238 | 7627704 | This group also had higher levels of endothelial cell-derived factors (vWF, TPA-PAI-1 complex, and PAI-1) than the control group. |
| 239 | 7648824 | Haemostatic parameters measured were fibrinogen, prothrombin time, activated partial thromboplastin time (APTT), factor VIIc, factor VIIIc, antithrombin III, and plasminogen. |
| 240 | 7726824 | Bovine estrogen receptor binding cyclophilin (ERBC), a cyclophilin component of the unactivated estrogen receptor, has been efficiently expressed in Escherichia coli as a fusion with glutathione S-transferase (GST) and purified by single-step chromatography on glutathione-agarose. |
| 241 | 7726824 | Thrombin cleavage from GST allowed the isolation of purified, recombinant ERBC. |
| 242 | 7740463 | Mg2+ (4 mM) prolonged in vitro BT by 30% and inhibited Fg-mediated aggregation significantly, independent of the agonist used to initiate platelet aggregation (ADP, collagen, epinephrine, thrombin, phorbol ester). |
| 243 | 7740463 | Moreover, Mg2+ reduced Fg binding to ADP- or collagen-stimulated platelets as well as surface expression of GMP-140 with an IC50 of approximately 3 mM. |
| 244 | 7744231 | The biological activity of thrombin and coagulation factor Xa was assessed in 62 insulin-dependent diabetic patients. |
| 245 | 7744231 | Compared to non-diabetic control subjects an increase in the biological activity of factor Xa was observed in all groups of diabetic patients (prothrombin fragment 1 + 2 levels were 1.14 +/- 0.38 nmol/l in group 2, p < 0.005; 1.06 +/- 0.45 nmol/l in group 3, p < 0.05 and 1.03 +/- 0.31 nmol/l in group 4, p < 0.05 vs 0.75 +/- 0.34 nmol/l in group 1). |
| 246 | 7744231 | The biological activity of thrombin and coagulation factor Xa was assessed in 62 insulin-dependent diabetic patients. |
| 247 | 7744231 | Compared to non-diabetic control subjects an increase in the biological activity of factor Xa was observed in all groups of diabetic patients (prothrombin fragment 1 + 2 levels were 1.14 +/- 0.38 nmol/l in group 2, p < 0.005; 1.06 +/- 0.45 nmol/l in group 3, p < 0.05 and 1.03 +/- 0.31 nmol/l in group 4, p < 0.05 vs 0.75 +/- 0.34 nmol/l in group 1). |
| 248 | 7773734 | Factor V Leiden gene mutation and thrombin generation in relation to the development of acute stroke. |
| 249 | 7778057 | The following haemostatic factors were measured in two representative groups of clinically healthy subjects, 28 with microalbuminuria (UAER of 6.6-150 micrograms/min) and 60 age- and sex-matched controls with normoalbuminuria (UAER < 6.6 micrograms/min): Coagulation factors: blood platelet count and mean volume, plasma Factor VII antigen concentration and coagulant activity, and plasma concentrations of prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, fibrinogen, and fibrinopeptide A; fibrinolytic and endothelial factors: plasma concentrations of tissue plasminogen activator antigen and plasminogen activator inhibitor type 1 antigen; and endothelial factor: plasma von Willebrand factor antigen concentration. |
| 250 | 7792737 | The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes. |
| 251 | 7792737 | In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. |
| 252 | 7792737 | A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. |
| 253 | 7792737 | The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes. |
| 254 | 7792737 | In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. |
| 255 | 7792737 | A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. |
| 256 | 7792737 | The effect of insulin-induced hypoglycaemia on factor VIII:C concentrations and thrombin activity in subjects with type 1 (insulin-dependent) diabetes. |
| 257 | 7792737 | In addition, factor VIII:C, thrombin-antithrombin III (TAT) complex and fibrinopeptide A (FPA) levels were measured. |
| 258 | 7792737 | A corresponding reduction in time to generate 50% maximal thrombin activity occurred from a pre-insulin value of 56 (6) s to a minimum reading of 46 (7) s at 15 min (p < 0.001) and remained low at 90 min [48 (6) s, p < 0.001]. |
| 259 | 7893927 | Plasminogen activator inhibitor, von Willebrand factor and thrombin/antithrombin complex were increased in the high-risk group with signs of cardiovascular disease in comparison with the low-risk group. |
| 260 | 7893927 | Clinical signs of cardiovascular disease were associated with increased plasma levels of fibrinogen, von Willebrand factor, plasminogen activator inhibitor, thrombin/antithrombin complex and prothrombin 1 + 2 fragment. |
| 261 | 7893927 | Plasminogen activator inhibitor, von Willebrand factor and thrombin/antithrombin complex were increased in the high-risk group with signs of cardiovascular disease in comparison with the low-risk group. |
| 262 | 7893927 | Clinical signs of cardiovascular disease were associated with increased plasma levels of fibrinogen, von Willebrand factor, plasminogen activator inhibitor, thrombin/antithrombin complex and prothrombin 1 + 2 fragment. |
| 263 | 7898603 | The following parameters were measured on admission: blood pressure, blood glucose, cholesterol, triglycerides, hematocrit, fibrinogen, prothrombin levels, platelet counts, prothrombin time, bilirubin, transaminases, gamma-glutamyltransferase, and alkaline phosphatase. |
| 264 | 7924884 | A high concentration of glucose alters the production of tPA, uPA and PAI-1 antigens from human mesangial cells. |
| 265 | 7924884 | To elucidate a role of tPA, uPA and PAI-1 for the development of diabetic glomerulosclerosis, the effect of high glucose concentration on the production of both basal and thrombin-mediated tPA, uPA and PAI-1 antigens from human mesangial cells was investigated. |
| 266 | 7924884 | The culture of mesangial cells in the presence of high glucose (33 mM) for 11 days resulted in an increase in the synthesis of tPA and uPA when compared with that in normal glucose concentration (5 mM). |
| 267 | 7924884 | Thrombin stimulated dose-dependently the production of tPA, uPA and PAI-1 from the cells grown in either 5 or 33 mM glucose. |
| 268 | 7924884 | However, the magnitude of the increase in tPA, uPA and PAI-1 from the cells grown in high glucose was less than that in normal glucose. |
| 269 | 7924884 | A high concentration of glucose alters the production of tPA, uPA and PAI-1 antigens from human mesangial cells. |
| 270 | 7924884 | To elucidate a role of tPA, uPA and PAI-1 for the development of diabetic glomerulosclerosis, the effect of high glucose concentration on the production of both basal and thrombin-mediated tPA, uPA and PAI-1 antigens from human mesangial cells was investigated. |
| 271 | 7924884 | The culture of mesangial cells in the presence of high glucose (33 mM) for 11 days resulted in an increase in the synthesis of tPA and uPA when compared with that in normal glucose concentration (5 mM). |
| 272 | 7924884 | Thrombin stimulated dose-dependently the production of tPA, uPA and PAI-1 from the cells grown in either 5 or 33 mM glucose. |
| 273 | 7924884 | However, the magnitude of the increase in tPA, uPA and PAI-1 from the cells grown in high glucose was less than that in normal glucose. |
| 274 | 7926350 | On the other hand, in platelets incubated with [32P]orthophosphate, thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) was significantly lower in the sulphonylurea and insulin groups than in the diet group. |
| 275 | 7926350 | There were no differences in thrombin-induced 47 kDa protein phosphorylation between platelets from the diet, sulphonylurea, or insulin groups. |
| 276 | 7926350 | These results suggest that sulphonylureas and insulin induce suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP2 and production of PA, which leads to inhibition of platelet aggregation. |
| 277 | 7926350 | On the other hand, in platelets incubated with [32P]orthophosphate, thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) was significantly lower in the sulphonylurea and insulin groups than in the diet group. |
| 278 | 7926350 | There were no differences in thrombin-induced 47 kDa protein phosphorylation between platelets from the diet, sulphonylurea, or insulin groups. |
| 279 | 7926350 | These results suggest that sulphonylureas and insulin induce suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP2 and production of PA, which leads to inhibition of platelet aggregation. |
| 280 | 7926350 | On the other hand, in platelets incubated with [32P]orthophosphate, thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) was significantly lower in the sulphonylurea and insulin groups than in the diet group. |
| 281 | 7926350 | There were no differences in thrombin-induced 47 kDa protein phosphorylation between platelets from the diet, sulphonylurea, or insulin groups. |
| 282 | 7926350 | These results suggest that sulphonylureas and insulin induce suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP2 and production of PA, which leads to inhibition of platelet aggregation. |
| 283 | 7968593 | The effects of contraceptive steroids on the expression of endothelial homeostasis were examined by direct and indirect measures in women with insulin-dependent diabetes mellitus (IDDM) in a prospective nonrandomized controlled study. |
| 284 | 7968593 | In the indirect assessment of endothelial function, we found a proportionate increase in plasma levels of thrombin-antithrombin III (TAT) complexes and D-dimer during treatment. |
| 285 | 7968593 | Hormonal intake was followed by decreased antigen concentrations of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (type 1 [PAI-1]), whereas the activities of t-PA and PAI-1 were unchanged. |
| 286 | 7968593 | Plasma levels of plasminogen and histidine-rich glycoprotein (HRG) increased and decreased, respectively, whereas an increase in von Willebrand factor was observed in the treatment group. |
| 287 | 8032574 | A 62-year-old male patient, suffering from a hypertensive cardiopathy, an arteriopathy of the lower extremities and a type II insulin independent diabetes had a prothrombin time ratio R of 2.15 (therapeutic range: 2.1-1.45) during a daily treatment of 4-6 mg acenocoumarin. |
| 288 | 8051797 | Thrombomodulin is an endothelial cell surface glycoprotein that forms a 1:1 complex with thrombin. |
| 289 | 8051797 | Thus thrombomodulin converts thrombin from a procoagulant protease to an anticoagulant. |
| 290 | 8051797 | Thrombomodulin is an endothelial cell surface glycoprotein that forms a 1:1 complex with thrombin. |
| 291 | 8051797 | Thus thrombomodulin converts thrombin from a procoagulant protease to an anticoagulant. |
| 292 | 8088128 | Prothrombin fragment 1 + 2 and antithrombin III-thrombin complex in microalbuminuric type 2 diabetic patients. |
| 293 | 8088128 | To investigate whether or not microalbuminuria is associated with haemostatic abnormalities in Type 2 diabetic patients, we measured the prothrombin fragment 1 + 2, a marker of thrombin generation, and the thrombin-antithrombin complex, a marker of thrombin neutralization. |
| 294 | 8088128 | Plasma levels of prothrombin fragment 1 + 2 and thrombin-antithrombin complex were assayed in 17 microalbuminuric patients (albumin excretion rate, AER 20-200 micrograms min-1) and in 17 comparable normoalbuminuric (AER < 20 micrograms min-1) Type 2 diabetic patients. |
| 295 | 8088128 | Plasma thrombin-antithrombin complex values were not significantly different in the two groups and were not correlated with AER. |
| 296 | 8088128 | Prothrombin fragment 1 + 2 and antithrombin III-thrombin complex in microalbuminuric type 2 diabetic patients. |
| 297 | 8088128 | To investigate whether or not microalbuminuria is associated with haemostatic abnormalities in Type 2 diabetic patients, we measured the prothrombin fragment 1 + 2, a marker of thrombin generation, and the thrombin-antithrombin complex, a marker of thrombin neutralization. |
| 298 | 8088128 | Plasma levels of prothrombin fragment 1 + 2 and thrombin-antithrombin complex were assayed in 17 microalbuminuric patients (albumin excretion rate, AER 20-200 micrograms min-1) and in 17 comparable normoalbuminuric (AER < 20 micrograms min-1) Type 2 diabetic patients. |
| 299 | 8088128 | Plasma thrombin-antithrombin complex values were not significantly different in the two groups and were not correlated with AER. |
| 300 | 8088128 | Prothrombin fragment 1 + 2 and antithrombin III-thrombin complex in microalbuminuric type 2 diabetic patients. |
| 301 | 8088128 | To investigate whether or not microalbuminuria is associated with haemostatic abnormalities in Type 2 diabetic patients, we measured the prothrombin fragment 1 + 2, a marker of thrombin generation, and the thrombin-antithrombin complex, a marker of thrombin neutralization. |
| 302 | 8088128 | Plasma levels of prothrombin fragment 1 + 2 and thrombin-antithrombin complex were assayed in 17 microalbuminuric patients (albumin excretion rate, AER 20-200 micrograms min-1) and in 17 comparable normoalbuminuric (AER < 20 micrograms min-1) Type 2 diabetic patients. |
| 303 | 8088128 | Plasma thrombin-antithrombin complex values were not significantly different in the two groups and were not correlated with AER. |
| 304 | 8088128 | Prothrombin fragment 1 + 2 and antithrombin III-thrombin complex in microalbuminuric type 2 diabetic patients. |
| 305 | 8088128 | To investigate whether or not microalbuminuria is associated with haemostatic abnormalities in Type 2 diabetic patients, we measured the prothrombin fragment 1 + 2, a marker of thrombin generation, and the thrombin-antithrombin complex, a marker of thrombin neutralization. |
| 306 | 8088128 | Plasma levels of prothrombin fragment 1 + 2 and thrombin-antithrombin complex were assayed in 17 microalbuminuric patients (albumin excretion rate, AER 20-200 micrograms min-1) and in 17 comparable normoalbuminuric (AER < 20 micrograms min-1) Type 2 diabetic patients. |
| 307 | 8088128 | Plasma thrombin-antithrombin complex values were not significantly different in the two groups and were not correlated with AER. |
| 308 | 8115982 | The experiments comprised functional assays of factor Xa and thrombin generation in the presence of normal or diabetic platelets, using saturating amounts of coagulation factors. |
| 309 | 8115982 | The results showed that, in contrast to the low prothrombin and factor X converting activity of normal platelets, the thrombin and FXa generation on diabetic platelets was increased by 3-7 times for either humans or hamsters. |
| 310 | 8115982 | The experiments comprised functional assays of factor Xa and thrombin generation in the presence of normal or diabetic platelets, using saturating amounts of coagulation factors. |
| 311 | 8115982 | The results showed that, in contrast to the low prothrombin and factor X converting activity of normal platelets, the thrombin and FXa generation on diabetic platelets was increased by 3-7 times for either humans or hamsters. |
| 312 | 8128458 | Microalbuminuria in insulin-dependent diabetes is associated with high levels of prothrombin fragment 1 + 2. |
| 313 | 8250495 | Microalbuminuria in insulin-dependent diabetes mellitus (IDDM) patients has been related to abnormalities in haemostasis, poor glycaemic control, disadvantageous alterations in the lipid spectrum and elevated concentrations of lipoprotein(a), another independent risk factor for cardiovascular disease. |
| 314 | 8250495 | No significant differences were found in blood lipids (Lp(a), serum cholesterol, low-density lipoprotein and high-density lipoprotein cholesterol and triglycerides), glycaemic control (HbA1c) and several haemostasis parameters (factor VII, VIII, fibrin monomer, thrombin-antithrombin III, D-dimer, tissue plasminogen activator antigen and plasminogen activator inhibitor-1) between the micro- and normoalbuminuric subgroups. |
| 315 | 8250495 | In the microalbuminuric subgroup increased concentrations for plasminogen and alpha 2-antiplasmin were measured. |
| 316 | 8329566 | Accordingly, we investigated the effects of increasing FVIII:C levels on coagulation in vitro using a computer-assisted measurement of thrombin activity. |
| 317 | 8329566 | Increasing FV concentrations resulted in an additive effect with high FVIII:C levels on the rate of thrombin generation. |
| 318 | 8329566 | The results showed that increasing plasma FVIII:C and FV concentrations accelerate rate of generation of thrombin activity independently, and in an additive manner. |
| 319 | 8329566 | Accordingly, we investigated the effects of increasing FVIII:C levels on coagulation in vitro using a computer-assisted measurement of thrombin activity. |
| 320 | 8329566 | Increasing FV concentrations resulted in an additive effect with high FVIII:C levels on the rate of thrombin generation. |
| 321 | 8329566 | The results showed that increasing plasma FVIII:C and FV concentrations accelerate rate of generation of thrombin activity independently, and in an additive manner. |
| 322 | 8329566 | Accordingly, we investigated the effects of increasing FVIII:C levels on coagulation in vitro using a computer-assisted measurement of thrombin activity. |
| 323 | 8329566 | Increasing FV concentrations resulted in an additive effect with high FVIII:C levels on the rate of thrombin generation. |
| 324 | 8329566 | The results showed that increasing plasma FVIII:C and FV concentrations accelerate rate of generation of thrombin activity independently, and in an additive manner. |
| 325 | 8340422 | Mitogen regulation of c-Raf-1 protein kinase activity toward mitogen-activated protein kinase-kinase. |
| 326 | 8340422 | The c-raf-1 protooncogene encodes a Ser/Thr protein kinase. |
| 327 | 8340422 | A mitogen-activated protein kinase-kinase (MAPKK) purified from bovine brain is phosphorylated and activated 4-9-fold in vitro by c-Raf-1 from mitogen-treated cells. c-Raf-1 protein kinase activity, measured by the phosphorylation of brain MAPKK substrate, is detectably activated within 1 min after addition of platelet-derived growth factor (PDGF) to 3T3 cells, increasing more rapidly than the endogenous NIH 3T3 cell MAPKK activity. c-Raf-1 activation is also induced by insulin, phorbol ester, thrombin, and endothelin. |
| 328 | 8340422 | PDGF-, epidermal groth factor-, and insulin-stimulated 32P-c-Raf-1 yield very similar, complex tryptic 32P-peptide maps, wherein only 2 of 10 32P-peptides appear entirely de novo after growth factor addition. |
| 329 | 8340422 | Mitogen-activated protein kinase/extracellular signal-regulated kinase-2 can phosphorylate c-Raf-1 in vitro on 4-6 tryptic 32P-peptides, all of which comigrate with tryptic 32P-peptides derived from c-Raf-1 labeled in situ. |
| 330 | 8340422 | Mitogen-activated protein kinase phosphorylation of c-Raf-1 in vitro, however, does not 1) generate 32P-peptides that comigrate with those that appear de novo after PDGF or insulin treatment in situ; 2) does not convert c-Raf-1 polypeptides to a slower mobility on SDS-polyacrylamide gel electrophoresis as is seen after PDGF or insulin; 3) does not alter c-Raf-1 kinase activity toward MAPKK. |
| 331 | 8340422 | Thus, based on overlapping site specificity, Erk-2 is a viable candidate to be among the PDGF-stimulated c-Raf-1 kinases. |
| 332 | 8340422 | Although PDGF/insulin-stimulated c-Raf-1 Ser/Thr phosphorylation may be necessary to sustain the active state, a role for mitogen-activated protein kinase/extracellular signal-regulated kinase-2 phosphorylation in the initiation of c-Raf-1 activation is unlikely. |
| 333 | 8362378 | In addition, APTT, factor VIII and thrombin-antithrombin III (TAT) complex levels were measured. |
| 334 | 8362378 | A greater increase in FVIII:C than vWF levels occurred in controls [0.2 (0.1); 0.1 (0.1) IU ml-1; (p = 0.005)] and patients [0.3 (0.4); 0.2 (0.1) IU ml-1; (p = 0.032)]. |
| 335 | 8382139 | The coagulation parameters (fibrinogen, prothrombin time, partial thromboplastin time with kaolin, von Willebrand factor antigen) did not differ between patients and control subjects either before or after 20 min of venous occlusion. |
| 336 | 8382139 | In the diabetic patients, chronic activation of the fibrinolytic system was found at baseline, which was indicated by a shortened euglobulin lysis time (P < 0.01), increased tissue plasminogen activator activity (P < 0.05) and decreased plasminogen activator inhibitor type 1 antigen level (P < 0.05), when compared with control subjects. |
| 337 | 8400336 | Elevated levels of fibrinogen, fibrin monomers, thrombin-antithrombin III complex, and factor VIIIc were found in the diabetic patients and factor VII in male diabetic patients. |
| 338 | 8445010 | Insulin (100 microU/mL) decreased thrombin-induced platelet aggregation (washed platelets resuspended in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-Tyrode buffer). |
| 339 | 8495717 | Thrombin also partially reversed the effects of H-7, a protein kinase C inhibitor, which on its own also caused cell retraction and disruption of microfilaments. |
| 340 | 8495717 | In conclusion, thrombin promotes endothelial activities which are associated with long-term endothelial repair; however, these effects do not appear to be directly due to the involvement of conventional isoforms of protein kinase C or the phosphotidylinositol system. |
| 341 | 8495717 | Thrombin also partially reversed the effects of H-7, a protein kinase C inhibitor, which on its own also caused cell retraction and disruption of microfilaments. |
| 342 | 8495717 | In conclusion, thrombin promotes endothelial activities which are associated with long-term endothelial repair; however, these effects do not appear to be directly due to the involvement of conventional isoforms of protein kinase C or the phosphotidylinositol system. |
| 343 | 8518538 | Endothelial cell damage, which is associated with local thrombin formation and inflammation, can lead to the release of endothelium-synthesized factors into plasma, such as vWFAg, TM, ACE and ET-1. |
| 344 | 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. |
| 345 | 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. |
| 346 | 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. |
| 347 | 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. |
| 348 | 8574252 | This study was designed to examine the balance between coagulation activity and fibrinolytic activity--an indirect measure of endothelial cell function--in women with insulin-dependent diabetes mellitus (IDDM) during long-term use of OCs. |
| 349 | 8574252 | There was a proportionate increase in the concentrations of thrombin-antithrombin III complexes and D-dimer. |
| 350 | 8596745 | In 53 diabetic patients and 33 healthy subjects as controls the following parameters have been assessed: plasma prekallikrein, serum fructosamine, glycated haemoglobin HbA1c, prothrombin time, partial thromboplastin time and antithrombin III (AT III). |
| 351 | 8607100 | Increased plasma thrombin-antithrombin III complex levels in non-insulin dependent diabetic patients with albuminuria are reduced by ethyl icosapentatenoate. |
| 352 | 8607100 | Plasma thrombin-anti-thrombin III complex (TAT) levels, representing a functional state of clotting system, were studied in one hundred and fifteen non-insulin-dependent diabetic (NIDDM) patients. |
| 353 | 8607100 | Increased plasma thrombin-antithrombin III complex levels in non-insulin dependent diabetic patients with albuminuria are reduced by ethyl icosapentatenoate. |
| 354 | 8607100 | Plasma thrombin-anti-thrombin III complex (TAT) levels, representing a functional state of clotting system, were studied in one hundred and fifteen non-insulin-dependent diabetic (NIDDM) patients. |
| 355 | 8645373 | Median levels of fibrinogen (P < 0.0001), thrombin-antithrombin III complex (TAT) (P < 0.005), and plasminogen activator inhibitor-1 (PAI-1) activity (P < 0.05) in plasma were significantly elevated in diabetic patients compared with controls. |
| 356 | 8674873 | Levels of fibrinogen, tissue factor pathway inhibitor (TFPI), thrombin-anti-thrombin complex, and plasminogen activator inhibitor 1 in plasma increased significantly in the diabetic patients. |
| 357 | 8777997 | Blood samples for measurement of plasma glucose, insulin, prothrombin fragments 1 + 2 and D-dimer were drawn at 0, 60, 120 and 240 min. |
| 358 | 8777997 | Acarbose administration significantly reduced the rise of glucose, insulin, prothrombin fragments 1 + 2 and D-dimer from 0 to 240 min in comparison to placebo. |
| 359 | 8777997 | Blood samples for measurement of plasma glucose, insulin, prothrombin fragments 1 + 2 and D-dimer were drawn at 0, 60, 120 and 240 min. |
| 360 | 8777997 | Acarbose administration significantly reduced the rise of glucose, insulin, prothrombin fragments 1 + 2 and D-dimer from 0 to 240 min in comparison to placebo. |
| 361 | 8870813 | We determined the plasma levels of prothrombin fragment 1 + 2, D-dimer, fibrinogen, plasminogen activator inhibitor type 1, tissue plasminogen activator, von Willebrand factor and coagulation factors VII and VIII. |
| 362 | 8890605 | Thrombomodulin (TM) is a thrombin receptor on endothelial cells. |
| 363 | 8904933 | Protein C and S activity, antithrombin III, thrombomodulin and prothrombin fragments 1 + 2 (F 1 + 2) were assessed together with fibrinogen, triglycerides, total and high density lipoprotein (HDL)-cholesterol concentrations. |
| 364 | 8904933 | The coagulation parameters were as follows: normoalbuminuric group: protein C activity 109% +/- 5%, protein S 95.4% +/- 5%, thrombomodulin 49.3 +/- 3 ng/ml, antithrombin III 93.3% +/- 3%, F 1 + 2 1.05 +/- 0.04 nmol/l; microalbuminuric group: protein C activity 107% +/- 4%, protein S 98.4% +/- 4%, thrombomodulin 64.4 +/- 4 ng/ml, antithrombin III 93.3% +/- 3%, F 1 + 2 1.03 +/- 0.05 nmol/l. |
| 365 | 8941058 | Antibodies to beta 2-glycoprotein I and prothrombin in habitual abortion. |
| 366 | 8960826 | The plasma levels of fibrinogen (p < 0.02), prothrombin fragment 1 + 2 (p < 0.05), fibrin monomer (p < 0.0001), protein C antigen (p < 0.005), total protein S antigen (p < 0.02), soluble thrombomodulin (p < 0.005) and soluble E-selectin (p < 0.005) were significantly higher in diabetic patients than in healthy subjects. |
| 367 | 8960826 | The plasma level of activated protein C-protein C inhibitor complex (7.4 +/- 3.8 vs 3.0 +/- 0.4 pmol/l) was significantly higher (p < 0.0001) and the anticoagulant response to exogenous thrombomodulin (23.4 +/- 2.6 vs 35.3 +/- 3.0 ng/ml) was markedly lower (p = 0.005) in all diabetic patients than in healthy subjects. |
| 368 | 8960826 | Cases with microalbuminuria presented low plasma levels of activated protein C-protein C inhibitor complex (5.5 +/- 0.6 vs 8.6 +/- 0.7 pmol/l, p < 0.05) and significantly decreased values of the anticoagulant response to exogenous thrombomodulin (16.5 +/- 2.9 vs 23.4 +/- 2.6%, p = 0.03) as compared to those with normoalbuminuria. |
| 369 | 9065996 | Increased tissue factor pathway inhibitor (TFPI) and coagulation in patients with insulin-dependent diabetes mellitus. |
| 370 | 9065996 | Recently, we found an increase in tissue factor pathway inhibitor (TFPI) activity in patients with insulin-dependent diabetes mellitus (IDDM). |
| 371 | 9065996 | This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans. |
| 372 | 9065996 | We studied TFPI activity (chromogenic assay) in relation to prothrombin F1 + 2 fragments and endogenous thrombin potential (ETP), in 46 IDDM patients, and 18 age and sex-matched healthy controls. |
| 373 | 9065996 | Prothrombin, antithrombin and thrombomodulin were also determined. |
| 374 | 9065996 | In IDDM patients, TFPI activity and F1 + 2 levels were significantly higher, while ETP, prothrombin antigen levels, and antithrombin activity were lower as compared to the controls. |
| 375 | 9065996 | In IDDM patients with microalbuminuria, a manifestation of generalized angiopathy, TFPI activity, F1 + 2 and thrombomodulin levels were higher than in patients with only retinopathy or patients without complications. |
| 376 | 9065996 | No correlation between TFPI activity, F1 + 2 levels and thrombomodulin was found, while TFPI activity was negatively correlated with ETP (r = -0.27). |
| 377 | 9065996 | Microalbuminuria was significantly correlated with TFPI activity (r = 0.46), F1 + 2 (r = 0.56), and thrombomodulin (r = 0.52). |
| 378 | 9065996 | In conclusion, the increase in TFPI activity in IDDM patients may not be considered to be a reaction on a procoagulant state. |
| 379 | 9065996 | Increased tissue factor pathway inhibitor (TFPI) and coagulation in patients with insulin-dependent diabetes mellitus. |
| 380 | 9065996 | Recently, we found an increase in tissue factor pathway inhibitor (TFPI) activity in patients with insulin-dependent diabetes mellitus (IDDM). |
| 381 | 9065996 | This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans. |
| 382 | 9065996 | We studied TFPI activity (chromogenic assay) in relation to prothrombin F1 + 2 fragments and endogenous thrombin potential (ETP), in 46 IDDM patients, and 18 age and sex-matched healthy controls. |
| 383 | 9065996 | Prothrombin, antithrombin and thrombomodulin were also determined. |
| 384 | 9065996 | In IDDM patients, TFPI activity and F1 + 2 levels were significantly higher, while ETP, prothrombin antigen levels, and antithrombin activity were lower as compared to the controls. |
| 385 | 9065996 | In IDDM patients with microalbuminuria, a manifestation of generalized angiopathy, TFPI activity, F1 + 2 and thrombomodulin levels were higher than in patients with only retinopathy or patients without complications. |
| 386 | 9065996 | No correlation between TFPI activity, F1 + 2 levels and thrombomodulin was found, while TFPI activity was negatively correlated with ETP (r = -0.27). |
| 387 | 9065996 | Microalbuminuria was significantly correlated with TFPI activity (r = 0.46), F1 + 2 (r = 0.56), and thrombomodulin (r = 0.52). |
| 388 | 9065996 | In conclusion, the increase in TFPI activity in IDDM patients may not be considered to be a reaction on a procoagulant state. |
| 389 | 9065996 | Increased tissue factor pathway inhibitor (TFPI) and coagulation in patients with insulin-dependent diabetes mellitus. |
| 390 | 9065996 | Recently, we found an increase in tissue factor pathway inhibitor (TFPI) activity in patients with insulin-dependent diabetes mellitus (IDDM). |
| 391 | 9065996 | This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans. |
| 392 | 9065996 | We studied TFPI activity (chromogenic assay) in relation to prothrombin F1 + 2 fragments and endogenous thrombin potential (ETP), in 46 IDDM patients, and 18 age and sex-matched healthy controls. |
| 393 | 9065996 | Prothrombin, antithrombin and thrombomodulin were also determined. |
| 394 | 9065996 | In IDDM patients, TFPI activity and F1 + 2 levels were significantly higher, while ETP, prothrombin antigen levels, and antithrombin activity were lower as compared to the controls. |
| 395 | 9065996 | In IDDM patients with microalbuminuria, a manifestation of generalized angiopathy, TFPI activity, F1 + 2 and thrombomodulin levels were higher than in patients with only retinopathy or patients without complications. |
| 396 | 9065996 | No correlation between TFPI activity, F1 + 2 levels and thrombomodulin was found, while TFPI activity was negatively correlated with ETP (r = -0.27). |
| 397 | 9065996 | Microalbuminuria was significantly correlated with TFPI activity (r = 0.46), F1 + 2 (r = 0.56), and thrombomodulin (r = 0.52). |
| 398 | 9065996 | In conclusion, the increase in TFPI activity in IDDM patients may not be considered to be a reaction on a procoagulant state. |
| 399 | 9065996 | Increased tissue factor pathway inhibitor (TFPI) and coagulation in patients with insulin-dependent diabetes mellitus. |
| 400 | 9065996 | Recently, we found an increase in tissue factor pathway inhibitor (TFPI) activity in patients with insulin-dependent diabetes mellitus (IDDM). |
| 401 | 9065996 | This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans. |
| 402 | 9065996 | We studied TFPI activity (chromogenic assay) in relation to prothrombin F1 + 2 fragments and endogenous thrombin potential (ETP), in 46 IDDM patients, and 18 age and sex-matched healthy controls. |
| 403 | 9065996 | Prothrombin, antithrombin and thrombomodulin were also determined. |
| 404 | 9065996 | In IDDM patients, TFPI activity and F1 + 2 levels were significantly higher, while ETP, prothrombin antigen levels, and antithrombin activity were lower as compared to the controls. |
| 405 | 9065996 | In IDDM patients with microalbuminuria, a manifestation of generalized angiopathy, TFPI activity, F1 + 2 and thrombomodulin levels were higher than in patients with only retinopathy or patients without complications. |
| 406 | 9065996 | No correlation between TFPI activity, F1 + 2 levels and thrombomodulin was found, while TFPI activity was negatively correlated with ETP (r = -0.27). |
| 407 | 9065996 | Microalbuminuria was significantly correlated with TFPI activity (r = 0.46), F1 + 2 (r = 0.56), and thrombomodulin (r = 0.52). |
| 408 | 9065996 | In conclusion, the increase in TFPI activity in IDDM patients may not be considered to be a reaction on a procoagulant state. |
| 409 | 9092031 | Membrane thrombomodulin (TM) is a very efficient natural anti-thrombin glycoprotein with anticoagulant properties expressed on endothelial cell surface. |
| 410 | 9092031 | Circulating plasmatic thrombomodulin (TMp) detected by enzyme immunoassay in plasma is considered as a cell marker of endothelial injury. |
| 411 | 9092031 | In cases of collagen vascular diseases, where vascular endothelium damage is suspected, TMp is increased particularly in systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). |
| 412 | 9175236 | Moreover, after stimulation with thrombin, collagen, phorbol myristate acetate (PMA) and platelet activating factor (PAF), platelets of diabetic subjects generated significantly higher amounts of hydrogen peroxide than controls. |
| 413 | 9219324 | Effect of bezafibrate on hypercoagulability assessed by fluorogenic prothrombin time in hyperlipidemic patients with non-insulin-dependent diabetes mellitus. |
| 414 | 9219324 | We investigated the usefulness of the fluorogenic prothrombin time (FPT) for detection of hypercoagulability and its association with hyperlipidemia in 19 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 10 healthy control subjects, compared with plasma levels of fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and D-dimer. |
| 415 | 9219324 | Six-months therapy with bezafibrate reduced the levels of FPT, triglycerides and basal insulin, but did not alter levels of fibrinogen, PAI-1 and D-dimer. |
| 416 | 9219324 | Effect of bezafibrate on hypercoagulability assessed by fluorogenic prothrombin time in hyperlipidemic patients with non-insulin-dependent diabetes mellitus. |
| 417 | 9219324 | We investigated the usefulness of the fluorogenic prothrombin time (FPT) for detection of hypercoagulability and its association with hyperlipidemia in 19 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 10 healthy control subjects, compared with plasma levels of fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and D-dimer. |
| 418 | 9219324 | Six-months therapy with bezafibrate reduced the levels of FPT, triglycerides and basal insulin, but did not alter levels of fibrinogen, PAI-1 and D-dimer. |
| 419 | 9222867 | In the present study, mean levels of plasma Lp(a) and parameters of coagulation and fibrinolysis such as thrombin-antithrombin III complex (TAT) and alpha 2 plasmin inhibitor-plasmin complex (alpha 2PIC) were elevated in diabetic patients with nephropathy compared to healthy controls. |
| 420 | 9225230 | Plasma levels of thrombin-antithrombin III complex (TAT), which reflects activation of coagulation system, were slightly but significantly higher in type IIb hyperlipidemia, although they were within normal range. |
| 421 | 9225230 | In the diabetics, the levels of Lp(a) as well as levels of tissue-type plasminogen activator (t-PA) antigen and PAI activity were significantly higher than normal controls. |
| 422 | 9254523 | The actions of S2-receptor antagonist naftidrofuril (Duzodril-retard, Byk Gulden, FRG) on both basal and thrombin-induced levels of malondialdehyde in platelets as well as platelet aggregability in patients with insulin-dependent diabetes mellitus with or without angiopathies were studied. |
| 423 | 9254523 | The treatment with Duzodril-retard at daily dose of 200 mg during 40 days was not shown to decrease in platelet hyperfunction in response to the inductors: ADP, 1 and 5 microM; adrenaline, 1 microM; collagen, 4 mu/ml; ristomycin, 0.9 and 1.2 mg/ml; and thrombin 0.5 U/ml). |
| 424 | 9254523 | The actions of S2-receptor antagonist naftidrofuril (Duzodril-retard, Byk Gulden, FRG) on both basal and thrombin-induced levels of malondialdehyde in platelets as well as platelet aggregability in patients with insulin-dependent diabetes mellitus with or without angiopathies were studied. |
| 425 | 9254523 | The treatment with Duzodril-retard at daily dose of 200 mg during 40 days was not shown to decrease in platelet hyperfunction in response to the inductors: ADP, 1 and 5 microM; adrenaline, 1 microM; collagen, 4 mu/ml; ristomycin, 0.9 and 1.2 mg/ml; and thrombin 0.5 U/ml). |
| 426 | 9258277 | All subjects were tested on the following parameters: fibrinogen, factor VII, prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), tissue plasminogen activator (t-PA) antigen (Ag) before and after venous occlusion (VO), and plasminogen activator inhibitor type-1 (PAI-1) activity pre- and post-VO. |
| 427 | 9258277 | At baseline, obese nondiabetic subjects, lean NIDDM patients, and especially obese NIDDM patients displayed significantly (P < .01) higher levels of fibrinogen, factor VII, F1 + 2, TAT, t-PA(Ag) pre-VO, and PAI-1 pre- and post-VO and significantly (P < .01) lower levels of t-PA(Ag) post-VO. |
| 428 | 9258277 | In obese NIDDM patients treated with heparin fibrinogen, factor VII, F1 + 2, TAT, t-PA(Ag) pre-VO, and PAI-1 pre- and post-VO levels significantly (P < .01) decreased and t-PA(Ag) post-VO levels significantly (P < .01) increased at the end of treatment. |
| 429 | 9258280 | Intracellular calcium ([Ca2+]i) and phorbol ester binding were studied in intact platelets of young patients with insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. |
| 430 | 9258280 | [Ca2+]i in platelets of the IDDM group (135 +/- 20 nmol/L) under basal conditions was significantly higher than that of the control group (81 +/- 8 nmol/L, P = .019), whereas at 60 seconds after stimulation with 0.1 National Institutes of Health (NIH) U/mL thrombin, [Ca2+]i in the NIDDM group (484 +/- 36 nmol/L) was significantly higher than that of the controls (347 +/- 22 nmol/L, P = .003) and IDDM group (360 +/- 45 nmol/L, P = .04), respectively. |
| 431 | 9258280 | Phorbol 12,13-dibutyrate (PdBu) maximal binding capacity (Bmax) in the IDDM group was significantly lower than that in the control group either under basal conditions or after stimulation with thrombin (P = .0034 and P = .015, respectively). |
| 432 | 9258280 | Intracellular calcium ([Ca2+]i) and phorbol ester binding were studied in intact platelets of young patients with insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. |
| 433 | 9258280 | [Ca2+]i in platelets of the IDDM group (135 +/- 20 nmol/L) under basal conditions was significantly higher than that of the control group (81 +/- 8 nmol/L, P = .019), whereas at 60 seconds after stimulation with 0.1 National Institutes of Health (NIH) U/mL thrombin, [Ca2+]i in the NIDDM group (484 +/- 36 nmol/L) was significantly higher than that of the controls (347 +/- 22 nmol/L, P = .003) and IDDM group (360 +/- 45 nmol/L, P = .04), respectively. |
| 434 | 9258280 | Phorbol 12,13-dibutyrate (PdBu) maximal binding capacity (Bmax) in the IDDM group was significantly lower than that in the control group either under basal conditions or after stimulation with thrombin (P = .0034 and P = .015, respectively). |
| 435 | 9282795 | Increased soluble fibrin monomer and soluble thrombomodulin levels in non-insulin-dependent diabetes mellitus. |
| 436 | 9282795 | We measured the plasma levels of fibrinogen, D-dimer, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), soluble fibrin monomer (SFM), tissue-type plasminogen activator (t-PA) and thrombomodulin (TM) in patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 437 | 9282795 | There were no significant differences in the hemostatic parameters between the 77 patients with NIDDM and healthy control subjects, although the plasma levels of fibrinogen, D-dimer, TAT, and PPIC in the NIDDM patients were slightly higher than those in the healthy controls. |
| 438 | 9282795 | There was no significant difference in activated partial thromboplastin time, prothrombin time, fibrinogen, TAT, PPIC, D-dimer, or t-PA among these three groups. |
| 439 | 9282795 | Increased soluble fibrin monomer and soluble thrombomodulin levels in non-insulin-dependent diabetes mellitus. |
| 440 | 9282795 | We measured the plasma levels of fibrinogen, D-dimer, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), soluble fibrin monomer (SFM), tissue-type plasminogen activator (t-PA) and thrombomodulin (TM) in patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 441 | 9282795 | There were no significant differences in the hemostatic parameters between the 77 patients with NIDDM and healthy control subjects, although the plasma levels of fibrinogen, D-dimer, TAT, and PPIC in the NIDDM patients were slightly higher than those in the healthy controls. |
| 442 | 9282795 | There was no significant difference in activated partial thromboplastin time, prothrombin time, fibrinogen, TAT, PPIC, D-dimer, or t-PA among these three groups. |
| 443 | 9283213 | We measured thrombin.antithrombin III complex (TAT), alpha 2-plasmin inhibitor plasmin complex (PIC), D-dimer, protein C, protein S, thrombomodulin (TM), vitronectin, tissue plasminogen activator.plasminogen activator inhibitor-1 complex (tPAI-C) in theses two groups. |
| 444 | 9326350 | Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: a prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus. |
| 445 | 9326350 | Patients showed triglyceride enrichment in low (P = 0.00002) and high density lipoproteins (P = 0.004) and increased levels of D-dimer (P < 0.00001), prothrombin fragment 1 + 2 (P < 0.00001), and thrombin-antithrombin III complex (P = 0.0001). |
| 446 | 9326350 | Patients with clinically detectable microangiopathy had increased type 1 plasminogen activator inhibitor (P = 0.00001), thrombomodulin (P = 0.02), and induced monocyte tissue factor expression (P < 0.00001). |
| 447 | 9342018 | The following laboratory tests were performed on serum specimens from all subjects: albumin (ALB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, total bilirubin, and prothrombin time. |
| 448 | 9342018 | However, the concentrations of ALB, ALT, AST, AST/ALT, and prothrombin time were substantially different among the four groups. |
| 449 | 9342018 | The following laboratory tests were performed on serum specimens from all subjects: albumin (ALB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, total bilirubin, and prothrombin time. |
| 450 | 9342018 | However, the concentrations of ALB, ALT, AST, AST/ALT, and prothrombin time were substantially different among the four groups. |
| 451 | 9409313 | Significantly increased levels of thrombin-antithrombin III complexes (P < .01), prothrombin fragments 1 + 2 (P < .01), and D-dimers (P < .01) were found 1 hour, as well as 24 to 48 hours, after PTA. |
| 452 | 9409313 | Restenotic patients as a whole had higher plasma fibrinogen (3.46 +/- 1.12 versus 2.95 +/- 0.62 g/L, P < .01) and C-reactive protein (25.4 +/- 46.7 versus 7.9 +/- 6.9 mg/L, P < .05) at baseline, as well as higher fibrinogen (P < .05) and prothrombin fragments 1 + 2 (P < .01) during months 3 to 6 after PTA. |
| 453 | 9409313 | There was a nonsignificant tendency for higher values of von Willebrand factor (206 +/- 98% versus 184 +/- 100%, P = .2) at baseline in patients with restenosis, whereas tissue plasminogen activator, plasminogen activator inhibitor, coagulation screening tests, blood cell counts, and serum lipids showed no significant difference between the two groups. |
| 454 | 9409313 | Patients with critical limb ischemia (stage III/IV, Fontaine) had significantly higher fibrinogen and von Willebrand factor at repeated points of time, as well as significantly higher C-reactive protein and lower creatinine clearance at entry. |
| 455 | 9409313 | Significantly increased levels of thrombin-antithrombin III complexes (P < .01), prothrombin fragments 1 + 2 (P < .01), and D-dimers (P < .01) were found 1 hour, as well as 24 to 48 hours, after PTA. |
| 456 | 9409313 | Restenotic patients as a whole had higher plasma fibrinogen (3.46 +/- 1.12 versus 2.95 +/- 0.62 g/L, P < .01) and C-reactive protein (25.4 +/- 46.7 versus 7.9 +/- 6.9 mg/L, P < .05) at baseline, as well as higher fibrinogen (P < .05) and prothrombin fragments 1 + 2 (P < .01) during months 3 to 6 after PTA. |
| 457 | 9409313 | There was a nonsignificant tendency for higher values of von Willebrand factor (206 +/- 98% versus 184 +/- 100%, P = .2) at baseline in patients with restenosis, whereas tissue plasminogen activator, plasminogen activator inhibitor, coagulation screening tests, blood cell counts, and serum lipids showed no significant difference between the two groups. |
| 458 | 9409313 | Patients with critical limb ischemia (stage III/IV, Fontaine) had significantly higher fibrinogen and von Willebrand factor at repeated points of time, as well as significantly higher C-reactive protein and lower creatinine clearance at entry. |
| 459 | 9430016 | No other blood tests results, including albumin, cholinesterase, and prothrombin time, or lipid profile and nutritional status, in terms of rapid turnover proteins, prealbumin, retinol binding protein, and transferin, were altered throughout the study period. |
| 460 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 461 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 462 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 463 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 464 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 465 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 466 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 467 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 468 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 469 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 470 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 471 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 472 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 473 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 474 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 475 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 476 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 477 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 478 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 479 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 480 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 481 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 482 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 483 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 484 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 485 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 486 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 487 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 488 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 489 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 490 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 491 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 492 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 493 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 494 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 495 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 496 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 497 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 498 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 499 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 500 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 501 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 502 | 9439534 | Comparative catabolism of prothrombin and antithrombin in normal and alloxan-diabetic rabbits. |
| 503 | 9439534 | In the present study, the catabolism of two hemostatic proteins, prothrombin and antithrombin, are compared in alloxan-induced diabetic rabbits (of 6 months' duration) and age-matched control rabbits. |
| 504 | 9439534 | Differentially radiolabeled prothrombin and antithrombin were injected intravenously, and arterial blood was sampled over a 7-day period to measure the clearance from plasma. |
| 505 | 9439534 | As observed for other plasma proteins, the whole-body fractional catabolic rates (jt) for prothrombin and antithrombin were significantly less in diabetic rabbits (prothrombin, 0.33 d-1; antithrombin, 0.27 d-1) than in control rabbits (prothrombin, 0.37 d-1; antithrombin, 0.30 d-1; P < .001 and P < .005, respectively). |
| 506 | 9439534 | In absolute terms, the catabolism of antithrombin and prothrombin in diabetic rabbits was 5.1 and 6.2 mg.kg-1.d-1, respectively, equivalent to a molar ratio for antithrombin to prothrombin of 0.94. |
| 507 | 9439534 | For the control rabbits, catabolism accounted for 6.3 mg.kg-1.d-1 of antithrombin and 7.3 mg.kg-1.d-1 of prothrombin, equivalent to a molar ratio of 1.01. |
| 508 | 9439534 | The decreased catabolic rates observed for prothrombin and antithrombin in diabetic rabbits conform with results obtained previously for other plasma proteins, and probably reflect a generally decreased rate of plasma protein production by diabetic rabbit liver compared with control liver. |
| 509 | 9483170 | FXIIa was measured as a marker of contact activation, and thrombin generation was evaluated using the two markers thrombin-antithrombin III complex and prothrombin fragment 1 + 2. |
| 510 | 9531249 | Interaction of coagulation defects and cardiovascular risk factors: increased risk of myocardial infarction associated with factor V Leiden or prothrombin 20210A. |
| 511 | 9541421 | Beginning at least 6 months after transplantation, we analysed hemostatic factors (fibrinogen, thrombin, and prothrombin times), coagulation inhibitors (proteins C and S), fibrinolysis (plasminogen activator inhibitor) and endothelial cell abnormalities (Von Willebrand factor: VWf). |
| 512 | 9583351 | Eight weeks after the injection, we observed increases in thrombin-antithrombin III complex and tissue type plasminogen activator activity, decreases in plasma levels of antithrombin III, plasminogen and alpha2-plasmin inhibitor, and significant shortening of activated partial thromboplastin time. |
| 513 | 9587911 | [Coefficient of linear correlation between levels of fibrinogen, antithrombin III, thrombin-antithrombin complex and lipid fractions in women exposed chronically to carbon disulfide]. |
| 514 | 9601894 | Elevated PAI-1 levels were described in different insulin resistant conditions, incl. diabetes mellitus type II. |
| 515 | 9601894 | Hitherto accomplished studies suggest not only the important effect of insulin acting synergically with very low density. lipoproteins (VLDL) on hepatocytes but also the importance of the endothelial pool where the action of proinsulin, VLDL and cytokines in synergy with Cai-dependent stimuli (oxidation stress, thrombin) is involved. |
| 516 | 9601894 | Under certain circumstances also another adipocyte compartment may play a role, and a significant role of thrombocytes in raising the PAI-1 level cannot be ruled out either. |
| 517 | 9647334 | Plasma concentrations of plasminogen activator inhibitor (PAI-1), prothrombin fragment F1+2, fibrinogen, and von Willebrand Factor (vWF) activity were measured. |
| 518 | 9714135 | Before the patients underwent PTCA, blood was obtained by venipuncture for measurement of Lp(a), total cholesterol, thrombin-antithrombin (TAT) complex, alpha2-antiplasmin-plasmin (APP) complex, and plasminogen activator inhibitor-1 (PAI-1). |
| 519 | 9714135 | The Lp(a) level was not correlated significantly with TAT, APP, PAI-1, or the TAT-APP ratio. |
| 520 | 9714135 | Levels of TAT, APP, and PAI-1 were not statistically different in the patients with versus those without restenosis. |
| 521 | 9726240 | Accordingly, we studied the effect of troglitazone, pioglitazone, and vitamin E on thrombin-induced platelet aggregation, metabolism of phosphoinositide, protein phosphorylation, protein kinase C (PKC)-alpha and -beta, and phosphatidylinositol (PI) 3-kinase activation in vitro in human platelets. |
| 522 | 9726240 | Maximum platelet aggregation by ADP, collagen, and thrombin decreased in the presence of 0.1-1 micromol/l troglitazone and 500 nmol/l vitamin E for 60 min compared with controls. |
| 523 | 9726240 | However, pioglitazone did not inhibit ADP-, collagen-, or thrombin-induced platelet aggregation. |
| 524 | 9726240 | Pretreatment with troglitazone and vitamin E, but not with pioglitazone, resulted in decreases in thrombin-induced phosphatidic acid production, hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C, and 47-kDa protein phosphorylation. |
| 525 | 9726240 | Thrombin-induced PKC-alpha and -beta activation in membrane fraction was suppressed by pretreatment with troglitazone and vitamin E, but not with pioglitazone. |
| 526 | 9726240 | Accordingly, we studied the effect of troglitazone, pioglitazone, and vitamin E on thrombin-induced platelet aggregation, metabolism of phosphoinositide, protein phosphorylation, protein kinase C (PKC)-alpha and -beta, and phosphatidylinositol (PI) 3-kinase activation in vitro in human platelets. |
| 527 | 9726240 | Maximum platelet aggregation by ADP, collagen, and thrombin decreased in the presence of 0.1-1 micromol/l troglitazone and 500 nmol/l vitamin E for 60 min compared with controls. |
| 528 | 9726240 | However, pioglitazone did not inhibit ADP-, collagen-, or thrombin-induced platelet aggregation. |
| 529 | 9726240 | Pretreatment with troglitazone and vitamin E, but not with pioglitazone, resulted in decreases in thrombin-induced phosphatidic acid production, hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C, and 47-kDa protein phosphorylation. |
| 530 | 9726240 | Thrombin-induced PKC-alpha and -beta activation in membrane fraction was suppressed by pretreatment with troglitazone and vitamin E, but not with pioglitazone. |
| 531 | 9726240 | Accordingly, we studied the effect of troglitazone, pioglitazone, and vitamin E on thrombin-induced platelet aggregation, metabolism of phosphoinositide, protein phosphorylation, protein kinase C (PKC)-alpha and -beta, and phosphatidylinositol (PI) 3-kinase activation in vitro in human platelets. |
| 532 | 9726240 | Maximum platelet aggregation by ADP, collagen, and thrombin decreased in the presence of 0.1-1 micromol/l troglitazone and 500 nmol/l vitamin E for 60 min compared with controls. |
| 533 | 9726240 | However, pioglitazone did not inhibit ADP-, collagen-, or thrombin-induced platelet aggregation. |
| 534 | 9726240 | Pretreatment with troglitazone and vitamin E, but not with pioglitazone, resulted in decreases in thrombin-induced phosphatidic acid production, hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C, and 47-kDa protein phosphorylation. |
| 535 | 9726240 | Thrombin-induced PKC-alpha and -beta activation in membrane fraction was suppressed by pretreatment with troglitazone and vitamin E, but not with pioglitazone. |
| 536 | 9726240 | Accordingly, we studied the effect of troglitazone, pioglitazone, and vitamin E on thrombin-induced platelet aggregation, metabolism of phosphoinositide, protein phosphorylation, protein kinase C (PKC)-alpha and -beta, and phosphatidylinositol (PI) 3-kinase activation in vitro in human platelets. |
| 537 | 9726240 | Maximum platelet aggregation by ADP, collagen, and thrombin decreased in the presence of 0.1-1 micromol/l troglitazone and 500 nmol/l vitamin E for 60 min compared with controls. |
| 538 | 9726240 | However, pioglitazone did not inhibit ADP-, collagen-, or thrombin-induced platelet aggregation. |
| 539 | 9726240 | Pretreatment with troglitazone and vitamin E, but not with pioglitazone, resulted in decreases in thrombin-induced phosphatidic acid production, hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C, and 47-kDa protein phosphorylation. |
| 540 | 9726240 | Thrombin-induced PKC-alpha and -beta activation in membrane fraction was suppressed by pretreatment with troglitazone and vitamin E, but not with pioglitazone. |
| 541 | 9726240 | Accordingly, we studied the effect of troglitazone, pioglitazone, and vitamin E on thrombin-induced platelet aggregation, metabolism of phosphoinositide, protein phosphorylation, protein kinase C (PKC)-alpha and -beta, and phosphatidylinositol (PI) 3-kinase activation in vitro in human platelets. |
| 542 | 9726240 | Maximum platelet aggregation by ADP, collagen, and thrombin decreased in the presence of 0.1-1 micromol/l troglitazone and 500 nmol/l vitamin E for 60 min compared with controls. |
| 543 | 9726240 | However, pioglitazone did not inhibit ADP-, collagen-, or thrombin-induced platelet aggregation. |
| 544 | 9726240 | Pretreatment with troglitazone and vitamin E, but not with pioglitazone, resulted in decreases in thrombin-induced phosphatidic acid production, hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C, and 47-kDa protein phosphorylation. |
| 545 | 9726240 | Thrombin-induced PKC-alpha and -beta activation in membrane fraction was suppressed by pretreatment with troglitazone and vitamin E, but not with pioglitazone. |
| 546 | 9776869 | There was no significant change in the levels of AST, ALT, alkaline phosphatase, total protein, albumin-globulin ratio and prothrombin time. |
| 547 | 9788646 | Antithrombin III, thrombin-antithrombin III complexes, heparin cofactor II, protein C, protein S, tissue plasminogen activator, (t-PA) D-dimer and plasminogen activator inhibitor (PAI-1 and PAI-2) activities in normal and gestational diabetes pregnancies were determined. |
| 548 | 9788646 | Thrombin-antithrombin III complexes increased and coagulation inhibitors decreased in gestational diabetes. |
| 549 | 9788646 | Antithrombin III, thrombin-antithrombin III complexes, heparin cofactor II, protein C, protein S, tissue plasminogen activator, (t-PA) D-dimer and plasminogen activator inhibitor (PAI-1 and PAI-2) activities in normal and gestational diabetes pregnancies were determined. |
| 550 | 9788646 | Thrombin-antithrombin III complexes increased and coagulation inhibitors decreased in gestational diabetes. |
| 551 | 9814671 | Since it has been reported that such factors involved in coagulation/fibrinolysis as tissue factor, tissue factor pathway inhibitor (TFPI), thrombin receptor and urokinase receptor are also localized in the caveolae, this membrane structure may act as a special component to regulate coagulation/fibrinolysis on the endothelial membrane surface. |
| 552 | 9814671 | Next we demonstrate the signaling pathway of the thrombin receptor. |
| 553 | 9814671 | We have identified that the signal from the thrombin receptor activates NF-kappaB through the activation of protein C kinase, tyrosine kinase and MAP kinase, and results in proliferation of the cells. |
| 554 | 9814671 | Since it has been reported that such factors involved in coagulation/fibrinolysis as tissue factor, tissue factor pathway inhibitor (TFPI), thrombin receptor and urokinase receptor are also localized in the caveolae, this membrane structure may act as a special component to regulate coagulation/fibrinolysis on the endothelial membrane surface. |
| 555 | 9814671 | Next we demonstrate the signaling pathway of the thrombin receptor. |
| 556 | 9814671 | We have identified that the signal from the thrombin receptor activates NF-kappaB through the activation of protein C kinase, tyrosine kinase and MAP kinase, and results in proliferation of the cells. |
| 557 | 9814671 | Since it has been reported that such factors involved in coagulation/fibrinolysis as tissue factor, tissue factor pathway inhibitor (TFPI), thrombin receptor and urokinase receptor are also localized in the caveolae, this membrane structure may act as a special component to regulate coagulation/fibrinolysis on the endothelial membrane surface. |
| 558 | 9814671 | Next we demonstrate the signaling pathway of the thrombin receptor. |
| 559 | 9814671 | We have identified that the signal from the thrombin receptor activates NF-kappaB through the activation of protein C kinase, tyrosine kinase and MAP kinase, and results in proliferation of the cells. |
| 560 | 9873092 | An ultrasound obtained for evaluation of a prolonged prothrombin time and decreased serum albumin level showed a suspicious nodular lesion in the left lobe of the liver. |
| 561 | 9950260 | The parameters assayed were: prothrombin fragment 1+2 (F1+2), thrombin-antithrombin III complexes (TAT), fibrinopeptide A (FPA), plasmin-alpha2 antiplasmin complexes (PAP) and D-Dimer. |
| 562 | 10073949 | In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37). |
| 563 | 10073949 | PAP was negatively related to factors associated with the insulin resistance syndrome (IRS) (eg, fasting insulin, r=-0.26; body mass index, r=-0.26), possibly reflecting an association with plasminogen activator inhibitor-1 (r=-0.29). |
| 564 | 10073949 | Although our study did not have sufficient power to detect a significant interaction, PAP and AAI appeared to be more weakly associated in subjects with more manifestations of the IRS: PAP appeared more strongly associated with AAI in the subgroup with 0 or 1 metabolic disorders (P</=0.001; slope estimate, -0.14) compared with the subgroup with 2 or more metabolic disorders (P=0.10; slope estimate, -0.08) and in those with non-insulin-dependent diabetes mellitus (P=0.46; slope estimate, -0.04). |
| 565 | 10073949 | Although PAP reflects reactive fibrinolysis and is associated with subclinical atherosclerosis, this relationship may be weaker in populations with characteristics of the IRS, possibly reflecting the inhibitory effects of plasminogen activator inhibitor-1 on PAP. |
| 566 | 10077454 | To clarify the relationship between circulating thrombomodulin (TM) and endothelial cell damage in diabetes mellitus, plasma levels of TM were quantitated by an enzyme linked immunoabsorbant assay (ELISA) in 164 type 2 diabetes mellitus and 72 normal control subjects, and these levels were compared with those of von Willebrand factor antigen (vWf: Ag), thrombin antithrombin III complexes (TAT), plasmin-alpha2-plasmin inhibitor complexes (PIC), fibrinogen, D-dimer, urinary albumin excretion rate (AER), intima-media thickness (IMT) and plaque score of the common carotid artery assessed with high resolution B-mode ultrasonography. |
| 567 | 10077739 | Furthermore, thrombin increased TSP1 mRNA in mesangial and epithelial cells in culture, indicating that thrombin may contribute to elevated TSP1 expression in renal disease. |
| 568 | 10077739 | Thrombin increased TSP1 mRNA within 30 min after treatment which required de novo synthesis of protein. |
| 569 | 10077739 | The thrombin receptor tethered ligand peptide, SFLLRN, increased TSP1 mRNA, indicating that the thrombin-induced increase in TSP1 mRNA was due to direct thrombin receptor (PAR1) stimulation. |
| 570 | 10077739 | Furthermore, thrombin increased TSP1 mRNA in mesangial and epithelial cells in culture, indicating that thrombin may contribute to elevated TSP1 expression in renal disease. |
| 571 | 10077739 | Thrombin increased TSP1 mRNA within 30 min after treatment which required de novo synthesis of protein. |
| 572 | 10077739 | The thrombin receptor tethered ligand peptide, SFLLRN, increased TSP1 mRNA, indicating that the thrombin-induced increase in TSP1 mRNA was due to direct thrombin receptor (PAR1) stimulation. |
| 573 | 10077739 | Furthermore, thrombin increased TSP1 mRNA in mesangial and epithelial cells in culture, indicating that thrombin may contribute to elevated TSP1 expression in renal disease. |
| 574 | 10077739 | Thrombin increased TSP1 mRNA within 30 min after treatment which required de novo synthesis of protein. |
| 575 | 10077739 | The thrombin receptor tethered ligand peptide, SFLLRN, increased TSP1 mRNA, indicating that the thrombin-induced increase in TSP1 mRNA was due to direct thrombin receptor (PAR1) stimulation. |
| 576 | 10098579 | Stepwise regression analysis and Cox proportional hazards model were used to assess the relationship between fistula dysfunction and age, sex, duration of hemodialysis, diabetes mellitus, hematocrit, serum creatinine, blood urea nitrogen, Kt/V, prothrombin time, blood pressure, anticoagulant therapy, dose of erythropoietin, calcium channel blocker therapy, and angiotensin-converting enzyme inhibitor therapy. |
| 577 | 10192656 | Levels of antithrombin decreased during treatment with oestradiol, whereas no changes were seen in levels of fibrinogen, von Willebrand factor, prothrombin fragment 1+2, protein S, protein C or resistance to activated protein C. |
| 578 | 10213277 | Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis. |
| 579 | 10213277 | We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. |
| 580 | 10213277 | Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis. |
| 581 | 10213277 | We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. |
| 582 | 10226869 | PPAR gamma-ligands inhibit migration mediated by multiple chemoattractants in vascular smooth muscle cells. |
| 583 | 10226869 | The purpose of this study was to determine the effect of the peroxisome proliferator-activated receptor gamma-(PPAR gamma) ligands troglitazone (TRO), rosiglitazone (RSG), and 15-deoxy-delta prostaglandin J2 (15d-PGJ2) on vascular smooth muscle cell (VSMC) migration directed by multiple chemoattractants. |
| 584 | 10226869 | Migration of rat aortic VSMCs was induced 5.4-fold by PDGF, 4.6-fold by thrombin, and 2.3-fold by insulin-like growth factor I (IGF-I; all values of p < 0.05). |
| 585 | 10226869 | The PPAR gamma ligands 15d-PGJ2, RSG, or TRO all inhibited VSMC migration with the following order of potency: 15d-PGJ2 > RSG > TRO. |
| 586 | 10226869 | Inhibition of MAPK signaling with PD98059 completely blocked PDGF-, thrombin-, and IGF-I-induced migration. |
| 587 | 10226869 | PPAR gamma ligands did not inhibit MAPK activation, suggesting a nuclear effect of these ligands downstream of MAPK. |
| 588 | 10226869 | We conclude that PPAR gamma ligands are potent inhibitors of VSMC migration pathways, dependent on MAPK and nuclear events. |
| 589 | 10226869 | PPAR gamma ligands act downstream of the cytoplasmic activation of MAPK and appear to exert their effects in the nucleus. |
| 590 | 10226869 | Because VSMC migration plays an important role in the formation of atherosclerotic lesions and restenosis, PPAR gamma ligands like TRO and RSG, which ameliorate insulin resistance in humans, also may protect the vasculature from diabetes-enhanced injury. |
| 591 | 10226869 | PPAR gamma-ligands inhibit migration mediated by multiple chemoattractants in vascular smooth muscle cells. |
| 592 | 10226869 | The purpose of this study was to determine the effect of the peroxisome proliferator-activated receptor gamma-(PPAR gamma) ligands troglitazone (TRO), rosiglitazone (RSG), and 15-deoxy-delta prostaglandin J2 (15d-PGJ2) on vascular smooth muscle cell (VSMC) migration directed by multiple chemoattractants. |
| 593 | 10226869 | Migration of rat aortic VSMCs was induced 5.4-fold by PDGF, 4.6-fold by thrombin, and 2.3-fold by insulin-like growth factor I (IGF-I; all values of p < 0.05). |
| 594 | 10226869 | The PPAR gamma ligands 15d-PGJ2, RSG, or TRO all inhibited VSMC migration with the following order of potency: 15d-PGJ2 > RSG > TRO. |
| 595 | 10226869 | Inhibition of MAPK signaling with PD98059 completely blocked PDGF-, thrombin-, and IGF-I-induced migration. |
| 596 | 10226869 | PPAR gamma ligands did not inhibit MAPK activation, suggesting a nuclear effect of these ligands downstream of MAPK. |
| 597 | 10226869 | We conclude that PPAR gamma ligands are potent inhibitors of VSMC migration pathways, dependent on MAPK and nuclear events. |
| 598 | 10226869 | PPAR gamma ligands act downstream of the cytoplasmic activation of MAPK and appear to exert their effects in the nucleus. |
| 599 | 10226869 | Because VSMC migration plays an important role in the formation of atherosclerotic lesions and restenosis, PPAR gamma ligands like TRO and RSG, which ameliorate insulin resistance in humans, also may protect the vasculature from diabetes-enhanced injury. |
| 600 | 10331423 | Measured were plasma activated factor VII activity (FVIIa), FVII coagulant (FVIIC) activity, FVIII coagulant (FVIIIC) activity, tissue factor pathway inhibitor (TFPI) antigen, and thrombin markers; and serum glucose, insulin, and electrolytes. |
| 601 | 10422516 | Hypofibrinolysis caused by increased PAI-1 levels in patients with insulin resistance (IR) is one of the most common acquired prothrombotic states with higher risk of arterial thrombosis associated with atherosclerosis. |
| 602 | 10422516 | Vascular compartment, including mainly endothelium, is sensitive on thrombin, angiotensin IV, cytokines, biological active lipids and oxidative stress effect, while insulin inhibits cytokine induced PAI-1 production on contrary. |
| 603 | 10442089 | Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine, thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca2+. |
| 604 | 10468143 | Recent studies have shown that patients with the 20210 A prothrombin mutation display remarkably similar characteristics compared with patients with Factor V Leiden mutation. |
| 605 | 10468143 | It is evident that neither the Factor V Leiden mutation nor the 20210 A prothrombin mutation is a major risk factor for myocardial infarction or stroke, unless accompanied by other classical risk factors, including diabetes mellitus, hypertension and smoking. |
| 606 | 10468143 | Recent studies have shown that patients with the 20210 A prothrombin mutation display remarkably similar characteristics compared with patients with Factor V Leiden mutation. |
| 607 | 10468143 | It is evident that neither the Factor V Leiden mutation nor the 20210 A prothrombin mutation is a major risk factor for myocardial infarction or stroke, unless accompanied by other classical risk factors, including diabetes mellitus, hypertension and smoking. |
| 608 | 10517305 | Blood VK status of the low VK intake group tended to be poorer than that of the high intake group (median of 5 samples: prothrombin time; 12.5 vs 12.2s and protein-induced VK absence-factor-II; 23 vs 15 mAU/ml), but fasting plasma glucose status was not markedly different between both groups: [plasma glucose (PG); 87 vs 86 mg/dl, immunoreactive insulin (IRI); 6.7 vs 5.3 microU/ml, HbA1c; 4.8 vs 4.9%]. |
| 609 | 10540156 | In addition, these antibody findings were studied for associations with prothrombin degradation products, activated factor VII and activated protein C, and with the incidence of diabetic complications. |
| 610 | 10578022 | In all patients levels of total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol, lipoprotein (a) (Lpa) C reactive protein (CRP), fibrinogen, thrombin/antithrombin III complex (TAT), plasminogen activator inhibitor type 1(PAI-1), tissue plasminogen activator (t-PA) and von Willebrand antigen were measured. |
| 611 | 10578022 | After H. pylori eradication, the levels of CRP and TAT decreased (48+/-0.7 ng/l vs 3.3+/-0.4 ng/l;P << 0.05), (27.7+/-44.7 microg/ml vs 2.1+/-1.4 microg/ml, P << 0.05), respectively. |
| 612 | 10578022 | Eradication of H. pylori infection in type 1 diabetic patients modifies some parameters of lipid and haemostasis patterns, (increase of HDL-cholesterol, reduction of Lpa and decrease of CRP and TAT) and so contributes to improvement of cardiovascular risk factors in these patients. |
| 613 | 10589686 | In addition, thrombin, which may play a role in the progression of renal disease, increased Sgk message in cell culture. |
| 614 | 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). |
| 615 | 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. |
| 616 | 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). |
| 617 | 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. |
| 618 | 10805277 | In all subjects, the frequency by which hemostatic markers exceeded their upper limit of normal range was 35.9% for thrombin-antithrombin HI complex (> or = 3.7 ng/ml), 38.3% for soluble fibrin monomer (> or = 4.0 microg/ml), 41.8% for D-dimer (> or = 1.0 microg/ml), 49.0% for plasmin-alpha2 plasmin inhibitor complex (> or = 1.0 microg/ml), and 53.7% for thrombomodulin (> or = 20 ng/ml). |
| 619 | 10808060 | To critically evaluate the relative importance of coagulation abnormalities over other clinical variables for micro- and macrovascular diabetic complications, prothrombin fragment (F1+2), thrombin-antithrombin III complex (TAT), fibrin degradation product d-dimer, and alpha2 plasmin inhibitor complex were determined in 101 stable, relatively well controlled patients with Type 2 diabetes (the mean HbA1c, age and duration of diabetes, 7.1%, 61 and 7.5 years, respectively). |
| 620 | 10870477 | Prevalence of prothrombin 20210A allele and methylenetetrahydrofolate reductase C677T genetic mutations in the Chinese population. |
| 621 | 10870477 | We suggested that the Chinese race dose not have the prothrombin 20210A allele, but can carry the 677 C-->T mutation of the methylenetetrahydrofolate reductase gene. |
| 622 | 10870477 | Prevalence of prothrombin 20210A allele and methylenetetrahydrofolate reductase C677T genetic mutations in the Chinese population. |
| 623 | 10870477 | We suggested that the Chinese race dose not have the prothrombin 20210A allele, but can carry the 677 C-->T mutation of the methylenetetrahydrofolate reductase gene. |
| 624 | 10899350 | As changes in coagulation parameters, the data indicated significant increases in factors II, V, VII, VIII, IX, X, and XII activities; a significant decrease in antithrombin III activity in rats more than 6 months of age; significant increases in fibrinogen level and factor XI activity; and significant decreases in prothrombin time and activated partial thromboplastin time in those more than 9 months of age. |
| 625 | 10910004 | Furthermore, EPA-E significantly and dose-dependently ameliorated coagulation-related parameters, including the prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen level, and factor II, V, VII, VIII, IX, X, XI, and XII and antithrombin III (AT III) activities, and fibrinolysis-related parameters, including plasminogen, tissue-type plasminogen activator (t-PA), alpha2-plasmin inhibitor (alpha2-PI), and plasminogen activator inhibitor (PAI), and also suppressed ADP- or collagen-induced platelet aggregation and the cholesterol to phospholipid (C/P) molar ratio in platelet membranes at a dose of 0.1 g/kg or higher. |
| 626 | 10976915 | Regulation of myosin-bound protein phosphatase by insulin in vascular smooth muscle cells: evaluation of the role of Rho kinase and phosphatidylinositol-3-kinase-dependent signaling pathways. |
| 627 | 10976915 | Insulin-mediated MBP activation was accompanied by a rapid time-dependent reduction in the phosphorylation state of the myosin-bound regulatory subunit (MBS) of MBP. |
| 628 | 10976915 | The decrease observed in MBS phosphorylation was due to insulin-induced inhibition of Rho kinase activity. |
| 629 | 10976915 | Insulin also prevented a thrombin-mediated increase in Rho kinase activation and abolished the thrombin-induced increase in MBS phosphorylation and MBP inactivation. |
| 630 | 10976915 | These data are consistent with the notion that insulin inactivates Rho kinase and decreases MBS phosphorylation to activate MBP in VSMCs. |
| 631 | 10976915 | Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation. |
| 632 | 10976915 | We conclude that insulin stimulates MBP via its regulatory subunit, MBS partly by inactivating Rho kinase and stimulating NO/cGMP signaling via PI3-kinase as part of a complex signaling network that controls 20-kDa myosin light chain (MLC20) phosphorylation and VSMC contraction. |
| 633 | 10989319 | Elevation of fibrinogen and thrombin-antithrombin III complex levels of type 2 diabetes mellitus patients with retinopathy and nephropathy. |
| 634 | 10989319 | Thrombin-antithrombin III complex (TAT) and fibrinogen levels are parameters of coagulation and fibrinolysis. |
| 635 | 10989319 | Elevation of fibrinogen and thrombin-antithrombin III complex levels of type 2 diabetes mellitus patients with retinopathy and nephropathy. |
| 636 | 10989319 | Thrombin-antithrombin III complex (TAT) and fibrinogen levels are parameters of coagulation and fibrinolysis. |
| 637 | 11059059 | At univariate analysis, activated protein C resistance (odds ratio 5.8) and factor V Leiden (odds ratio 4.4) were significantly associated with central retinal vein occlusion whereas G20210A polymorphism of the prothrombin gene was not. |
| 638 | 11078228 | Thrombomodulin is an endothelial glycoprotein that decreases thrombin activity and activates protein C. |
| 639 | 11083070 | The plasma levels of tissue-type plasminogen activator antigen (t-PA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) were measured by ELISA. |
| 640 | 11120454 | Univariate analyses showed that in all patients, age at examination, duration of diabetes, thrombin-antithrombin III complex (TAT) level, fibrinogen level, lipoprotein (a) (Lp(a)) level, total cholesterol (T-Chol) level, and existence of microagiopathy were risk factors for PVD. |
| 641 | 11247757 | We found that thrombin- and collagen-induced increases in [Ca(2+)](i) and aggregation were not acutely affected by high glucose concentrations of 45 mM. |
| 642 | 11257274 | Thrombomodulin is an important endothelial anticoagulant protein that decreases thrombin activity and activates protein C. |
| 643 | 11257732 | Thrombomodulin--endothelial thrombin receptor in blood of patients with unstable angina pectoris. |
| 644 | 11302472 | Soluble P-selectin, von Willebrand factor antigen and markers of thrombin generation in plasma were determined by immunoassays, and platelet P-selectin expression (unstimulated and agonist-stimulated) by flow cytometry in whole blood. |
| 645 | 11302472 | Plasma levels of von Willebrand factor and thrombin generation were similar in patients and controls, and were not altered by hyperglycemia. |
| 646 | 11302472 | Soluble P-selectin, von Willebrand factor antigen and markers of thrombin generation in plasma were determined by immunoassays, and platelet P-selectin expression (unstimulated and agonist-stimulated) by flow cytometry in whole blood. |
| 647 | 11302472 | Plasma levels of von Willebrand factor and thrombin generation were similar in patients and controls, and were not altered by hyperglycemia. |
| 648 | 11317648 | All individuals in the three study groups have normal platelet count, thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (aPTT), clot retraction, Factor VIII activity (FVIIIc) and von Willebrand factor antigen (vWAg). |
| 649 | 11317648 | Bleeding diathesis is a new additional feature to the clinical spectrum of WS, which is probably a feature of the disorder WFS2 and not WFS1, as bleeding has never been reported in the latter. |
| 650 | 11415460 | We have previously shown that unsaturated fatty acids amplify platelet-derived-growth-factor (PDGF)-induced protein kinase C (PKC) activation in vascular smooth-muscle cells (VSMCs). |
| 651 | 11415460 | Fractionation of VSMC extracts demonstrated that the DGK alpha isoform was the major DGK activity present. |
| 652 | 11415460 | PDGF markedly increased the DGK activity of cultured cells. |
| 653 | 11415460 | An inhibitor selective for the DGK alpha isoform, R59949 [3-[2-[4-(bis-(4-fluorophenyl)methylene]piperidin-1-yl)ethyl]-2,3-dihydro-2-thioxo-4(1H)-quinazolinone], abolished the growth-factor-induced increase in DGK activity, but had little effect on basal activity. |
| 654 | 11415460 | PDGF thus selectively activates DGKalpha. |
| 655 | 11415460 | Epidermal growth factor and alpha-thrombin stimulated total DGK activity similarly to PDGF. |
| 656 | 11415460 | Activation by epidermal growth factor was sensitive to R59949, again suggesting involvement of DGKalpha. |
| 657 | 11509551 | Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle. |
| 658 | 11509551 | Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L. |
| 659 | 11509551 | In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation. |
| 660 | 11509551 | Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation. |
| 661 | 11509551 | Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation. |
| 662 | 11509551 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695). |
| 663 | 11509551 | Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP. |
| 664 | 11509551 | Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS. |
| 665 | 11509551 | Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle. |
| 666 | 11509551 | Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L. |
| 667 | 11509551 | In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation. |
| 668 | 11509551 | Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation. |
| 669 | 11509551 | Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation. |
| 670 | 11509551 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695). |
| 671 | 11509551 | Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP. |
| 672 | 11509551 | Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS. |
| 673 | 11509551 | Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle. |
| 674 | 11509551 | Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L. |
| 675 | 11509551 | In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation. |
| 676 | 11509551 | Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation. |
| 677 | 11509551 | Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation. |
| 678 | 11509551 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695). |
| 679 | 11509551 | Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP. |
| 680 | 11509551 | Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS. |
| 681 | 11509551 | Selected contribution: insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle. |
| 682 | 11509551 | Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L. |
| 683 | 11509551 | In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway may inactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBS(Thr695)) of MBP and in its activation. |
| 684 | 11509551 | Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases in membrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBS(Thr695) of MBP and caused MBP activation. |
| 685 | 11509551 | Preexposure to N(G)-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio)cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBS(Thr695) phosphorylation, resulting in MBP inactivation. |
| 686 | 11509551 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylation of MBS(Thr695). |
| 687 | 11509551 | Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBS(Thr695) phosphorylation and caused insulin activation of MBP. |
| 688 | 11509551 | Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS. |
| 689 | 11558626 | Thrombomodulin is a glycoprotein that can bind to thrombin and activate protein C, thus mitigating the effects of cytokines produced by inflammatory and immunological processes. |
| 690 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 691 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 692 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 693 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 694 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 695 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 696 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 697 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 698 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 699 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 700 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 701 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 702 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 703 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 704 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 705 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 706 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 707 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 708 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 709 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 710 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 711 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 712 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 713 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 714 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 715 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 716 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 717 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 718 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 719 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 720 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 721 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 722 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 723 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 724 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 725 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 726 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 727 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 728 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 729 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 730 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 731 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 732 | 11606309 | Thrombin-induced platelet endostatin release is blocked by a proteinase activated receptor-4 (PAR4) antagonist. |
| 733 | 11606309 | Endostatin is a potent endogenous inhibitor of angiogenesis that was recently shown to be stored in platelets and released in response to thrombin, but not ADP. |
| 734 | 11606309 | In the present study, we have tested the hypothesis that thrombin-induced endostatin release from rat platelets is mediated via proteinase-activated receptor-4 (PAR4). |
| 735 | 11606309 | Aggregation and release of endostatin could be elicited by thrombin (0.5 - 1.0 U ml(-1)) or by specific PAR4 agonist (AYPGKF-NH(2); AY-NH(2); 15 - 50 microM). |
| 736 | 11606309 | Significant release of endostatin could be induced by a dose of thrombin below that necessary for induction of aggregation. |
| 737 | 11606309 | In contrast, a selective PAR4 antagonist (trans-cinnamoyl-YPGKF-NH(2); tcY-NH(2)) prevented endostatin release and aggregation induced by thrombin or by AY-NH(2). |
| 738 | 11606309 | We conclude that thrombin-induced endostatin release from rat platelets is PAR4-mediated via an ADP-independent mechanism that can occur independently of platelet aggregation. |
| 739 | 11739083 | IGFBP-3 binding to endothelial cells inhibits plasmin and thrombin proteolysis. |
| 740 | 11739083 | Insulin-like growth factor-binding protein (IGFBP)-3 contains a highly basic COOH-terminal heparin-binding region, the P3 region, which is thought to be important in the binding of IGFBP-3 to endothelial cells. |
| 741 | 11739083 | IGFBP-3 and IGFBP-4, and their chimeras IGFBP-3(4) and IGFBP-4(3), were treated with plasmin and with thrombin, proteases known to cleave IGFBP-3. |
| 742 | 11739083 | IGFBP-3 was highly susceptible to plasmin, whereas IGFBP-4 was less so. |
| 743 | 11739083 | Substitution of the P3 region for the P4 region in IGFBP-4 (IGFBP-4(3)) increased the ability of the protease to digest IGFBP-4(3); substitution of the P4 region for the P3 region in IGFBP-3 (IGFBP-3(4)) decreased the digestion of IGFBP-3(4). |
| 744 | 11739083 | When 125I-labeled IGFBP-3 or 125I-IGFBP-4(3) was first bound to vascular endothelial cells, subsequent proteolysis by either plasmin or thrombin was substantially inhibited. |
| 745 | 11739083 | We conclude that the P3 region is central to proteolysis of IGFBP-3 by plasmin and thrombin, processes which were inhibited by association of IGFBP-3 with endothelial cells. |
| 746 | 11739083 | IGFBP-3 binding to endothelial cells inhibits plasmin and thrombin proteolysis. |
| 747 | 11739083 | Insulin-like growth factor-binding protein (IGFBP)-3 contains a highly basic COOH-terminal heparin-binding region, the P3 region, which is thought to be important in the binding of IGFBP-3 to endothelial cells. |
| 748 | 11739083 | IGFBP-3 and IGFBP-4, and their chimeras IGFBP-3(4) and IGFBP-4(3), were treated with plasmin and with thrombin, proteases known to cleave IGFBP-3. |
| 749 | 11739083 | IGFBP-3 was highly susceptible to plasmin, whereas IGFBP-4 was less so. |
| 750 | 11739083 | Substitution of the P3 region for the P4 region in IGFBP-4 (IGFBP-4(3)) increased the ability of the protease to digest IGFBP-4(3); substitution of the P4 region for the P3 region in IGFBP-3 (IGFBP-3(4)) decreased the digestion of IGFBP-3(4). |
| 751 | 11739083 | When 125I-labeled IGFBP-3 or 125I-IGFBP-4(3) was first bound to vascular endothelial cells, subsequent proteolysis by either plasmin or thrombin was substantially inhibited. |
| 752 | 11739083 | We conclude that the P3 region is central to proteolysis of IGFBP-3 by plasmin and thrombin, processes which were inhibited by association of IGFBP-3 with endothelial cells. |
| 753 | 11739083 | IGFBP-3 binding to endothelial cells inhibits plasmin and thrombin proteolysis. |
| 754 | 11739083 | Insulin-like growth factor-binding protein (IGFBP)-3 contains a highly basic COOH-terminal heparin-binding region, the P3 region, which is thought to be important in the binding of IGFBP-3 to endothelial cells. |
| 755 | 11739083 | IGFBP-3 and IGFBP-4, and their chimeras IGFBP-3(4) and IGFBP-4(3), were treated with plasmin and with thrombin, proteases known to cleave IGFBP-3. |
| 756 | 11739083 | IGFBP-3 was highly susceptible to plasmin, whereas IGFBP-4 was less so. |
| 757 | 11739083 | Substitution of the P3 region for the P4 region in IGFBP-4 (IGFBP-4(3)) increased the ability of the protease to digest IGFBP-4(3); substitution of the P4 region for the P3 region in IGFBP-3 (IGFBP-3(4)) decreased the digestion of IGFBP-3(4). |
| 758 | 11739083 | When 125I-labeled IGFBP-3 or 125I-IGFBP-4(3) was first bound to vascular endothelial cells, subsequent proteolysis by either plasmin or thrombin was substantially inhibited. |
| 759 | 11739083 | We conclude that the P3 region is central to proteolysis of IGFBP-3 by plasmin and thrombin, processes which were inhibited by association of IGFBP-3 with endothelial cells. |
| 760 | 11739083 | IGFBP-3 binding to endothelial cells inhibits plasmin and thrombin proteolysis. |
| 761 | 11739083 | Insulin-like growth factor-binding protein (IGFBP)-3 contains a highly basic COOH-terminal heparin-binding region, the P3 region, which is thought to be important in the binding of IGFBP-3 to endothelial cells. |
| 762 | 11739083 | IGFBP-3 and IGFBP-4, and their chimeras IGFBP-3(4) and IGFBP-4(3), were treated with plasmin and with thrombin, proteases known to cleave IGFBP-3. |
| 763 | 11739083 | IGFBP-3 was highly susceptible to plasmin, whereas IGFBP-4 was less so. |
| 764 | 11739083 | Substitution of the P3 region for the P4 region in IGFBP-4 (IGFBP-4(3)) increased the ability of the protease to digest IGFBP-4(3); substitution of the P4 region for the P3 region in IGFBP-3 (IGFBP-3(4)) decreased the digestion of IGFBP-3(4). |
| 765 | 11739083 | When 125I-labeled IGFBP-3 or 125I-IGFBP-4(3) was first bound to vascular endothelial cells, subsequent proteolysis by either plasmin or thrombin was substantially inhibited. |
| 766 | 11739083 | We conclude that the P3 region is central to proteolysis of IGFBP-3 by plasmin and thrombin, processes which were inhibited by association of IGFBP-3 with endothelial cells. |
| 767 | 11739394 | Active Rho kinase (ROK-alpha ) associates with insulin receptor substrate-1 and inhibits insulin signaling in vascular smooth muscle cells. |
| 768 | 11739394 | Recent studies from our laboratory have shown that insulin stimulates myosin-bound phosphatase (MBP) in vascular smooth muscle cells (VSMCs) by decreasing site-specific phosphorylation of the myosin-bound subunit (MBS) of MBP via nitric oxide/cGMP-mediated Rho/Rho kinase inactivation. |
| 769 | 11739394 | Here we tested potential interactions between Rho kinase and insulin signaling pathways. |
| 770 | 11739394 | In control VSMCs, insulin inactivates ROK-alpha, the major Rho kinase isoform in VSMCs, and inhibits thrombin-induced increase in ROK-alpha association with the insulin receptor substrate-1 (IRS-1). |
| 771 | 11739394 | Hypertension (in spontaneous hypertensive rats) or expression of an active RhoA(V14) up-regulates Rho kinase activity and increases ROK-alpha/IRS-1 association resulting in IRS-1 serine phosphorylation that leads to inhibition of both insulin-induced IRS-1 tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3-kinase) activation. |
| 772 | 11739394 | In contrast, expression of dominant negative RhoA or cGMP-dependent protein kinase type I alpha inactivates Rho kinase, abolishes ROK-alpha/IRS-1 association, and potentiates insulin-induced tyrosine phosphorylation and PI3-kinase activation leading to decreased MBS(T695) phosphorylation and decreased MBP inhibition. |
| 773 | 11739394 | Collectively, these results suggest a novel function for ROK-alpha in insulin signal transduction at the level of IRS-1 and potential cross-talk between cGMP-dependent protein kinase type I alpha, Rho/Rho kinase signaling, and insulin signaling at the level of IRS-1/PI3-kinase. |
| 774 | 11796180 | The fibrinogen and thrombin-antithrombin III complex (TAT) levels significantly correlated with VFA only in the female patients. |
| 775 | 11805236 | We have identified two peptides, FSLLRY-NH(2) (FSY-NH(2)) and LSIGRL-NH(2) (LS-NH(2)) that block the ability of trypsin to activate PAR(2) either in PAR(2)-expressing Kirsten virus-transformed kidney (KNRK) cell lines or in a rat aorta ring preparation. |
| 776 | 11805236 | The reverse PAR(2) peptide, LRGILS-NH(2) (LRG-NH(2)) did not do so and FSY-NH(2) failed to block thrombin activation of PAR(1) in the aorta ring or in PAR(1)-expressing human embryonic kidney cells. |
| 777 | 11805236 | Half-maximal inhibition (IC(50)) by FSY-NH(2) and LS-NH(2) of the activation of PAR(2) by trypsin in a PAR(2) KNRK calcium-signaling assay was observed at about 50 and 200 microM, respectively. |
| 778 | 11805236 | In contrast, the activation of PAR(2) by the PAR(2)-activating peptide, SLIGRL-NH(2) (SL-NH(2)) was not inhibited by FSY-NH(2), LS-NH(2), or LRG-NH(2). |
| 779 | 11805236 | In addition, FSY-NH(2) and LS-NH(2) were unable to prevent trypsin from hydrolyzing a 20-amino acid peptide, GPNSKGR/SLIGRLDTPYGGC representing the trypsin cleavage/activation site of rat PAR(2). |
| 780 | 11805236 | Similarly, FSY-NH(2) and LS-NH(2) failed to block the ability of trypsin to release the PAR(2) N-terminal epitope that is cleaved from the receptor upon proteolytic activation of receptor-expressing KNRK cells. |
| 781 | 11805236 | We conclude that the peptides FSY-NH(2) and LS-NH(2) block the ability of trypsin to activate PAR(2) by a mechanism that does not involve a simple inhibition of trypsin proteolytic activity, but possibly by interacting with a tethered ligand receptor-docking site. |
| 782 | 11836301 | Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients. |
| 783 | 11836301 | Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma. |
| 784 | 11836301 | The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate). |
| 785 | 11836301 | This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance. |
| 786 | 11836301 | Insulin resistance is associated with increased circulating level of thrombin-activatable fibrinolysis inhibitor in type 2 diabetic patients. |
| 787 | 11836301 | Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI) has been isolated and characterized from human plasma. |
| 788 | 11836301 | The plasma levels of TAFI were independently and significantly correlated with glucose intolerance (HbA(1c)), with obesity (BMI, visceral fat area), and with an indicator of insulin resistance (glucose infusion rate). |
| 789 | 11836301 | This study showed that increased circulating level of TAFI may be an important causative factor of hypofibrinolysis in patients with type 2 diabetes, obesity and insulin resistance. |
| 790 | 11848462 | Thrombomodulin is an endothelial cell surface receptor for thrombin. |
| 791 | 11861803 | Close relationship between the platelet activation marker CD62 and the granular release of platelet-derived growth factor. |
| 792 | 11861803 | We characterized the relationship between CD62 expression and platelet-derived growth factor (PDGF)(AB) and PDGF(BB) secretion in response to thrombin-receptor activating peptide (TRAP). |
| 793 | 11861803 | The principal findings were 1) expression of CD62 as a constituent of platelet alpha-granule membrane and secretion of PDGF, an important ingredient of alpha-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion. |
| 794 | 11861803 | Although CD62 is perceived as an activation marker of platelets indicating enhanced aggregability and secretion of alpha-granular content, the proof that the CD62 status and its modifications reflect directly the actual secretion of the most important platelet mitogen, PDGF, has so far not been given. |
| 795 | 11861803 | This ex vivo-in vitro study shows that at least for the activation pathway provided by the PAR-1 receptor for which TRAP is the selective agonist, CD62 expression on platelets could be a surrogate for their secretory activity. |
| 796 | 11889219 | Insulin inhibits the pro-inflammatory transcription factor early growth response gene-1 (Egr)-1 expression in mononuclear cells (MNC) and reduces plasma tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) concentrations. |
| 797 | 11889219 | We have recently demonstrated that an infusion of a low dose of insulin reduces the intranuclear NF-kappa B (a pro-inflammatory transcription factor) content in MNC while also reducing the plasma concentration of NF-kappa B dependent pro-inflammatory cytokines and adhesion molecules. |
| 798 | 11889219 | We have now tested the effect of insulin on the pro-inflammatory transcription factor, early growth response-1 (Egr-1) and plasma concentration of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1), two major proteins whose expression is modulated by Egr-1. |
| 799 | 11889219 | PAI-1 levels (basal = 100%) decreased significantly after insulin infusion at 2 h (57 +/- 6.7% of the basal level) and at 4 h (58 +/- 8.3% of the basal level; P<0.001). |
| 800 | 11889219 | Thus, insulin reduces intranuclear Egr-1 and the expression of TF and PAI-1. |
| 801 | 11889219 | These data provide further evidence that insulin has an anti-inflammatory effect including the inhibition of TF and PAI-1 expression. |
| 802 | 11889219 | These effects suggest a potential beneficial effect of insulin in thrombin formation and fibrinolysis in atherothrombosis. |
| 803 | 11919159 | RhoA- and RhoD-dependent regulatory switch of Galpha subunit signaling by PAR-1 receptors in cellular invasion. |
| 804 | 11919159 | We recently reported that thrombin inhibits cellular invasion induced by src, hepatocyte growth factor (HGF), and leptin in kidney and colonic epithelial cells via predominant activation of the pertussis toxin (PTx) -sensitive G-proteins Galphao/Galphai. |
| 805 | 11919159 | We provide pharmacological and biochemical evidence that in the presence of PTx, PAR-1 induced cellular invasion through Galpha12/Galpha13- and RhoA/Rho kinase (ROCK) -dependent signaling. |
| 806 | 11919159 | However, inhibition of the endogenous small GTPase RhoA by the C3 exoenzyme, dominant-negative N19-RhoA, activated G26V-RhoD, and activators of the nitric oxide/cGMP pathways conferred invasive activity to PAR-1 via a signaling cascade using Galphaq, phospholipase C (PLC), Ca(2+)/calmodulin myosin light chain kinase (CaM-MLCK), and phosphorylation of MLC. |
| 807 | 11919159 | Our data demonstrate that the RhoA and RhoD small GTPases are acting as a molecular switch of cellular invasion and reveal a novel critical mechanism by which PAR-1 bypass Galphao/i and RhoA inhibition via differential coupling to heterotrimeric G-proteins linked to divergent or convergent biological responses. |
| 808 | 11919159 | We conclude that dynamic regulation of Rho GTPases activation and inactivation by oncogenes, growth factors, cGMP-inducing agents, and adhesion molecules can initiate convergent invasion signals controlled by the thrombin PAR-1 in cancer cells. |
| 809 | 11919159 | RhoA- and RhoD-dependent regulatory switch of Galpha subunit signaling by PAR-1 receptors in cellular invasion. |
| 810 | 11919159 | We recently reported that thrombin inhibits cellular invasion induced by src, hepatocyte growth factor (HGF), and leptin in kidney and colonic epithelial cells via predominant activation of the pertussis toxin (PTx) -sensitive G-proteins Galphao/Galphai. |
| 811 | 11919159 | We provide pharmacological and biochemical evidence that in the presence of PTx, PAR-1 induced cellular invasion through Galpha12/Galpha13- and RhoA/Rho kinase (ROCK) -dependent signaling. |
| 812 | 11919159 | However, inhibition of the endogenous small GTPase RhoA by the C3 exoenzyme, dominant-negative N19-RhoA, activated G26V-RhoD, and activators of the nitric oxide/cGMP pathways conferred invasive activity to PAR-1 via a signaling cascade using Galphaq, phospholipase C (PLC), Ca(2+)/calmodulin myosin light chain kinase (CaM-MLCK), and phosphorylation of MLC. |
| 813 | 11919159 | Our data demonstrate that the RhoA and RhoD small GTPases are acting as a molecular switch of cellular invasion and reveal a novel critical mechanism by which PAR-1 bypass Galphao/i and RhoA inhibition via differential coupling to heterotrimeric G-proteins linked to divergent or convergent biological responses. |
| 814 | 11919159 | We conclude that dynamic regulation of Rho GTPases activation and inactivation by oncogenes, growth factors, cGMP-inducing agents, and adhesion molecules can initiate convergent invasion signals controlled by the thrombin PAR-1 in cancer cells. |
| 815 | 11965826 | Other factors in patients with type 2 diabetes include alterations in serum fibrinogen, PAI-1, tissue-type plasminogen activator (tPa) and factors V, II and VII, which have all been linked to the risk of myocardial infarction. |
| 816 | 11965826 | Increased D-dimer, von Willebrand factor (vWf) antigen, A-II anti-plasmin and decreased anti-thrombin III were also reported in patients with type 2 diabetes. |
| 817 | 12031965 | In this study, the hypothesis that a specific thrombin inhibitor, Melagatran, could reduce IBMIR in an in vitro model in which human islets are exposed to ABO-compatible blood was tested. |
| 818 | 12062538 | A high fibrinogen level was not associated with other markers of hypercoagulability, Thrombin-Antithrombin (TAT), Prothrombin Fragment 1+2 (F 1+2) and D-dimer although the latter three correlated with each other. |
| 819 | 12062538 | There was also a correlation between von Willebrand antigen (vWF) and CRP, also in this case the relationship was dependent on the findings in patients with diabetes. |
| 820 | 12086958 | Recent studies from our laboratory have shown that insulin induces relaxation of vascular smooth muscle cells (VSMCs) via stimulation of myosin phosphatase and inhibition of Rho kinase activity. |
| 821 | 12086958 | In this study, we examined the mechanism whereby insulin inhibits Rho signaling and its impact on actin cytoskeleton organization. |
| 822 | 12086958 | Incubation of confluent serum-starved VSMCs with thrombin or phenylephrine (PE) caused a rapid increase in glutathione S-transferase-Rhotekin-Rho binding domain-associated RhoA, Rho kinase activation, and actin cytoskeleton organization, which was blocked by preincubation with insulin. |
| 823 | 12086958 | Preexposure to N(G)-monomethyl L-arginine acetate (L-NMMA), a nitric oxide synthase inhibitor, and Rp-8 CPT-cyclic guanosine monophosphate (RpcGMP), a cyclic guanosine monophosphate (cGMP) antagonist, attenuated the inhibitory effect of insulin on RhoA activation and restored thrombin-induced Rho kinase activation, and site-specific phosphorylation of the myosin-bound regulatory subunit (MBS(Thr695)) of myosin-bound phosphatase (MBP), and caused actin fiber reorganization. |
| 824 | 12086958 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked the inhibitory effects of insulin and abolished thrombin-mediated Rho activation. |
| 825 | 12086958 | We conclude that insulin may inhibit Rho signaling by affecting posttranslational modification of RhoA via nitric oxide/cGMP signaling pathway to cause MBP activation, actin cytoskeletal disorganization, and vasodilation. |
| 826 | 12086958 | Recent studies from our laboratory have shown that insulin induces relaxation of vascular smooth muscle cells (VSMCs) via stimulation of myosin phosphatase and inhibition of Rho kinase activity. |
| 827 | 12086958 | In this study, we examined the mechanism whereby insulin inhibits Rho signaling and its impact on actin cytoskeleton organization. |
| 828 | 12086958 | Incubation of confluent serum-starved VSMCs with thrombin or phenylephrine (PE) caused a rapid increase in glutathione S-transferase-Rhotekin-Rho binding domain-associated RhoA, Rho kinase activation, and actin cytoskeleton organization, which was blocked by preincubation with insulin. |
| 829 | 12086958 | Preexposure to N(G)-monomethyl L-arginine acetate (L-NMMA), a nitric oxide synthase inhibitor, and Rp-8 CPT-cyclic guanosine monophosphate (RpcGMP), a cyclic guanosine monophosphate (cGMP) antagonist, attenuated the inhibitory effect of insulin on RhoA activation and restored thrombin-induced Rho kinase activation, and site-specific phosphorylation of the myosin-bound regulatory subunit (MBS(Thr695)) of myosin-bound phosphatase (MBP), and caused actin fiber reorganization. |
| 830 | 12086958 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked the inhibitory effects of insulin and abolished thrombin-mediated Rho activation. |
| 831 | 12086958 | We conclude that insulin may inhibit Rho signaling by affecting posttranslational modification of RhoA via nitric oxide/cGMP signaling pathway to cause MBP activation, actin cytoskeletal disorganization, and vasodilation. |
| 832 | 12086958 | Recent studies from our laboratory have shown that insulin induces relaxation of vascular smooth muscle cells (VSMCs) via stimulation of myosin phosphatase and inhibition of Rho kinase activity. |
| 833 | 12086958 | In this study, we examined the mechanism whereby insulin inhibits Rho signaling and its impact on actin cytoskeleton organization. |
| 834 | 12086958 | Incubation of confluent serum-starved VSMCs with thrombin or phenylephrine (PE) caused a rapid increase in glutathione S-transferase-Rhotekin-Rho binding domain-associated RhoA, Rho kinase activation, and actin cytoskeleton organization, which was blocked by preincubation with insulin. |
| 835 | 12086958 | Preexposure to N(G)-monomethyl L-arginine acetate (L-NMMA), a nitric oxide synthase inhibitor, and Rp-8 CPT-cyclic guanosine monophosphate (RpcGMP), a cyclic guanosine monophosphate (cGMP) antagonist, attenuated the inhibitory effect of insulin on RhoA activation and restored thrombin-induced Rho kinase activation, and site-specific phosphorylation of the myosin-bound regulatory subunit (MBS(Thr695)) of myosin-bound phosphatase (MBP), and caused actin fiber reorganization. |
| 836 | 12086958 | In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked the inhibitory effects of insulin and abolished thrombin-mediated Rho activation. |
| 837 | 12086958 | We conclude that insulin may inhibit Rho signaling by affecting posttranslational modification of RhoA via nitric oxide/cGMP signaling pathway to cause MBP activation, actin cytoskeletal disorganization, and vasodilation. |
| 838 | 12087030 | Association between plasma thrombin-activatable fibrinolysis inhibitor levels and activated protein C in normotensive type 2 diabetic patients. |
| 839 | 12180730 | Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies. |
| 840 | 12372926 | In 78 non-diabetic, normotensive first-degree relatives of type 2 diabetic patients (47 without a family history of hypertension and 31 with a family history of hypertension) and in 36 normoglycemic, normotensive subjects with no family history of hypertension, we evaluated plasma levels of fasting glucose and insulin, tissue-type plasminogen activator (t-PA), plasminogen activator-inhibitor (PAI-1), D-dimer (DD) and prothrombin fragment 1 + 2 (F1+2). |
| 841 | 12372926 | Insulin resistance, calculated by the HOMA model, and plasma levels of t-PA and PAI-1 were significantly higher in relatives of diabetics compared to controls. |
| 842 | 12430899 | However, in contrast to healthy postmenopausal women, we recently reported that HRT did not significantly decrease PAI-1 antigen levels and rather, increased tissue factor activity and prothrombin fragment F(1+2) levels from baseline in hypertensive and/or overweight postmenopausal women. |
| 843 | 12441907 | The concentration of serum sialic acid showed significant positive correlations with blood platelet count and with plasma concentrations of fibrinogen, D-dimer, thrombin-antithrombin III complex and plasmin-alpha2 plasmin inhibitor complex. |
| 844 | 12441907 | The correlation coefficient of blood fibrinogen with serum sialic acid was still significant after adjustment for D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex. |
| 845 | 12441907 | On the contrary, blood fibrinogen showed no significant correlation with D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex, although an increase in blood fibrinogen is known to be an atherosclerotic risk factor. |
| 846 | 12441907 | The concentration of serum sialic acid showed significant positive correlations with blood platelet count and with plasma concentrations of fibrinogen, D-dimer, thrombin-antithrombin III complex and plasmin-alpha2 plasmin inhibitor complex. |
| 847 | 12441907 | The correlation coefficient of blood fibrinogen with serum sialic acid was still significant after adjustment for D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex. |
| 848 | 12441907 | On the contrary, blood fibrinogen showed no significant correlation with D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex, although an increase in blood fibrinogen is known to be an atherosclerotic risk factor. |
| 849 | 12441907 | The concentration of serum sialic acid showed significant positive correlations with blood platelet count and with plasma concentrations of fibrinogen, D-dimer, thrombin-antithrombin III complex and plasmin-alpha2 plasmin inhibitor complex. |
| 850 | 12441907 | The correlation coefficient of blood fibrinogen with serum sialic acid was still significant after adjustment for D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex. |
| 851 | 12441907 | On the contrary, blood fibrinogen showed no significant correlation with D-dimer, thrombin-antithrombin III complex or plasmin-alpha2 plasmin inhibitor complex, although an increase in blood fibrinogen is known to be an atherosclerotic risk factor. |
| 852 | 12451315 | Oxidized low-density lipoproteins (LDLs) induce atherosclerosis in the vascular wall, as well as endothelin-1 secretion in endothelial cells and are activators of both peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and PPAR-gamma. |
| 853 | 12451315 | PPAR-alpha (fibric acids) and PPAR-gamma (glitazones) activators are used to treat dyslipoproteinemias and type 2 diabetes, respectively. |
| 854 | 12451315 | Furthermore, these drugs induce numerous pleiotropic effects, such as inhibiting thrombin-induced endothelin-1 secretion in endothelial cells. |
| 855 | 12451315 | This study shows that both PPAR-alpha (Wy 14643) and PPAR-gamma activation (rosiglitazone) partially inhibit oxidized LDL-induced protein kinase C activity and endothelin-1 secretion in endothelial cells at the transcriptional levels and suggests that synthetic PPAR activators are stronger PPAR activators than oxidized LDL. |
| 856 | 12479881 | Activated platelet membrane provides an anchor, phosphatidylserine, for the attachment of the prothrombinase complex, which allows increased thrombin formation. |
| 857 | 12574207 | Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria. |
| 858 | 12574207 | Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma. |
| 859 | 12574207 | In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria. |
| 860 | 12574207 | The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients. |
| 861 | 12574207 | Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01). |
| 862 | 12574207 | Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria. |
| 863 | 12574207 | Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma. |
| 864 | 12574207 | In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria. |
| 865 | 12574207 | The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients. |
| 866 | 12574207 | Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01). |
| 867 | 12574207 | Increased plasma thrombin-activatable fibrinolysis inhibitor levels in normotensive type 2 diabetic patients with microalbuminuria. |
| 868 | 12574207 | Recently, a new potent inhibitor of fibrinolysis, the thrombin-activatable fibrinolysis inhibitor (TAFI), has been isolated from human plasma. |
| 869 | 12574207 | In the present study, we investigated the plasma levels of TAFI and its relation to urinary albumin excretion in normotensive diabetic patients with normo- and microalbuminuria. |
| 870 | 12574207 | The plasma level of thrombin-antithrombin complex was significantly increased (22.1 +/- 2.6 vs. 8.3 +/- 1.0 nmol/liter; P < 0.05), whereas the D-dimer/thrombin-antithrombin complex ratio was significantly decreased (15.7 +/- 1.4 vs. 26.5 +/- 2.2; P < 0.05), showing the occurrence of hypercoagulability and hypofibrinolysis in diabetic patients. |
| 871 | 12574207 | Univariate analysis showed that the plasma TAFI levels are significantly and proportionally correlated with urinary albumin excretion rate (r = 0.58; P < 0.005) and with plasma soluble thrombomodulin level, a marker of endothelial cell damage, in all diabetic patients (r = 0.42; P < 0.01). |
| 872 | 12616982 | We observed significant increases of Factor VII (FVII) and von Willebrand factor (vWF) after oERT and no change in the already high fibrinogen. |
| 873 | 12616982 | Prothrombin fragment 1 + 2 (F1 + 2) increased after oERT, whereas thrombin-antithrombin (TAT) complexes was unchanged, but increments of F1 + 2 and TAT correlated. |
| 874 | 12616982 | In fibrinolysis, a clear reduction in plasminogen activator inhibitor 1 (PAI-1) was observed, but no significant change in tissue-type plasminogen activator antigen (t-PA-Ag) or activity was found, although fibrinolytic activity assessed as t-PA activity (t-PA-Act) tended to increase after oERT. |
| 875 | 12766367 | Prothrombin G20210A mutation, but not factor V Leiden, is a risk factor in patients with persistent foramen ovale and otherwise unexplained cerebral ischemia. |
| 876 | 12871543 | Race-adjusted odds ratios for the associations of factor V Leiden and prothrombin G20210A mutations were 3.1 (1.5, 6.7) and 1.9 (0.8, 4.4), respectively. |
| 877 | 12877676 | In 217 women with a first myocardial infarction before the age of 50 years and 763 healthy control women from a population-based case-control study, factor V Leiden and prothrombin 20210A status were determined. |
| 878 | 12877676 | Among women who smoked cigarettes, factor V Leiden presence versus absence increased the risk of myocardial infarction by 2.0 (95% CI 0.9-4.6), and prothrombin 20210A presence versus absence had an odds ratio of 1.0 (95% CI 0.3-3.5). |
| 879 | 12877676 | We conclude that factor V Leiden and prothrombin 20210A do not add substantially to the overall risk of myocardial infarction in young women. |
| 880 | 12877676 | In 217 women with a first myocardial infarction before the age of 50 years and 763 healthy control women from a population-based case-control study, factor V Leiden and prothrombin 20210A status were determined. |
| 881 | 12877676 | Among women who smoked cigarettes, factor V Leiden presence versus absence increased the risk of myocardial infarction by 2.0 (95% CI 0.9-4.6), and prothrombin 20210A presence versus absence had an odds ratio of 1.0 (95% CI 0.3-3.5). |
| 882 | 12877676 | We conclude that factor V Leiden and prothrombin 20210A do not add substantially to the overall risk of myocardial infarction in young women. |
| 883 | 12877676 | In 217 women with a first myocardial infarction before the age of 50 years and 763 healthy control women from a population-based case-control study, factor V Leiden and prothrombin 20210A status were determined. |
| 884 | 12877676 | Among women who smoked cigarettes, factor V Leiden presence versus absence increased the risk of myocardial infarction by 2.0 (95% CI 0.9-4.6), and prothrombin 20210A presence versus absence had an odds ratio of 1.0 (95% CI 0.3-3.5). |
| 885 | 12877676 | We conclude that factor V Leiden and prothrombin 20210A do not add substantially to the overall risk of myocardial infarction in young women. |
| 886 | 12888875 | To investigate the association between the risk of MI at a young age and genetic thrombogenic disorders (G20210A mutation in the prothrombin gene, G1691A mutation in the factor V gene and deficiencies of protein C, protein S and antithrombin III) we conducted a case-control study among 70 survivors of MI who had experienced the event before the age of 36 and 260 healthy subjects. |
| 887 | 12941040 | Onset of force development as a marker of thrombin generation in whole blood: the thrombin generation time (TGT). |
| 888 | 12941040 | Other markers of thrombin generation, prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complex, are typically measured after the fact. |
| 889 | 12941040 | The time between assay start and PCF onset is termed the thrombin generation time (TGT). |
| 890 | 12941040 | TGT is prolonged in clotting factor deficiencies and in the presence of direct and indirect thrombin inhibitors. |
| 891 | 12941040 | Onset of force development as a marker of thrombin generation in whole blood: the thrombin generation time (TGT). |
| 892 | 12941040 | Other markers of thrombin generation, prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complex, are typically measured after the fact. |
| 893 | 12941040 | The time between assay start and PCF onset is termed the thrombin generation time (TGT). |
| 894 | 12941040 | TGT is prolonged in clotting factor deficiencies and in the presence of direct and indirect thrombin inhibitors. |
| 895 | 12941040 | Onset of force development as a marker of thrombin generation in whole blood: the thrombin generation time (TGT). |
| 896 | 12941040 | Other markers of thrombin generation, prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complex, are typically measured after the fact. |
| 897 | 12941040 | The time between assay start and PCF onset is termed the thrombin generation time (TGT). |
| 898 | 12941040 | TGT is prolonged in clotting factor deficiencies and in the presence of direct and indirect thrombin inhibitors. |
| 899 | 12941040 | Onset of force development as a marker of thrombin generation in whole blood: the thrombin generation time (TGT). |
| 900 | 12941040 | Other markers of thrombin generation, prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complex, are typically measured after the fact. |
| 901 | 12941040 | The time between assay start and PCF onset is termed the thrombin generation time (TGT). |
| 902 | 12941040 | TGT is prolonged in clotting factor deficiencies and in the presence of direct and indirect thrombin inhibitors. |
| 903 | 12960608 | Thrombin activatable fibrinolysis inhibitor and hemostatic changes in patients with type I diabetes mellitus with and without microvascular complications. |
| 904 | 12960608 | We investigated thrombin activatable fibrinolysis inhibitor (TAFI) and its influence on fibrinolysis by measuring pro-TAFI activity and total TAFI antigen in 38 patients with type I diabetes mellitus (18 with and 20 without microvascular complications), as well as in 20 healthy controls. |
| 905 | 12960608 | Thrombin activatable fibrinolysis inhibitor and hemostatic changes in patients with type I diabetes mellitus with and without microvascular complications. |
| 906 | 12960608 | We investigated thrombin activatable fibrinolysis inhibitor (TAFI) and its influence on fibrinolysis by measuring pro-TAFI activity and total TAFI antigen in 38 patients with type I diabetes mellitus (18 with and 20 without microvascular complications), as well as in 20 healthy controls. |
| 907 | 14524361 | More recently the presence of NO synthase (ecNOS, iNOS) have been recognized in human platelets. |
| 908 | 14524361 | In the present report washed platelets isolated from healthy persons and patients with chronic myeloproliferative diseases (CMPD) were exposed to common and physiologically relevant activators (i.e., thrombin, collagen, epinephrine etc.). |
| 909 | 14652638 | Therefore, first of all the aim was to investigate if differences in blood coagulation and fibrinolysis can be demonstrated in subjects with insulin-dependent diabetes mellitus (IDDM) compared to controls and secondly, if differences concerning exercise induced changes can be seen in diabetics. 16 moderately fit subjects with IDDM and 16 matched controls underwent a maximal step test. |
| 910 | 14652638 | The rest values (mean of the two rest samples) in extrinsic total thrombin potential (TTPex, P=0.049), tPA-activity (P=0.007) were significantly higher and in PAI-1-antigen (P=0.002) -activity (P=0.049) lower in the diabetic group. |
| 911 | 14652638 | IDDM led to higher extrinsic total thrombin and fibrinolytic potential at rest, and reducing the exercise provoked distribution of tPA-antigen and decrease of PAI-1-antigen. |
| 912 | 14652638 | Therefore, first of all the aim was to investigate if differences in blood coagulation and fibrinolysis can be demonstrated in subjects with insulin-dependent diabetes mellitus (IDDM) compared to controls and secondly, if differences concerning exercise induced changes can be seen in diabetics. 16 moderately fit subjects with IDDM and 16 matched controls underwent a maximal step test. |
| 913 | 14652638 | The rest values (mean of the two rest samples) in extrinsic total thrombin potential (TTPex, P=0.049), tPA-activity (P=0.007) were significantly higher and in PAI-1-antigen (P=0.002) -activity (P=0.049) lower in the diabetic group. |
| 914 | 14652638 | IDDM led to higher extrinsic total thrombin and fibrinolytic potential at rest, and reducing the exercise provoked distribution of tPA-antigen and decrease of PAI-1-antigen. |
| 915 | 14681844 | Activities of pyruvate dehydrogenase (PDH), adenosine triphosphate (ATP)-citrate lyase (ATPCL), acetyl-coenzyme A (acetyl-CoA) content, malonyl dialdehyde (MDA), synthesis, and platelet aggregation in resting conditions and after activation with thrombin were measured in diabetic subjects and in age- and sex-matched healthy subjects. |
| 916 | 14681844 | Activities of ATPCL and PDH, acetyl-CoA content, and thrombin-evoked MDA synthesis as well as platelet aggregation in diabetes were 31%, 51%, 62%, 35%, and 21%, respectively, higher than in healthy subjects. |
| 917 | 14681844 | Activities of pyruvate dehydrogenase (PDH), adenosine triphosphate (ATP)-citrate lyase (ATPCL), acetyl-coenzyme A (acetyl-CoA) content, malonyl dialdehyde (MDA), synthesis, and platelet aggregation in resting conditions and after activation with thrombin were measured in diabetic subjects and in age- and sex-matched healthy subjects. |
| 918 | 14681844 | Activities of ATPCL and PDH, acetyl-CoA content, and thrombin-evoked MDA synthesis as well as platelet aggregation in diabetes were 31%, 51%, 62%, 35%, and 21%, respectively, higher than in healthy subjects. |
| 919 | 14682222 | It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis. |
| 920 | 14682222 | We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits. |
| 921 | 14682222 | All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration. |
| 922 | 14682222 | It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis. |
| 923 | 14682222 | We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits. |
| 924 | 14682222 | All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration. |
| 925 | 14757134 | Protein kinase C (PKC)-beta and other PKC isozymes have been implicated in the loss of endothelial barrier function in diabetic microangiopathy. |
| 926 | 14757134 | The effects of a PKC-beta-specific inhibitor, LY379196, on hyperpermeability responses to high-glucose, angiotensin II, alpha-thrombin and endothelin-1 were evaluated using an in vitro model of human pulmonary artery endothelial cell monolayers. |
| 927 | 14757134 | LY379196 attenuated the increase in transendothelial albumin flux induced by glucose 40 mM (e.g. 411+/-160% [high-glucose] vs. 167+37% [high-glucose+LY379196], P<0.001) and angiotensin II 10 microM (e.g. 121+/-12% vs. 246+/-35%, P<0.01); endothelin-1 had no significant effect on monolayer permeability. |
| 928 | 14961163 | We evaluated the prothrombotic status of DM and non-DM (NDM) patients at days 1 and 6 after MI, by measurement of circulating procoagulant MP and soluble GPV (sGPV), the platelet glycoprotein V major fragment released upon thrombin cleavage. |
| 929 | 14983223 | Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy. |
| 930 | 14983223 | It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients. |
| 931 | 14983223 | We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment. |
| 932 | 14983223 | Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group. |
| 933 | 14983223 | Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy. |
| 934 | 14983223 | It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients. |
| 935 | 14983223 | We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment. |
| 936 | 14983223 | Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group. |
| 937 | 14983223 | Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy. |
| 938 | 14983223 | It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients. |
| 939 | 14983223 | We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment. |
| 940 | 14983223 | Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group. |
| 941 | 15040606 | Bilirubin, alkaline phosphatase, prothrombin time, and APTT stayed within normal range. |
| 942 | 15055239 | The incubation of platelets with glycated LDL enhanced the reactivity of platelets by 32-44% depending on the aggregating agents (thrombin, collagen, ADP). |
| 943 | 15130939 | Human bone marrow megakaryocytes and platelets express PPARgamma, and PPARgamma agonists blunt platelet release of CD40 ligand and thromboxanes. |
| 944 | 15130939 | Platelets are essential not only for clotting, but have an emerging role in inflammation in part due to their release or production of the proinflammatory and proatherogenic mediators CD40 ligand (CD40L) and thromboxanes (TXs). |
| 945 | 15130939 | Platelet incubation with a natural PPARgamma agonist, 15d-PGJ(2), or with a potent synthetic PPARgamma ligand, rosiglitazone, prevented thrombin-induced CD40L surface expression and release of CD40L and thromboxane B(2) (TXB(2)). 15d-PGJ(2) also inhibited platelet aggregation and adenosine triphosphate (ATP) release. |
| 946 | 15134466 | Inheritance of the factor V Leiden (FVL), prothrombin G20210A mutation, or the presence of antiphospholipid antibodies (APA) may increase the risk of renal allograft thrombosis approximately 3-fold in selected patients. |
| 947 | 15134466 | Patients with APA, FVL, or prothrombin G20210A mutation also appear to have greater graft loss due to vascular rejection, possibly reflecting immunological injury upon the vascular wall exacerbated or induced by the prothrombotic state. |
| 948 | 15134466 | Inheritance of the factor V Leiden (FVL), prothrombin G20210A mutation, or the presence of antiphospholipid antibodies (APA) may increase the risk of renal allograft thrombosis approximately 3-fold in selected patients. |
| 949 | 15134466 | Patients with APA, FVL, or prothrombin G20210A mutation also appear to have greater graft loss due to vascular rejection, possibly reflecting immunological injury upon the vascular wall exacerbated or induced by the prothrombotic state. |
| 950 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 951 | 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. |
| 952 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 953 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 954 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 955 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 956 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 957 | 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. |
| 958 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 959 | 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. |
| 960 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 961 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 962 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 963 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 964 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 965 | 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. |
| 966 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 967 | 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. |
| 968 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 969 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 970 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 971 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 972 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 973 | 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. |
| 974 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 975 | 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. |
| 976 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 977 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 978 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 979 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 980 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 981 | 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. |
| 982 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 983 | 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. |
| 984 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 985 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 986 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 987 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 988 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 989 | 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. |
| 990 | 15201277 | Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun. |
| 991 | 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. |
| 992 | 15201277 | We observed a remarkable synergy in the expression of tissue factor by thrombin plus TNFalpha. |
| 993 | 15201277 | This was due to altered regulation of the transcription factors c-Jun and c-Fos. |
| 994 | 15201277 | The activation of c-Jun was greater and more sustained than that obtained with either thrombin or TNFalpha alone. |
| 995 | 15201277 | Thrombin-stimulated expression of c-Fos was both enhanced and prolonged by the concurrent presence of TNFalpha. |
| 996 | 15201277 | These changes support the increased availability of c-Jun/c-Fos AP-1 complexes for mediating transcription at the tissue factor promoter. |
| 997 | 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. |
| 998 | 15320820 | Antithrombin (AT), activated protein C (APC), and tissue factor pathway inhibitor (TFPI) mainly constitute the natural anticoagulant system apart from the recently reported physiological components such as lipoproteins, sphingosine, thrombomodulin (TM) or cellular Marcks protein. |
| 999 | 15320820 | Pharmacological anticoagulants include warfarin, FVIIa inhibitors, FXa inhibitors, and thrombin inhibition by its direct inhibitors or heparins. |
| 1000 | 15351860 | Our results showed that in Ca 2(+)-containing media, there was no significant differences in the basal [Ca(2+)](i), but the maximal increases of [Ca(2+)](i) of platelets were higher (p <0.05) in group 1 than in group 2 after stimulating with PAF and ADP, but not with thrombin and arachidonic acid. |
| 1001 | 15382171 | There were no differences between both groups regarding age, gender, diabetes, hyperlipidemia, ALT levels, AST-to-ALT ratio levels, albumin levels, prothrombin activity, steatosis, or inflammation. |
| 1002 | 15543340 | High heparin cofactor II (HCII) activity has recently been described to protect from coronary instent restenosis, presumably by inactivating thrombin in injured arteries. |
| 1003 | 15555528 | DHA activates a number of nuclear hormone receptors that operate as transcription factors for molecules that modulate reduction-oxidation-sensitive and proinflammatory genes; these include the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and the retinoid X receptor. |
| 1004 | 15555528 | In the case of PPAR-alpha, this action is thought to prevent endothelial cell dysfunction and vascular remodeling through inhibition of: vascular smooth muscle cell proliferation, inducible nitric oxide synthase production, interleukin-1 induced cyclooxygenase (COX)-2 production, and thrombin-induced endothelin 1 production. |
| 1005 | 15555528 | EPA depresses vascular endothelial growth factor (VEGF)-specific tyrosine kinase receptor activation and expression. |
| 1006 | 15555528 | The mechanism of VEGF receptor down-regulation is believed to occur at the tyrosine kinase nuclear factor-kappa B (NFkappaB). |
| 1007 | 15555528 | NFkappaB is a nuclear transcription factor that up-regulates COX-2 expression, intracellular adhesion molecule, thrombin, and nitric oxide synthase. |
| 1008 | 15555528 | DHA activates a number of nuclear hormone receptors that operate as transcription factors for molecules that modulate reduction-oxidation-sensitive and proinflammatory genes; these include the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and the retinoid X receptor. |
| 1009 | 15555528 | In the case of PPAR-alpha, this action is thought to prevent endothelial cell dysfunction and vascular remodeling through inhibition of: vascular smooth muscle cell proliferation, inducible nitric oxide synthase production, interleukin-1 induced cyclooxygenase (COX)-2 production, and thrombin-induced endothelin 1 production. |
| 1010 | 15555528 | EPA depresses vascular endothelial growth factor (VEGF)-specific tyrosine kinase receptor activation and expression. |
| 1011 | 15555528 | The mechanism of VEGF receptor down-regulation is believed to occur at the tyrosine kinase nuclear factor-kappa B (NFkappaB). |
| 1012 | 15555528 | NFkappaB is a nuclear transcription factor that up-regulates COX-2 expression, intracellular adhesion molecule, thrombin, and nitric oxide synthase. |
| 1013 | 15615851 | Proteinase-activated receptors 1 and 4 counter-regulate endostatin and VEGF release from human platelets. |
| 1014 | 15615851 | Among these is the release of factors that regulate the process of angiogenesis, such as endostatin and VEGF, which, respectively, inhibit and promote angiogenesis. |
| 1015 | 15615851 | PAR1 and PAR4 are expressed on the surface of human platelets and can be activated by thrombin. |
| 1016 | 15615851 | In the present study, we have attempted to determine the roles of PAR1 and PAR4 in regulating release of endostatin and VEGF from human platelets. |
| 1017 | 15615851 | Aggregation and endostatin release could be elicited by a specific PAR4 agonist (AYPGKF-NH(2)). |
| 1018 | 15615851 | The PAR4 agonist concentration dependently suppressed VEGF release. |
| 1019 | 15615851 | A selective PAR1 agonist (TFLLR-NH(2)) induced platelet aggregation and VEGF release but suppressed endostatin release. |
| 1020 | 15615851 | Thrombin did not affect endostatin or VEGF release. |
| 1021 | 15615851 | However, in the presence of a selective PAR1 antagonist (SCH79797), thrombin stimulated endostatin release and suppressed VEGF release. |
| 1022 | 15615851 | Conversely, in the presence of a selective PAR4 antagonist (transcinnamoyl-YPGKF-NH(2)), thrombin stimulated VEGF release. |
| 1023 | 15615851 | In vivo, treatment of rats with established gastric ulcers with a PAR1 antagonist each day for 1 wk resulted in a significant retardation of healing. |
| 1024 | 15615851 | We conclude that PAR1 and PAR4 counter-regulate the release of endostatin and VEGF from platelets. |
| 1025 | 15615851 | Proteinase-activated receptors 1 and 4 counter-regulate endostatin and VEGF release from human platelets. |
| 1026 | 15615851 | Among these is the release of factors that regulate the process of angiogenesis, such as endostatin and VEGF, which, respectively, inhibit and promote angiogenesis. |
| 1027 | 15615851 | PAR1 and PAR4 are expressed on the surface of human platelets and can be activated by thrombin. |
| 1028 | 15615851 | In the present study, we have attempted to determine the roles of PAR1 and PAR4 in regulating release of endostatin and VEGF from human platelets. |
| 1029 | 15615851 | Aggregation and endostatin release could be elicited by a specific PAR4 agonist (AYPGKF-NH(2)). |
| 1030 | 15615851 | The PAR4 agonist concentration dependently suppressed VEGF release. |
| 1031 | 15615851 | A selective PAR1 agonist (TFLLR-NH(2)) induced platelet aggregation and VEGF release but suppressed endostatin release. |
| 1032 | 15615851 | Thrombin did not affect endostatin or VEGF release. |
| 1033 | 15615851 | However, in the presence of a selective PAR1 antagonist (SCH79797), thrombin stimulated endostatin release and suppressed VEGF release. |
| 1034 | 15615851 | Conversely, in the presence of a selective PAR4 antagonist (transcinnamoyl-YPGKF-NH(2)), thrombin stimulated VEGF release. |
| 1035 | 15615851 | In vivo, treatment of rats with established gastric ulcers with a PAR1 antagonist each day for 1 wk resulted in a significant retardation of healing. |
| 1036 | 15615851 | We conclude that PAR1 and PAR4 counter-regulate the release of endostatin and VEGF from platelets. |
| 1037 | 15615851 | Proteinase-activated receptors 1 and 4 counter-regulate endostatin and VEGF release from human platelets. |
| 1038 | 15615851 | Among these is the release of factors that regulate the process of angiogenesis, such as endostatin and VEGF, which, respectively, inhibit and promote angiogenesis. |
| 1039 | 15615851 | PAR1 and PAR4 are expressed on the surface of human platelets and can be activated by thrombin. |
| 1040 | 15615851 | In the present study, we have attempted to determine the roles of PAR1 and PAR4 in regulating release of endostatin and VEGF from human platelets. |
| 1041 | 15615851 | Aggregation and endostatin release could be elicited by a specific PAR4 agonist (AYPGKF-NH(2)). |
| 1042 | 15615851 | The PAR4 agonist concentration dependently suppressed VEGF release. |
| 1043 | 15615851 | A selective PAR1 agonist (TFLLR-NH(2)) induced platelet aggregation and VEGF release but suppressed endostatin release. |
| 1044 | 15615851 | Thrombin did not affect endostatin or VEGF release. |
| 1045 | 15615851 | However, in the presence of a selective PAR1 antagonist (SCH79797), thrombin stimulated endostatin release and suppressed VEGF release. |
| 1046 | 15615851 | Conversely, in the presence of a selective PAR4 antagonist (transcinnamoyl-YPGKF-NH(2)), thrombin stimulated VEGF release. |
| 1047 | 15615851 | In vivo, treatment of rats with established gastric ulcers with a PAR1 antagonist each day for 1 wk resulted in a significant retardation of healing. |
| 1048 | 15615851 | We conclude that PAR1 and PAR4 counter-regulate the release of endostatin and VEGF from platelets. |
| 1049 | 15636223 | Levels of anti-proteases were similar in DM1, DM2 and control group, with one exception: anti-thrombin level was lower in DM2 patients' sera than this in the control group. |
| 1050 | 15647842 | Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway. |
| 1051 | 15647842 | Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis. |
| 1052 | 15647842 | We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes. |
| 1053 | 15647842 | Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI. |
| 1054 | 15647842 | To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes. |
| 1055 | 15647842 | TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes. |
| 1056 | 15647842 | PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects. |
| 1057 | 15647842 | These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway. |
| 1058 | 15647842 | Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt. |
| 1059 | 15647842 | In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes. |
| 1060 | 15647842 | It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance. |
| 1061 | 15647842 | Insulin enhanced thrombin-activable fibrinolysis inhibitor expression through PI3 kinase/Akt pathway. |
| 1062 | 15647842 | Thrombin-activable fibrinolysis inhibitor (TAFI) is a key modulator of fibrinolysis. |
| 1063 | 15647842 | We have reported the elevated levels of plasma TAFI and their correlation with visceral fat area and insulin resistance in the patients with type 2 diabetes. |
| 1064 | 15647842 | Thus, we hypothesized that TAFI secreted from adipose tissues might be an important causative factor of hypofibrinolysis in patients with insulin resistance and that insulin was a modulator of the gene expression of TAFI. |
| 1065 | 15647842 | To evaluate this hypothesis, we examined the regulation of TAFI expression by insulin in adipocytes. |
| 1066 | 15647842 | TAFI mRNA was induced dose-dependently by insulin in 3T3-L1 adipocytes. |
| 1067 | 15647842 | PI3 kinase inhibitor wortmannin inhibited insulin-induced expression, but MEK1 inhibitor PD98059 had no effects. |
| 1068 | 15647842 | These data suggested that the gene expression of TAFI was regulated by PI3 kinase signaling pathway. |
| 1069 | 15647842 | Moreover, activated Akt induced the expression of TAFI mRNA to a similar extent by insulin in 3T3-L1 adipocytes expressing tamoxifen-regulatable Akt. |
| 1070 | 15647842 | In conclusion, TAFI was induced by insulin through PI3 kinase/Akt pathway in adipocytes. |
| 1071 | 15647842 | It is supposed that plasma TAFI levels are regulated at least in part by transcription levels in adipose tissues of patients with insulin resistance. |
| 1072 | 15668188 | Thrombin activatable fibrinolysis inhibitor in Behçet's disease. |
| 1073 | 15678662 | The below main parameters, which matter in progression of thrombohemorrhagic conditions should be determined, apart from D-dimer, for choosing an adequate medicamental therapy: aggregation ability of platelets, activated partial thromboplastin time, antithrombin-III, protein-C, prothrombin time, soluble complexes of fibrinmonomer, thrombin time, plasma fibrinogen and fibrinolytic plasma activity. |
| 1074 | 15714993 | Associated factors included age, sex, hypertension, diabetes mellitus, dyslipidemia, smoking, extracranial and intra-cranial vascular lesions, extent of lacunes and white matter lesions, progression status and blood pressure in the acute stage, and coagulation markers such as fibrinogen, thrombin-antithrombin complex, D-dimer, beta-thromboglobulin, platelet factor 4. |
| 1075 | 15791889 | In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. |
| 1076 | 15886665 | Factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations are not associated with chronic limb ischemia: the Linz Peripheral Arterial Disease (LIPAD) study. |
| 1077 | 15919797 | Thrombin-antithrombin complex (TAT) and FVIIa-antithrombin complex (FVIIa-AT) were measured in nine patients who together received 20 infusions of isolated human islets. |
| 1078 | 15963463 | Pretreatment of platelets with catalase or trolox, an analog of vitamin E, reversed the enhanced Ca2+ entry, evoked by thapsigargin plus ionomycin or thrombin, observed in platelets from diabetic subjects, so that in the presence of these scavengers Ca2+ entry was similar in platelets from healthy and diabetic subjects. |
| 1079 | 15963463 | Catalase and trolox reduced thrombin-induced aggregation in platelets from type 2 diabetic subjects, while mannitol did not modify thrombin-induced platelet hyperaggregability. |
| 1080 | 15963463 | Pretreatment of platelets with catalase or trolox, an analog of vitamin E, reversed the enhanced Ca2+ entry, evoked by thapsigargin plus ionomycin or thrombin, observed in platelets from diabetic subjects, so that in the presence of these scavengers Ca2+ entry was similar in platelets from healthy and diabetic subjects. |
| 1081 | 15963463 | Catalase and trolox reduced thrombin-induced aggregation in platelets from type 2 diabetic subjects, while mannitol did not modify thrombin-induced platelet hyperaggregability. |
| 1082 | 15968383 | Thrombophilic risk factors analyzed were hyperhomocysteinemia, MTHFR gene mutation, factor V Leiden mutation, protein C and S deficiency, antithrombin deficiency, prothrombin gene mutation, anticardiolipin antibodies and lupus anticoagulant. |
| 1083 | 15968383 | The odds ratios were 8.9 (95% CI 5.7 - 13.7) for hyperhomocysteinemia, 3.9 (95% CI 2.3 - 6.7) for anticardiolipin antibodies, 1.2 (95% CI 0.9 - 1.6) for MTHFR, 1.5 (95% CI 1.0 - 2.2) for factor V Leiden mutation and 1.6 (95% CI 0.8 - 3.2) for prothrombin gene mutation. |
| 1084 | 15968383 | Thrombophilic risk factors analyzed were hyperhomocysteinemia, MTHFR gene mutation, factor V Leiden mutation, protein C and S deficiency, antithrombin deficiency, prothrombin gene mutation, anticardiolipin antibodies and lupus anticoagulant. |
| 1085 | 15968383 | The odds ratios were 8.9 (95% CI 5.7 - 13.7) for hyperhomocysteinemia, 3.9 (95% CI 2.3 - 6.7) for anticardiolipin antibodies, 1.2 (95% CI 0.9 - 1.6) for MTHFR, 1.5 (95% CI 1.0 - 2.2) for factor V Leiden mutation and 1.6 (95% CI 0.8 - 3.2) for prothrombin gene mutation. |
| 1086 | 15968399 | Platelet P2Y12 receptors enhance signalling towards procoagulant activity and thrombin generation. |
| 1087 | 15968399 | We established that, in PRP from healthy subjects, ADP accelerated and potentiated tissue factor induced thrombin generation exclusively via stimulation of P2Y(12) and not via P2Y(1) receptors. |
| 1088 | 15968399 | The P2Y(12) receptors also mediated the potentiating effect of PAR-1 stimulation on thrombin generation. |
| 1089 | 15968399 | Platelet P2Y12 receptors enhance signalling towards procoagulant activity and thrombin generation. |
| 1090 | 15968399 | We established that, in PRP from healthy subjects, ADP accelerated and potentiated tissue factor induced thrombin generation exclusively via stimulation of P2Y(12) and not via P2Y(1) receptors. |
| 1091 | 15968399 | The P2Y(12) receptors also mediated the potentiating effect of PAR-1 stimulation on thrombin generation. |
| 1092 | 15968399 | Platelet P2Y12 receptors enhance signalling towards procoagulant activity and thrombin generation. |
| 1093 | 15968399 | We established that, in PRP from healthy subjects, ADP accelerated and potentiated tissue factor induced thrombin generation exclusively via stimulation of P2Y(12) and not via P2Y(1) receptors. |
| 1094 | 15968399 | The P2Y(12) receptors also mediated the potentiating effect of PAR-1 stimulation on thrombin generation. |
| 1095 | 16021635 | Because we found that hIPCs, PANC-1 cells, human fetal pancreas, and human adult islets express two protease-activated receptors (PARs), PAR-1 and PAR-2, we tested whether the effects of thrombin and trypsin were mediated, at least in part, by these receptors. |
| 1096 | 16114812 | Von Willebrand factor (VWF), thrombin activatable fibrinolysis inhibitor, activated protein C (APC) ratio, factor V, and prothrombin time had heritabilities greater than 0.50. |
| 1097 | 16114812 | Significant (p < or = 0.05) positive genetic correlations (0.37-0.51) occurred with factors II and VIII, VWF, total protein S (tPS), and tissue factor pathway inhibitor. |
| 1098 | 16123492 | Metabolic syndrome accompanied by hypercholesterolemia is strongly associated with proinflammatory state and impairment of fibrinolysis in patients with type 2 diabetes: synergistic effects of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor. |
| 1099 | 16138347 | The association of the single nucleotide polymorphisms (SNPs) G1691A in coagulation factor V (FV)-Leiden and G20210A in prothrombin (PRT) genes with type 2 diabetes mellitus (T2DM) were analyzed in 112 T2DM patients (58 males, 54 females; mean age 55.24 +/- 13.5 years) and 249 healthy control subjects (118 males, 131 females; mean age 53.03 +/- 13.8 years). |
| 1100 | 16142016 | Both treatments significantly declined plasma glucose, total-cholesterol, LDL-cholesterol, triglycerides, PAI-1, PAP levels and increased HDL-cholesterol. |
| 1101 | 16142016 | Lowering in plasma PAI-1 and PAP levels was significantly greater in repaglinide group. |
| 1102 | 16142016 | Furthermore, repaglinide administration resulted in a significant decrease in fasting plasma free fatty acids, fibrinogen, thrombin-antithrombin complex and reaction product of malondialdehyde with thiobarbituric acid (TBARS) levels, in absence of significant difference in fasting plasma insulin levels. |
| 1103 | 16142016 | At time 120' of meal test, repaglinide vs glimepiride administration was associated with a significant decline in plasma triglycerides, free fatty acids, fibrinogen, Plasminogen Activator Inhibitor-1, plasmin-alpha(2)-antiplasmin complex, thrombin-antithrombin complex, TBARS levels and increase in plasma HDL-cholesterol levels. |
| 1104 | 16142016 | Both treatments significantly declined plasma glucose, total-cholesterol, LDL-cholesterol, triglycerides, PAI-1, PAP levels and increased HDL-cholesterol. |
| 1105 | 16142016 | Lowering in plasma PAI-1 and PAP levels was significantly greater in repaglinide group. |
| 1106 | 16142016 | Furthermore, repaglinide administration resulted in a significant decrease in fasting plasma free fatty acids, fibrinogen, thrombin-antithrombin complex and reaction product of malondialdehyde with thiobarbituric acid (TBARS) levels, in absence of significant difference in fasting plasma insulin levels. |
| 1107 | 16142016 | At time 120' of meal test, repaglinide vs glimepiride administration was associated with a significant decline in plasma triglycerides, free fatty acids, fibrinogen, Plasminogen Activator Inhibitor-1, plasmin-alpha(2)-antiplasmin complex, thrombin-antithrombin complex, TBARS levels and increase in plasma HDL-cholesterol levels. |
| 1108 | 16188573 | Levels of prothrombin fragment 1+2 (F1+2), factor VII, plasminogen activator inhibitor-1 (PAI-1) and tissue factor pathway inhibitor (TFPI) antigens, but not tissue plasminogen activator (tPA) antigen, in the pre-simvastatin plasmas of the diabetic patients were significantly higher than the levels found in plasmas of healthy subjects. |
| 1109 | 16188573 | Levels of total tPA, TFPI, FVII, hemoglobin A1c, fasting blood glucose, and insulin in the diabetic patients' plasma were not significantly altered by simvastatin treatment. |
| 1110 | 16188573 | The results suggest that simvastatin reduces in vivo prothrombinase activity and PAI-1 levels in type 2 DM patients. |
| 1111 | 16193199 | Fibrinogen, fibrin D-dimer, and thrombin-antithrombin III levels reflecting coagulation system activity were found to be increased in the patients with atypical AFl when compared with those with typical AFl and the control group (p < 0.001). |
| 1112 | 16303885 | Impact of age, CYP2C9 genotype and concomitant medication on the rate of rise for prothrombin time during the first 30 days of warfarin therapy. |
| 1113 | 16308911 | The pro-inflammatory CD40/CD40L dyad participates in atherogenesis. |
| 1114 | 16308911 | This study compared CD40/CD40L surface expression on platelets and T lymphocytes of diabetic and control subjects, and tested whether glucose and advanced glycation end products (AGEs) stimulate sCD40L release. |
| 1115 | 16308911 | Constitutive and inducible surface expression of CD40/CD40L on platelets or T lymphocytes did not differ between diabetic patients (n = 9) and controls (n = 13). |
| 1116 | 16308911 | Platelets from diabetic patients contained higher intracellular CD40L than controls (p < 0.05) and thrombin stimulated greater platelet sCD40L release in diabetic patients (15.11 +/- 16.77 ng/ml) compared to controls (3.64 +/- 2.03 ng/ml; p < 0.05). |
| 1117 | 16369752 | In view of the possible association between clear cell histology and VTE in endometrial cancer, we measured the plasma levels of thrombin-antithrombin III complex (TAT) and D-dimer (DD) in the preoperative examinations of a patient with clear cell adenocarcinoma of the endometrium. |
| 1118 | 16377281 | Platelet aggregation, after adenosine diphosphate (6 and 20 micromol/L) and collagen (6 microg/ml) stimuli, and platelet activation (glycoprotein IIb/IIIa activation and P-selectin expression), after adenosine diphosphate (2 micromol/L) and thrombin receptor-activating peptide (50 micromol/L) stimuli, were assessed by light transmittance aggregometry and flow cytometry, respectively. |
| 1119 | 16380494 | Effects of hyperglycemia and hyperinsulinemia on circulating tissue factor procoagulant activity and platelet CD40 ligand. |
| 1120 | 16380494 | Combined elevations of plasma insulin and glucose levels for 24 h produced a ninefold increase in tissue factor PCA, which was associated with an increase in monocyte tissue factor protein (flow cytometry) and mRNA (RT-PCR), increases in plasma thrombin-antithrombin complexes, prothrombin fragment 1.2, factor VIII coagulant activity, and platelet CD40 ligand as well as decreases in factor VIIa, factor VII coagulant activities, and factor VII antigen. |
| 1121 | 16380494 | We conclude that hyperinsulinemia and hyperglycemia but particularly the combination of both create a prothrombotic state and in addition may be proinflammatory and proatherogenic because of the proinflammatory actions of CD40 ligand and tissue factor. |
| 1122 | 16389166 | Thrombin-activatable fibrinolysis inhibitor activity and global fibrinolytic capacity in Type 1 diabetes: evidence for normal fibrinolytic state. |
| 1123 | 16389166 | There is little information, however, regarding the status of fibrinolytic system in Type 1 diabetes, in particular as reflected by thrombin-activatable fibrinolysis inhibitor (TAFI) activity and global fibrinolytic capacity (GFC). |
| 1124 | 16389166 | TAFI activity did not significantly correlate with age, albumin excretion, fasting plasma glucose, HbA(1c), D-dimer, and fibrinogen by Spearman rank correlation test. |
| 1125 | 16389166 | Thrombin-activatable fibrinolysis inhibitor activity and global fibrinolytic capacity in Type 1 diabetes: evidence for normal fibrinolytic state. |
| 1126 | 16389166 | There is little information, however, regarding the status of fibrinolytic system in Type 1 diabetes, in particular as reflected by thrombin-activatable fibrinolysis inhibitor (TAFI) activity and global fibrinolytic capacity (GFC). |
| 1127 | 16389166 | TAFI activity did not significantly correlate with age, albumin excretion, fasting plasma glucose, HbA(1c), D-dimer, and fibrinogen by Spearman rank correlation test. |
| 1128 | 16425373 | An 85-year-old man with HCV infection and diabetes mellitus was diagnosed as having hepatocellular carcinoma (HCC, 13 cm in diameter) based on high serum alpha-fetoprotein (AFP), AFP-L3, and des-gamma-carboxy prothrombin levels as well as typical enhancement pattern on contrast-enhanced CT. |
| 1129 | 16458385 | Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients. |
| 1130 | 16458385 | We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients. |
| 1131 | 16458385 | The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects. |
| 1132 | 16458385 | The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects. |
| 1133 | 16458385 | There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04). |
| 1134 | 16458385 | These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus. |
| 1135 | 16458385 | Different metabolic correlations of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 in non-obese type 2 diabetic patients. |
| 1136 | 16458385 | We investigated the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) and their relation with clinical and metabolic parameters in non-obese type 2 diabetic patients. |
| 1137 | 16458385 | The plasma levels of TAFI and PAI-1 were evaluated in 47 non-obese type 2 diabetic patients and 31 normal subjects. |
| 1138 | 16458385 | The plasma levels of TAFI (169.0+/-108.8% versus 103.7+/-52.3%; p<0.001, mean+/-S.D.) and PAI-1 (82.7+/-54.5ng/ml versus 52.9+/-51.7ng/ml; p<0.05) were significantly higher in non-obese type 2 diabetic patients than in normal subjects. |
| 1139 | 16458385 | There was no significant correlation between plasma levels of TAFI and PAI-1 (r=0.04). |
| 1140 | 16458385 | These results show that the plasma levels of TAFI and PAI-1 differently correlate with insulin resistance and visceral fat accumulation, suggesting that different factors are implicated in the plasma elevation of TAFI and PAI-1 in non-obese type 2 diabetes mellitus. |
| 1141 | 16643434 | High glucose levels enhanced adenosine diphosphate (ADP)- and thrombin receptor-activating peptide (TRAP)-induced platelet P-selectin expression, and TRAP-induced platelet fibrinogen binding. |
| 1142 | 16643434 | Blockade of cyclo-oxygenase (COX), phosphotidylinositol-3 (PI3) kinase, or nitric oxide synthase, or the addition of insulin did not influence the effect of hyperglycaemia. |
| 1143 | 16679086 | Serial biomarkers C-reactive protein, troponin, creatine kinase-MB, soluble CD40 ligand, interleukin-6, prothrombin fragment F1.2, and RANTES (regulated on activation, normal T-cell expressed and secreted) were assessed through 24 hours after PCI. |
| 1144 | 16679086 | Creatine kinase-MB, soluble sCD40 ligand, prothrombin fragment F1.2, and RANTES did not differ by DES use. |
| 1145 | 16679086 | Serial biomarkers C-reactive protein, troponin, creatine kinase-MB, soluble CD40 ligand, interleukin-6, prothrombin fragment F1.2, and RANTES (regulated on activation, normal T-cell expressed and secreted) were assessed through 24 hours after PCI. |
| 1146 | 16679086 | Creatine kinase-MB, soluble sCD40 ligand, prothrombin fragment F1.2, and RANTES did not differ by DES use. |
| 1147 | 16709900 | An osteopontin-NADPH oxidase signaling cascade promotes pro-matrix metalloproteinase 9 activation in aortic mesenchymal cells. |
| 1148 | 16709900 | By zymography, OPN and tumor necrosis factor (TNF)-alpha preferentially upregulate pro-matrix metalloproteinase 9 (pro-MMP9) activity. |
| 1149 | 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. |
| 1150 | 16709900 | OPN treatment of VSMCs enhanced pro-MMP9 activity, and TNF-alpha induction of pro-MMP9 was inhibited by anti-OPN antibody and apocynin. |
| 1151 | 16709900 | Like OPN and TNF-alpha, 8-IsoP preferentially activated pro-MMP9. |
| 1152 | 16709900 | Superoxide, 8-IsoP, and NADPH oxidase 2 (Nox2) subunits were reduced in OPN(-/-) AMFs. |
| 1153 | 16709900 | Treatment of A7r5 VSMCs with OPN upregulated NADPH oxidase subunit accumulation. |
| 1154 | 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). |
| 1155 | 16709900 | Treatment of aortic VSMCs with SVVYGLR upregulated pro-MMP9 activity and restored TNF-alpha activation of pro-MMP9 in OPN(-/-) AMFs. |
| 1156 | 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). |
| 1157 | 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. |
| 1158 | 16709900 | Thus, OPN provides a paracrine signal that augments vascular pro-MMP9 activity, mediated in part via superoxide generation and oxylipid formation. |
| 1159 | 16731846 | Hyperglycemia exerted a procoagulant effect irrespective of insulin levels, as reflected by mean twofold rises in thrombin-antithrombin complexes and soluble tissue factor, whereas hyperinsulinemia inhibited fibrinolysis irrespective of glucose levels, as reflected by a decrease in plasminogen activator activity levels due to a mean 2.5-fold rise in plasminogen activator inhibitor type 1. |
| 1160 | 16760910 | However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. |
| 1161 | 16760910 | Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. |
| 1162 | 16760910 | Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. |
| 1163 | 16760910 | In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. |
| 1164 | 16760910 | However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. |
| 1165 | 16760910 | Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. |
| 1166 | 16760910 | Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. |
| 1167 | 16760910 | In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. |
| 1168 | 16760910 | However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. |
| 1169 | 16760910 | Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. |
| 1170 | 16760910 | Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. |
| 1171 | 16760910 | In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. |
| 1172 | 16760910 | However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. |
| 1173 | 16760910 | Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. |
| 1174 | 16760910 | Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. |
| 1175 | 16760910 | In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. |
| 1176 | 16779662 | The significant (P<0.001) decreases by garlic oil of plasma concentration factors, V, VII, VIII: C, IX and X in diabetic rats may be interpreted to mean that there was a modulation of factor VII similar to that brought about by thrombin on factors V and VIII: C. |
| 1177 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1178 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1179 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1180 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1181 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1182 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1183 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1184 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1185 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1186 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1187 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1188 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1189 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1190 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1191 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1192 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1193 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1194 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1195 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1196 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1197 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1198 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1199 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1200 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1201 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1202 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1203 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1204 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1205 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1206 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1207 | 16801070 | We previously reported the effects of diet, sulphonylureas or insulin on thrombin-induced platelet aggregation, phosphoinositide metabolism and protein phosphorylation in non-insulin-dependent diabetes mellitus (NIDDM) patients. |
| 1208 | 16801070 | To clarify the mechanism of glyburide and insulin on platelet function, here we studied the in vitro effects of glyburide and insulin on thrombin-induced metabolic changes using normal human platelets. |
| 1209 | 16801070 | Platelet aggregation stimulated with <0.5 U/ml thrombin, 0.75-3 microM adenosine diphosphate (ADP) or 1 microg/ml collagen was significantly lower in glyburide-treated platelets, but not in insulin-treated platelets, than in untreated ones (control). |
| 1210 | 16801070 | Thrombin-induced incorporation of 32P radioactivity into phosphatidic acid (PA) in glyburide-treated platelets was lower than that in control but not in insulin-treated platelets. |
| 1211 | 16801070 | Phosphorylated proteins of platelets induced by thrombin and 12- O -tetradecanoylphorbol 13-acetate (TPA) in glyburide-treated platelets were suppressed, but not in insulin-treated platelets, compared with control. |
| 1212 | 16801070 | These results suggest that glyburide induces suppression of thrombin-induced activation of phospholipase C, which mediates hydrolysis of PIP and PIP(2) and production of PA, and subsequently inhibits platelet aggregation. |
| 1213 | 16801071 | The shifts in platelet volume distributions were paralleled by decreased expression of the alpha subunit of glycoprotein Ib (by up to 17%, P < 0.01) in platelet membranes from diabetic patients, increased expression of P-selectin in thrombin-stimulated diabetic platelets (P< 0.02), an increased number of platelet microparticles in diabetic individuals (P< 0.05 or P< 0.03 for resting or stimulated platelets, respectively), and reduced platelet membrane fluidity (by 5.2 +/- 0.6%, P< 0.01). |
| 1214 | 16831022 | Currently, the PPARgamma ligands rosiglitazone and pioglitazone are used for the treatment of type 2 diabetes mellitus because they are potent insulin sensitizers. |
| 1215 | 16831022 | In particular, release of soluble CD40 ligand (sCD40L) and thromboxane (TXA(2)) was inhibited by PPARgamma ligands in thrombin-activated platelets. |
| 1216 | 16877877 | The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. |
| 1217 | 16877877 | Thrombin induces thrombin activatable fibrinolysis inhibitor. |
| 1218 | 16877877 | Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. |
| 1219 | 16877877 | The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. |
| 1220 | 16877877 | Thrombin induces thrombin activatable fibrinolysis inhibitor. |
| 1221 | 16877877 | Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. |
| 1222 | 16877877 | The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. |
| 1223 | 16877877 | Thrombin induces thrombin activatable fibrinolysis inhibitor. |
| 1224 | 16877877 | Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. |
| 1225 | 17006373 | In a matched, controlled study, we defined the major genetic predispositions that increase the risk of venous thromboembolism after total hip arthroplasty: deficiency of antithrombin III (< 75%) and protein C (< 70%), and prothrombin gene mutation. |
| 1226 | 17018519 | Adipocyte-derived "adipokines" such as adiponectin, leptin, and visceral adipose tissue-derived serine protease inhibitor (vaspin) exert hormone-like activities at the systemic level. |
| 1227 | 17018519 | Moreover we detected a number of established adipokines such as adiponectin and plasminogen activator inhibitor 1. |
| 1228 | 17018519 | In addition to plasminogen activator inhibitor 1, these included pigment epithelium-derived factor (confirmed by Western immunoblot), placental thrombin inhibitor, pregnancy zone protein, and protease C1 inhibitor. |
| 1229 | 17046544 | Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients. |
| 1230 | 17046544 | The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients. |
| 1231 | 17046544 | Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls. |
| 1232 | 17046544 | Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured. |
| 1233 | 17046544 | This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose. |
| 1234 | 17046544 | Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase. |
| 1235 | 17046544 | Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients. |
| 1236 | 17046544 | The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients. |
| 1237 | 17046544 | Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls. |
| 1238 | 17046544 | Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured. |
| 1239 | 17046544 | This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose. |
| 1240 | 17046544 | Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase. |
| 1241 | 17064853 | Oxidation of methionine 388 in thrombomodulin is known to slow the rate at which the thrombomodulin-thrombin complex activates protein C, a protein which, in turn, degrades the factors which activate thrombin and lead to clot formation. |
| 1242 | 17164134 | Upon activation, platelets synthesize eicosanoids such as thromboxane A2 (TXA2) and PGE2 and release pro-inflammatory mediators including CD40 ligand (CD40L). |
| 1243 | 17164134 | Treatment with eicosanoid and synthetic PPARgamma ligands blunts platelet release of the bioactive mediators, soluble (s) CD40L and TXA2, in thrombin-activated platelets. |
| 1244 | 17182793 | In both studies, multivariate analysis indicated a strong clustering of fasting concentrations of triacylglycerols, prothrombin, factor V, factor VII, and factor X with one another at baseline. |
| 1245 | 17182793 | In both healthy subjects and diabetes patients, high triacylglycerol concentrations (>1.69 mmol/L) at baseline were closely linked to a strong fish oil-induced lowering of triacylglycerol and coagulation factor V, VII, and X concentrations, and thrombin generation. |
| 1246 | 17182793 | In both studies, multivariate analysis indicated a strong clustering of fasting concentrations of triacylglycerols, prothrombin, factor V, factor VII, and factor X with one another at baseline. |
| 1247 | 17182793 | In both healthy subjects and diabetes patients, high triacylglycerol concentrations (>1.69 mmol/L) at baseline were closely linked to a strong fish oil-induced lowering of triacylglycerol and coagulation factor V, VII, and X concentrations, and thrombin generation. |
| 1248 | 17184758 | Thrombin activatable fibrinolysis inhibitor (TAFI): a role in pre-eclampsia? |
| 1249 | 17184758 | Pro-thrombin activatable fibrinolysis inhibitor (pro-TAFI) is a relatively recently described glycoprotein that can be converted into its active form (TAFIa) by thrombin, thrombin-thrombomodulin and plasmin. |
| 1250 | 17184758 | Thrombin activatable fibrinolysis inhibitor (TAFI): a role in pre-eclampsia? |
| 1251 | 17184758 | Pro-thrombin activatable fibrinolysis inhibitor (pro-TAFI) is a relatively recently described glycoprotein that can be converted into its active form (TAFIa) by thrombin, thrombin-thrombomodulin and plasmin. |
| 1252 | 17213471 | Circulating TF procoagulant activity (TF-PCA), factor VIIa activity (FVIIa; clotting assays), TF antigen (TF-Ag; ELISA), prothrombin fragment 1.2 (F1.2), thrombin-antithrombin complexes (ELISAs), CD40 ligand expression on platelets, and monocyte-platelet aggregates (flow cytometry) were determined in blood from normal volunteers undergoing 24 h of basal glucose/basal insulin (BG/BI) clamps and high-glucose/high-insulin (HG/HI) clamps with and without SMS. |
| 1253 | 17229985 | Superoxide production was significantly increased in patients with cardiovascular risk profile when compared to controls, while platelet aggregation in response to either collagen or thrombin were borderline higher, and did not reach statistical significance. |
| 1254 | 17365861 | Maximum platelets aggregation rate (MPAR) in control and diabetic subjects by adenosine diphosphate (ADP), collagen and thrombin were measured by aggregometer after pretreatment with 100 ng/ml leptin for 60 min. |
| 1255 | 17365861 | The MPAR by 0.15 U/ml thrombin stimulation in leptin-treated platelet in the controls was significantly increased compared with that in non-treated platelets, but not by ADP and collagen stimulation. |
| 1256 | 17365861 | Maximum platelets aggregation rate (MPAR) in control and diabetic subjects by adenosine diphosphate (ADP), collagen and thrombin were measured by aggregometer after pretreatment with 100 ng/ml leptin for 60 min. |
| 1257 | 17365861 | The MPAR by 0.15 U/ml thrombin stimulation in leptin-treated platelet in the controls was significantly increased compared with that in non-treated platelets, but not by ADP and collagen stimulation. |
| 1258 | 17395187 | Men in lower social classes had higher mean levels of C-reactive protein, fibrinogen, interleukin-6, white blood cell count, von Willebrand factor (vWF), factor VIII, activated protein C (APC) resistance, plasma viscosity, fibrin D-dimer and platelet count, compared to higher social class groups; but not of tissue plasminogen activator antigen, haematocrit or activated partial prothrombin time. |
| 1259 | 17682344 | One of the main anti-inflammatory response mediators is bikunin (Bik) that is responsible for inhibiting the activity of many serine proteases such as trypsin, thrombin, chymotrypsin, kallikrein, plasmin, elastase, cathepsin, Factors IXa, Xa, XIa, and XlIa. |
| 1260 | 17785358 | Circulating tissue factor procoagulant activity and thrombin generation in patients with type 2 diabetes: effects of insulin and glucose. |
| 1261 | 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. |
| 1262 | 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. |
| 1263 | 17957564 | To these purposes, we performed: (i) measurement of basal and thrombin-stimulated [Ca(2+)](i) in platelets isolated from type 2 diabetic patients and from normal subjects of young (27 +/- 7 years), mature (48 +/- 12 years) and older (>60 years) age, and (ii) quantitation of [Ca(2+)](i) when platelets of young healthy subjects were exposed to 25.5 mM glucose (vs. 11 mM glucose), 0.23-1.7 mM AGE-poly-L-lysine (vs. poly-L-lysine), 0.3-2.26 mM AGE-albumin (vs. albumin), and to 10 mM and 100 mM H(2)O(2). |
| 1264 | 17957564 | The results showed that: (i) in physiological conditions, [Ca(2+)](i) was approximately 10% increased in the platelets of the mature subjects, and approximately 33% enhanced at the older group (vs. young), sustaining that biological ageing is associated with accumulation of free [Ca(2+)](i) within the platelets cytoplasm; (ii) in type 2 diabetes, [Ca(2+)](i) was approximately 16% and approximately 27% higher in the platelets of mature and older patients, respectively (vs. age-matched normals), demonstrating that ageing of diabetics is accompanied by alterations in calcium balance (vs. physiological ageing); (iii) thrombin (1U/ml) induced approximately 39% increase of [Ca(2+)](i) in platelets of matures and approximately 29% at older normals, and approximately 34% increase at the mature diabetics, approximately 84% at the older diabetics (vs. no thrombin condition), indicating that under thrombin stimulation simultaneous insults of diabetes and advanced age produced a higher thrombin-evoked mobilization of Ca(2+) from intracellular stores; (iv) the components of the diabetic milieu had various effects on platelet free [Ca(2+)](i): high enhancement ( approximately 73%) in 25.5 mM glucose (vs. 11 mM glucose), a minor increase ( approximately 15%) in 100 mM H(2)O(2), and a decrease (by approximately 56% and approximately 132%) in 1.7 mM AGE- poly-L-lysine (vs. poly-L-lysine) and 2.26 mM AGE- albumin (vs. albumin), respectively. |
| 1265 | 17957564 | To these purposes, we performed: (i) measurement of basal and thrombin-stimulated [Ca(2+)](i) in platelets isolated from type 2 diabetic patients and from normal subjects of young (27 +/- 7 years), mature (48 +/- 12 years) and older (>60 years) age, and (ii) quantitation of [Ca(2+)](i) when platelets of young healthy subjects were exposed to 25.5 mM glucose (vs. 11 mM glucose), 0.23-1.7 mM AGE-poly-L-lysine (vs. poly-L-lysine), 0.3-2.26 mM AGE-albumin (vs. albumin), and to 10 mM and 100 mM H(2)O(2). |
| 1266 | 17957564 | The results showed that: (i) in physiological conditions, [Ca(2+)](i) was approximately 10% increased in the platelets of the mature subjects, and approximately 33% enhanced at the older group (vs. young), sustaining that biological ageing is associated with accumulation of free [Ca(2+)](i) within the platelets cytoplasm; (ii) in type 2 diabetes, [Ca(2+)](i) was approximately 16% and approximately 27% higher in the platelets of mature and older patients, respectively (vs. age-matched normals), demonstrating that ageing of diabetics is accompanied by alterations in calcium balance (vs. physiological ageing); (iii) thrombin (1U/ml) induced approximately 39% increase of [Ca(2+)](i) in platelets of matures and approximately 29% at older normals, and approximately 34% increase at the mature diabetics, approximately 84% at the older diabetics (vs. no thrombin condition), indicating that under thrombin stimulation simultaneous insults of diabetes and advanced age produced a higher thrombin-evoked mobilization of Ca(2+) from intracellular stores; (iv) the components of the diabetic milieu had various effects on platelet free [Ca(2+)](i): high enhancement ( approximately 73%) in 25.5 mM glucose (vs. 11 mM glucose), a minor increase ( approximately 15%) in 100 mM H(2)O(2), and a decrease (by approximately 56% and approximately 132%) in 1.7 mM AGE- poly-L-lysine (vs. poly-L-lysine) and 2.26 mM AGE- albumin (vs. albumin), respectively. |
| 1267 | 17966595 | [Factors influencing thrombin generation measured as thrombin-antithrombin complexes levels and using calibrated automated thrombogram in patients with advanced coronary artery disease]. |
| 1268 | 18075282 | Plasminogen activator inhibitor-1 and thrombin activatable fibrinolysis inhibitor levels in non-alcoholic steatohepatitis. |
| 1269 | 18223196 | BI 1356 was >/=10,000-fold more selective for DPP-4 than DPP-8, DPP-9, amino-peptidases N and P, prolyloligopeptidase, trypsin, plasmin, and thrombin and was 90-fold more selective than for fibroblast activation protein in vitro. |
| 1270 | 18316629 | Hyperglycemia reduced neutrophil degranulation (plasma elastase levels, P < .001) and exaggerated coagulation (plasma concentrations of thrombin-antithrombin complexes and soluble tissue factor, both P < .001). |
| 1271 | 18320477 | These disorders include deficiencies of anticoagulant proteins such as protein C, protein S, and antithrombin III, abnormalities of factor V and prothrombin resulting from genetic mutations, and hyperhomocysteinemia. |
| 1272 | 18350479 | Thrombin-activatable fibrinolysis inhibitor and cardiovascular risk factors in polycystic ovary syndrome. |
| 1273 | 18406001 | Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy. |
| 1274 | 18406001 | The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels. |
| 1275 | 18406001 | Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes. |
| 1276 | 18406001 | Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking. |
| 1277 | 18406001 | Gestational diabetes has no additional effect on plasma thrombin-activatable fibrinolysis inhibitor antigen levels beyond pregnancy. |
| 1278 | 18406001 | The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels. |
| 1279 | 18406001 | Plasma TAFI and PAI-1 antigen levels were measured in 26 pregnant women with gestational diabetes, 25 pregnant women with normal glucose tolerance, and age-matched 24 non-pregnant women with no history of gestational diabetes. |
| 1280 | 18406001 | Despite increased PAI-1 antigen levels associated with gestational diabetes, the effect of gestational diabetes on TAFI antigen levels is lacking. |
| 1281 | 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. |
| 1282 | 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. |
| 1283 | 18433156 | PDR vitreous also had increased levels of peroxiredoxin-1 and decreased levels of extracellular superoxide dismutase, compared with noDR or NDM vitreous. |
| 1284 | 18439569 | STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets. |
| 1285 | 18439569 | Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation. |
| 1286 | 18439569 | Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation. |
| 1287 | 18439569 | The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody. |
| 1288 | 18439569 | The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores. |
| 1289 | 18439569 | These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3. |
| 1290 | 18439569 | STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets. |
| 1291 | 18439569 | Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation. |
| 1292 | 18439569 | Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation. |
| 1293 | 18439569 | The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody. |
| 1294 | 18439569 | The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores. |
| 1295 | 18439569 | These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3. |
| 1296 | 18439569 | STIM1 regulates acidic Ca2+ store refilling by interaction with SERCA3 in human platelets. |
| 1297 | 18439569 | Electrotransjection of cells with anti-STIM1 (Y(231)-K(243)) antibody, directed towards a cytoplasmic sequence of STIM1, significantly reduced acidic store refilling, which was tested by remobilizing Ca(2+) from the acidic stores using 2,5-di-(t-butyl)-1,4-hydroquinone (TBHQ) after a brief refilling period that followed thrombin stimulation. |
| 1298 | 18439569 | Platelet treatment with thrombin or thapsigargin in combination with ionomycin, to induce extensive Ca(2+) store depletion, resulted in a transient increase in the interaction between STIM1 and SERCA3, reaching a maximum 30 s after stimulation. |
| 1299 | 18439569 | The coupling between STIM1 and SERCA3 was abolished by electrotransjection with anti-STIM1 antibody. |
| 1300 | 18439569 | The interaction between STIM1 and SERCA3 induced by thrombin or by treatment with thapsigargin plus ionomycin is reduced in platelets from type 2 diabetic patients, as well as Ca(2+) reuptake into the acidic Ca(2+) stores. |
| 1301 | 18439569 | These findings provide evidence for a role of STIM1 in acidic store refilling in platelets probably acting as a Ca(2+) sensor and regulating the activity of SERCA3. |
| 1302 | 18571697 | Thrombin regulates vascular smooth muscle cell proteoglycan synthesis via PAR-1 and multiple downstream signalling pathways. |
| 1303 | 18612541 | Patients with DM exhibited higher baseline platelet activity by adenosine diphosphate (ADP)- (p = 0.0002), and collagen-induced (p = 0.03) aggregometry; Ultegra- (p = 0.0001), and PFA-100 (p = 0.02) analyzers; and expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) (p = 0.01), glycoprotein (GP) IIb/IIIa antigen (p = 0.001), and activity (p = 0.02), vitronectin receptor (p = 0.03), P selectin (p = 0.02), and intact epitope of PAR-1 thrombin receptor (p = 0.02). |
| 1304 | 18619595 | In the present report, we describe the effects of these alterations on the transfers of phospholipids (PL) from VLDL to platelets in basal conditions or after thrombin (0.1U/mL) or lipoprotein lipase (LPL, 500ng/mL)-mediated platelet activation. |
| 1305 | 18619595 | When we compared the platelets from either diabetic patients or control subjects, we observed that the transfers of PL from control VLDL to diabetic platelets were 20-30% higher than those to control platelets, whether in basal conditions or under LPL or thrombin stimulations. |
| 1306 | 18619595 | In the present report, we describe the effects of these alterations on the transfers of phospholipids (PL) from VLDL to platelets in basal conditions or after thrombin (0.1U/mL) or lipoprotein lipase (LPL, 500ng/mL)-mediated platelet activation. |
| 1307 | 18619595 | When we compared the platelets from either diabetic patients or control subjects, we observed that the transfers of PL from control VLDL to diabetic platelets were 20-30% higher than those to control platelets, whether in basal conditions or under LPL or thrombin stimulations. |
| 1308 | 18639910 | Derangement of laboratory features such as prothrombin time, activated partial thromboplastin time and serum albumin level was common on presentation. |
| 1309 | 18673157 | The assay is based on repeated spectrophotometric registration of fibrin-aggregation in citrated plasma, to which small amounts of exogenous thrombin, tissue type plasminogen activator and calcium chloride have been added. |
| 1310 | 19069453 | The parameters measured in the study included results of the auticoagulation test, hemolysate of the aggregation test, thrombin time, fibrinogen level, fibrinolytic activity, fibrinolygase activity, and antithrombin III level at 07 h 00 min, 11 hr 00 min, 15 hr 00 min, 19 hr 00 min, 23 hr 00 min, and 03 hr 00 min in 20 healthy subjects and 30 patients with type 1 diabetes mellitus. |
| 1311 | 19249500 | We assessed visfatin markers of coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2; fibrinolysis: tissue plasminogen activator, plasminogen activator inhibitor, plasmin-antiplasmin complexes; endothelial function/injury: von Willebrand factor, thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule (VCAM); inflammation: hsCRP and interleukin-6. |
| 1312 | 19249500 | On univariate analysis, visfatin correlated positively with prothrombin fragments 1 + 2, VCAM, creatinine, high-sensitivity C-reactive protein, and negatively with albumin. |
| 1313 | 19249500 | We assessed visfatin markers of coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2; fibrinolysis: tissue plasminogen activator, plasminogen activator inhibitor, plasmin-antiplasmin complexes; endothelial function/injury: von Willebrand factor, thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule (VCAM); inflammation: hsCRP and interleukin-6. |
| 1314 | 19249500 | On univariate analysis, visfatin correlated positively with prothrombin fragments 1 + 2, VCAM, creatinine, high-sensitivity C-reactive protein, and negatively with albumin. |
| 1315 | 19349859 | Factor V G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase polymorphism C677T are not associated with coronary artery disease and type 2 diabetes mellitus in western Iran. |
| 1316 | 19349859 | There are controversial results related to the contribution of factor V Leiden G1691A, prothrombin gene G20210A and methylentetrahydrofolate reductase (MTHFR) C677T mutations in the development of coronary artery disease (CAD) and their association with diabetes. |
| 1317 | 19349859 | Genotyping was done by polymerase chain reaction (PCR)-restriction fragment length polymorphism using Mnl I, Hind III and Hinf I for factor V Leiden, prothrombin G20210A and MTHFR C677T, respectively. |
| 1318 | 19349859 | Our results indicate that there is no significant difference between the prevalence of thrombophilic mutations of factor V Leiden, prothrombin G20210A variant and MTHFR C677T in CAD patients with or without diabetes compared with controls. |
| 1319 | 19349859 | Factor V G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase polymorphism C677T are not associated with coronary artery disease and type 2 diabetes mellitus in western Iran. |
| 1320 | 19349859 | There are controversial results related to the contribution of factor V Leiden G1691A, prothrombin gene G20210A and methylentetrahydrofolate reductase (MTHFR) C677T mutations in the development of coronary artery disease (CAD) and their association with diabetes. |
| 1321 | 19349859 | Genotyping was done by polymerase chain reaction (PCR)-restriction fragment length polymorphism using Mnl I, Hind III and Hinf I for factor V Leiden, prothrombin G20210A and MTHFR C677T, respectively. |
| 1322 | 19349859 | Our results indicate that there is no significant difference between the prevalence of thrombophilic mutations of factor V Leiden, prothrombin G20210A variant and MTHFR C677T in CAD patients with or without diabetes compared with controls. |
| 1323 | 19349859 | Factor V G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase polymorphism C677T are not associated with coronary artery disease and type 2 diabetes mellitus in western Iran. |
| 1324 | 19349859 | There are controversial results related to the contribution of factor V Leiden G1691A, prothrombin gene G20210A and methylentetrahydrofolate reductase (MTHFR) C677T mutations in the development of coronary artery disease (CAD) and their association with diabetes. |
| 1325 | 19349859 | Genotyping was done by polymerase chain reaction (PCR)-restriction fragment length polymorphism using Mnl I, Hind III and Hinf I for factor V Leiden, prothrombin G20210A and MTHFR C677T, respectively. |
| 1326 | 19349859 | Our results indicate that there is no significant difference between the prevalence of thrombophilic mutations of factor V Leiden, prothrombin G20210A variant and MTHFR C677T in CAD patients with or without diabetes compared with controls. |
| 1327 | 19349859 | Factor V G1691A, prothrombin G20210A and methylenetetrahydrofolate reductase polymorphism C677T are not associated with coronary artery disease and type 2 diabetes mellitus in western Iran. |
| 1328 | 19349859 | There are controversial results related to the contribution of factor V Leiden G1691A, prothrombin gene G20210A and methylentetrahydrofolate reductase (MTHFR) C677T mutations in the development of coronary artery disease (CAD) and their association with diabetes. |
| 1329 | 19349859 | Genotyping was done by polymerase chain reaction (PCR)-restriction fragment length polymorphism using Mnl I, Hind III and Hinf I for factor V Leiden, prothrombin G20210A and MTHFR C677T, respectively. |
| 1330 | 19349859 | Our results indicate that there is no significant difference between the prevalence of thrombophilic mutations of factor V Leiden, prothrombin G20210A variant and MTHFR C677T in CAD patients with or without diabetes compared with controls. |
| 1331 | 19436948 | Serum VEGF and plasma von Willebrand factor, soluble thrombomodulin, plasminogen activator inhibitor 1, thrombin-activatable fibrinolysis inhibitor (TAFI) and tissue plasminogen activator (t-PA) were measured using enzyme-linked immunosorbent assay in all subjects. |
| 1332 | 19436948 | Only TAFI correlated with VEGF in MAU. |
| 1333 | 19437339 | Thrombin receptor agonist peptide 6 (TRAP(6), residues 42-47 of the thrombin receptor) and collagen I induced platelet aggregation was measured as a time course of glycated albumin incubation. |
| 1334 | 19437339 | The thrombogenicity of platelets incubated with glycated albumin was also measured under static and dynamic flow conditions using the modified prothrombinase assay. |
| 1335 | 19437339 | CD41 and CD62P expression was examined using flow cytometry to validate aggregation and activation studies. |
| 1336 | 19437339 | Platelets subjected to glycated albumin were more susceptible to TRAP(6)- and collagen-induced aggregation and flow induced activation. |
| 1337 | 19705255 | Antithrombin, Protein C, Protein S and homocysteine levels, lupus anticoagulant, anticardiolipin antibodies, FV G1691A and prothrombin G20210A polymorphisms were comparable in the two groups, nor were different according to RVO localization or to the age at event. |
| 1338 | 19718465 | The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor. |
| 1339 | 19718465 | The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI). |
| 1340 | 19718465 | Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential. |
| 1341 | 19718465 | This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected. |
| 1342 | 19718465 | The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor. |
| 1343 | 19718465 | The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI). |
| 1344 | 19718465 | Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential. |
| 1345 | 19718465 | This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected. |
| 1346 | 19718465 | The effects of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor. |
| 1347 | 19718465 | The aim of this study was to determine the effect of hyperglycaemia on thrombin-activatable fibrinolysis inhibitor (TAFI). |
| 1348 | 19718465 | Glycated TAFI showed decreased activity after activation by thrombin-thrombomodulin in a glyceraldehyde-dose-dependent manner and a reduced anti-fibrinolytic potential. |
| 1349 | 19718465 | This is in contrast to fibrinolytic factors as plasminogen-activator inhibitor I and tissue-type plasminogen activator, which are affected. |
| 1350 | 19755774 | Serious venous thromboembolism, heterozygous factor V Leiden and prothrombin G20210A mutations in a patient with Klinefelter syndrome and type 2 diabetes. |
| 1351 | 19755774 | Here, we present the youngest KS case with pulmonary thromboembolism with the heterozygous mutations in factor V Leiden and prothrombin genes, as detected by further tests. |
| 1352 | 19755774 | Serious venous thromboembolism, heterozygous factor V Leiden and prothrombin G20210A mutations in a patient with Klinefelter syndrome and type 2 diabetes. |
| 1353 | 19755774 | Here, we present the youngest KS case with pulmonary thromboembolism with the heterozygous mutations in factor V Leiden and prothrombin genes, as detected by further tests. |
| 1354 | 19787562 | Inherited variations of the vitamin K epoxide reductase C1 enzyme and of the cytochrome P450 2C9 system influence the dosage as well as exogenous factors such as food and drug intake or intercurrent diseases. |
| 1355 | 19787562 | Indirect systemic and oral direct factor Xa and oral direct thrombin inhibitors are currently being developed for the prevention of embolism in patients with AF. |
| 1356 | 19806938 | The following parameters were assessed: patency of the bypasses and major arteries of the lower limbs (LL), homocysteine (Hey), fibrinolytic activity, fibrinogen, activated partial thromboplastin time (aPTT), factor XIII, thrombin time, prothrombin index, activity of antithrombin III (AIII), platelet aggregation with ADP, and glycosylated haemoglobin (Hb Aic). |
| 1357 | 19966184 | Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice. |
| 1358 | 19966184 | The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. |
| 1359 | 19966184 | Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. |
| 1360 | 19966184 | The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. |
| 1361 | 19966184 | The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. |
| 1362 | 19966184 | These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. |
| 1363 | 19966184 | Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice. |
| 1364 | 19966184 | The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. |
| 1365 | 19966184 | Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. |
| 1366 | 19966184 | The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. |
| 1367 | 19966184 | The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. |
| 1368 | 19966184 | These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. |
| 1369 | 19966184 | Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice. |
| 1370 | 19966184 | The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. |
| 1371 | 19966184 | Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. |
| 1372 | 19966184 | The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. |
| 1373 | 19966184 | The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. |
| 1374 | 19966184 | These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. |
| 1375 | 19966184 | Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice. |
| 1376 | 19966184 | The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. |
| 1377 | 19966184 | Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. |
| 1378 | 19966184 | The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. |
| 1379 | 19966184 | The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. |
| 1380 | 19966184 | These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. |
| 1381 | 19966184 | Inhibition of thrombin action ameliorates insulin resistance in type 2 diabetic db/db mice. |
| 1382 | 19966184 | The binding of thrombin to its receptor stimulates inflammatory cytokines including IL-6 and monocyte chemoattractant protein-1 (MCP-1); both are associated with the development of insulin resistance. |
| 1383 | 19966184 | Because increased adiposity enhanced the expression of coagulation factor VII that stimulates the coagulation pathway in adipose tissue, we tested whether the inhibition of thrombin action ameliorates insulin resistance in obese diabetic (Lpr(-/-):db/db) mice. |
| 1384 | 19966184 | The 4-wk administration of argatroban, a selective thrombin inhibitor, reduced fasting plasma glucose and ameliorated insulin resistance in these mice. |
| 1385 | 19966184 | The aberrant gene expression of MCP-1, IL-6, adiponectin, and factor VII and suppressed insulin receptor substrate-1-Akt signaling in adipose tissue of db/db mice were reversed by argatroban treatment. |
| 1386 | 19966184 | These results demonstrate that increased adiposity enhances the production of thrombin in adipose tissue by stimulating factor VII expression and suggest that increased thrombin activity in adipose tissue plays an important role in the development of insulin resistance via enhancing MCP-1 production, leading to macrophage infiltration and insulin receptor substrate-1-Akt pathway inactivation. |
| 1387 | 20070990 | The body mass index, fasting plasma glucose, immunoreactive insulin, homeostasis model assessment of insulin resistance, hemoglobin A(1c) (HbA(1c)), total cholesterol, triglycerides, high-density lipoprotein cholesterol, prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin-antithrombin III complex, plasmin-alpha2-plasmin inhibitor complex, and plasma plasminogen activator inhibitor type 1 (PAI-1) were not changed. |
| 1388 | 20070990 | The other independent variants, like the final dose of gliclazide, homeostasis model assessment of insulin resistance, percentage change of prothrombin time, activated partial thromboplastin time, and total cholesterol, were not significantly associated with the percentage change of plasma PAI-1 level. |
| 1389 | 20070990 | The body mass index, fasting plasma glucose, immunoreactive insulin, homeostasis model assessment of insulin resistance, hemoglobin A(1c) (HbA(1c)), total cholesterol, triglycerides, high-density lipoprotein cholesterol, prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin-antithrombin III complex, plasmin-alpha2-plasmin inhibitor complex, and plasma plasminogen activator inhibitor type 1 (PAI-1) were not changed. |
| 1390 | 20070990 | The other independent variants, like the final dose of gliclazide, homeostasis model assessment of insulin resistance, percentage change of prothrombin time, activated partial thromboplastin time, and total cholesterol, were not significantly associated with the percentage change of plasma PAI-1 level. |
| 1391 | 20082095 | The best characterized endothelium-derived relaxing factor is nitric oxide (NO), which is synthesized by the endothelial isoform of nitric oxide synthase (eNOS). |
| 1392 | 20082095 | Endothelium-dependent relaxations involve both pertussis-toxin-sensitive G(i) (e.g., responses to serotonin, sphingosine 1-phosphate, alpha(2)-adrenergic agonists, and thrombin) and pertussis-toxin-insensitive G(q) (e.g., adenosine diphosphate and bradykinin) coupling proteins. eNOS undergoes a complex pattern of intracellular regulation, including post-translational modifications involving enzyme acylation and phosphorylation. eNOS is reversibly targeted to signal-transducing plasmalemmal caveolae where the enzyme interacts with a number of regulatory proteins, many of which are modified in cardiovascular disease states. |
| 1393 | 20102751 | Thrombomodulin (TM) acts as an important regulator of thrombosis and inflammation through its capacity to channel the catalytic activity of thrombin towards generation of activated protein C (APC), a potent anticoagulant and anti-inflammatory agent. |
| 1394 | 20216989 | Association between the Thr325Ile polymorphism of the thrombin-activatable fibrinolysis inhibitor and stroke in the Ludwigshafen Risk and Cardiovascular Health Study. |
| 1395 | 20216989 | The thrombin-activatable fibrinolysis inhibitor (TAFI) is a key mediator in the regulation of endogenous fibrinolysis, down-regulating clot lysis by degrading the C-terminal lysine residues from fibrin, which are important for binding and activating plasminogen. |
| 1396 | 20216989 | Association between the Thr325Ile polymorphism of the thrombin-activatable fibrinolysis inhibitor and stroke in the Ludwigshafen Risk and Cardiovascular Health Study. |
| 1397 | 20216989 | The thrombin-activatable fibrinolysis inhibitor (TAFI) is a key mediator in the regulation of endogenous fibrinolysis, down-regulating clot lysis by degrading the C-terminal lysine residues from fibrin, which are important for binding and activating plasminogen. |
| 1398 | 20494125 | Since long, the structure of the fibrin network has been evaluated, and recently the influence of aspirin and new thrombin and factor Xa inhibitors has been investigated. |
| 1399 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 1400 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 1401 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 1402 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 1403 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 1404 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 1405 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 1406 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 1407 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 1408 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 1409 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 1410 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 1411 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 1412 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 1413 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 1414 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 1415 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 1416 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 1417 | 20575037 | Blacks had a significantly higher mean BMI and a significantly lower proportion with recent surgery, trauma or infection, family history of VTE, and documented thrombophilia (solely from reduced factor V Leiden and prothrombin G20210A prevalence). |
| 1418 | 20723798 | With numerous novel factor Xa and direct thrombin inhibitor drugs completing phase III clinical trials, it is likely that additional oral anticoagulant drugs will be clinically available for stroke prevention soon. |
| 1419 | 20828799 | The role of thrombin-activatable fibrinolysis inhibitor in diabetic wound healing. |
| 1420 | 20978998 | The assay is based on repeated spectrophotometric registration of the fibrin-aggregation curve in platelet-poor plasma containing small amounts of exogenous thrombin, tissue-type plasminogen activator, and calcium. |
| 1421 | 21389321 | In diabetic patients, the FVL mutation, but not the plasminogen activator inhibitor-1 4G/5G polymorphism, is associated with reduced albuminuria, which is consistent with a nephroprotective role of low but sustained thrombin generation. |
| 1422 | 21389321 | These results identify a nephroprotective function of low but sustained thrombin levels in FVL carriers, supporting a dual, context-dependent function of thrombin in chronic diseases. |
| 1423 | 21389321 | In diabetic patients, the FVL mutation, but not the plasminogen activator inhibitor-1 4G/5G polymorphism, is associated with reduced albuminuria, which is consistent with a nephroprotective role of low but sustained thrombin generation. |
| 1424 | 21389321 | These results identify a nephroprotective function of low but sustained thrombin levels in FVL carriers, supporting a dual, context-dependent function of thrombin in chronic diseases. |
| 1425 | 21406417 | Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes. |
| 1426 | 21406417 | We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis. |
| 1427 | 21406417 | Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed. |
| 1428 | 21406417 | Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT. |
| 1429 | 21406417 | Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes. |
| 1430 | 21406417 | We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis. |
| 1431 | 21406417 | Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed. |
| 1432 | 21406417 | Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT. |
| 1433 | 21406417 | Plasma thrombin-activatable fibrinolysis inhibitor levels are not associated with glucose intolerance and subclinical atherosclerosis in women with previous gestational diabetes. |
| 1434 | 21406417 | We aimed to determine plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels in women with previous gestational diabetes mellitus (GDM) and to evaluate the possible association of plasma TAFI with glucose intolerance and markers of subclinical atherosclerosis. |
| 1435 | 21406417 | Circulating lipids, interleukin-6, matrix metalloproteinase-1, fibrinogen, plasminogen activator inhibitor-1, and TAFI antigen levels were assayed. |
| 1436 | 21406417 | Thrombin-activatable fibrinolysis inhibitor was not associated with the indices of insulin resistance, glucose intolerance, markers of atherosclerosis, and carotid IMT. |
| 1437 | 21517734 | On the other hand, TF upregulation may facilitate inflammation by enhancing intravascular fibrin deposition, formation of proinflammatory fragments of fibrin, and by generating coagulation proteases, including FVIIa, FXa and thrombin, that activate protease-activated receptors. |
| 1438 | 21519232 | The relationship among TAFI, t-PA, PAI-1 and F1 + 2 in type 2 diabetic patients with normoalbuminuria and microalbuminuria. |
| 1439 | 21519232 | The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria. |
| 1440 | 21519232 | TAFI, PAI-1, t-PA and F1+2 were assessed by enzyme-linked immunosorbent assay (ELISA) in all patients. |
| 1441 | 21519232 | TAFI was significantly increased in the MAU group, PAI-1 and F1+2 were increased in both groups and t-PA was not elevated in either group compared to controls. |
| 1442 | 21519232 | We found positive correlations in the NAU: TAFI and fibrinogen (r=0.65, P=0.02), PAI-1 and triglycerides (r=0.67, P=0.01), in the MAU: TAFI and F1+2 (r=0.48, P=0.02), TAFI and systolic blood pressure (r=0.53, P=0.01), PAI-1 and BMI (r=0.43, P<0.05). |
| 1443 | 21519232 | TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1. |
| 1444 | 21574459 | A polymerase chain reaction was used to diagnose single-nucleotide substitution of C6777T in the MTHFR gene, a point mutation in the coagulation factor V (FV) gene, and a factor II (FII) G20210A gene mutation in the coagulation factor II (FII) gene. |
| 1445 | 21615248 | General characteristics of the patients and hematological parameters (platelet count, white blood cell count, prothrombin time, partial thromboplastin time (PTT), bleeding time, coagulation time, protein C, protein S, antithrombin III, fibrinogen, D-dimer, factor VIII, factor IX, and factor X levels) at diagnosis (0th hour) and 96th hour after the initiation of treatment were determined. |
| 1446 | 21691748 | The mean age and duration of DM1 of patients also affected by CD were similar to those of only diabetic patients, but the metabolic control and the hemocoagulative parameters were significantly different between the two groups: DM1 patients also affected by CD presented significantly lower concentrations of glycosylated hemoglobin (HbA1c) (P < 0.05), cholesterol (P < 0.001), triglycerides (P < 0.001), factor VII antigen (FVII:ag) (P < 0.005), factor VII coagulant activity (FVII:c) (P < 0.05), and prothrombin degradation fragments (F1+2) (P < 0.001), as well as higher values of activated C protein (APC) (<0.001). |
| 1447 | 21935671 | Valvular tissue factor (TF), TF pathway inhibitor (TFPI), prothrombin, C-reactive protein (CRP) expression were evaluated by immunostaining and TF, prothrombin, and CRP transcripts were analyzed by real-time PCR. |
| 1448 | 21935671 | In DM group, TF-, TFPI-, and prothrombin expression within valves was not related to demographics, body mass index, and concomitant diseases, whereas increased expression related to DM was found for CRP on both protein (2.87 [0.5-9]% vs. 0.94 [0-4]%, p = 0.01) and transcript levels (1.3 ± 0.61 vs. 0.22 ± 0.43, p = 0.009). |
| 1449 | 21935671 | Valvular tissue factor (TF), TF pathway inhibitor (TFPI), prothrombin, C-reactive protein (CRP) expression were evaluated by immunostaining and TF, prothrombin, and CRP transcripts were analyzed by real-time PCR. |
| 1450 | 21935671 | In DM group, TF-, TFPI-, and prothrombin expression within valves was not related to demographics, body mass index, and concomitant diseases, whereas increased expression related to DM was found for CRP on both protein (2.87 [0.5-9]% vs. 0.94 [0-4]%, p = 0.01) and transcript levels (1.3 ± 0.61 vs. 0.22 ± 0.43, p = 0.009). |
| 1451 | 22028447 | Heparin-binding EGF-like growth factor (HB-EGF) mediates 5-HT-induced insulin resistance through activation of EGF receptor-ERK1/2-mTOR pathway. |
| 1452 | 22028447 | Although an inverse correlation between insulin sensitivity and the level of Gq/11-coupled receptor agonists, such as endothelin-1, thrombin, and 5-hydroxytryptamine (5-HT), has been reported, its precise mechanism remains unclear. |
| 1453 | 22028447 | In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. |
| 1454 | 22028447 | In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. |
| 1455 | 22028447 | HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. |
| 1456 | 22028447 | Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. |
| 1457 | 22028447 | Pharmacological inhibition of either Gq/11-coupled receptors or metalloproteinases, as well as either inhibition or knockdown of HB-EGF or Gαq/11, restored insulin signal transduction impaired by 5-HT. |
| 1458 | 22028447 | Inhibition of metalloproteinase activity also abolished HB-EGF production and subsequent EGF receptor activation by other Gq/11-coupled receptor agonists known to cause insulin resistance, such as endothelin-1 and thrombin. |
| 1459 | 22028447 | These results suggest that transactivation of the EGF receptor through HB-EGF processing plays a pivotal role in 5-HT-induced insulin resistance. |
| 1460 | 22072096 | New direct thrombin inhibitors and direct Factor Xa inhibitors in development offer the possibility of simplifying treatment and management although offering similar or better efficacy and safety profiles to warfarin. |
| 1461 | 22198859 | The latter complication has been consistently associated with inherited (i.e., the prothrombin 20210 polymorphism, and polymorphisms in the genes encoding for transforming growth factor-β1, nitric oxide synthase, plasminogen activator inhibitor-1, angiotensin converting enzyme, and methylene tetrahydrofolate reductase), and acquired thrombotic risk factors (i.e., diabetes, obesity, atrial fibrillation, hypertension, hyperhomocysteinemia, hyperlipoproteinemia(a), low serum albumin, antiphospholipid antibodies, autoantibodies against protein C and S, erythropoietin administration, malnutrition, and cytomegalovirus infection). |
| 1462 | 22484367 | Fasting glucose level, insulin, prothrombin time (PT), fibrinogen, activated partial thromboplastin time (aPTT), D-dimer, endogenous thrombin potential (ETP), C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon-γ-inducible-protein (IP-10), monocyte chemoattractant protein 1 (MCP-1), and interleukin-1 receptor antagonist (IL-1Ra) were measured. |
| 1463 | 22484367 | Anti- (IL-1Ra) and proinflammatory cytokines (MCP-1, IL-6) were significantly increased in obese children in comparison to the control group, even before puberty. |
| 1464 | 22484367 | The cytokines IL-1Ra and MCP-1 were most significantly increased in obese children. |
| 1465 | 22528331 | Factor V leiden G1691A/R506Q (FVL), prothrombin G20210A (FII) and methylenetetrahydrofolate reductase (MTHFR) C677T are related genetic risk factors for venous thromboembolism. |
| 1466 | 22551736 | There were no interaction between glycated hemoglobin level or glycemia on admission and platelet reactivity measured with collagen, arachidonic acid or thrombin receptor agonist peptide-induced aggregation. |
| 1467 | 22585309 | Beyond hyperglycemia in diabetes: role of statin treatment on thrombogenesis triggered by inflammation: Editorial to: "Impact of statins on the coagulation status of type 2 diabetes patients evaluated by a novel thrombin-generations assay" by P. |
| 1468 | 22752805 | We tested 140 with MI individuals for factor V (FV) Leiden, FV H1299R, Prothrombin G20210A, factor XIII (FXIII) V34L, β-fibrinogen b-455G/A, plasminogen activator inhibitor-1 (PAI-1)-675 4G/5G, human platelet antigens 1 (HPA-1) a/b, apolipoprotein B (ApoB) R3500Q, apolipoprotein E (ApoE), E2, E3, and E4, angiotensin-converting enzyme (ACE) D/I, 5,10 methylenetetrahydrofolate reductase (MTHFR) 677C/T, and MTHFR 1298A/C polymorphisms using a ViennaLab CVD strip assay. |
| 1469 | 22859370 | Defining the cellular repertoire of GPCRs identifies a profibrotic role for the most highly expressed receptor, protease-activated receptor 1, in cardiac fibroblasts. |
| 1470 | 22859370 | We discovered that adult rat CFs express 190 GPCRs and that activation of protease-activated receptor 1 (PAR1), the most highly expressed receptor, raises the expression of profibrotic markers in rat CFs, resulting in a 60% increase in collagen synthesis and conversion to a profibrogenic myofibroblast phenotype. |
| 1471 | 22859370 | We use siRNA knockdown of PAR1 (90% decrease in mRNA) to show that the profibrotic effects of thrombin are PAR1-dependent. |
| 1472 | 22859370 | These findings, which define the expression of GPCRs in CFs, provide a proof of principle of an approach to discover previously unappreciated, functionally relevant GPCRs and reveal a potential role for thrombin and PAR1 in wound repair and pathophysiology of the adult heart. |
| 1473 | 22859370 | Defining the cellular repertoire of GPCRs identifies a profibrotic role for the most highly expressed receptor, protease-activated receptor 1, in cardiac fibroblasts. |
| 1474 | 22859370 | We discovered that adult rat CFs express 190 GPCRs and that activation of protease-activated receptor 1 (PAR1), the most highly expressed receptor, raises the expression of profibrotic markers in rat CFs, resulting in a 60% increase in collagen synthesis and conversion to a profibrogenic myofibroblast phenotype. |
| 1475 | 22859370 | We use siRNA knockdown of PAR1 (90% decrease in mRNA) to show that the profibrotic effects of thrombin are PAR1-dependent. |
| 1476 | 22859370 | These findings, which define the expression of GPCRs in CFs, provide a proof of principle of an approach to discover previously unappreciated, functionally relevant GPCRs and reveal a potential role for thrombin and PAR1 in wound repair and pathophysiology of the adult heart. |
| 1477 | 22886693 | Endothelial hyperpermeability is increased by actomyosin contractile activity in response to phosphorylation of myosin light chain by myosin light chain kinase (MLCK). |
| 1478 | 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.). |
| 1479 | 22969847 | To assess whether hepatic capacity of protein synthesis varies with the etiology of cirrhosis, serum albumin and cholinesterase levels, and prothrombin time were compared between alcoholic cirrhosis and hepatitis C virus (HCV)-related cirrhosis. |
| 1480 | 23059602 | The group of patients receiving intra-arterial administration of urokinase showed that the examined parameters on day 20 of treatment as compared with basic therapy alone increased: those of coagulability by 6% (p<0.05), activated partial thromboplastin time by 14% (p<0.01), thrombin time by 9.2% (p<0.01), antithrombin III by 7% (p<0.001). |
| 1481 | 23059602 | The fibrinogen level decreased by 9% (p<0.05), malonic dialdehyde concentration dropped by 30% (p<0.001), the concentrations of catalase and superoxide dismutase elevated by 55% (p<0.001) and 42%, respectively (p<0.05). |
| 1482 | 23066003 | Treatment of a life-threatening laryngeal bradykinin angio-oedema precipitated by dipeptidylpeptidase-4 inhibitor and angiotensin-I converting enzyme inhibitor with prothrombin complex concentrates. |
| 1483 | 23086579 | Ex vivo plasma fibrin clot permeability (K(s)) and lysis time (t(50%)) induced by 1 μg/mL recombinant tissue plasminogen activator (tPA), along with plasma levels of plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tPA, von Willebrand factor (vWF), P-selectin, soluble CD40 ligand (sCD40L), were measured. |
| 1484 | 23086579 | Concomitant DM2 was associated with higher glucose (+24.3%, p < 0.001), fibrinogen (+9.0%, p = 0.037), PAI-1 (+58.7%, p < 0.001), tPA (+24.0%, p < 0.001) and P-selectin (+12.2%, p < 0.001). |
| 1485 | 23086579 | Multiple regression analysis of the whole study group showed that vWF, PAI-1, fibrinogen and DM2 were the independent predictors of t(50%) (R(2) = 0.58, p < 0.001), while only vWF was an independent predictor of K(s) (R(2) = 0.22, p < 0.001). |
| 1486 | 23490299 | Plasma thrombin-antithrombin complex, prothrombin fragments 1 and 2, and D-dimer levels are elevated after endovascular but not open repair of infrarenal abdominal aortic aneurysm. |
| 1487 | 23514988 | New oral anticoagulants targeting thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban and edoxaban) may replace warfarin in many patients with atrial fibrillation due to convincing data both on efficacy and safety as well as convenience. |
| 1488 | 23527528 | NR also had higher arachidonic acid-induced platelet aggregation than R, and a tendency towards higher aggregation induced by thrombin receptor agonist peptide (TRAP), indicating that HPR reflects a global platelet hyper-reactivity. |
| 1489 | 23578325 | Thrombin is also added to whole blood exposed to iron, glucose and blood from diabetes and hemochromatosis patients. |
| 1490 | 23583575 | GPCR signalling is well known to proceed through several linear pathways involving activation of G proteins and their downstream signalling pathways such as activation of phospholipase C. |
| 1491 | 23583575 | In addition, GPCRs signal via transactivation of Protein Tyrosine Kinase receptors such as that for Epidermal Growth Factor (EGF) and Platelet-Derived Growth Factor (PDGF) where GPCR agonists mediate increase levels of phosphorylated Erk (pErk) the immediate downstream product of the activation of EGF receptor. |
| 1492 | 23583575 | It has recently been shown that this paradigm can be extended to include the GPCR transactivation of a Protein Serine/Threonine Kinase receptor, specifically the Transforming Growth Factor β Type I receptor (also known as Alk V) (TβRI) in which case GPCR activation leads to the formation of carboxy terminal polyphosphorylated Smad2 (phosphoSmad2) being the immediate downstream product of the activation of TβRI. |
| 1493 | 23583575 | In the example of proteoglycan synthesis stimulated by GPCR agonists such as thrombin and endothelin-1, the transactivation pathways for the EGF receptor and TβRI are both active and together account for essentially all of the response to the GPCRs. |
| 1494 | 23583575 | In contrast, signalling downstream of GPCRs such as increased inositol 1,4,5 trisphosphate (IP3) and intracellular calcium do not have any effect on GPCR stimulated proteoglycan synthesis. |
| 1495 | 23650948 | Thiazolidinediones (TZDs) represent a class of peroxisome proliferator-activated receptor (PPAR)γ agonists widely used as insulin-sensitizers in the treatment of type 2 diabetes mellitus (T2DM). |
| 1496 | 23650948 | Upon activation platelets synthesize and release many bioactive substances such as thromboxane A2 (TXA2) or pro-inflammatory mediators including CD40 ligand (CD40L) that exert autocrine and paracrine activation processes in vascular inflammation leading to cardiovascular disease (CVD). |
| 1497 | 23650948 | Although PPARγ is a nuclear hormone receptor, anucleate platelets also highly express this receptor and treatment with synthetic PPARγ ligands dampens the release of soluble(s)CD40L and TXA2 in thrombin-activated platelets. |
| 1498 | 23737314 | Family history of dyslipidemia was a predictor for hypertriglyceridemia (P=0.02), higher prothrombin time levels (P=0.013), lower albumin (P=0.024) and T4 (P=0.043) levels. |
| 1499 | 23945058 | Thrombin activatable fibrinolysis inhibitor (TAFI) is an important procoagulant factor. |