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diagnostics
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the activation peptide of procarboxypeptidase B, set free during activation of procarboxypeptidase B, is a marker for acute pancreatitis
pharmacology
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enzyme inhibitors are valid as enhancer of physiological fibrinolysis in microcirculation and as adjunctive agent to tissue-type plasminogen activator for thromboembolic diseases in humans while maintaining a small effect on primary hemostasis
medicine
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agents that improve the efficiency of TAFI to downregulate fibrinolysis might become available for the treatment of bleeding disorders such as hemophilias A and B
medicine
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a range of fibrinolytic kinetic values and the contribution of thrombin activatable fibrinolysis inhibitor in normal subjects are established. Study of disease states involving potential hypofibrinolysis can be conducted using this system to link fibrinolytic vulnerability and thrombophilia
medicine
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argatroban enhances fibrinolysis via a differential inhibition of thrombin-mediated activation of TAFI and factor XIII
medicine
coagulation pathway in patients with non-small-cell lung cancer (NSCLC) is investigated: The TAFI activity, prothrombin fragment 1 + 2 levels, and tissue factor pathway inhibitor activity are significantly higher in patients with lung cancer than in subjects in the control group. There is no statistically significant associations between TAFI activity levels and patient age, sex, body mass index, histopathology, or stage of disease
medicine
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important differences in the hemostatic parameters between the patients with hypothyroidism and healthy controls are found. Increased FVII, TM, and TAFI and decreased FV, FVIII, vWF, protein C, protein S, and TFPI in these patients represent a potential hypercoagulable and hypofibrinolytic state, possible endothelial dysfunction, which might augment the risk for atherosclerotic and atherothrombotic complications in patients with hypothyroidism
medicine
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in Hashimoto thyroiditis, patients have high levels of TAFI activity compared to controls. A high level of TAFI activity suggests fibrinolytic deficit or thrombotic tendency in hypothyroid patients and this deficit is persistent after L-thyroxine replacement
medicine
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it is investigated whether it is possible to detect the activation of the proCPU/CPU system during therapeutic thrombolysis of patients with acute ischemic stroke: activation of the proCPU system during intravenous recombinant tissue plasminogen activator and intra-arterial administration of urokinase in patients with acute ischemic stroke is shown
medicine
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no significant difference in lipid parameters is determined between patients with polycystic ovary syndrome and healthy controls. In addition, no difference in CIMT measurements and TAFI levels between patients with polycystic ovary syndrome and healthy controls is shown
medicine
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pregnancy is associated with elevated plasma TAFI antigen levels but no additional effect of gestational diabetes is found on plasma TAFI antigen levels beyond pregnancy
medicine
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proCPU activation and its relatedness to efficacy and safety of thrombolytic therapy in ischemic stroke patients is investigated. In 12 patients with ischemic stroke who are treated with intravenous or intraarterial thrombolysis, venous blood samples are taken at different time points before, during and after thrombolytic therapy. No correlations between maximal CPU activity or proCPU consumption and patient or stroke characteristics are found. Maximal CPU activity is associated with evolution of the clinical deficit and achieved recanalisation. ProCPU consumption is related to the risk of intracranial hemorrhage, mortality and final infarct volume
medicine
results provide evidence for a role of TAFI in arterial thrombosis in rats and suggest that TAFI inhibition could be explored as an attractive target for the development of new antithrombotic drugs
medicine
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results suggest that women with polycystic ovary syndrome have impaired fibrinolysis, as reflected by increased TAFI. This impairment can contribute to the risk of cardiovascular disease in polycystic ovary syndrome
medicine
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TAFI as well as plasminogen activator inhibitor-1 plasma levels in inflammatory bowel disease patients are compared with healthy controls. Mean plasma plasminogen activator inhibitor-1 levels are significantly higher in both ulcerative colitis patients and Crohns disease patients compared with healthy controls. Mean plasma TAFI levels are significantly lower in both ulcerative colitis patients and Crohns disease patients compared with healthy controls. These results suggest an imbalance of fibrinolysis in inflammatory bowel disease patients
medicine
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TAFI is present in the gastric mucosa and it may play a role in the pathogenesis of Helicobacter pylori infection-associated gastroduodenal disorders
medicine
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TAFI plays an important role in the deterioration of organ dysfunction in sepsis and the inhibitor of TAFIa protects against sepsis-induced tissue damage through regulation of fibrinolysis and inflammation
medicine
TAFI-mediated inhibition of plasmin generation plays a role in the pathogenesis of glomerulonephritis, and it might constitute a novel molecular target for therapy
medicine
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the absolute risk of venous and arterial thromboembolism in subjects with high TAFI levels versus subjects with normal levels, and the contribution of other concomitant thrombophilic defects is assessed. Relatives from four identical cohort studies in families with either deficiencies of antithrombin, protein C or protein S, prothrombin 20210A, high factor VIII levels, or hyperhomocysteinemia are pooled. Only high factor VIII levels are associated with an increased risk of venous and arterial thrombosis, independently of TAFI levels. None of these concomitant defects shows interaction with high TAFI levels. High TAFI levels are not associated with an increased risk of venous and arterial thromboembolism in thrombophilic families
medicine
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the extent of TAFI activation over time in normal plasma and factor VIII deficient plasma (FVIII-DP) is analysed and it is determined whether soluble thrombomodulin can correct the lysis defect in factor VIII deficient plasma. TAFI activation increases as the concentration of factor VIII increases. Factor VIII at a level of 10% fully corrects the lysis defect in spite of the extent of TAFI activation being only one half that obtained with 100% factor VIII. In addition, thrombomodulin increases TAFI activation sufficiently to correct the premature lysis defect in factor VIII-deficient plasma
medicine
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the increased risk of thrombosis in thrombophilia patients is not only ascribable to an increased thrombin generation, but also high levels of proCPU and the presence of the 325Ile genotype tip the balance towards thrombotic tendency even further
medicine
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the proCPU system is not of major importance in the bleeding pathogenesis of these patients. The higher proCPU levels in the patients may even modestly counteract the bleeding tendency
medicine
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this study aims to assess concomitantly the effects of fenofibrate therapy on thrombin-activatable fibrinolysis inhibitor concentrations and endothelial functions in patients with metabolic syndrome. Twenty-five patients are enrolled in the study. Fenofibrate decreases thrombin-activatable fibrinolysis inhibitor levels and improves endothelial function in metabolic syndrome and, thus, suggests a potential for protection against cardiovascular effects
medicine
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the decrease in proCPU concentration in the first 72 h after stroke onset correlates with more severe stroke, unfavourable stroke evolution, and poor longterm stroke outcome
molecular biology
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results demonstrate that the activation peptide is not required for TAFIa activity or for stabilization of the enzyme, but solely for stabilization of the zymogen
molecular biology
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thrombomodulin suppresses pericellular fibrinolysis and plasma-induced tumor cell invasion which is mediated by plasma TAFI activation