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thrombophilia/protease
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Thromboelastographic assessment of the contribution of platelets and clotting proteases to the hypercoagulable state of dogs with immune-mediated hemolytic anemia.
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BACKGROUND
Hypercoagulability is a well-known feature of canine immune-mediated hemolytic anemia (IMHA) and is believed to increase the risk of thrombosis. This study was undertaken to differentiate the relative contribution of platelets and clotting proteases to this hypercoagulability using
Mutations within the protein Z-dependent protease inhibitor gene are associated with venous thromboembolic disease: a new form of thrombophilia.
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Protein Z-dependent protease inhibitor (ZPI) is a serpin that inhibits the activated coagulation factors X and XI. The precise physiological significance of ZPI in the control of haemostasis is unknown although a deficiency of ZPI may be predicted to alter this balance. The coding region of the ZPI
Protective effect of a thrombin receptor (protease-activated receptor 1) gene polymorphism toward venous thromboembolism.
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The human protease-activated receptor 1 (PAR-1) is activated by thrombin at the surface of platelets and endothelial cells, 2 cells that are implicated in hemostasis and thrombosis. We studied the PAR-1 gene in a large case-control study from the Paris Thrombosis Study (PATHROS), and the possible
Nafamostat mesilate, a synthetic protease inhibitor, attenuated hypercoagulability in a canine model of hemorrhagic shock.
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Hypercoagulability is known to occur in the early phase of hemorrhagic shock. The prolongation of excessive clot formation after recovery from a shock state leads to the formation of microthrombi or disseminated intravascular coagulation which disturbs microcirculation, damaging organ function. The
Marburg I polymorphism of factor VII-activating protease and risk of recurrent venous thromboembolism.
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Whether a single nucleotide polymorphism (1601 G > A) in the factor VII-activating protease gene (FSAP Marburg I) is a risk factor for venous thromboembolism (VTE) is unclear. We investigated the relevance of the variant with respect to recurrentVTE. 854 patients with a first unprovoked VTE were
Marburg I polymorphism of factor VII-activating protease is associated with idiopathic venous thromboembolism.
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The factor VII-activating protease (FSAP) variant Marburg I is known to attenuate the profibrinolytic system in vitro and was recently shown to be a significant predictor for the evolution and progression of carotid stenosis. The objective of this case-control study was to assess FSAP Marburg I's
Polymorphisms of the Z protein protease inhibitor and risk of venous thromboembolism: a meta-analysis.
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Two nonsense polymorphisms of Z-dependent protease inhibitor (ZPI; Serpina10) have been identified. To assess the risk of venous thromboembolism (VTE) associated with W303x and R67X Serpina10 mutations, we performed a meta-analysis of studies comparing the prevalence of these two mutations in VTE
Hypercoagulability inhibits monocyte transendothelial migration through protease-activated receptor-1-, phospholipase-Cbeta-, phosphoinositide 3-kinase-, and nitric oxide-dependent signaling in monocytes and promotes plaque stability.
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BACKGROUND
Clinical studies failed to provide clear evidence for a proatherogenic role of hypercoagulability. This is in contrast to the well-established detrimental role of hypercoagulability and thrombin during acute atherosclerotic complications. These seemingly opposing data suggest that
Warm ischemia provokes inflammation and regional hypercoagulability within the heart during off-pump coronary artery bypass: a possible target for serine protease inhibition.
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OBJECTIVE
Accumulating evidence suggests that a hypercoagulable state influences early graft failure after off-pump coronary artery bypass (OPCAB). We hypothesized that regional myocardial ischemia caused by obligatory periods of coronary occlusion during OPCAB is an important trigger for this
The Marburg I polymorphism of factor VII-activating protease and the risk of venous thromboembolism.
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Marburg I polymorphism of factor VII-activating protease and risk of venous thromboembolism.
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Marburg I polymorphism of factor VII-activating protease and risk of recurrent venous thromboembolism.
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Prospective study of polymorphisms of the protein Z-dependent protease inhibitor and risk of venous thromboembolism.
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Polymorphisms of the protein Z-dependent protease inhibitor (ZPI) gene and the risk of venous thromboembolism.
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Prominent protein Z-induced thrombin inhibition in cirrhosis: a new functional assay for hypercoagulability assessment.
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OBJECTIVE
Protein Z (PZ) is an anticoagulant that accelerates the inhibitory effect of PZ-dependent protease inhibitor (ZPI) on coagulation factor Xa. We assessed functional status of PZ system in 158 patients with liver cirrhosis and 59 healthy controls.
METHODS
Plasma PZ and ZPI levels were
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