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Activated protein C (APC) is a serine protease with potent anticoagulant properties, which is formed in blood on the endothelium from an inactive precursor. During normal haemostasis, APC limits clot formation by proteolytic inactivation of factors Va and VIIIa (ref. 2). To do this efficiently the enzyme needs a nonenzymatic cofactor, protein S (ref. 3).(More)
This article continues the review begun in a previous issue of the Journal, which considered the molecular basis and epidemiology of thrombophilia. In order to evaluate the contribution of genetic defects in the patho-genesis of thrombosis, the laboratory investigation should include a functional APC-R lest, determination of the factor V genotype and(More)
We undertook a population-based case-control study to test the clinical importance of a hereditary abnormality in the coagulation system, characterised by poor anticoagulant response to activated protein C (APC), which is associated with familial thrombophilia. The abnormality was detected in 64 (21%) of 301 unselected consecutive patients younger than 70(More)
We investigated whether the occurrence of venous thrombosis in young women who use oral contraceptives might be explained by the factor V Leiden mutation, which leads to resistance to activated protein C and enhances susceptibility to thrombosis. We compared 155 consecutive premenopausal women, aged 15 to 49, who had developed deep venous thrombosis in the(More)
BACKGROUND Microparticles (MPs) are small vesicles released from cells of different origin, bearing surface antigens from parental cells. Elevated numbers of blood MPs have been reported in (cardio)vascular disorders and cancer. Most of these MPs are derived from platelets. OBJECTIVES To investigate whether atomic force microscopy (AFM) can be used to(More)
I n vivo, a delicate balance exists between fibrin formation and fibrinolysis. Reduced blood flow, changes in the vessel wall, and changes in blood composition (hypercoagulability) 1 may all result in a disturbance of this balance, which favors fibrin formation and ultimately may lead to the formation of occlusive thrombi. Venous thromboembolism is the(More)
BACKGROUND A genetic variation located in the 3'-untranslated region of the prothrombin gene (prothrombin 20210 G-->A) was recently described as a risk factor for venous thrombosis. We examined how the presence of this mutation affected the risk of myocardial infarction in a population-based case-control study. Furthermore, we studied the risk of myocardial(More)
Thrombin activatable fibrinolysis inhibitor (TAFI, or procarboxypeptidase B) is the precursor of a recently described carboxypeptidase that potently attenuates fibrinolysis. Therefore, we hypothesized that elevated plasma TAFI levels induce a hypofibrinolytic state associated with an increased risk for venous thrombosis. To evaluate this hypothesis, we(More)
Several studies have found an association between high plasminogen activator inhibitor-1 (PAI-1) levels and myocardial infarction. Whether this is causal or a consequence of atherosclerosis or tissue damage, remains unclear. Homozygous carriers of the 4G allele of the 4G/5G polymorphism in the PAI-1 gene have higher PAI-1 levels compared to carriers of the(More)
Results of plasma microparticles (MPs) measurements reported in the literature vary widely. This is clearly not only related to the lack of well-standardised MP assays, but also to variations in pre-analytical conditions. In this review we will discuss the pre-analytical variables related to plasma and MP preparation which may affect MP analysis.(More)