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Wolfgang Speiser

Researcher at University of Vienna

Publications -  76
Citations -  3700

Wolfgang Speiser is an academic researcher from University of Vienna. The author has contributed to research in topics: Endothelial stem cell & Fibrinolysis. The author has an hindex of 32, co-authored 76 publications receiving 3591 citations. Previous affiliations of Wolfgang Speiser include University of Giessen & University of Tromsø.

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High plasma levels of factor viii and the risk of recurrent venous thromboembolism

TL;DR: Patients with a high plasma level of factor VIII have an increased risk of recurrent venous thromboembolism, and the likelihood of recurrence at two years was higher than among patients with lower levels.
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Leptin Induces Endothelin-1 in Endothelial Cells In Vitro

TL;DR: Leptin upregulates ET-1 production in HUVECs via a mechanism potentially involving jun binding members of the bZIP family, and is responsible for the increase in serum leptin levels observed in obese subjects.
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Monitoring of aspirin (ASA) pharmacodynamics with the platelet function analyzer PFA-100

TL;DR: The PFA-100 system appears suitable to demonstrate an aspirin-induced platelet effect in a longitudinal study, and may be adequate to monitor a patient's compliance, however, prospective trials have to be conducted to demonstrate whether the EPI-CT achieved under ASA-intake has predictive value for cardiovascular outcome.
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Clinical Studies and Thrombin Generation in Patients Homozygous or Heterozygous for the G20210A Mutation in the Prothrombin Gene

TL;DR: Hobbitosity for the G20210A mutation in the prothrombin gene is associated with a severe, albeit more benign, thrombotic diathesis compared with homozygosity for deficiencies of antithrombin, protein C, or protein S.
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Morning hypercoagulability and hypofibrinolysis. Diurnal variations in circulating activated factor VII, prothrombin fragment F1+2, and plasmin-plasmin inhibitor complex

TL;DR: The data suggest that the diurnal changes in the plasma levels of activators and inhibitors of coagulation and fibrinolysis lead to correspondingChanges in the activity state of these systems, leading to morning hypercoagulability and hypofibrinoleysis.