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Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate: A Randomized, Placebo-Controlled, Crossover Study in Healthy Subjects
TLDR
Prothrombin complex concentrate immediately and completely reverses the anticoagulant effect of rivaroxaban in healthy subjects but has no influence on the anticonvulsant action of dabigatran at the PCC dose used in this study. Expand
Prospective validation of the International Society of Thrombosis and Haemostasis scoring system for disseminated intravascular coagulation*
TLDR
A diagnosis of DIC based on a simple scoring system, using widely available routine coagulation tests, is sufficiently accurate to make or reject a diagnosis ofDIC in intensive care patients with a clinical suspicion of this condition. Expand
Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.
TLDR
A potential role for glycocalyx perturbation in mediating vascular dysfunction during hyperglycemia is indicated, thereby increasing vascular vulnerability and indicating a potential roles for N-acetylcysteine and mannitol infusion. Expand
Beta2-glycoprotein I can exist in 2 conformations: implications for our understanding of the antiphospholipid syndrome.
TLDR
It is shown that beta(2)GPI can exist in at least 2 different conformations: a circular plasma conformation and an "activated" open conformation, and that the closed, circular conformation is maintained by interaction between the first and fifth domain of beta( 2)G PI. Expand
KLF2 provokes a gene expression pattern that establishes functional quiescent differentiation of the endothelium.
TLDR
It is established that KLF2 acts as a central transcriptional switch point between the quiescent and activated states of the adult endothelial cell. Expand
ROLE OF TOLL-LIKE RECEPTORS 2 AND 4, AND THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS IN HIGH-MOBILITY GROUP BOX 1-INDUCED INFLAMMATION IN VIVO
TLDR
Data indicate that HMGB-1 induces release of cytokines, activation of coagulation, and neutrophil recruitment in vivo via a mechanism that at least in part depends on TLR-4 and RAGE. Expand
Thrombin‐activatable fibrinolysis inhibitor (TAFI, plasma procarboxypeptidase B, procarboxypeptidase R, procarboxypeptidase U)
TLDR
Activated TAFI (TAFIa) downregulates fibrinolysis by the removal of carboxy‐terminal lysines from fibrin, resulting in a decreased rate of plasmin generation and thus downregulation of fibrinelysis. Expand
Reduced plasma fibrinolytic potential is a risk factor for venous thrombosis.
TLDR
The results indicate that plasma hypofibrinolysis constitutes a risk factor for venous thrombosis, with a doubling of the risk at clot lysis times that are present in 10% of the population. Expand
Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease
TLDR
The authors conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoAGulant properties of circulating erythrocyte-derived microparticles. Expand
Venous thrombosis risk associated with plasma hypofibrinolysis is explained by elevated plasma levels of TAFI and PAI-1.
TLDR
In conclusion, CLT reflects levels of all fibrinolytic factors except t-PA, which are associated with venous thrombosis, however, plasminogen and t- PA levels may reflect underlying risk factors. Expand
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