In this study we hypothesized that anthrax infection modulates the activity of von Willebrand factor (VWF) and its endogenous regulator ADAMTS13, which play important roles in hemostasis and thrombosis, including interaction of endothelial cells with platelets.
Of the 76 patients with thrombosis, 29 were positive for LAC, 9 for aCL, 7 for anti-beta(2)GPI, 3 for LAC+aCL, 9 for aCL+anti-beta(2)GPI, 11 for LAC+anti-beta(2)GPI, and 8 for LAC+aCL+anti-beta(2)GPI.
Valine/valine genotype at position 247 of the beta2-glycoprotein I gene in Mexican patients with primary antiphospholipid syndrome: association with anti-beta2-glycoprotein I antibodies.
The ability of gC1qR to bind proteins involved in complement, coagulation, and kinin systems, as well as viral and bacterial pathogens including S. aureus protein A, supports the hypothesis that gC1qR expressed on activated platelets may contribute directly to thrombosis, inflammation, and endovascular infections.
Combining the hDAF transgene with the GP IIb/IIIa inhibitor tirofiban improves heart performance and reduces myocardial damage following hyperacute rejection in an ex vivo perfusion model.
A high TAFI level (75th or higher percentile in thrombosis patients) was associated with a 2-fold higher risk for recurrence compared with lower levels.
Collectively, these data demonstrate that decorin can regulate fibrin organization and reveal a novel mechanism by which extracellular matrix components can participate in hemostasis, thrombosis, and wound repair.
For the first time, we show a strong association between endoglin and EGR-1, increased collagen and SMCs expression, decreased levels of intraplaque thrombosis, and a stable plaque phenotype.
For the first time, we show a strong association between endoglin and EGR-1, increased collagen and SMCs expression, decreased levels of intraplaque thrombosis, and a stable plaque phenotype.
A single-base change (G to A) at position 20210 in the 3' untranslated region of the prothrombin gene is associated with increased plasma levels of prothrombin and might therefore increase the risk for thrombosis.
Group 1: A total of 377 children with thrombosis were analyzed during 7 years between January 1997 and 2004 and screened for prothrombin G20210A mutation.