Publications by authors named "Z Bereczky"
Article Synopsis
- The study investigates the structure and evolution of coronary thrombi in STEMI, focusing on the role of activated protein C (APC/PC) and factors like factor XIII (FXIII) and α2 plasmin inhibitor (α2-PI).
- Histopathological analysis of thrombi from 24 male patients revealed that thrombus age (fresh, lytic, organized) affects the levels and distribution of APC/PC, FXIII, and α2-PI.
- Key findings indicate that FXIII is highly co-localized with fibrin, while α2-PI increases during thrombus lysis, and NET markers are most prominent in the lytic phase, highlighting potential therapeutic strategies for STEMI.
Article Synopsis
- Direct oral anticoagulants (DOACs) are the preferred choice for preventing venous thromboembolism (VTE) in most patients, but their effectiveness and safety in those with severe inherited thrombophilias are not well understood.
- Current research primarily comes from small studies, and there's insufficient data on how well patients stick to their treatment plans.
- Although DOACs and vitamin K antagonists show similar effectiveness and bleeding risks for preventing VTE in these patients, caution is advised with low-dose DOACs, and more extensive studies are needed for a definitive treatment strategy.
Antithrombin (AT) is a critical regulator of the coagulation cascade by inhibiting multiple coagulation factors including thrombin and FXa. Binding of heparinoids to this serpin enhances the inhibition considerably. Mutations located in the heparin binding site of AT result in thrombophilia in affected individuals.
View Article and Find Full Text PDFAntithrombin (AT) is the major plasma inhibitor of thrombin (FIIa) and activated factor X (FXa), and antithrombin deficiency (ATD) is one of the most severe thrombophilic disorders. In this study, we identified nine novel AT mutations and investigated their genotype-phenotype correlations. Clinical and laboratory data from patients were collected, and the nine mutant AT proteins (p.
View Article and Find Full Text PDFBackground: The rs867186 single-nucleotide polymorphism in the gene (g.6936A > G, c.4600A > G) results in a serine-to-glycine substitution at codon 219 of endothelial protein C receptor (EPCR).
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