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Introduction: This article discusses the current role of sports practice in people with hemophilia (PWH).

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Improvement in XIa Selectivity of Snake Venom Peptide Analogue BF9-N17K Using P2' Amino Acid Replacements.

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Institute of Biomedicine, Hubei Key Laboratory of Embryonic Stem Cell Research, College of Basic Medicine, Hubei University of Medicine, Shiyan 442000, China.

Coagulation factor XIa is a new serine-protease family drug target for next-generation anticoagulants. With the snake venom Kunitz-type peptide BF9 as the scaffold, we obtained a highly active XIa inhibitor BF9-N17K in our previous work, but it also inhibited the hemostatic target plasmin. Here, in order to enhance the selectivity of BF9-N17K toward XIa, four mutants, BF9-N17K-L19A, BF9-N17K-L19S, BF9-N17K-L19D, and BF9-N17K-L19K, were further designed using the P2' amino acid classification scanning strategy.

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Paradoxical embolism occurs when a clot originates in the venous system and traverses through a pulmonary or intracardiac shunt into the systemic circulation, with a mortality rate of around 18%. The risk factors for arterial embolism and venous thrombosis are similar, but different disease entities can lead to a hypercoagulable state of the blood, including antithrombin III (AT III) deficiency. We report the case of a 43-year-old man with a massive central pulmonary embolism with a rider embolus and concomitant aortic arch embolism with involvement of the brachiocephalic trunk, bilateral subclavian and axillary arteries, and the right vertebral artery, followed by a secondary ischaemic stroke.

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Hemophilia A (HA) is associated with FVIII coagulation insufficiency or inactivity leading to excessive bleeding. Elevated FVIII, on the contrary, is associated with thrombophilia, thrombosis, myocardial infarctions, and stroke. Active FVIII (aFVIII) uses its C2 domain to bind to blood cells' membranes, consequently carrying out its coagulative function.

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Background: Chronic spontaneous urticaria (CSU) appears to share some pathomechanisms with metabolic syndrome (MS), such as proinflammatory state, increased oxidative stress, changes in adipokine profile, and coagulation system activation.

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