Temat: anticoagulant factor

Skocz do pozycji: 1.

Tytuł:: Isolation and partial purification of anticoagulant fractions from the venom of the Iranian snake Echis carinatus
Autorzy:: Babaie, Mahdi
Zolfagharian, Hossein
Salmanizadeh, Hossein
Mirakabadi, Abbas
Alizadeh, Hafezeh
Tematy:: anticoagulant factor
snake venom
Iranian Echis carinatus
chromatography; Pokaż więcej
Wydawca:: Polskie Towarzystwo Biochemiczne
Powiązania:: https://bibliotekanauki.pl/articles/1039597.pdf Link otwiera się w nowym oknie
Opis:: Many snake venoms comprise different factors, which can either promote or inhibit the blood coagulation pathway. Coagulation disorders and hemorrhage belong to the most prominent features of bites of the many vipers. A number of these factors interact with components of the human blood coagulation. This study is focused on the effect of Echis carinatus snake venom on blood coagulation pathway. Anticoagulant factors were purified from the Iranian Echis carinatus venom by two steps: gel filtration (Sephadex G-75) and ion-exchange (DEAE-Sephadex) chromatography, in order to study the anticoagulant effect of crude venom and their fractions. The prothrombin time was estimated on human plasma for each fraction. Our results showed that protrombin time value was increase from 13.4 s to 170 s for F2C and to 280 s for F2D. Our study showed that these fractions of the venom delay the prothrombine time and thus can be considered as anticoagulant factors. They were shown to exhibit proteolytic activity. The molecular weights of these anticoagulants (F2C, F2D) were estimated by SDS/PAGE electrophoresis. F2C comprises two protein bands with molecular weights of 50 and 79 kDa and F2D a single band with a molecular weight of 42 kDa.
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Autorzy:: ten Cate, Hugo
Spronk, Henri M.H.
Eikelboom, John
Guzik, Tomasz
Opis:: Atherosclerosis is a chronic inflammatory disease in which atherothrombotic complications lead to cardiovascular morbidity and mortality. At advanced stages, myocardial infarction, ischaemic stroke, and peripheral artery disease, including major adverse limb events, are caused either by acute occlusive atherothrombosis or by thromboembolism. Endothelial dysfunction, vascular smooth muscle cell activation, and vascular inflammation are essential in the development of acute cardiovascular events. Effects of the coagulation system on vascular biology extend beyond thrombosis. Under physiological conditions, coagulation proteases in blood are pivotal in maintaining haemostasis and vascular integrity. Under pathological conditions, including atherosclerosis, the same coagulation proteases (including factor Xa, factor VIIa, and thrombin) become drivers of atherothrombosis, working in concert with platelets and vessel wall components. While initially atherothrombosis was attributed primarily to platelets, recent advances indicate the critical role of fibrin clot and plasma coagulation factors. Mechanisms of atherothrombosis and hypercoagulability vary depending on plaque erosion or plaque rupture. In addition to contributing to thrombus formation, factor Xa and thrombin can affect endothelial dysfunction, oxidative stress, vascular smooth muscle cell function as well as immune cell activation and vascular inflammation. By these mechanisms, they promote atherosclerosis and contribute to plaque instability. In this review, we first discuss the postulated vasoprotective mechanisms of protease-activated receptor signalling induced by coagulation enzymes under physiological conditions. Next, we discuss preclinical studies linking coagulation with endothelial cell dysfunction, thromboinflammation, and atherogenesis. Understanding these mechanisms is pivotal for the introduction of novel strategies in cardiovascular prevention and therapy. We therefore translate these findings to clinical studies of direct oral anticoagulant drugs and discuss the potential relevance of dual pathway inhibition for atherothrombosis prevention and vascular protection.
Dostawca treści:: Repozytorium Uniwersytetu Jagiellońskiego

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Skocz do pozycji: 3.

Autorzy:: Baran, Beata
Windyga, Jerzy
Odnoczko, Edyta
Grodzicki, Tomasz
Opis:: Acquired hemophilia A is an autoimmune disease caused by antibodies against coagulationfactor VIII (FVIII). These antibodies, called circulating FVIII anticoagulant or FVIII inhibitor,reduce plasma FVIII activity, which results in excessive bleeding. Acquired hemophilia A isclassified as severe hemorrhagic disorder. Typical for this disease are extensive subcutaneousspontaneous blood extravasations, intramuscular and retroperitoneal hematomas, and post--traumatic bleeds, including post-surgery bleeding. In approximately 30% of cases, acquiredhemophilia A is initially manifested merely by minor bleeding, which may be often overlookedby physician, but as long as FVIII inhibitor is detected, patient is at risk of severe, sometimesfatal, hemorrhage. Acquired hemophilia A is most common in people aged 60–90 years. Patientsin this age group often take anticoagulants, antiplatelet and non-steroidal anti-inflammatorydrugs, and bruising and purpura are relatively common among them, so acquired hemophiliaA can easily be overlooked. On the other hand, the delay in the diagnosis of the disorder mayresult in delayed initiation of hemostatic treatment and elimination of the FVIII inhibitor, whichputs the patient at risk of premature death. The aim of this publication is to present the principlesof diagnosis of acquired hemophilia A, the use of hemostatic drugs to inhibit and preventbleeding, and immunosuppressive drugs to eliminate the FVIII inhibitor in elderly patients.
Dostawca treści:: Repozytorium Uniwersytetu Jagiellońskiego

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