Ramadan intermittent fasting is associated with improved anticoagulant activity among healthy people: a case-control study.

Data on the pathophysiological mechanisms of hemostatic alterations in the thrombotic events that occur during Ramadan intermittent fasting (RIF), particularly in the natural coagulation inhibitors, are very limited. Thus, our objective was to evaluate the effect of RIF on the natural anticoagulants level, antithrombin, protein C, and total and free protein S (PS) in healthy participants. Participants were divided into two groups.

Camel platelet aggregation responses and the antiplatelet effect of camel urine: comparison between black and white camels.

Human black and white-skinned races exhibited differences in platelet aggregation. However, no similar differences were described on white and black camels. This study aims to find out whether black and white camel skin color is associated with differences in camel platelet aggregation responses or the platelet inhibitory activity of their urine Platelet aggregometry was undertaken in black and white camels, in response to adenosine diphosphate (ADP), Arachidonic acid (AA), Epinephrine (EPN), collagen, and Ristocetin.

Natural anticoagulants and fibrinolytic activity following interferon therapy in chronic viral hepatitis.

Chronic liver disease is accompanied by derangement of hepatocyte function including the synthesis of haemostastic factors. It is, however, not known whether the improvement in liver functions as a result of interferon (IFN)-alpha therapy would be reflected in the plasma levels of these factors. To evaluate the effect of IFN-alpha therapy on the plasma levels of natural anticoagulants and on the fibrinolytic parameters, in patients with chronic viral hepatitis.

The liver and the haemeostatic system.

The liver plays a central role in the control of haemostasis being the site of synthesis of most of the coagulation factors and natural anticoagulants, as well as fibrinolytic factors except the main activators of the fibrinolytic system (t-PA and u-PA). The liver also clears many of the activated clotting and fibrinolytic factors, as well as haemostatic activation complexes (TAT and PAP) and end product of fibrin degradation, FDP. Therefore, liver disease results in a complex and multifactorial pattern of defects in haemostatic function in the form of: (i) decreased synthesis of coagulation factors (ii) Abnormal protein synthesis e.