Changes in the Biorhythms of Biochemical Parameters in Animals with Modeled Acute Desynchronosis.

This article describes models for the study of acute desynchronosis: jetlag syndrome and acute desynchronosis under physical stress for possible pharmacological correction of these disorders. The cosinor analysis allowed assessing significance of changes in biological rhythms in 2 biological models: the jetlag-type diurnal rhythm shift model and the model with changed light mode. The revealed changes in the rhythms of biochemical parameters in the blood serum of animals with acute desynchronosis indicate significant changes in the intensity of carbohydrate-lipid metabolism, which affected the processes of cell bioenergetics.

Platelet Activation in Heparin-Induced Thrombocytopenia is Followed by Platelet Death via Complex Apoptotic and Non-Apoptotic Pathways.

Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous or arterial thrombosis. HIT is caused by antibodies that recognize complexes of platelet factor 4 and heparin. The pathogenic mechanisms of this condition are not fully understood.

In systemic lupus erythematosus anti-dsDNA antibodies can promote thrombosis through direct platelet activation.

Systemic lupus erythematosus (SLE) is associated with a high risk of venous and arterial thrombosis, not necessarily associated with prothrombotic antiphospholipid antibodies (Abs). Alternatively, thrombosis may be due to an increased titer of anti-dsDNA Abs that presumably promote thrombosis via direct platelet activation. Here, we investigated effects of purified anti-dsDNA Abs from the blood of SLE patients, alone or in a complex with dsDNA, on isolated normal human platelets.

Platelet factor 4-containing immune complexes induce platelet activation followed by calpain-dependent platelet death.

Heparin-induced thrombocytopenia (HIT) is a complication of heparin therapy sometimes associated with thrombosis. The hallmark of HIT is antibodies to the heparin/platelet factor 4 (PF4) complex that cause thrombocytopenia and thrombosis through platelet activation. Despite the clinical importance, the molecular mechanisms and late consequences of immune platelet activation are not fully understood.

Fatal dysfunction and disintegration of thrombin-stimulated platelets.

Platelets play a key role in the formation of hemostatic clots and obstructive thrombi as well as in other biological processes. In response to physiological stimulants, including thrombin, platelets change shape, express adhesive molecules, aggregate, and secrete bioactive substances, but their subsequent fate is largely unknown. Here we examined late-stage structural, metabolic, and functional consequences of thrombin-induced platelet activation.