ITP is an autoimmune disease which results in low blood platelet counts.

The present investigation has studied the influence of A23187 on blood platelet aggregation and secretion.

Heparin-induced thrombocytopenia refers to the decrease in blood platelet count following the administration of heparin, which is an anticoagulant.

However, a low dose of cyclosporine A resulted in a sustained normal range of blood platelet count and negative proteinuria.

Whole blood platelet aggregometry and clot signature analyzer parameters did not show any sign of activation of platelets or the coagulation system.

Results: During treatment the leukocyte count decreased remarkably, and the patient developed lymphopenia together with a paradoxical increase in her blood platelet count.

The low peripheral blood platelet count is caused by premature platelet destruction by self-reacting antibodies in addition to an impairment of platelet production.

The discoid form of blood platelets is important to their function in hemostasis.

Blood platelets are notoriously difficult to preserve in vitro for long periods of time.

The hemophiliac, or H gene, produces male issue with a lack of blood platelets.

One of these compounds is thromboxane, which encourages blood platelets to aggregate into clots.

Photoreceptor rod cells and blood platelets are remarkably different, yet both illustrate a similar phenomenon.

Both medicines help stimulate the production of blood platelets.

Unstimulated blood platelets have a characteristic discoid form supported by a circumferential band of microtubules.

Nanomolar concentrations of cerastocytin induce aggregation of blood platelets.

Blood platelets and fibrinolytic activity may play an important role in the development of these complications.