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ITP is an autoimmune disease which results in low bloodplatelet counts.
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The present investigation has studied the influence of A23187 on bloodplatelet aggregation and secretion.
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Heparin-induced thrombocytopenia refers to the decrease in bloodplatelet count following the administration of heparin, which is an anticoagulant.
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However, a low dose of cyclosporine A resulted in a sustained normal range of bloodplatelet count and negative proteinuria.
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Whole bloodplatelet aggregometry and clot signature analyzer parameters did not show any sign of activation of platelets or the coagulation system.
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Results: During treatment the leukocyte count decreased remarkably, and the patient developed lymphopenia together with a paradoxical increase in her bloodplatelet count.
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The low peripheral bloodplatelet count is caused by premature platelet destruction by self-reacting antibodies in addition to an impairment of platelet production.
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The discoid form of bloodplatelets is important to their function in hemostasis.
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Bloodplatelets are notoriously difficult to preserve in vitro for long periods of time.
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The hemophiliac, or H gene, produces male issue with a lack of bloodplatelets.
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One of these compounds is thromboxane, which encourages bloodplatelets to aggregate into clots.
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Photoreceptor rod cells and bloodplatelets are remarkably different, yet both illustrate a similar phenomenon.
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Both medicines help stimulate the production of bloodplatelets.
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Unstimulated bloodplatelets have a characteristic discoid form supported by a circumferential band of microtubules.
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Nanomolar concentrations of cerastocytin induce aggregation of bloodplatelets.
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Bloodplatelets and fibrinolytic activity may play an important role in the development of these complications.