PLATELET ANTIGENS AND PLATELET ACTIVATION

我们已经开发了几种方法来研究体外血小板激活和 在试管中。这些研究是由于发展和 从人血中分离血小板的技术实现 诱导血小板活化或分泌。我们已经开发了九个 仅与激活的血小板发生反应的单抗。我们的 结果表明，在某些形式的von Willebrand病中， 存在血小板活化，并导致血小板减少。在病人中 患有动脉硬化性心脏病的患者，血小板活化增加 在运动之后。这一发现表明，一些自发的内毒素 血小板活化或增强激动剂诱导的血小板活化不是 观察到的。轻度或轻度动脉粥样硬化患者的运动可以 不会引起血小板活化。 我们已经确认了阵发性睡眠性血红蛋白尿(PNM)患者 血小板被激活。活化表现为α颗粒的释放 蛋白质和增加的纤维蛋白原结合到血小板表面。新的 观察到凝血激活的证据。这些发现表明 血小板活化可能是静脉血栓形成的主要机制 在PNH。检验这一假说的研究正在实施中。

We have developed several methods to study platelet activation ex vivo and in vitro. These studies were made possible by the development and implementation of techniques to isolate platelets from human blood without inducing platelet activation or secretion. We have developed nine monoclonal antibodies that react only with activated platelets. Our results have shown that in some forms of von Willebrand's disease, platelet activation is present and causes thrombocytopenia. In patients with arteriosclerotic heart disease, platelet activation is increased after exercise. This finding suggests that some endotoxin, spontaneous platelet activation or enhances agonist-induced platelet activation is not observed. Exercise in individuals with minor or mild atherosclerosis does not induce platelet activation. We have identified patients with paroxysmal nocturnal hemoglobinuria (PNM) platelet activation. The activation was shown by release of alpha granule protein and increased fibrinogen binding to the platelet surface. New evidence of coagulation activation was observed. These findings suggest that platelet activation may be the primary mechanism of venous thrombosis in PNH. Studies to test this hypothesis are being implemented.