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Evidence for a platelet membrane defect in the myeloproliferative syndromes.

作者信息

Castaldi P A, Berndt M C, Booth W, Gregory C, Bull H, Greaves M

出版信息

Thromb Res. 1982 Sep 1;27(5):601-9. doi: 10.1016/0049-3848(82)90307-3.

DOI:10.1016/0049-3848(82)90307-3
PMID:6960545
Abstract

Bleeding and abnormal platelet aggregation occur in patients with myeloproliferative disorders. In this study, twenty patients were examined, some sequentially, and a proportion found to have defective aggregation toward adrenaline, adenosine diphosphate (ADP), and collagen. In these seven patients, the abnormality in platelet response with defective collagen-induced [14C]serotonin release correlated with poor collagen-stimulated thromboxane B2 (TXB2) production. In contrast, five of these patients showed a normal threshold aggregation response to arachidonic acid. The combined results suggest that in these patients, there is a defect between receptor-stimulus coupling and the mobilization of arachidonic acid from membrane phospholipid.

摘要

相似文献

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Evidence for a platelet membrane defect in the myeloproliferative syndromes.
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[Defects in the prostaglandin system. VIII. A pathologic thrombocyte population in myeloproliferative syndrome, which forms no thromboxane from exogenous arachidonic acid].[前列腺素系统的缺陷。VIII. 骨髓增殖综合征中的病理性血小板群体,其不能从外源性花生四烯酸形成血栓素]
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Surface expression of fatty acid translocase (FAT/CD36) on platelets in myeloproliferative disorders and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake.骨髓增殖性疾病和非胰岛素依赖型糖尿病患者血小板上脂肪酸转运蛋白(FAT/CD36)的表面表达:对花生四烯酸摄取的影响
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An altered platelet granule glycoprotein in patients with essential thrombocythemia.
原发性血小板增多症患者血小板颗粒糖蛋白的改变
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