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首页> 外文期刊>British Journal of Cancer >Evidence that cells from experimental tumours can activate coagulation factor X
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Evidence that cells from experimental tumours can activate coagulation factor X

机译:来自实验肿瘤的细胞可以激活凝血因子X的证据

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The procoagulant activity of cells from some experimental tumours isolated in culture or in single-cell suspensions from ascitic fluid was investigated. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, Factor VIII- and Factor VII-deficient but not of Factor X-deficient human plasma. The same cells generated thrombin when mixed with a source of prothrombin and Factor X, absorbed bovine serum (as a source of Factor V), phospholipid and calcium chloride. Thrombin formation was not influenced by the presence of Factor VII. Cells from Sarcoma 180 ascites were completely inactive in both test systems. It is concluded that cells from some experimental tumours have the capacity to activate Coagulation Factor X directly. These findings suggest the existence of an alternative "cellular" pathway in the initiation of blood clotting distinct from both the intrinsic and extrinsic mechanisms.
机译:研究了从腹水中培养或分离的单细胞悬液中某些实验性肿瘤细胞的促凝血活性。来自Lewis肺癌(原发性和转移性),Ehrlich癌性腹水和JW肉瘤腹水的细胞能够显着缩短正常的,缺乏VIII因子和VII因子的血浆的重新钙化时间,而不能缩短缺乏X因子的人类血浆的钙化时间。当与凝血酶原和凝血因子X混合,吸收牛血清(作为凝血因子V的来源),磷脂和氯化钙混合时,相同的细胞会产生凝血酶。凝血酶的形成不受因子VII的存在的影响。肉瘤180腹水的细胞在两个测试系统中都完全失活。结论是来自一些实验性肿瘤的细胞具有直接激活凝血因子X的能力。这些发现表明,在血液凝固的起始中存在与内在和外在机制不同的替代“细胞”途径。

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