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高β脂蛋白血症中激肽释放酶系统的激活。

Activation of the kallikrein system in hyperbetalipoproteinemia.

作者信息

Carvalho A C, Lees R S, Vaillancourt R A, Cabral R B, Colman R W

出版信息

J Lab Clin Med. 1978 Jan;91(1):117-22.

PMID:201701
Abstract

In 30 patients with hyperlipoproteinemia (19 type II and 11 type IV), the role of the intrinsic coagulation pathway was evaluated by assays of preK, Kl's, and Hageman factor (factor XII). Analysis of the plasma of type II patients suggested activation of the intrinsic pathway characterized by a 40% decrease in preK (p less than 0.01) and a 50% decrease Kl (p less than 0.01); in contrast, analysis of the plasma of type IV patients showed no activation of the intrinsic pathway. In type II patients C-1INH was present in normal concentrations as measured by immunochemical techniques. The findings of normal levels of C-1INH by immunoassay, in association with altered electrophoretic mobility, are suggestive of formation of a kallikrein-C-1INH complex in vivo.

摘要

在30例高脂蛋白血症患者(19例Ⅱ型和11例Ⅳ型)中,通过检测前激肽释放酶、激肽释放酶原(Kl's)和哈格曼因子(因子Ⅻ)来评估内源性凝血途径的作用。对Ⅱ型患者血浆的分析提示内源性途径被激活,其特征为前激肽释放酶降低40%(p<0.01)和激肽释放酶原降低50%(p<0.01);相比之下,对Ⅳ型患者血浆的分析显示内源性途径未被激活。通过免疫化学技术检测,Ⅱ型患者血浆中C-1酯酶抑制物(C-1INH)浓度正常。免疫测定显示C-1INH水平正常,但电泳迁移率改变,提示体内形成了激肽释放酶-C-1INH复合物。

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