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[凝血因子 XII(哈格曼因子)]

[Factor XII (HAGEMAN FACTOR)].

作者信息

Kase F, Klír P, Pospísil J, Poucková P

出版信息

Folia Haematol Int Mag Klin Morphol Blutforsch. 1978;105(1):1-19.

PMID:77809
Abstract

The discovery of factor XII (Hageman factor), the attempts of characterizing it, the knowledge of its presence of absence in the various vertebrate classes are represented in a survey and recent opinions of molecular biology about its structure and composition are discussed. The effect of the activating substances for transferring the Hageman factor into its active form are represented with the role of the pre-kallikrein (Fletcher factor) and of the highly molecular kininogen (Fitzgerald factor) being referred to. Furthermore, the following systems influenced by factor XII are dealt with: 1. The endogenous and exogenous activating system of blood clotting and possible reasons for lower bleedings with factor XII deficiency. 2. Role of the Hageman factor in activating fibrinolysis. 3. Influence on the liberation of kinin. 4. Correlations towards the complement system. 5. Possible inhibitory effect of platelet aggregation. Finally the close connection of all these systems is referred to and the necessity of considering these complicated events in a complex way is stressed.

摘要

本文综述了凝血因子 XII(哈格曼因子)的发现过程、对其进行特性描述的尝试,以及不同脊椎动物类群中该因子存在与否的相关知识,并讨论了分子生物学对其结构和组成的最新观点。文中阐述了将哈格曼因子转化为活性形式的激活物质的作用,同时提及了前激肽释放酶(弗莱彻因子)和高分子量激肽原(菲茨杰拉德因子)的作用。此外,还探讨了受凝血因子 XII 影响的以下系统:1. 内源性和外源性凝血激活系统以及凝血因子 XII 缺乏时出血减少的可能原因。2. 哈格曼因子在激活纤溶中的作用。3. 对激肽释放的影响。4. 与补体系统的相关性。5. 对血小板聚集可能的抑制作用。最后,本文指出了所有这些系统之间的紧密联系,并强调了以综合方式考虑这些复杂事件的必要性。

相似文献

1
[Factor XII (HAGEMAN FACTOR)].[凝血因子 XII(哈格曼因子)]
Folia Haematol Int Mag Klin Morphol Blutforsch. 1978;105(1):1-19.
2
Hageman-factor-dependent coagulation, fibrinolysis, and kinin generation.哈格曼因子依赖性凝血、纤维蛋白溶解和激肽生成。
Transplant Proc. 1974 Mar;6(1):39-45.
3
Fletcher factor deficiency. A diminished rate of Hageman factor activation caused by absence of prekallikrein with abnormalities of coagulation, fibrinolysis, chemotactic activity, and kinin generation.弗莱彻因子缺乏症。由于缺乏前激肽释放酶导致哈格曼因子激活速率降低,伴有凝血、纤维蛋白溶解、趋化活性和激肽生成异常。
J Clin Invest. 1974 Feb;53(2):622-33. doi: 10.1172/JCI107597.
4
Kininogen deficiency in Fitzgerald trait: role of high molecular weight kininogen in clotting and fibrinolysis.菲茨杰拉德性状中的激肽原缺乏:高分子量激肽原在凝血和纤维蛋白溶解中的作用。
J Lab Clin Med. 1976 Feb;87(2):327-37.
5
The intrinsic coagulation-kinin pathway, complement cascades, plasma renin-angiotensin system, and their interrelationships.内源性凝血-激肽途径、补体级联反应、血浆肾素-血管紧张素系统及其相互关系。
Crit Rev Immunol. 1981 Sep;3(1):75-93.
6
Inhibition by C1INH of Hagemann factor fragment activation of coagulation, fibrinolysis, and kinin generation.C1抑制物对凝血因子片段激活凝血、纤维蛋白溶解和激肽生成的抑制作用。
J Clin Invest. 1973 Jun;52(6):1402-9. doi: 10.1172/JCI107313.
7
The Hageman factor dependent pathways of coagulation, fibrinolysis, and kinin-generation.接触因子依赖的凝血、纤维蛋白溶解和激肽生成途径。
Semin Thromb Hemost. 1976 Jul;3(1):1-26. doi: 10.1055/s-0028-1087162.
8
Hageman complement and factor.哈格曼补体与因子
Ann Allergy. 1977 Mar;38(3):211-4.
9
The "Hageman" connection: interrelationships of blood coagulation, fibrino(geno)lysis, kinin generation, and complement activation.
Am J Hematol. 1978;4(4):409-17. doi: 10.1002/ajh.2830040412.
10
The "Hageman" connection: interrelationships of blood coagulation, fibrinogenolysis, kinin generation, and complement activation.“哈格曼”关联:凝血、纤维蛋白溶解、激肽生成与补体激活之间的相互关系。
Przegl Lek. 1981;38(10):709-13.