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The "Hageman" connection: interrelationships of blood coagulation, fibrino(geno)lysis, kinin generation, and complement activation.

作者信息

Murano G

出版信息

Am J Hematol. 1978;4(4):409-17. doi: 10.1002/ajh.2830040412.

DOI:10.1002/ajh.2830040412
PMID:362910
Abstract

The activation pathways for the generation of enzymes involved in blood clotting, clot lysis, complement activation, and kinin generation are briefly reviewed. The interrelationship of the four systems is illustrated by the multiple functions of four key enzymes: Factor XIIa, kallikrein, plasmin, and C1 esterase. The pivotal role of Factor XIIa in establishing this connection is elucidated.

摘要

相似文献

1
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.
2
[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.
3
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.
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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.
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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.
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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.
7
[Correlation of complement system with coagulation, fibrinolysis, and kinin generation].补体系统与凝血、纤维蛋白溶解及激肽生成的相关性
Rinsho Ketsueki. 1976 Jan;17(1):1-14.
8
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.
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Interaction of the clotting, kinin-forming, complement, and fibrinolytic pathways in inflammation.炎症中凝血、激肽形成、补体和纤溶途径的相互作用。
Ann N Y Acad Sci. 1982;389:25-38. doi: 10.1111/j.1749-6632.1982.tb22123.x.
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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.

引用本文的文献

1
Coagulation Factor XII Levels and Intrinsic Thrombin Generation in Multiple Sclerosis.多发性硬化症中的凝血因子 XII 水平与内源性凝血酶生成
Front Neurol. 2018 Apr 20;9:245. doi: 10.3389/fneur.2018.00245. eCollection 2018.
2
A history of late and very late stent thrombosis is not associated with increased activation of the contact system, a case control study.支架血栓形成时间晚和很晚的病史与接触系统的过度激活无关:一项病例对照研究。
Thromb J. 2010 Apr 15;8:6. doi: 10.1186/1477-9560-8-6.
3
Immunological characterisation of plasminogen activators in the human vessel wall.
人血管壁中纤溶酶原激活剂的免疫学特性分析
J Clin Pathol. 1983 Sep;36(9):1046-9. doi: 10.1136/jcp.36.9.1046.
4
Immunological comparison between human and rat plasminogen activators in blood and the vessel wall.人和大鼠血液及血管壁中纤溶酶原激活剂的免疫学比较。
J Clin Pathol. 1984 Oct;37(10):1153-6. doi: 10.1136/jcp.37.10.1153.
5
Hematologic and oncologic complications in the critically ill child.危重症患儿的血液学和肿瘤学并发症
Yale J Biol Med. 1984 Mar-Apr;57(2):199-242.
6
Liquoid-induced disseminated intravascular coagulation in the blue fox.蓝狐中液体诱导的弥散性血管内凝血
Acta Vet Scand. 1982;23(4):570-80. doi: 10.1186/BF03546776.
7
Antithrombin III activity (residual thrombin activity) in plasma from non-medicated or heparinized horses.来自未用药或肝素化马匹的血浆中的抗凝血酶III活性(残余凝血酶活性)。
Vet Res Commun. 1989;13(1):31-46. doi: 10.1007/BF00366851.