• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

人类恶性和良性腹水中的接触系统

The contact system in human malignant and benign ascites.

作者信息

Buø L, Karlsrud T S, Johansen H T, Aasen A O

机构信息

Institute for Surgical Research, Rikshospitalet, Oslo, Norway.

出版信息

Scand J Clin Lab Invest. 1993 Apr;53(2):117-24. doi: 10.3109/00365519309088398.

DOI:10.3109/00365519309088398
PMID:7682333
Abstract

The plasma contact system was studied in ascites and plasma from patients with gastrointestinal cancer and patients with liver failure. Our study demonstrates the presence of factor XII, factor XI, and prekallikrein and their main inhibitors in ascites and plasma from both patient groups. Both factor XII-like and plasma kallikrein-like activities were detected in the malignant ascites. The kallikrein-like activity in malignant ascites was found in complex with alpha 2-macroglobulin. In plasma samples from the patients functional values of factor XII and prekallikrein were decreased compared to controls. In benign ascites the proenzyme levels were significantly lower than in malignant ascites. Functional inhibition values in ascites and plasma from patients were unexpectedly high. Our findings indicate that the plasma contact system is activated in the ascites from cancer patients. Activation of the contact system generates vasoactive mediators, which may play a role in the accumulation of malignant ascites.

摘要

对胃肠道癌患者和肝衰竭患者的腹水及血浆中的血浆接触系统进行了研究。我们的研究表明,两组患者的腹水和血浆中均存在因子 XII、因子 XI 和前激肽释放酶及其主要抑制剂。在恶性腹水中检测到了类似因子 XII 和类似血浆激肽释放酶的活性。在恶性腹水中发现类似激肽释放酶的活性与α2-巨球蛋白结合。与对照组相比,患者血浆样本中因子 XII 和前激肽释放酶的功能值降低。在良性腹水中,酶原水平显著低于恶性腹水。患者腹水和血浆中的功能抑制值意外地高。我们的研究结果表明,癌症患者腹水中的血浆接触系统被激活。接触系统的激活产生血管活性介质,这可能在恶性腹水的积聚中起作用。

相似文献

1
The contact system in human malignant and benign ascites.人类恶性和良性腹水中的接触系统
Scand J Clin Lab Invest. 1993 Apr;53(2):117-24. doi: 10.3109/00365519309088398.
2
Activation of the contact system in ascites from patients with gastrointestinal cancer.胃肠道癌患者腹水中接触系统的激活。
Agents Actions Suppl. 1992;38 ( Pt 2):237-48.
3
Plasma kallikrein activation and inhibition during typhoid fever.伤寒热期间血浆激肽释放酶的激活与抑制
J Clin Invest. 1978 Feb;61(2):287-96. doi: 10.1172/jci108938.
4
Cold promoted activation and factor XII, prekallikrein and C1-inhibitor.寒冷促进活化以及因子 XII、前激肽释放酶和 C1 抑制剂。
Thromb Haemost. 1985 Apr 22;53(2):242-4.
5
Simple chromogenic peptide substrate assays for determining prekallikrein, kallikrein inhibition and kallikrein "like" activity in human plasma.用于测定人血浆中前激肽释放酶、激肽释放酶抑制作用及类激肽释放酶活性的简单显色肽底物检测法。
Thromb Res. 1982 Feb 1;25(3):293-8.
6
Factor XII-independent activation of the bradykinin-forming cascade: Implications for the pathogenesis of hereditary angioedema types I and II.旁路途径 XII 因子非依赖性激活动脉紧张素转化酶形成级联反应:对遗传性血管性水肿 I 型和 II 型发病机制的影响。
J Allergy Clin Immunol. 2013 Aug;132(2):470-5. doi: 10.1016/j.jaci.2013.03.026. Epub 2013 May 11.
7
Effect of heparin on the activation of factor XII and the contact system in plasma.肝素对血浆中因子 XII 激活及接触系统的影响。
Thromb Haemost. 1991 Nov 1;66(5):540-7.
8
Structural and functional characterization of factor XII.凝血因子XII的结构与功能特性
Semin Thromb Hemost. 1987 Jan;13(1):1-14. doi: 10.1055/s-2007-1003471.
9
Computerized immunoblot analyses (CIBA) of the distribution of prekallikrein and its activation products in vivo and in vitro.
Agents Actions Suppl. 1992;38 ( Pt 1):166-73. doi: 10.1007/978-3-0348-7321-5_22.
10
Studies on components of the plasma kallikrein-kinin system in plasma samples from normal individuals and patients with septic shock.对正常个体和脓毒性休克患者血浆样本中血浆激肽释放酶-激肽系统成分的研究。
Adv Shock Res. 1980;4:1-10.

引用本文的文献

1
The contact system in liver injury.肝脏损伤中的接触系统。
Semin Immunopathol. 2021 Aug;43(4):507-517. doi: 10.1007/s00281-021-00876-7. Epub 2021 Jun 14.