COMPLEMENT AND HAGEMAN FACTOR IN ANGIOEDEMA

血管性水肿中的补体和哈格曼因子

• 批准号: 6307378
• 负责人: Bruce L. Zuraw
• 金额: $ 2.74万
• 依托单位: SCRIPPS RESEARCH INSTITUTE, THE
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-12-01 至 2001-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6307378
• 关键词: clinical research; clinical trials; coagulation factor XII; complement inhibitors; hereditary angioneurotic edema; human subject; inflammation; urticaria

Deficiencies of C1 inhibitor occur on both a hereditary and acquired basis, are associated with potentially fata angioedema, and may contribute to uncontrolled inflammation in certain conditions. Our studies are designed to elucidate the regulation of C1 inhibitor synthesis as well as its catabolic pathways, ultimately to allow therapeutic manipulation of its plasama level.

C1抑制剂的缺陷发生在遗传和获得的基础上，与潜在的fata血管性水肿相关，并可能导致某些条件下不受控制的炎症。 我们的研究旨在阐明C1抑制剂合成的调节以及其分解代谢途径，最终允许其血浆水平的治疗操作。