BLOOD COAGULATION AND HEMORRHAGIC DISEASE

凝血和出血性疾病

• 批准号: 3337888
• 负责人: WILLIAM R JR BELL
• 金额: $ 13.93万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1981
• 资助国家: 美国
• 起止时间: 1981-09-30 至 1986-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3337888
• 关键词: biological information processing; fibrin; fibrinogen; gel electrophoresis; hemorrhagic disorders; infant animal; liver cells; radiotracer; sialate; spectrometry

The long term goal of the proposed research is increased understanding of certain aspects of fibrinogen biosynthesis, the carbohydrate content (sialic acid) of fibrinogen and its relationship to synthesis. Studies are designed to increase understanding of the basic mechanisms involved in the regulation of fibrinogen synthesis by parenchymal cells of the liver. Particular attention will be directed at the mechanism by which the plasma degradative fibrinogen fragments D and E increase the synthesis of fibrinogen in the intact rabbit. To directly answer this question, the hepatic parenchymal cells will be isolated and studied in a controlled environment, in vitro. Of particular interest is the observation that fibrinogen fragments D and E stimulate fibrinogen synthesis, while the same fragments from fibrin do not. Studies have been designed to determine whether the polypeptide or carbohydrate portion of fragments D and E are responsible for their stimulatory capacity. These studies will provide further understanding of fibrinogen biosynthesis and the clottability of this protein.

拟议研究的长期目标是增加对 纤维蛋白原生物合成的某些方面，碳水化合物含量 纤维蛋白原的唾液酸及其与合成的关系。 研究是 目的是增加对有关的基本机制的了解， 肝实质细胞对纤维蛋白原合成的调节。 将特别注意等离子体 降解的纤维蛋白原片段D和E增加了 纤维蛋白原在完整的兔子。 为了直接回答这个问题， 肝实质细胞将被分离并在一个受控的 环境，体外。 特别令人感兴趣的是， 纤维蛋白原片段D和E刺激纤维蛋白原合成，而相同的 纤维蛋白碎片则不能。 研究旨在确定 片段D和E的多肽或碳水化合物部分是否 负责他们的刺激能力。 这些研究将提供 进一步了解纤维蛋白原的生物合成和 这种蛋白质。