MECHANISMS OF ACUTE VASCULAR REACTION TO INJURY

急性血管损伤反应的机制

• 批准号: 3097359
• 负责人: EARL P BENDITT
• 金额: $ 100.05万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-03-01 至 1988-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3097359
• 关键词: atherosclerosis; hypertension; vascular endothelium; vascular smooth muscle

This program has a common interest in responses of large and small vessels and of their endothelial and smooth muscle cells to injury. Fundamental questions are being asked related to basic pathologic processes that may be involved in atherosclerosis. Mechanisms that permit or stimulate cell replication, cell migration and cellular interactions are being investigated. The potential role of mechanical and toxic injuries, of the metabolic products of xenobiotics and the mechanism whereby herpesviruses may produce proliferative lesions in animals and human beings are being investigated. The program includes studies of the nature of changes in ploidy of smooth muscle with age and hypertension studies. Mechanisms of interaction of leukocytes, endothelial cells, of the HDL apoprotein and ApoSAA are also being investigated. A wide range of methods are being used including cell culture, histoimmunocytochemistry, flow cytophotometry, scanning electron microscopy and molecular probes for viral and amyloid protein genes in cells.

该计划对大型和小型船只的反应有共同的兴趣 及其内皮细胞和平滑肌细胞的损伤。 基本的 正在提出与基本病理过程相关的问题，这些过程可能是 参与动脉粥样硬化。 允许或刺激细胞的机制 复制、细胞迁移和细胞相互作用 调查了。 机械性和毒性损伤的潜在作用 异生物质的代谢产物及疱疹病毒的作用机制 可能在动物和人类中产生增殖性病变 调查了。 该计划包括对变化性质的研究 平滑肌倍性与年龄和高血压的研究。 机制 白细胞、内皮细胞、HDL 脱辅基蛋白和 ApoSAA 也正在接受调查。 正在使用多种方法 包括细胞培养、组织免疫细胞化学、流式细胞光度测定、 病毒和淀粉样蛋白的扫描电子显微镜和分子探针 细胞中的蛋白质基因。