MOLECULAR MECHANISTIC BASIS FOR RADIATION INDUCED PULMONARY LATE EFFECTS

辐射引起的肺迟发效应的分子机制基础

• 批准号: 6563658
• 负责人: Jacob N Finkelstein
• 金额: $ 15.75万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-02-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6563658
• 关键词: RNase protection assay; allergic pneumonitis; alveolar macrophages; cell cell interaction; cell type; chemokine; cytokine; enzyme linked immunosorbent assay; fibroblast growth factor; gene expression; genetic strain; immunocytochemistry; in situ hybridization; ionizing radiation; laboratory mouse; medical complication; molecular pathology; neoplasm /cancer radiation therapy; protein biosynthesis; pulmonary fibrosis /granuloma; radiation dosage; radiation genetics; radiation sensitivity; respiratory epithelium; vascular endothelium

Description: (Applicant?s Description)The general goal of this program is directed at gaining a deeper understanding of the molecular mechanisms which are the basis for the normal tissue late effects which are observed in the lung following radiation. Previous CERRIS programs have led to the paradigm of radiation late effects being dependent upon the "conversation" which takes place between a number of injured cells, rather than the classic concept of a single target cell. In pursuit of this goal, they mean to further define the conversation, which they have hypothesized as a "cytokine cascade", in terms of the spatial and temporal release of proinflammatory and profibrotic cytokines and growth factors, and their genetic context. Expansion of this paradigm has led them to postulate the role of the immune system in the development of late tissue effects and this will be explored in more detail. Modulation of the cytokine cascade(s) and/or the immune system will be investigated as a means of both elucidating the roles of specific cytokines, as well as suggesting routes of amelioration.

描述：（申请人？s Description）本计划的总体目标是 旨在更深入地了解分子机制， 是正常组织晚期效应的基础， 放射后的肺部。以前的CERRIS计划已经导致了这种范式 辐射的后期效应取决于“对话”， 在许多受伤的细胞之间放置，而不是经典的概念， 单个靶细胞。为了实现这一目标，他们打算进一步界定 对话，他们假设为“细胞因子级联反应”， 促炎性和促纤维化的空间和时间释放 细胞因子和生长因子，以及它们的遗传背景。扩大这一 这种模式使他们假设免疫系统在免疫系统中的作用。 后期组织效应的发展，这将进行更详细的探讨。 细胞因子级联反应和/或免疫系统的调节将是一种有效的方法。 作为阐明特定细胞因子作用的手段， 以及提出改善的途径。