CLINICAL TRIAL: TOBACCO SMOKE INDUCED CELL INJURY IN LUNG COMPARTMENTS

临床试验：烟草烟雾引起的肺室细胞损伤

• 批准号: 7717092
• 负责人: MARK Louis BRANTLY
• 金额: $ 2.49万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7717092
• 关键词: Alveolar Macrophages; Biopsy; Blood Tests; Bronchoscopy; Chronic Obstructive Airway Disease; Clinical Trials; Computer Retrieval of Information on Scientific Projects Database; Development; Funding; Grant; Institution; Lung; Lung Lavage Fluid; Mediating; Nitric Oxide; Oxidants; Pilot Projects; Production; Pulmonary function tests; Research; Research Personnel; Resources; Role; Smoke; Source; Structure of parenchyma of lung; Tobacco smoke; Transcriptional Activation; United States National Institutes of Health; Up-Regulation; alpha 1-Antitrypsin; alpha 1-Antitrypsin Deficiency; cell injury; concept; healthy volunteer; lung injury; novel; prevent

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Determining the role of tobacco smoke (TS) induced alveolar macrophage (AM) mediated lung injury and the protective role of alpha 1-antitrypsin (AAT) in modulating the extent of lung injury caused by TS may allow for the development of more specific therapies to prevent or reduce the lung damage. AM are a source of nitric oxide (NO) through up-regulation of iNOS. NO production may continue long after the initial insult (TS) has been eliminated. The concept that AAT may function to inhibit oxidant damage, such as iNOS, to the lung tissue is novel and the subject of this project. This is a pilot project with 20 subjects undergoing bronchoscopy. Bronchial lavage fluid, biopsy/brushings, pulmonary function testing and research blood tests will be compared in four subject groups?healthy volunteers who smoke, healthy volunteers who do not smoke, subjects with documented chronic obstructive pulmonary disease (COPD) and subjects with alpha 1-antitrypsin deficiency (AATD).

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 确定烟草烟雾（TS）诱导的肺泡巨噬细胞（AM）介导的肺损伤以及Alpha 1-抗抗蛋白酶（AAT）在调节由TS引起的肺损伤程度的保护作用可能允许开发更具体的疗法以预防或减少肺损伤。 AM是iNOS上调的一氧化氮（NO）的来源。 最初的侮辱（TS）被消除后很长一段时间都不会持续生产。 AAT可能在抑制氧化剂损伤（例如iNOS）对肺组织的氧化剂损伤的概念是新颖的，并且是该项目的主题。 这是一个试点项目，有20名受试者进行支气管镜检查。 在四个受试者中，将比较支气管灌洗液，活检/刷子，肺功能测试和研究血液检查？健康的志愿者，不吸烟的健康志愿者，不吸烟的健康志愿者，患有慢性阻塞性肺部疾病（COPD）的受试者以及患有Alpha 1-抗抗肽缺乏症的受试者（AATD）。