QUANTUM

量子

• 批准号: 7950755
• 负责人: MARK Louis BRANTLY
• 金额: $ 0.44万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-12-01 至 2009-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7950755
• 关键词: Address; Biological Markers; Chronic Obstructive Airway Disease; Clinical Research; Computer Retrieval of Information on Scientific Projects Database; DNA; Development; Foundations; Funding; Grant; Individual; Inflammatory; Institution; Link; Longitudinal Studies; Lung; Lung Inflammation; Measures; Monitor; Outcome Study; Pulmonary Function Test/Forced Expiratory Volume 1; Research; Research Personnel; Resolution; Resources; Respiratory physiology; Single Nucleotide Polymorphism; Source; Structure of parenchyma of lung; Susceptibility Gene; Techniques; Tissue Banking; Tissue Banks; United States National Institutes of Health; Visit; density; improved; quantum

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. Hypotheses are: AATD subjects with normal lung function-FEV1 greater or equal to 80 percent predicted, and abnormal QCT have a greater rate of decline in FEV1- ml/year than AATD subjects with a normal QCT; loss of lung parenchyma determined by QCT significantly correlates with lung function decline and COPD progression; lung inflammation as measured by CRP correlates with loss of lung function and lung parenchyma determined by QCT. Secondary analyses will evaluate the correlation of QTC with other measures of lung function, and inflammatory biomarkers. Participation of these subjects in the Alpha-1 Foundation DNA and Tissue Bank will be encouraged to link the CT outcomes of this study to single nucleotide polymorphisms of candidate COPD susceptibility genes that are being evaluated in current AATD studies. To address these hypotheses, we will conduct a 3-year longitudinal study in 50 individuals with AATD with normal lung function. The baseline QCT will define the percentage of lung less than-910 Hounsfield units and the median value will be chosen to divide the subjects into those with greater lung density and those with less lung density. We will monitor inspiratory QCTs at a high and low resolution at every visit and expiratory QCTs at visit 1 and at the end of year 2. Secondary and exploratory analyses will assess the optimal radiographic technique for correlation with FEV1 decline. This study will pilot the development of a more accurate assessment of lung tissue loss and may improve the understanding of the lung destruction in AATD individuals.

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。 假设是：正常肺功能-FEV1的AATD受试者的预测大于或等于80％，而异常QCT的FEV1-mL/年降低率要比具有正常QCT的AATD受试者高。 由QCT确定的肺实质的丧失与肺功能下降和COPD进展显着相关； 通过CRP测量的肺部炎症与肺功能的丧失和由QCT确定的肺实质的丧失相关。 次要分析将评估QTC与肺功能的其他度量和炎症生物标志物的相关性。这些受试者将鼓励这些受试者参与Alpha-1基础DNA和组织库，将本研究的CT结局与当前AATD研究中正在评估的候选COPD易感基因的单核苷酸多态性联系起来。 为了解决这些假设，我们将对50名具有正常肺功能的AATD患者进行3年的纵向研究。 基线QCT将定义小于910 Hounsfield单位的肺百分比，并选择中位数以将受试者分为肺部密度较高和肺部密度较小的受试者。 我们将在每次访问和访问1年底和第二年末以高分辨率和低分辨率监视Insperation QCT。次级和探索性分析将评估与FEV1下降相关的最佳放射学技术。这项研究将通过对肺组织损失进行更准确的评估发展，并可能提高对AATD个体肺破坏的理解。