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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 假设是：肺功能正常-FEV 1大于或等于80%预测值且QCT异常的AATD受试者的FEV 1- ml/年下降率大于QCT正常的AATD受试者;通过QCT确定的肺实质损失与肺功能下降和COPD进展显著相关;通过CRP测量的肺部炎症与通过QCT确定的肺功能和肺实质损失相关。 次要分析将评价QTC与其他肺功能指标和炎症生物标志物的相关性。将鼓励这些受试者参与Alpha-1基金会DNA和组织库，以将本研究的CT结果与当前AATD研究中正在评价的候选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，我们将在50名肺功能正常的AATD患者中进行为期3年的纵向研究。 基线QCT将定义肺部小于-910 Hounsfield单位的百分比，并将选择中位数将受试者分为肺密度较高和肺密度较低的受试者。 我们将在每次访视时以高分辨率和低分辨率监测吸气QCT，并在访视1和第2年结束时监测呼气QCT。 次要和探索性分析将评估最佳放射学技术与FEV 1下降的相关性。这项研究将引导开发一种更准确的肺组织损失评估方法，并可能提高对AATD个体肺破坏的理解。