镰状细胞贫血症中的哮喘和夜间低氧血症-猫眼课题宝

镰状细胞贫血症中的哮喘和夜间低氧血症

批准号：

7457787

负责人：

Michael R. DeBaun

金额：

$184.15万

依托单位：

WASHINGTON UNIVERSITY

依托单位国家：

美国

项目类别：

财政年份：

2005

资助国家：

美国

项目状态：

已结题

起止时间：

2005-08-25 至 2010-06-30

来源：

https://reporter.nih.gov/project-details/7457787

关键词：

Accounting Age Anemia Asthma Basic Science Biological Markers Biopsy Bronchoalveolar Lavage Candidate Disease Gene Case-Control Studies Cell Adhesion Molecules Cells Cerebrum Child Childhood Chronic Classification Clinical Clinical Research Cohort Studies Collaborations Condition Coupled Data Disease Eczema Enrollment Epidemiology Epithelial Cells Evaluation Forced expiratory volume function Foundations Funding Gender Genes Genomics Goals Height Hemoglobin SS Human Hypersensitivity skin testing Hypoxia Immunohistochemistry Incidence Individual Infarction Laboratories Link Lung Lung diseases Masks Measures Modeling Molecular Molecular Genetics Morbidity - disease rate Mus Nitric Oxide Nocturnal Asthma Oxygen Pain Participant Pathologic Pathology Patients Pattern Phenotype Physiological Plasma Platelet Activation Polysomnography Population Predisposition Pulmonary function tests Race Rate Recording of previous events Research Personnel Risk Risk Factors STAT1 gene Scientist Sendai virus Sickle Cell Anemia Sleep Sleep disturbances Staining method Stains Structure of parenchyma of lung Subgroup Testing Tissues Transgenic Organisms United States National Institutes of Health Universities Virus Diseases Washington acute chest syndrome airway inflammation airway obstruction base bench to bedside cooperative study genome sequencing inflammatory pain insight lung injury neutrophil nocturnal Hypoxemia novel therapeutics positional cloning programs repository research facility research study

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Our overall goal is to elucidate the physiologic, genetic, and molecular aspects of two common co-morbid conditions, asthma and nocturnal oxygen desaturation, that increase the incidence rate of pain in sickle cell anemia (SCA). In separate studies, we have shown children with SCA and either asthma or nocturnal desaturation have an increased pajn rate when compared to children without the condition. Also, our group demonstrated that in a murine model of SCA there was significant susceptibility to hypoxia-induced pulmonary vasocongestion when compared to mice without SCA. Unfortunately, we do not know the interrelationship if any, between asthma, nocturnal desaturation and lung disease in SCA. We propose three interrelated projects. The first and second clinical projects will delineate the physiological basis for the association of asthma and nocturnal desaturation with SCA related morbidity. The first project will also obtain DMA and clinical information from 1800 children with SCA participating in the Silent Cerebral Infarct (SIT) Trial. We will perform a case-control study evaluating whether genes associated with asthma increase the risk of pain and ACS episodes. The basic science project will have experiments aimed at defining the molecular mechanisms by which asthma and nocturnal hypoxemia, separately and together, increase lung injury in a transgenic SCA murine model. We will test three global hypotheses: 1) phenotypic and genotypic features of asthma are risk factors for pain and ACS episodes in children with SCA; 2) nocturnal desaturation in children with SCA modifies the effect of asthma on morbidity in SCA; and 3) chronic airway inflammation and nocturnal hypoxia, separately and together, increase HbSS-induced lung injury in a murine SCA model. Taken together, the results of this highly interactive collaboration of clinical and basic scientists will permit new insights into the mechanisms of lung disease, thus providing a strong foundation for targeted therapy for this vulnerable group.

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