Mechanisms of Transfusion-Induced Lung Injury in

输血所致肺损伤的机制

• 批准号: 7531182
• 负责人: MICHAEL A. MATTHAY
• 金额: $ 31.81万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7531182
• 关键词: Activities of Daily Living; Acute Lung Injury; Adhesions; Adrenergic Agents; Adrenergic Agonists; Agonist; Alveolar; Alveolar Macrophages; Animal Model; Antibodies; Antigen-Antibody Complex; Antigens; Blood; Blood Vessels; Cell Adhesion Molecules; Cells; Complement Receptor; Cyclic AMP; Development; Dissection; Edema; Environmental air flow; Epithelial; Epithelium; Experimental Models; Extravascular Lung Water; Histologic; Individual; Intercellular adhesion molecule 1; Ions; Knockout Mice; Leukocytes; Lipids; Liquid substance; Lung; Lung Capacity; Measures; Mediator of activation protein; Modeling; Monoclonal Antibodies; Mus; Mutation; Pathogenesis; Permeability; Plasma; Play; Proteins; Pulmonary Edema; Resolution; Role; Serum; Testing; TimeLine; Transfusion; Transgenic Mice; adrenergic; alveolar epithelium; base; clinically relevant; in vivo; in vivo Model; insight; lung injury; macrophage; mortality; mouse model; neutrophil; polyclonal antibody; pressure; receptor; reconstitution; research study; response; restoration; src-Family Kinases