Inflammatory mechanisms in the toxicity of ricin

蓖麻毒素毒性的炎症机制

• 批准号: 8084854
• 负责人: BRUCE E. MAGUN
• 金额: $ 38.5万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-21 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8084854
• 关键词: Acute; Adenine; Aerosols; Alveolar Macrophages; Antibodies; Apoptosis; Biological; Bioterrorism; Bone Marrow; Breathing; Caspase-1; Cell Death; Cells; Cessation of life; Complex; Depurination; Development; Edema; Environment; Event; Gene Expression; Genes; Genetic Transcription; Goals; Human; Immunoprecipitation; Inflammation; Inflammation Mediators; Inflammatory; Inflammatory Response; Injury; Interleukin-1; Interleukin-1 Receptors; Lead; Life; Lung; Lung Inflammation; MAP Kinase Gene; MAPK14 gene; MAPK8 gene; Mass Spectrum Analysis; Measures; Mediating; Mediator of activation protein; Molecular; Molecular Sieve Chromatography; Molecular Target; Mus; NADPH Oxidase; Pathology; Pathway interactions; Phosphorylation; Phosphotransferases; Pneumonia; Population; Process; Production; Proteasome Inhibitor; Protein Inhibition; Protein Synthesis Inhibitors; Proteins; Proteomics; Publishing; RNA, Ribosomal, 28S; Reactive Oxygen Species; Research; Residual state; Ricin; Role; Signal Pathway; Signal Transduction; Testing; Therapeutic; Toxic effect; Toxin; Transducers; Translations; aerosolized; anakinra; chemokine; cytokine; efficacy testing; extracellular; in vivo; inhibitor/antagonist; lung injury; macrophage; mortality; neutrophil; novel; pathogen; receptor; response; secretion process; stem; stress activated protein kinase; upstream kinase