Core J: MOUSE MODELS

核心 J：鼠标模型

• 批准号: 8126768
• 负责人: COLIN D. FUNK
• 金额: $ 31.14万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-08-01 至 2017-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8126768
• 关键词: Address; Animal Experimentation; Animals; Biochemical; Biology; Biomedical Research; Cardiovascular system; Controlled Clinical Trials; Dose; Drug effect disorder; Genetic; Heart failure; Human; Hypertension; Integration Host Factors; Knowledge; Mus; Non-Steroidal Anti-Inflammatory Agents; Output; Pathway interactions; Prostaglandin-Endoperoxide Synthase; Regimen; Resources; Risk; Signal Pathway; Stratification; Therapeutic; Thrombosis; Time; Treatment Efficacy; base; cyclooxygenase 2; hazard; member; microbiome; mouse model; non-genetic; response

The mouse is the most commonly used animal in biomedical research comprising >90% of all animal experimentation. This mammalian species is often the prime choice to flesh out mechanisms of action of drugs and to establish biochemical signaling pathways prior to entering human trials. Directly relevant to PENTACON, mice were used to predict and then assign mechanistic understanding to all recognized features ¿ thrombosis, hypertension, heart failure, dysrhythmia ¿ of the cardiovascular hazard in humans taking COX-2 selective NSAIDs (1,2). More than 20 genetic mouse models that disrupt or perturb the COX biosyntheticresponse pathway have been developed by PENTACON members, a unique resource for use in this proposal.

该小鼠是生物医学研究中最常用的动物，占所有动物的90％ 实验。这种哺乳动物物种通常是充实药物作用机制的主要选择 并在进入人类试验之前建立生化信号通路。与 Pentacon，小鼠被用于预测并将机械理解分配给所有公认的特征 »人类心血管危害COX-2的血栓形成，高血压，心力衰竭，心律失常 选择性NSAID（1,2）。超过20种破坏或扰动Cox BiosyntheticRespons的遗传小鼠模型 Pentacon成员已经开发了途径，这是该提案中的独特资源。