R35 Administrative Supplements to Recognize Excellencein Diversity, Equity, Inclusion, and Accessibility (DEIA)Mentorship

R35 表彰多元化、公平、包容性和可及性 (DEIA) 指导方面卓越表现的行政补充

• 批准号: 10630461
• 负责人: Eva S. Nozik
• 金额: $ 5.17万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-09-01 至 2025-05-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10630461
• 关键词: Administrative Supplement; Adult; Biomedical Research; Birth; Blood Circulation; Blood Vessels; Chronic; Colorado; Development; Development Plans; Doctor of Philosophy; Exercise; Fetal Liver; Foundations; Hypoxia; Impairment; Individual; Lead; Lung; Medical; Mentorship; Modeling; Mus; Neonatal; Oxidation-Reduction; Phenotype; Physiology; Pregnancy; Publishing; Pulmonary Hypertension; Rattus; Regulation; Research; Research Support; Role; Signal Transduction; Students; Superoxide Dismutase; United States National Institutes of Health; Universities; Work; antioxidant enzyme; base; career development; disadvantaged background; diversity and equity; doctoral student; extracellular; graduate student; hypoxia-induced pulmonary hypertension; interest; macrophage; mouse model; neonatal mice; neonatal pulmonary hypertension; offspring; pre-doctoral; pregnant; prenatal; programs; pulmonary vascular disorder; pup; young adult

Abstract This is a request for an administrative supplement to R35 HL139726 SOD3 regulation of redox sensitive signaling in pulmonary vascular diseases to increase diversity, equity and inclusion in biomedical research by supporting pre-doctoral student, Thi-Tina Nguyen. Thi-Tina Nguyen is a predoctoral student in the Integrative Physiology Graduate Program at the University of Colorado Anschutz Medical Campus and will be joining the Nozik lab in July 2022 for her PhD thesis work. She meets criteria for this program based on being from a disadvantaged background according to the NIH criteria. Ms Nguyen has identified an interest in studying how maternal factors that impair EC-SOD expression lead to dysregulated redox signaling in the lung and pulmonary vasculature of the offspring. Specifically, she plans to build upon the lab's published observations that 1) insufficient EC-SOD (SOD3) worsens neonatal lung and vascular development in neonatal mouse models, as well as chronic hypoxic pulmonary hypertension in adult mice; 2) prenatal hypoxic exposure of pregnant rats reduced pup lung EC-SOD content; 3) exercise increases placental derived EC-SOD in the maternal circulation and protects the fetal liver; and 3) low EC-SOD content modulates macrophage reprogramming in pulmonary vascular diseases. Based on these observations, Ms Nguyen has developed a research plan to investigate how hypoxia in late gestation impacts lung EC-SOD, lung and pulmonary vascular development and macrophage phenotype in the offspring after birth and into young adulthood. This work will provide a foundation for an individual F31 application to expand upon this work. The proposal outlines both the scientific proposal and a summary of the career development plan for Ms. Nguyen.

摘要 这是对R35 HL 139726 SOD 3氧化还原法规的行政补充请求 肺血管疾病的敏感信号，以增加多样性，公平性和包容性， 生物医学研究的支持博士前学生，阮蒂蒂娜。阮缇娜是一个 在综合生理学研究生课程的博士前学生在大学的 科罗拉多安舒茨医学院，并将于2022年7月加入Nozik实验室攻读博士学位 论文工作。她符合这个项目的标准，因为她来自一个弱势群体。 根据NIH的标准。阮女士已经确定了一个研究如何 母体因素损害EC-SOD的表达，导致细胞内氧化还原信号失调， 后代的肺和肺脉管系统。具体来说，她计划建立在实验室的基础上， 已发表的观察结果表明：1）EC-SOD（SOD 3）不足导致新生儿肺和血管损伤， 新生小鼠模型的发展，以及慢性缺氧性肺动脉高压， 孕鼠出生前低氧暴露可降低幼鼠肺EC-SOD含量; 运动增加母体循环中胎盘来源的EC-SOD并保护胎儿 低EC-SOD含量调节肺血管中巨噬细胞重编程 疾病基于这些观察，阮女士制定了一项研究计划， 探讨妊娠晚期缺氧对肺EC-SOD、肺及肺血管的影响 发育和巨噬细胞表型在出生后的后代和进入青年期。 这项工作将为个人F31应用程序扩展这项工作提供基础。 该提案既有科学的提案纲要，也有职业发展的总结 为阮女士制定的计划