The Contribution of Inflammation to Brain Injury after Stroke

炎症对中风后脑损伤的影响

基本信息

批准号：
7749995
负责人：
Helena Willington Morrison
金额：
$ 0.34万
依托单位：
UNIVERSITY OF ARIZONA
依托单位国家：
美国
项目类别：
财政年份：
2007
资助国家：
美国
起止时间：
2007-12-01 至 2010-04-02
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7749995
关键词：
Address Adhesions American American Heart Association Area Behavioral Biochemical Blood Blood Cells Brain Injuries Caring Cause of Death Cerebrum Complement Development Environment Experimental Designs Genetic Goals Infarction Inflammation Inflammation Mediators Inflammatory Inflammatory Response Injury Interdisciplinary Study Ischemic Stroke Knowledge Laboratories Left Leukocyte Adhesion Molecules Leukocyte-Adhesion Receptors Leukocytes Life Mannose Binding Lectin Mannose-Binding Lectins Measurement Mediating Mentors Methods Nervous System Physiology Nurses Operative Surgical Procedures Outcome Pathway interactions Process Production Public Health Reactive Oxygen Species Reperfusion Injury Reperfusion Therapy Research Research Project Grants Research Training Risk Science Scientist Staining method Stroke Students Supportive care Tissue Stains Transgenic Mice Translating career complement pathway disability experience improved inflammatory marker leukocyte activation mouse model neutrophil novel programs response stroke therapy

项目摘要

DESCRIPTION (provided by applicant): Stroke is the third leading cause of death in the US. About 700,000 Americans have a stroke each year (American Heart Association [AHA], 2006); 88% of these are ischemic strokes (AHA, 2006). Those able to recover and rehabilitate from ischemic stroke are often left with long-term disabilities requiring supportive care and are at increased risk for further illness and injury (AHA). It is known that inflammatory responses are increased after ischemic stroke and reperfusion. These responses increase brain injury (Crack & Taylor, 2005; D'Ambrosio et al., 2001; Ritter et al., 2000; Ritter et al., 2005; Ruehl et al., 2002). It is also known that leukocyte activation is one inflammatory mechanism that contributes to brain injury after stroke. However, the influence of other inflammatory mediators on leukocyte activation, and subsequent brain injury, remains unclear. To address this gap in knowledge, the overall goal of this research is to determine how novel inflammatory complement proteins contribute to leukocyte mediated brain injury after stroke. A quantitative experimental design using a transgenic mouse model, that does not express the complement protein mannose binding lectin complement, will be employed. Following a surgical method of ischemic stroke and reperfusion, behavioral analysis, measurement of infarct area using tissue staining methods, and biochemical analyses of blood markers of inflammation will be performed. The applicant and mentor are perfectly matched and the research environment strongly supports the applicant's research training plan. Dr. Leslie Ritter, the applicant's mentor, has an established program of research related to mechanisms of inflammation and stroke. She maintains a laboratory, a strong interdisciplinary research team, and has mentored successful doctoral students. Relevance of this research to public health: The outcomes of the specific proposed research project will serve the 700,000 people who suffer a stroke each year, by filling a gap in knowledge related to the understanding of the specific inflammatory mechanisms that contribute to brain injury after stroke. Subsequently, this contribution to science will translate into the development of new stroke therapies that will limit brain injury, extend healthy life, and reduce disability from ischemic stroke. The outcome of the proposed research training plan will be to prepare a nurse scientist who, over the course of her career, will continue to make significant contributions to the understanding of the ischemic stroke inflammatory process and the care of people who experience this kind of brain injury

描述（由申请人提供）：中风是美国第三大死亡原因。每年约有70万美国人中风（美国心脏协会[AHA]，2006年）；其中88％是缺血性中风（AHA，2006年）。那些能够从缺血性中风中恢复和康复的人通常会保留长期的残疾，需要支持性护理，并且面临进一步疾病和伤害的风险（AHA）。众所周知，缺血性中风和再灌注后炎症反应会增加。这些反应会增加脑损伤（Crack＆Taylor，2005; D'Ambrosio等，2001; Ritter等，2000; Ritter等，2005; Ruehl等，2002）。众所周知，白细胞激活是一种炎症机制，可导致中风后脑损伤。但是，其他炎症介质对白细胞激活以及随后的脑损伤的影响尚不清楚。为了解决这一知识的差距，这项研究的总体目标是确定新颖的炎症补体蛋白如何在中风后有助于白细胞介导的脑损伤。使用不表达补体蛋白甘露糖结合凝集素补体的转基因小鼠模型的定量实验设计。遵循缺血性中风和再灌注的手术方法，将使用组织染色方法对梗塞区域的测量以及炎症血液标记的生化分析进行测量。申请人和指导者完全匹配，研究环境强烈支持申请人的研究培训计划。申请人的导师莱斯利·里特（Leslie Ritter）博士拥有与炎症和中风机制有关的既定研究计划。她维护着一个实验室，一个强大的跨学科研究团队，并指导了成功的博士生。这项研究与公共卫生的相关性：特定提议的研究项目的结果将为每年遭受中风的700,000人服务，通过填补与对中风后有助于脑损伤的特定炎症机制有关的知识的差距。随后，这种对科学的贡献将转化为新的中风疗法的发展，这些疗法将限制脑损伤，延长健康生活并减少缺血性中风的残疾。拟议的研究培训计划的结果将是为护士科学家做好准备，在她的职业生涯中，她将继续为理解缺血性中风炎症过程以及经历这种脑损伤的人们的照顾做出重大贡献

项目成果

期刊论文数量（4）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Immunological methods for nursing research: from cells to systems.

DOI：
10.1177/1099800411402494
发表时间：
2011-07
期刊：
Biological research for nursing
影响因子：
2.5
作者：
Morrison HW;Downs CA
通讯作者：
Downs CA

Systemic neutrophil activation in a mouse model of ischemic stroke and reperfusion.

DOI：
10.1177/1099800410384500
发表时间：
2011-04
期刊：
Biological research for nursing
影响因子：
2.5
作者：
Morrison H;McKee D;Ritter L
通讯作者：
Ritter L

Exaggerated neutrophil-mediated reperfusion injury after ischemic stroke in a rodent model of type 2 diabetes.

DOI：
10.1111/j.1549-8719.2011.00115.x
发表时间：
2011-10
期刊：
Microcirculation (New York, N.Y. : 1994)
影响因子：
0
作者：
Ritter L;Davidson L;Henry M;Davis-Gorman G;Morrison H;Frye JB;Cohen Z;Chandler S;McDonagh P;Funk JL
通讯作者：
Funk JL

Beyond the PhD: putting the right tools in your research toolbox.

超越博士学位：将正确的工具放入您的研究工具箱中。