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

Agency
National Institute of Health (NIH)
Institute
National Institute of Nursing Research (NINR)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31NR010658-03
Application #
7749995
Study Section
National Institute of Nursing Research Initial Review Group (NRRC)
Program Officer
Banks, David
Project Start
2007-12-01
Project End
2010-04-02
Budget Start
2009-12-01
Budget End
2010-04-02
Support Year
3
Fiscal Year
2010
Total Cost
$3,375
Indirect Cost
Name
University of Arizona
Department
Type
Schools of Nursing
DUNS #
806345617
City
Tucson
State
AZ
Country
United States
Zip Code
85721
Morrison, Helena W; Downs, Charles A (2011) Immunological methods for nursing research: from cells to systems. Biol Res Nurs 13:227-34
Downs, Charles A; Morrison, Helena W (2011) Beyond the PhD: putting the right tools in your research toolbox. Biol Res Nurs 13:5-14
Morrison, Helena; Frye, Jennifer; Davis-Gorman, Grace et al. (2011) The contribution of mannose binding lectin to reperfusion injury after ischemic stroke. Curr Neurovasc Res 8:52-63
Morrison, Helena; McKee, Dana; Ritter, Leslie (2011) Systemic neutrophil activation in a mouse model of ischemic stroke and reperfusion. Biol Res Nurs 13:154-63