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dc.contributor.advisorGu, Zezongeng
dc.contributor.authorTomlinson, Brittany N.eng
dc.date.issued2013eng
dc.date.submitted2013 Springeng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on September 18, 2013).eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionThesis advisor: Dr. Zezong Gueng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionM.S. University of Missouri-Columbia 2013.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- pathology.eng
dc.description"May 2013"eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Traumatic brain injury (TBI) is a highly prevalent cause of death and disability in the US and has become a significant burden to our present healthcare system. Currently there are few biomarkers and clinical diagnostic tests to determine the severity of TBI in humans. In addition, there are few efficacious treatments at this time for TBI that do not have severe side effects. Matrix metalloproteinases (MMPs) represent the most prominent family of endopeptidases that are necessary for normal growth and development but are also involved in the disruption of the blood-brain barrier (BBB), neuronal cell death, neuroinflammation and/or neurodegeneration after TBI. Studies of mouse models from our laboratory and others have shown that there is an elevation of MMPs, specifically gelatinase MMP-9, in the brain tissue of mice with TBI. In the Gu laboratory, we have adopted an electromagnetic (EM) controlled cortical impact (CCI) mouse model along with refined surgical techniques and behavioral testing to mimic a precise, graded TBI. Here we compare our EM CCI mouse model of TBI to cerebrospinal fluid (CSF) from the severe human head trauma cases through examining matrix metalloproteinase-9 (MMP-9), which we have shown to be upregulated after TBI. We also examine the efficacy of selective MMP-9 inhibitors analog to the prototype mechanism-based MMP inhibitor SB-3CT, which is selective to gelatinases (MMP-2/-9). SB-3CT has been shown to attenuate MMP-9 and ameliorate neurological deficits after TBI.eng
dc.format.extentxii, 59 pageseng
dc.identifier.urihttp://hdl.handle.net/10355/38597
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartof2013 MU restricted theses (MU)eng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the University of Missouri - Columbia.eng
dc.source.originalSubmitted by the University of Missouri--Columbia Graduate Schooleng
dc.subjecttraumatic brain injuryeng
dc.subjectmatrix metalloproteinaseseng
dc.subjectcerebrospinal fluideng
dc.titleOf mice and men: can MMP-9 be a biomarker and a potential target for treatment after traumatic brain injury?eng
dc.typeThesiseng
thesis.degree.disciplinePathology (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.S.eng


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