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Novel Targets for Mitochondrial Dysfunction Following Traumatic Brain Injury

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서명/저자사항Novel Targets for Mitochondrial Dysfunction Following Traumatic Brain Injury.
개인저자Yonutas, Heather M.
단체저자명University of Kentucky. Neuroscience.
발행사항[S.l.]: University of Kentucky., 2016.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2016.
형태사항217 p.
기본자료 저록Dissertation Abstracts International 79-11B(E).
Dissertation Abstract International
ISBN9780438110953
학위논문주기Thesis (Ph.D.)--University of Kentucky, 2016.
일반주기 Source: Dissertation Abstracts International, Volume: 79-11(E), Section: B.
요약Mitochondrial dysfunction is a phenomenon observed in models of Traumatic Brain Injury (TBI). Loss of mitochondrial bioenergetics can result in diminished cellular homeostasis leading to cellular dysfunction and possible cellular death. Conseque
요약For this project, we tested the hypothesis that mitoNEET, a novel mitochondrial membrane protein, is a target for pioglitazone mediated neuroprotection. To test this, we used a severe Controlled Cortical Impact (CCI) injury model in mitoNEET nul
요약In addition to this specific hypothesis tested, our experiments provided insight casting doubt on the central dogma that mitochondrial dysfunction following TBI is the result of vast oxidative damage and consequential irreversible mitochondrial
요약These studies support the role of mitoNEET in the neuropathological sequelae of brain injury, supporting mitoNEET as a crucial target for pioglitazone mediated neuroprotection following TBI. Lastly, these studies propose a mechanism of TBI relat
일반주제명Neurosciences.
Pharmaceutical sciences.
언어영어
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