자료유형 | 학위논문 |
---|---|
서명/저자사항 | Novel Targets for Mitochondrial Dysfunction Following Traumatic Brain Injury. |
개인저자 | Yonutas, Heather M. |
단체저자명 | University of Kentucky. Neuroscience. |
발행사항 | [S.l.]: University of Kentucky., 2016. |
발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2016. |
형태사항 | 217 p. |
기본자료 저록 | Dissertation Abstracts International 79-11B(E). Dissertation Abstract International |
ISBN | 9780438110953 |
학위논문주기 | Thesis (Ph.D.)--University of Kentucky, 2016. |
일반주기 |
Source: Dissertation Abstracts International, Volume: 79-11(E), Section: B.
|
요약 | Mitochondrial 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 |
요약 | For 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 |
요약 | In 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 |
요약 | These 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 |
일반주제명 | Neurosciences. Pharmaceutical sciences. |
언어 | 영어 |
바로가기 |
: 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |