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008181129s2016 ||| | | | eng d
020 ▼a 9780438110953
035 ▼a (MiAaPQ)AAI10902434
040 ▼a MiAaPQ ▼c MiAaPQ ▼d 248032
0491 ▼f DP
0820 ▼a 616
1001 ▼a Yonutas, Heather M.
24510 ▼a Novel Targets for Mitochondrial Dysfunction Following Traumatic Brain Injury.
260 ▼a [S.l.] : ▼b University of Kentucky., ▼c 2016
260 1 ▼a Ann Arbor : ▼b ProQuest Dissertations & Theses, ▼c 2016
300 ▼a 217 p.
500 ▼a Source: Dissertation Abstracts International, Volume: 79-11(E), Section: B.
5021 ▼a Thesis (Ph.D.)--University of Kentucky, 2016.
520 ▼a 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
520 ▼a 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
520 ▼a 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
520 ▼a 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
590 ▼a School code: 0102.
650 4 ▼a Neurosciences.
650 4 ▼a Pharmaceutical sciences.
690 ▼a 0317
690 ▼a 0572
71020 ▼a University of Kentucky. ▼b Neuroscience.
7730 ▼t Dissertation Abstracts International ▼g 79-11B(E).
773 ▼t Dissertation Abstract International
790 ▼a 0102
791 ▼a Ph.D.
792 ▼a 2016
793 ▼a English
85640 ▼u http://www.riss.kr/pdu/ddodLink.do?id=T15000372 ▼n KERIS
980 ▼a 201812 ▼f 2019
990 ▼a 관리자 ▼b 관리자