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dc.contributor.authorKing, Melanie Dawn Ivester
dc.date.accessioned2014-05-23T19:13:06Z
dc.date.available2014-05-23T19:13:06Z
dc.date.issued2013-05en
dc.identifier.urihttp://hdl.handle.net/10675.2/317391
dc.description.abstractIntracerebral hemorrhage (ICH), the most common form of hemorrhagic stroke, exhibits the highest acute mortality and the worst long-term prognosis of all stroke subtypes. Unfortunately, treatment options for ICH are lacking due in part to a lack of feasible therapeutic targets. Inflammatory activation is associated with neurological deficits in pre-clinical ICH models and with patient deterioration after clinical ICH. In the present study, we tested the hypothesis that R-7050, a novel cell-permeable triazoloquinoxaline inhibitor of the tumor necrosis factor receptor (TNFR) complex, attenuates neurovascular injury after ICH in mice. Up to 2h post-injury administration of R-7050 significantly reduced blood-brain barrier opening and attenuated edema development at 24h post-ICH. Neurological outcomes were also improved over the first days after injury. In contrast, R-7050 did not reduce hematoma volume, suggesting the beneficial effects of TNFR inhibition were downstream of clot formation/resolution. These data suggest a potential clinical utility for TNFR antagonists as an adjunct therapy to reduce neurological injury and improve patient outcomes after ICH.
dc.language.isoen_USen
dc.relation.urlhttp://search.proquest.com/docview/1372291772?accountid=12365en
dc.titleThe Role of TNF-Alpha Signaling in the Pathophysiology of Intracerebral Hemorrageen
dc.typeDissertationen
dc.contributor.departmentDepartment of Neurosurgeryen
dc.description.advisorDhandapani, Krishnanen
dc.description.degreeDoctor of Philosophy (Ph.D.)en
dc.description.committeeAlleyne, Cargill Jr.; Brann, Darrell; El-Remessy, Azza; Ergul, Adviye.en


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