Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/71993
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dc.contributor.authorFinnie, J.-
dc.contributor.authorBlumbergs, P.-
dc.contributor.authorManavis, J.-
dc.date.issued2011-
dc.identifier.citationJournal of Clinical Neuroscience, 2011; 18(7):947-950-
dc.identifier.issn0967-5868-
dc.identifier.issn1532-2653-
dc.identifier.urihttp://hdl.handle.net/2440/71993-
dc.description.abstractCerebral contusions are one of the principal lesions of traumatic brain injury and the attendant oedema formation contributes substantially to the clinicopathological manifestations. While it is now recognised that the membrane channel protein aquaporin-4 (AQP-4) plays a major role in the development and resolution of cerebral oedema, assessments of its expression in and around contusions have produced conflicting results. We used an ovine impact-acceleration model of closed head injury to examine contusion-related AQP-4 expression and found that there was a heterogeneous AQP-4 response within contusions, with some astrocytes being nonviable and immunonegative, while others showed increased AQP-4 expression. Pericontusional astrocytes in the penumbra region generally showed more robust AQP-4 immunopositivity than intracontusional glia. Thus, manipulation of AQP-4 expression could have therapeutic applications in controlling cerebral oedema associated with contusions.-
dc.description.statementofresponsibilityJohn W. Finnie, Peter C. Blumbergs and Jim Manavis-
dc.language.isoen-
dc.publisherChurchill Livingstone-
dc.rights© 2011 Elsevier Ltd. All rights reserved.-
dc.subjectAstrocytes-
dc.subjectAnimals-
dc.subjectSheep-
dc.subjectBrain Edema-
dc.subjectBrain Injuries-
dc.subjectHead Injuries, Closed-
dc.subjectDisease Models, Animal-
dc.subjectImmunohistochemistry-
dc.subjectFemale-
dc.subjectAquaporin 4-
dc.titleAquaporin-4 expression after experimental contusional injury in an ovine impact-acceleration head injury model-
dc.typeJournal article-
dc.identifier.doi10.1016/j.jocn.2010.11.010-
pubs.publication-statusPublished-
dc.identifier.orcidFinnie, J. [0000-0003-2277-1693]-
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