Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12018
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dc.contributor.authorAntonic, Anaen
dc.contributor.authorDottori, Mirellaen
dc.contributor.authorLeung, Jessieen
dc.contributor.authorSidon, Kateen
dc.contributor.authorBatchelor, Peter Egertonen
dc.contributor.authorWilson, Williamen
dc.contributor.authorMacleod, Malcolm Ren
dc.contributor.authorHowells, David Williamen
dc.date.accessioned2015-05-16T01:39:15Z
dc.date.available2015-05-16T01:39:15Z
dc.date.issued2014-01-03en
dc.identifier.citationInternational Journal of Stroke 2014; 9(5): 544-52en
dc.identifier.govdoc24393199en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12018en
dc.description.abstractHypothermia provides neuroprotection after cardiac arrest, hypoxic-ischemic encephalopathy, and in animal models of ischemic stroke. However, as drug development for stroke has been beset by translational failure, we sought additional evidence that hypothermia protects human neurons against ischemic injury.Human embryonic stem cells were cultured and differentiated to provide a source of neurons expressing β III tubulin, microtubule-associated protein 2, and the Neuronal Nuclei antigen. Oxygen deprivation, oxygen-glucose deprivation, and H2 O2 -induced oxidative stress were used to induce relevant injury.Hypothermia to 33°C protected these human neurons against H2 O2 -induced oxidative stress reducing lactate dehydrogenase release and Terminal deoxynucleotidyl transferase dUTP nick end labeling-staining by 53% (P ≤ 0·0001; 95% confidence interval 34·8-71·04) and 42% (P ≤ 0·0001; 95% confidence interval 27·5-56·6), respectively, after 24 h in culture. Hypothermia provided similar protection against oxygen-glucose deprivation (42%, P ≤ 0·001, 95% confidence interval 18·3-71·3 and 26%, P ≤ 0·001; 95% confidence interval 12·4-52·2, respectively) but provided no protection against oxygen deprivation alone. Protection (21%) persisted against H2 O2 -induced oxidative stress even when hypothermia was initiated six-hours after onset of injury (P ≤ 0·05; 95% confidence interval 0·57-43·1).We conclude that hypothermia protects stem cell-derived human neurons against insults relevant to stroke over a clinically relevant time frame. Protection against H2 O2 -induced injury and combined oxygen and glucose deprivation but not against oxygen deprivation alone suggests an interaction in which protection benefits from reduction in available glucose under some but not all circumstances.en
dc.language.isoenen
dc.subject.otherbrainen
dc.subject.otherhypothermiaen
dc.subject.otherischemic strokeen
dc.subject.otherneuroprotectionen
dc.subject.otherstem cellsen
dc.subject.othertreatmenten
dc.subject.otherApoptosis.physiologyen
dc.subject.otherCell Death.physiologyen
dc.subject.otherCell Hypoxiaen
dc.subject.otherCells, Cultureden
dc.subject.otherEmbryonic Stem Cellsen
dc.subject.otherGlucose.deficiencyen
dc.subject.otherHumansen
dc.subject.otherHydrogen Peroxide.toxicityen
dc.subject.otherHypothermia.physiopathologyen
dc.subject.otherHypothermia, Induceden
dc.subject.otherLactate Dehydrogenases.metabolismen
dc.subject.otherNeurons.physiologyen
dc.subject.otherOxidative Stress.physiologyen
dc.subject.otherOxygen.metabolismen
dc.subject.otherTime Factorsen
dc.titleHypothermia protects human neurons.en
dc.typeJournal Articleen
dc.identifier.journaltitleInternational Journal of Strokeen
dc.identifier.affiliationFlorey Institute of Neuroscience and Mental Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1111/ijs.12224en
dc.description.pages544-52en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/24393199en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
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