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Article: Late measures of brain injury after neonatal hypoxia-ischemia in mice

TitleLate measures of brain injury after neonatal hypoxia-ischemia in mice
Authors
Issue Date2004
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://stroke.ahajournals.org
Citation
Stroke, 2004, v. 35 n. 9, p. 2183-2188 How to Cite?
AbstractBackground and Purpose-This work was undertaken to determine to what degree long-term neurofunctional outcome of neonatal hypoxic-ischemic (HI) brain injury in mice correlates with anatomical extent of cerebral damage assessed by magnetic resonance imaging (MRI) and histopathology. Methods-On postnatal day 7, mice were subjected to HI. At 7 to 9 weeks after HI neurofunctional outcome was assessed by water-maze, rota-rod, and open-field test performance, followed by cerebral MRI and histopathology evaluation. Results-At 10 weeks after HI, MRI revealed ipsilateral brain atrophy alone or with porencephalic cyst formation and contralateral ventriculomegaly. Adult HI-affected mice, especially those that developed a porencephalic cyst, demonstrated significant neurofunctional deficit compared with age-matched naïve mice. HI-affected mice with ipsilateral cerebral atrophy but without porencephaly demonstrated no or an intermediate level of neurofunctional deficit. Neurobehavioral assessment of mice subjected to HI insult revealed a strong correlation between degree of brain injury and functional neurohandicap. Conclusions-This is the first study to demonstrate that long-term neurofunctional outcome in mice after a neonatal HI correlates tightly with anatomical pattern/extent of cerebral damage, defined by MRI and histopathology.
Persistent Identifierhttp://hdl.handle.net/10722/73793
ISSN
2015 Impact Factor: 5.787
2015 SCImago Journal Rankings: 3.671
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTen, VSen_HK
dc.contributor.authorWu, EXen_HK
dc.contributor.authorTang, Hen_HK
dc.contributor.authorBradleyMoore, Men_HK
dc.contributor.authorFedarau, MVen_HK
dc.contributor.authorRatner, VIen_HK
dc.contributor.authorStark, RIen_HK
dc.contributor.authorGingrich, JAen_HK
dc.contributor.authorPinsky, DJen_HK
dc.date.accessioned2010-09-06T06:54:49Z-
dc.date.available2010-09-06T06:54:49Z-
dc.date.issued2004en_HK
dc.identifier.citationStroke, 2004, v. 35 n. 9, p. 2183-2188en_HK
dc.identifier.issn0039-2499en_HK
dc.identifier.urihttp://hdl.handle.net/10722/73793-
dc.description.abstractBackground and Purpose-This work was undertaken to determine to what degree long-term neurofunctional outcome of neonatal hypoxic-ischemic (HI) brain injury in mice correlates with anatomical extent of cerebral damage assessed by magnetic resonance imaging (MRI) and histopathology. Methods-On postnatal day 7, mice were subjected to HI. At 7 to 9 weeks after HI neurofunctional outcome was assessed by water-maze, rota-rod, and open-field test performance, followed by cerebral MRI and histopathology evaluation. Results-At 10 weeks after HI, MRI revealed ipsilateral brain atrophy alone or with porencephalic cyst formation and contralateral ventriculomegaly. Adult HI-affected mice, especially those that developed a porencephalic cyst, demonstrated significant neurofunctional deficit compared with age-matched naïve mice. HI-affected mice with ipsilateral cerebral atrophy but without porencephaly demonstrated no or an intermediate level of neurofunctional deficit. Neurobehavioral assessment of mice subjected to HI insult revealed a strong correlation between degree of brain injury and functional neurohandicap. Conclusions-This is the first study to demonstrate that long-term neurofunctional outcome in mice after a neonatal HI correlates tightly with anatomical pattern/extent of cerebral damage, defined by MRI and histopathology.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://stroke.ahajournals.orgen_HK
dc.relation.ispartofStrokeen_HK
dc.rightsStroke. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshAtaxia - etiology - pathologyen_HK
dc.subject.meshAtrophyen_HK
dc.subject.meshBrain - pathologyen_HK
dc.subject.meshBrain Damage, Chronic - etiology - pathologyen_HK
dc.subject.meshBrain Diseases - etiology - pathologyen_HK
dc.subject.meshCarotid Artery, Commonen_HK
dc.subject.meshCerebral Ventricles - pathologyen_HK
dc.subject.meshCysts - etiology - pathologyen_HK
dc.subject.meshExploratory Behavioren_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHypoxia-Ischemia, Brain - complications - pathologyen_HK
dc.subject.meshLearning Disorders - etiology - pathologyen_HK
dc.subject.meshLigationen_HK
dc.subject.meshMagnetic Resonance Imagingen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMaze Learningen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMotor Activityen_HK
dc.subject.meshNeuronal Plasticityen_HK
dc.subject.meshNeuropsychological Testsen_HK
dc.titleLate measures of brain injury after neonatal hypoxia-ischemia in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0039-2499&volume=35&spage=2183&epage=2188&date=2004&atitle=Late+measures+of+brain+injury+after+neonatal+hypoxia-ischemia+in+miceen_HK
dc.identifier.emailWu, EX:ewu1@hkucc.hku.hken_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1161/01.STR.0000137768.25203.dfen_HK
dc.identifier.pmid15272130-
dc.identifier.scopuseid_2-s2.0-4344634904en_HK
dc.identifier.hkuros141482en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4344634904&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue9en_HK
dc.identifier.spage2183en_HK
dc.identifier.epage2188en_HK
dc.identifier.isiWOS:000223537000035-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTen, VS=6701589562en_HK
dc.identifier.scopusauthoridWu, EX=7202128034en_HK
dc.identifier.scopusauthoridTang, H=36827331000en_HK
dc.identifier.scopusauthoridBradleyMoore, M=7801531717en_HK
dc.identifier.scopusauthoridFedarau, MV=36825777400en_HK
dc.identifier.scopusauthoridRatner, VI=7006500704en_HK
dc.identifier.scopusauthoridStark, RI=7202161406en_HK
dc.identifier.scopusauthoridGingrich, JA=35309966500en_HK
dc.identifier.scopusauthoridPinsky, DJ=7004815412en_HK

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