File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)

Article: Manganese-enhanced MRI detection of neurodegeneration in neonatal hypoxic-ischemic cerebral injury

TitleManganese-enhanced MRI detection of neurodegeneration in neonatal hypoxic-ischemic cerebral injury
Authors
KeywordsCerebral ischemia
Glutamate excitotoxicity
Glutamine synthetase
Hypoxia
Manganese-enhanced MRI
Mn-superoxide dismutase
Neonatal rat
Oxidative stress
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0740-3194/
Citation
Magnetic Resonance In Medicine, 2008, v. 59 n. 6, p. 1329-1339 How to Cite?
AbstractIn this study, we investigated the Mn-enhanced MRI (MEMRI) for detecting neurodegenerative processes in neonatal hypoxic-ischemic (H-I) cerebral injury. Seven-day-old rats were induced with H-I injury, and scanned for T 1-weighted image (T1WI) and T2-weighted image (T2WI) with and without systemic MnCl2 administration. Serial histological analysis was performed for Mn-superoxide dismutase (Mn-SOD) and glutamine synthetase (GS), which are Mn-binding enzymes against the oxidative stress and glutamate excitotoxicity in neurodegeneration. In the acute phase (first 2 days), the ipsilateral lesion exhibited no Mn enhancement in T1WIs, with histology showing no Mn-SOD and GS production. In the mid-phase (from day 3), Mn enhancement was found in the cortex, basal ganglia, and hippocampus, correlating with local Mn-SOD and GS increase. In the late phase, the enhancement became more localized to the pericyst basal ganglia and cortex, and then gradually diminished. In T2WIs, a signal decrease was observed from day 3 in the corresponding regions. Hypointense voids gradually formed in the late phase, correlating with the local iron accumulation. H-I rats without Mn2+ administration exhibited similar but weak changes in T1WIs and T2WIs from days 14 and 7, respectively. These results indicate that Mn2+ may be a useful in vivo probe for monitoring Mn-SOD and GS enzymatic activities. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/72404
ISSN
2015 Impact Factor: 3.782
2015 SCImago Journal Rankings: 2.197
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Jen_HK
dc.contributor.authorKhong, PLen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorChu, ACYen_HK
dc.contributor.authorHo, SLen_HK
dc.contributor.authorCheung, PTen_HK
dc.contributor.authorWu, EXen_HK
dc.date.accessioned2010-09-06T06:41:23Z-
dc.date.available2010-09-06T06:41:23Z-
dc.date.issued2008en_HK
dc.identifier.citationMagnetic Resonance In Medicine, 2008, v. 59 n. 6, p. 1329-1339en_HK
dc.identifier.issn0740-3194en_HK
dc.identifier.urihttp://hdl.handle.net/10722/72404-
dc.description.abstractIn this study, we investigated the Mn-enhanced MRI (MEMRI) for detecting neurodegenerative processes in neonatal hypoxic-ischemic (H-I) cerebral injury. Seven-day-old rats were induced with H-I injury, and scanned for T 1-weighted image (T1WI) and T2-weighted image (T2WI) with and without systemic MnCl2 administration. Serial histological analysis was performed for Mn-superoxide dismutase (Mn-SOD) and glutamine synthetase (GS), which are Mn-binding enzymes against the oxidative stress and glutamate excitotoxicity in neurodegeneration. In the acute phase (first 2 days), the ipsilateral lesion exhibited no Mn enhancement in T1WIs, with histology showing no Mn-SOD and GS production. In the mid-phase (from day 3), Mn enhancement was found in the cortex, basal ganglia, and hippocampus, correlating with local Mn-SOD and GS increase. In the late phase, the enhancement became more localized to the pericyst basal ganglia and cortex, and then gradually diminished. In T2WIs, a signal decrease was observed from day 3 in the corresponding regions. Hypointense voids gradually formed in the late phase, correlating with the local iron accumulation. H-I rats without Mn2+ administration exhibited similar but weak changes in T1WIs and T2WIs from days 14 and 7, respectively. These results indicate that Mn2+ may be a useful in vivo probe for monitoring Mn-SOD and GS enzymatic activities. © 2008 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0740-3194/en_HK
dc.relation.ispartofMagnetic Resonance in Medicineen_HK
dc.rightsMagnetic Resonance in Medicine. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectCerebral ischemiaen_HK
dc.subjectGlutamate excitotoxicityen_HK
dc.subjectGlutamine synthetaseen_HK
dc.subjectHypoxiaen_HK
dc.subjectManganese-enhanced MRIen_HK
dc.subjectMn-superoxide dismutaseen_HK
dc.subjectNeonatal raten_HK
dc.subjectOxidative stressen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshChlorides - diagnostic useen_HK
dc.subject.meshContrast Mediaen_HK
dc.subject.meshGlutamate-Ammonia Ligase - metabolismen_HK
dc.subject.meshHypoxia-Ischemia, Brain - enzymology - metabolism - pathologyen_HK
dc.subject.meshImage Processing, Computer-Assisted - methodsen_HK
dc.subject.meshMagnetic Resonance Imaging - methodsen_HK
dc.subject.meshManganese Compounds - diagnostic useen_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSuperoxide Dismutase - metabolismen_HK
dc.titleManganese-enhanced MRI detection of neurodegeneration in neonatal hypoxic-ischemic cerebral injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0740-3194&volume=59&spage=1329&epage=&date=2008&atitle=Manganese-enhanced+MRI+detection+of+neurodegeneration+in+neonatal+hypoxic-ischemic+cerebral+injuryen_HK
dc.identifier.emailKhong, PL: plkhong@hkucc.hku.hken_HK
dc.identifier.emailChu, ACY: bcccy@hkucc.hku.hken_HK
dc.identifier.emailHo, SL: slho@hku.hken_HK
dc.identifier.emailCheung, PT: ptcheung@hku.hken_HK
dc.identifier.emailWu, EX: ewu1@hkucc.hku.hken_HK
dc.identifier.authorityKhong, PL=rp00467en_HK
dc.identifier.authorityChu, ACY=rp00505en_HK
dc.identifier.authorityHo, SL=rp00240en_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/mrm.21484en_HK
dc.identifier.pmid18421694-
dc.identifier.scopuseid_2-s2.0-44949250938en_HK
dc.identifier.hkuros151263en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44949250938&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume59en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1329en_HK
dc.identifier.epage1339en_HK
dc.identifier.isiWOS:000256266400015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYang, J=10041733800en_HK
dc.identifier.scopusauthoridKhong, PL=7006693233en_HK
dc.identifier.scopusauthoridWang, Y=7601514650en_HK
dc.identifier.scopusauthoridChu, ACY=24343085700en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK
dc.identifier.scopusauthoridCheung, PT=7202595465en_HK
dc.identifier.scopusauthoridWu, EX=7202128034en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats