Linked Life Data

7609899

Source:http://linkedlifedata.com/resource/pubmed/id/7609899

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-8-11
pubmed:abstractText
To clarify the pathogenesis and molecular basis of ischemia-related nerve cell death, we examined the occurrence of DNA fragmentation as a hallmark of apoptotic cell death following incomplete ischemia in the rat brain by means of in situ end labeling of fragmented DNA. Incomplete ischemia was produced by permanently occluding one carotid artery, while temporarily occluding the other. The condensed nuclei of ischemic neurons in the neocortex, and in the subiculum and CA1 area of the hippocampus were positively stained 24 h and 3 days following vessel occlusion, respectively, and their morphology was typically apoptotic. The ischemic neurons with condensed nuclei gradually increased in number and were clearly stained for fragmented DNA in these areas. The labeled nuclei in the neocortex became pyknotic 72 h later, and in the hippocampus 7 days later incomplete ischemia. After attaining a peak, the number of labeled nuclei decreased with the duration of recovery in all areas. These results suggest that an apoptotic process plays, at least primarily, a role in the degeneration of neurons associated with incomplete forebrain ischemia in rat.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
188
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-62
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Detection of DNA damage induced by apoptosis in the rat brain following incomplete ischemia.
pubmed:affiliation
Department of Physiology, Okayama University Medical School, Japan.
pubmed:publicationType
Journal Article