Linked Life Data

9875281

Source:http://linkedlifedata.com/resource/pubmed/id/9875281

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-1-19
pubmed:abstractText
Defining the chronology and severity of cell damage in an evolving lesion after ischemia is important for understanding the underlying mechanisms in the development of therapeutic intervention. In the present study, we used a combination of histological and immunocytochemical methods to evaluate cell responses from 30 min to 48 h after permanent occlusion of the middle cerebral artery (MCAO) in the rat. Specific immunocytochemical markers clearly revealed acute early responses in neurons (neurofilament protein 200), astrocytes (glial fibrillary acidic protein), and microglia/macrophages (OX-42 and ED-1) such as enlarged, convoluted neuronal processes, and disintegration of glia. Progressive topographic changes in the developing lesion, pinpointed by immunolabeling, indicated the severity and extension of the cell damage. Proliferation and hypertrophy of astrocytes and microglia around the infarct, and contralaterally, occurred 24-48 h after MCAO and coincided with mass necrosis and infiltration of neutrophils and macrophages into the core. These observations corroborate the suggestion that the inflammatory process is involved in the progression of the infarct.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
154
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
199-212
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
An integrated analysis of the progression of cell responses induced by permanent focal middle cerebral artery occlusion in the rat.
pubmed:affiliation
School of Biological Sciences, University of Manchester, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't