| pubmed-article:14511328 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0291573 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0038220 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:14511328 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:14511328 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:14511328 | pubmed:dateCreated | 2003-9-26 | lld:pubmed |
| pubmed-article:14511328 | pubmed:abstractText | It is in dispute whether caspase 3 contributes to status epilepticus (SE)-induced cell loss. We hypothesized that caspase 3-mediated cell death continues beyond the acute phase of SE. We induced SE with either kainic acid or electrical stimulation of the amygdala in Wistar and Sprague-Dawley rats. Caspase 3 immunohistochemistry, Western blot analysis and enzyme activity measurements were used to determine cellular localization and the time course of caspase 3 expression and activation. Immunohistochemistry indicated that caspase 3 protein expression increased following SE, peaking at 16-24 h. Cleavage of procaspase 3 to active fragments (p20-17) was detected 2-7 days after SE. Caspase 3 enzyme activity was elevated at 8 h and further increased up to 19.4-fold at 7 days following SE. Activation of caspase 3 after SE occurred in the hippocampus and the extrahippocampal temporal lobe but not in the thalamus. Caspase 3-immunoreactive cells represented only a minority of degenerating cells as assessed by Fluoro-Jade B and TUNEL staining. Analysis of double-labelled sections indicated that active caspase 3 was located in astrocytes rather than neurons or microglia. There was increased caspase 3 expression in both rat strains, and it was independent of the method used to induce SE. These data demonstrate that caspase 3 contributes to the cell death occurring within the first week after SE, but in only a small proportion of degenerating cells. These results suggest that, contrary to expectations, caspase 3 inhibitors would have only limited benefits in the treatment of SE. | lld:pubmed |
| pubmed-article:14511328 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14511328 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14511328 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14511328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14511328 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14511328 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:14511328 | pubmed:issn | 0953-816X | lld:pubmed |
| pubmed-article:14511328 | pubmed:author | pubmed-author:PitkänenAslaA | lld:pubmed |
| pubmed-article:14511328 | pubmed:author | pubmed-author:PirttiläTerhi... | lld:pubmed |
| pubmed-article:14511328 | pubmed:author | pubmed-author:LukasiukKatar... | lld:pubmed |
| pubmed-article:14511328 | pubmed:author | pubmed-author:NarkilahtiSus... | lld:pubmed |
| pubmed-article:14511328 | pubmed:author | pubmed-author:TuunanenJarkk... | lld:pubmed |
| pubmed-article:14511328 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14511328 | pubmed:volume | 18 | lld:pubmed |
| pubmed-article:14511328 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14511328 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14511328 | pubmed:pagination | 1486-96 | lld:pubmed |
| pubmed-article:14511328 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:14511328 | pubmed:meshHeading | pubmed-meshheading:14511328... | lld:pubmed |
| pubmed-article:14511328 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14511328 | pubmed:articleTitle | Expression and activation of caspase 3 following status epilepticus in the rat. | lld:pubmed |
| pubmed-article:14511328 | pubmed:affiliation | A.I. Virtanen Institute for Molecular Sciences, University of Kuopio, PO Box 1627, FIN-70 211 Kuopio, Finland. | lld:pubmed |
| pubmed-article:14511328 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14511328 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:14511328 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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