| pubmed-article:15772780 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0027051 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0027061 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0225897 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0442800 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C1609982 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0536847 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:15772780 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:15772780 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15772780 | pubmed:dateCreated | 2005-3-17 | lld:pubmed |
| pubmed-article:15772780 | pubmed:abstractText | Left ventricular (LV) dilatation following myocardial infarction (MI) is a major determinant of the patient's prognosis, and myocardial energy metabolism may play a key role in LV remodeling. We aimed to investigate the relative timing of LV dilatation to LV function, myocardial energy regulation by uncoupling protein (UCP)-2, and cellular damage in the noninfarct zone. Myocardial infarction was produced in Sprague-Dawley rats by ligation of the coronary artery. The LV end-diastolic dimension (mm) increased (8.9+/-0.3 vs 6.8+/-0.8 in sham-operated rats, P<0.01) in association with elevation of the LV end-diastolic pressure (mmHg) (18+/-5 vs 6+/-2 in sham-operated rats) at 1 week following the ligation. At 4 weeks, the UCP-2 expression (180% of that in sham-operated rats) and LV end-diastolic dimension increased further (11.1+/-0.5, P<0.01) but there was no change in the LV end-diastolic pressure. The mechanisms for LV dilatation were quite different between the early and late stages after MI. In the late stage, augmentation of UCP-2 expression in the noninfarct zone may be related to the LV dilatation. Further examinations regarding the possibility of the protective role of UCP-2 are needed. | lld:pubmed |
| pubmed-article:15772780 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15772780 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15772780 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15772780 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15772780 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15772780 | pubmed:issn | 1615-2573 | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:PageN RNR | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:KimuraShojiS | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:NambaTsunetat... | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:MizushigeKats... | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:KohnoMasakazu... | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:TsujiTeppeiT | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:NomaTakahisaT | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:MurakamiKazus... | lld:pubmed |
| pubmed-article:15772780 | pubmed:author | pubmed-author:IshizawaMakot... | lld:pubmed |
| pubmed-article:15772780 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15772780 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:15772780 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15772780 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15772780 | pubmed:pagination | 61-5 | lld:pubmed |
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| pubmed-article:15772780 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15772780 | pubmed:articleTitle | Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction. | lld:pubmed |
| pubmed-article:15772780 | pubmed:affiliation | Second Department of Internal Medicine, School of Medicine, Kagawa University, Kagawa, Japan. | lld:pubmed |
| pubmed-article:15772780 | pubmed:publicationType | Journal Article | lld:pubmed |
| entrez-gene:54315 | entrezgene:pubmed | pubmed-article:15772780 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:15772780 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15772780 | lld:pubmed |
