| pubmed-article:15781740 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0019425 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0038836 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0015259 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0024708 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C0439801 | lld:lifeskim |
| pubmed-article:15781740 | lifeskim:mentions | umls-concept:C1516240 | lld:lifeskim |
| pubmed-article:15781740 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:15781740 | pubmed:dateCreated | 2005-3-29 | lld:pubmed |
| pubmed-article:15781740 | pubmed:abstractText | We have reported that there is a limitation of exercise capacity in mice with defects in the expression of endothelial nitric oxide (NO) synthase, which is associated with a greater increase in whole-body oxygen consumption (VO2). We hypothesized that in states in which superoxide anion (O2-) is increased, especially in the mitochondria, whole-body VO2 will be increased because of the inactivation of NO, and consequently, exercise capacity will be reduced. | lld:pubmed |
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| pubmed-article:15781740 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15781740 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15781740 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15781740 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15781740 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:15781740 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:HintzeThomas... | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:KaleyGaborG | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:KinugawaShint... | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:EdwardsJohn... | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:WolinMichael... | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:WangZipingZ | lld:pubmed |
| pubmed-article:15781740 | pubmed:author | pubmed-author:KaminskiPawel... | lld:pubmed |
| pubmed-article:15781740 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15781740 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:15781740 | pubmed:volume | 111 | lld:pubmed |
| pubmed-article:15781740 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15781740 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15781740 | pubmed:pagination | 1480-6 | lld:pubmed |
| pubmed-article:15781740 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15781740 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15781740 | pubmed:articleTitle | Limited exercise capacity in heterozygous manganese superoxide dismutase gene-knockout mice: roles of superoxide anion and nitric oxide. | lld:pubmed |
| pubmed-article:15781740 | pubmed:affiliation | Department of Physiology, New York Medical College, Valhalla, NY 10595, USA. | lld:pubmed |
| pubmed-article:15781740 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15781740 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15781740 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:20656 | entrezgene:pubmed | pubmed-article:15781740 | lld:entrezgene |
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