pubmed-article:18541744 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
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pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0669368 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0033095 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C1705165 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
pubmed-article:18541744 | lifeskim:mentions | umls-concept:C2700061 | lld:lifeskim |
pubmed-article:18541744 | pubmed:issue | 25 | lld:pubmed |
pubmed-article:18541744 | pubmed:dateCreated | 2008-6-24 | lld:pubmed |
pubmed-article:18541744 | pubmed:abstractText | Defects in cardiomyocyte Ca(2+) cycling are a signature feature of heart failure (HF) that occurs in response to sustained hemodynamic overload, and they largely account for contractile dysfunction. Neuronal nitric oxide synthase (NOS1) influences myocyte excitation-contraction coupling through modulation of Ca(2+) cycling, but the potential relevance of this in HF is unknown. | lld:pubmed |
pubmed-article:18541744 | pubmed:language | eng | lld:pubmed |
pubmed-article:18541744 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18541744 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:18541744 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18541744 | pubmed:month | Jun | lld:pubmed |
pubmed-article:18541744 | pubmed:issn | 1524-4539 | lld:pubmed |
pubmed-article:18541744 | pubmed:author | pubmed-author:RichardSylvai... | lld:pubmed |
pubmed-article:18541744 | pubmed:author | pubmed-author:ZhangWeiW | lld:pubmed |
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pubmed-article:18541744 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18541744 | pubmed:day | 24 | lld:pubmed |
pubmed-article:18541744 | pubmed:volume | 117 | lld:pubmed |
pubmed-article:18541744 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18541744 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18541744 | pubmed:pagination | 3187-98 | lld:pubmed |
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pubmed-article:18541744 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18541744 | pubmed:articleTitle | Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling. | lld:pubmed |
pubmed-article:18541744 | pubmed:affiliation | Institut National de Santé et de Recherché Médicale (INSERM), Unit 689, Centre de Recherché Cardiovasculaire Lariboisière, Paris, France. | lld:pubmed |
pubmed-article:18541744 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18541744 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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