| pubmed-article:11983548 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C1522564 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C1150130 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C0205088 | lld:lifeskim |
| pubmed-article:11983548 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:11983548 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11983548 | pubmed:dateCreated | 2002-5-1 | lld:pubmed |
| pubmed-article:11983548 | pubmed:abstractText | Apoptosis contributes to ventricular remodeling in heart failure (HF). Nitric oxide (NO) inhibits caspase 3, a key effector apoptotic enzyme. We hypothesized that reduced endogenous NO in HF disinhibits cardiac caspase 3 to promote apoptosis. | lld:pubmed |
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| pubmed-article:11983548 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11983548 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11983548 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11983548 | pubmed:month | May | lld:pubmed |
| pubmed-article:11983548 | pubmed:issn | 1053-2498 | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:HintzeThomas... | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:MitalSeemaS | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:OzMehmet CMC | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:BarboneAlessa... | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:AddonizioLind... | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:QuaegebeurJan... | lld:pubmed |
| pubmed-article:11983548 | pubmed:author | pubmed-author:MoscaRalph... | lld:pubmed |
| pubmed-article:11983548 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11983548 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:11983548 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11983548 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11983548 | pubmed:pagination | 576-85 | lld:pubmed |
| pubmed-article:11983548 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11983548 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11983548 | pubmed:articleTitle | Endogenous endothelium-derived nitric oxide inhibits myocardial caspase activity: implications for treatment of end-stage heart failure. | lld:pubmed |
| pubmed-article:11983548 | pubmed:affiliation | Division of Pediatric Cardiology, Babies Hospital, Columbia University, New York, New York 10032, USA. sm364@columbia.edu | lld:pubmed |
| pubmed-article:11983548 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11983548 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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