| pubmed-article:12354748 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0026820 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0013030 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12354748 | lifeskim:mentions | umls-concept:C1637379 | lld:lifeskim |
| pubmed-article:12354748 | pubmed:issue | 12 Suppl 1 | lld:pubmed |
| pubmed-article:12354748 | pubmed:dateCreated | 2002-9-30 | lld:pubmed |
| pubmed-article:12354748 | pubmed:abstractText | Ischemia and adrenergic stimulation of cardiomyocyte cultures have been shown to induce apoptotic cell death. We hypothesized that in a model of contractile dysfunction following ischemia, a commonly used catecholamine such as dopamine augments cardiomyocyte apoptosis via activation of calcium-dependent signaling cascades. | lld:pubmed |
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| pubmed-article:12354748 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12354748 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12354748 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12354748 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12354748 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:StammChristof... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:FriehsIngebor... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:del... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:DuebenerLenna... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:CowanDouglas... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:Cao-DanhHungH | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:ChoiYeong-Hoo... | lld:pubmed |
| pubmed-article:12354748 | pubmed:author | pubmed-author:McGowanFranci... | lld:pubmed |
| pubmed-article:12354748 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12354748 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:12354748 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:12354748 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12354748 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12354748 | pubmed:pagination | I290-8 | lld:pubmed |
| pubmed-article:12354748 | pubmed:dateRevised | 2011-4-22 | lld:pubmed |
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| pubmed-article:12354748 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12354748 | pubmed:articleTitle | Dopamine treatment of postischemic contractile dysfunction rapidly induces calcium-dependent pro-apoptotic signaling. | lld:pubmed |
| pubmed-article:12354748 | pubmed:affiliation | Department of Cardiac Surgery, Children's Hospital, Harvard Medical School, Boston, Mass 02115, USA. | lld:pubmed |
| pubmed-article:12354748 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12354748 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:12354748 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12354748 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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