pubmed-article:17289007 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0034705 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C1423552 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
pubmed-article:17289007 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
pubmed-article:17289007 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:17289007 | pubmed:dateCreated | 2007-3-13 | lld:pubmed |
pubmed-article:17289007 | pubmed:abstractText | A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology. | lld:pubmed |
pubmed-article:17289007 | pubmed:language | eng | lld:pubmed |
pubmed-article:17289007 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17289007 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17289007 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17289007 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17289007 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17289007 | pubmed:month | Apr | lld:pubmed |
pubmed-article:17289007 | pubmed:issn | 0008-6363 | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:EhmkeHeimoH | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:VolkTilmannT | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:WagnerMichael... | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:SchwoererAlex... | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:SchultzJobst-... | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:GoltzDianeD | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:BassalaýPeter... | lld:pubmed |
pubmed-article:17289007 | pubmed:author | pubmed-author:StuckeCarolin... | lld:pubmed |
pubmed-article:17289007 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17289007 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17289007 | pubmed:volume | 74 | lld:pubmed |
pubmed-article:17289007 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17289007 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17289007 | pubmed:pagination | 85-95 | lld:pubmed |
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pubmed-article:17289007 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17289007 | pubmed:articleTitle | Diminished Kv4.2/3 but not KChIP2 levels reduce the cardiac transient outward K+ current in spontaneously hypertensive rats. | lld:pubmed |
pubmed-article:17289007 | pubmed:affiliation | Institut für Vegetative Physiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf, 20246 Hamburg, Germany. | lld:pubmed |
pubmed-article:17289007 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17289007 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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