| pubmed-article:11376626 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11376626 | lifeskim:mentions | umls-concept:C0027061 | lld:lifeskim |
| pubmed-article:11376626 | lifeskim:mentions | umls-concept:C0033095 | lld:lifeskim |
| pubmed-article:11376626 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:11376626 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11376626 | pubmed:dateCreated | 2001-5-29 | lld:pubmed |
| pubmed-article:11376626 | pubmed:abstractText | Dystrophin provides mechanical reinforcement to the membranes of myocytes. Dystrophin abnormalities are known to cause cardiomyopathy and skeletal muscle disorders; however, the pathogenesis of these abnormalities remains unclear. Dystrophin-deficient skeletal muscle is vulnerable to stresses such as stretch and hypo-osmotic shock. We investigated whether the myocardium of dystrophin-deficient (mdx) mice shows increased vulnerability to acute pressure overload in vivo. | lld:pubmed |
| pubmed-article:11376626 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11376626 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11376626 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11376626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11376626 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11376626 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11376626 | pubmed:issn | 0008-6363 | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:YoshidaHH | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:MaedaMM | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:HirakawaTT | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:SetoguchiMM | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:BirkWW | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:TeiCC | lld:pubmed |
| pubmed-article:11376626 | pubmed:author | pubmed-author:KamogawaYY | lld:pubmed |
| pubmed-article:11376626 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11376626 | pubmed:volume | 50 | lld:pubmed |
| pubmed-article:11376626 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11376626 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11376626 | pubmed:pagination | 509-15 | lld:pubmed |
| pubmed-article:11376626 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11376626 | pubmed:meshHeading | pubmed-meshheading:11376626... | lld:pubmed |
| pubmed-article:11376626 | pubmed:meshHeading | pubmed-meshheading:11376626... | lld:pubmed |
| pubmed-article:11376626 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11376626 | pubmed:articleTitle | Dystrophin-deficient myocardium is vulnerable to pressure overload in vivo. | lld:pubmed |
| pubmed-article:11376626 | pubmed:affiliation | First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, 8908520, Kagoshima, Japan. | lld:pubmed |
| pubmed-article:11376626 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11376626 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:13405 | entrezgene:pubmed | pubmed-article:11376626 | lld:entrezgene |
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