| pubmed-article:12543879 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12543879 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:12543879 | lifeskim:mentions | umls-concept:C0011881 | lld:lifeskim |
| pubmed-article:12543879 | lifeskim:mentions | umls-concept:C0360714 | lld:lifeskim |
| pubmed-article:12543879 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:12543879 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12543879 | pubmed:dateCreated | 2003-1-24 | lld:pubmed |
| pubmed-article:12543879 | pubmed:abstractText | An inflammatory process may be one of the critical factors that contribute to the development of diabetic nephropathy (DN). We reported previously that intercellular adhesion molecule-1 (ICAM-1) is up-regulated and promotes macrophage infiltration in the glomeruli of diabetic rats. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have recently been emphasized to have anti-inflammatory effects; inhibition of leukocyte adhesion and migration, independent of the cholesterol-lowering effect. The present study was designed to test the hypothesis that statins prevent the development of DN by pleiotropic effects. | lld:pubmed |
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| pubmed-article:12543879 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12543879 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12543879 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12543879 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12543879 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:12543879 | pubmed:issn | 0931-0509 | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:WildD JDJ | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:MakinoHirofum... | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:YamashitaTets... | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:HidaKazuyukiK | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:ShikataKenich... | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:OkadaShinichi... | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:MatsudaMitsuh... | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:OgawaDaisukeD | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:SatohMinoruM | lld:pubmed |
| pubmed-article:12543879 | pubmed:author | pubmed-author:UsuiHitomiH | lld:pubmed |
| pubmed-article:12543879 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12543879 | pubmed:volume | 18 | lld:pubmed |
| pubmed-article:12543879 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12543879 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12543879 | pubmed:pagination | 265-72 | lld:pubmed |
| pubmed-article:12543879 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12543879 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12543879 | pubmed:articleTitle | HMG-CoA reductase inhibitor ameliorates diabetic nephropathy by its pleiotropic effects in rats. | lld:pubmed |
| pubmed-article:12543879 | pubmed:affiliation | Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. | lld:pubmed |
| pubmed-article:12543879 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12543879 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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