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| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0003483 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0038836 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:15490108 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:15490108 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:15490108 | pubmed:dateCreated | 2004-11-19 | lld:pubmed |
| pubmed-article:15490108 | pubmed:abstractText | Hyperglycaemia is a primary cause of vascular complications in diabetes. A hallmark of these vascular complications is endothelial cell dysfunction, which is partly due to the reduced production of nitric oxide. The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose. | lld:pubmed |
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| pubmed-article:15490108 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15490108 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15490108 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15490108 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:15490108 | pubmed:issn | 0012-186X | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:SrinivasanSS | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:BrownleeMM | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:EdelsteinDD | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:PalmerL ALA | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:HedrickC CCC | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:HatleyM EME | lld:pubmed |
| pubmed-article:15490108 | pubmed:author | pubmed-author:BolickD TDT | lld:pubmed |
| pubmed-article:15490108 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15490108 | pubmed:volume | 47 | lld:pubmed |
| pubmed-article:15490108 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15490108 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15490108 | pubmed:pagination | 1727-34 | lld:pubmed |
| pubmed-article:15490108 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15490108 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15490108 | pubmed:articleTitle | Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells. | lld:pubmed |
| pubmed-article:15490108 | pubmed:affiliation | Division of Endocrinology and Metabolism, Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA. | lld:pubmed |
| pubmed-article:15490108 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15490108 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15490108 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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