| pubmed-article:15998894 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15998894 | lifeskim:mentions | umls-concept:C0002895 | lld:lifeskim |
| pubmed-article:15998894 | lifeskim:mentions | umls-concept:C0020542 | lld:lifeskim |
| pubmed-article:15998894 | lifeskim:mentions | umls-concept:C0026565 | lld:lifeskim |
| pubmed-article:15998894 | lifeskim:mentions | umls-concept:C1156810 | lld:lifeskim |
| pubmed-article:15998894 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15998894 | pubmed:dateCreated | 2005-7-6 | lld:pubmed |
| pubmed-article:15998894 | pubmed:abstractText | Sickle cell disease is characterized by a state of nitric oxide resistance and limited bioavailability of l-arginine, the substrate for nitric oxide synthesis. We hypothesized that increased arginase activity and dysregulated arginine metabolism contribute to endothelial dysfunction, pulmonary hypertension, and patient outcomes. | lld:pubmed |
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| pubmed-article:15998894 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15998894 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15998894 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15998894 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:15998894 | pubmed:issn | 1538-3598 | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:MorrisSidney... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:GladwinMark... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:PoljakovicMir... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:BlackwelderWi... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:HazenStanley... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:VichinskyElli... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:KatoGregory... | lld:pubmed |
| pubmed-article:15998894 | pubmed:author | pubmed-author:WangXundeX | lld:pubmed |
