| pubmed-article:15718491 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C0003847 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C1522318 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C0012359 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C0031727 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C0068355 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C0006560 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C1366876 | lld:lifeskim |
| pubmed-article:15718491 | lifeskim:mentions | umls-concept:C1833235 | lld:lifeskim |
| pubmed-article:15718491 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15718491 | pubmed:dateCreated | 2005-5-2 | lld:pubmed |
| pubmed-article:15718491 | pubmed:abstractText | Elevated levels of C-reactive protein (CRP), a proinflammatory marker, are associated with reduced systemic endothelium-dependent NO-mediated dilation in patients with coronary artery disease; however, the direct effect of CRP on coronary microvascular reactivity remains unknown. Herein, we examined whether CRP can modulate endothelium-dependent NO-mediated dilation of coronary arterioles and whether proinflammatory signaling pathways such as stress-activated protein kinases (p38 and c-Jun N-terminal kinase [JNK]) and oxidative stress are involved in the CRP-mediated effect. | lld:pubmed |
| pubmed-article:15718491 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15718491 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15718491 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15718491 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15718491 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15718491 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15718491 | pubmed:month | May | lld:pubmed |
| pubmed-article:15718491 | pubmed:issn | 1524-4636 | lld:pubmed |
| pubmed-article:15718491 | pubmed:author | pubmed-author:MoyO JOJ | lld:pubmed |
| pubmed-article:15718491 | pubmed:author | pubmed-author:VALJJ | lld:pubmed |
| pubmed-article:15718491 | pubmed:author | pubmed-author:HeinTravis... | lld:pubmed |
| pubmed-article:15718491 | pubmed:author | pubmed-author:QamiraniErion... | lld:pubmed |
| pubmed-article:15718491 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15718491 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:15718491 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15718491 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15718491 | pubmed:pagination | 995-1001 | lld:pubmed |
| pubmed-article:15718491 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15718491 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15718491 | pubmed:articleTitle | C-reactive protein inhibits endothelium-dependent NO-mediated dilation in coronary arterioles by activating p38 kinase and NAD(P)H oxidase. | lld:pubmed |
| pubmed-article:15718491 | pubmed:affiliation | Department of Medical Physiology, Cardiovascular Research Institute, The Texas A&M University System Health Science Center, College Station, Tex, USA. | lld:pubmed |
| pubmed-article:15718491 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15718491 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:15718491 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15718491 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15718491 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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