pubmed-article:20590569 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0054594 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0022658 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C1413554 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0311404 | lld:lifeskim |
pubmed-article:20590569 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:20590569 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:20590569 | pubmed:dateCreated | 2010-7-1 | lld:pubmed |
pubmed-article:20590569 | pubmed:abstractText | Accumulating recent evidence suggests that cannabinoid-1 (CB(1)) receptor activation may promote inflammation and cell death and its pharmacological inhibition is associated with anti-inflammatory and tissue-protective effects in various preclinical disease models, as well as in humans. | lld:pubmed |
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pubmed-article:20590569 | pubmed:language | eng | lld:pubmed |
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pubmed-article:20590569 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20590569 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20590569 | pubmed:month | Jun | lld:pubmed |
pubmed-article:20590569 | pubmed:issn | 1476-5381 | lld:pubmed |
pubmed-article:20590569 | pubmed:author | pubmed-author:LeeS KSK | lld:pubmed |
pubmed-article:20590569 | pubmed:author | pubmed-author:PacherPálP | lld:pubmed |