| pubmed-article:1997652 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C0039736 | lld:lifeskim |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:1997652 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:1997652 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:1997652 | pubmed:dateCreated | 1991-4-2 | lld:pubmed |
| pubmed-article:1997652 | pubmed:abstractText | Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting. | lld:pubmed |
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| pubmed-article:1997652 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1997652 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1997652 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1997652 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1997652 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:1997652 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:1997652 | pubmed:author | pubmed-author:KaplanGG | lld:pubmed |
| pubmed-article:1997652 | pubmed:author | pubmed-author:CohnZ AZA | lld:pubmed |
| pubmed-article:1997652 | pubmed:author | pubmed-author:SarnoE NEN | lld:pubmed |
| pubmed-article:1997652 | pubmed:author | pubmed-author:SampaioE PEP | lld:pubmed |
| pubmed-article:1997652 | pubmed:author | pubmed-author:GalillyRR | lld:pubmed |
| pubmed-article:1997652 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1997652 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1997652 | pubmed:volume | 173 | lld:pubmed |
| pubmed-article:1997652 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1997652 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1997652 | pubmed:pagination | 699-703 | lld:pubmed |
| pubmed-article:1997652 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1997652 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1997652 | pubmed:articleTitle | Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes. | lld:pubmed |
| pubmed-article:1997652 | pubmed:affiliation | Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021. | lld:pubmed |
| pubmed-article:1997652 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1997652 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1997652 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1997652 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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