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| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0027078 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0332161 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0242210 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:16079165 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16079165 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16079165 | pubmed:dateCreated | 2006-2-13 | lld:pubmed |
| pubmed-article:16079165 | pubmed:abstractText | Insulin-like growth factor 1 (IGF1) is an important determinant of muscle mass because it promotes growth and suppresses protein degradation. IGF1 is decreased in rheumatoid arthritis and juvenile idiopathic arthritis because its synthesis is inhibited by inflammation. In parallel, glucocorticoids induce IGF1 resistance and add to muscle degradation. | lld:pubmed |
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| pubmed-article:16079165 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16079165 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16079165 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16079165 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16079165 | pubmed:issn | 0003-4967 | lld:pubmed |
| pubmed-article:16079165 | pubmed:author | pubmed-author:SchölmerichJJ | lld:pubmed |
| pubmed-article:16079165 | pubmed:author | pubmed-author:CutoloMM | lld:pubmed |
| pubmed-article:16079165 | pubmed:author | pubmed-author:StraubR HRH | lld:pubmed |
| pubmed-article:16079165 | pubmed:author | pubmed-author:AtzeniFF | lld:pubmed |
| pubmed-article:16079165 | pubmed:author | pubmed-author:Sarzi-Puttini... | lld:pubmed |
| pubmed-article:16079165 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16079165 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:16079165 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16079165 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16079165 | pubmed:pagination | 301-5 | lld:pubmed |
| pubmed-article:16079165 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:16079165 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16079165 | pubmed:articleTitle | Anti-TNF antibody treatment improves glucocorticoid induced insulin-like growth factor 1 (IGF1) resistance without influencing myoglobin and IGF1 binding proteins 1 and 3. | lld:pubmed |
| pubmed-article:16079165 | pubmed:affiliation | Laboratory of Experimental Rheumatology and Neuroendocrino-immunology, Department of Internal Medicine I, University Hospital, 93042 Regensburg, Germany. | lld:pubmed |
| pubmed-article:16079165 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16079165 | pubmed:publicationType | Clinical Trial | lld:pubmed |
| pubmed-article:16079165 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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