| pubmed-article:16299028 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0524979 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0021852 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0039215 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0013470 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0439662 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:16299028 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:16299028 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:16299028 | pubmed:dateCreated | 2006-3-13 | lld:pubmed |
| pubmed-article:16299028 | pubmed:abstractText | Gastrointestinal inflammation reduces food intake but the biological mechanisms explaining suppressed feeding during inflammation are unknown. We have used a model of upper gut infection (Trichinella spiralis in the mouse) to study the effect of inflammation on food intake, and explored the role of a key enteroendocrine cell (EEC) in the regulation of feeding by the immune response. | lld:pubmed |
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| pubmed-article:16299028 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16299028 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16299028 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16299028 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16299028 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:16299028 | pubmed:issn | 0017-5749 | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:McDermottJ... | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:ThompsonD GDG | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:McLaughlinJ... | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:D'AmateCC | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:GrencisR KRK | lld:pubmed |
| pubmed-article:16299028 | pubmed:author | pubmed-author:LeslieF CFC | lld:pubmed |
| pubmed-article:16299028 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16299028 | pubmed:volume | 55 | lld:pubmed |
| pubmed-article:16299028 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16299028 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16299028 | pubmed:pagination | 492-7 | lld:pubmed |
| pubmed-article:16299028 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16299028 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16299028 | pubmed:articleTitle | Immune control of food intake: enteroendocrine cells are regulated by CD4+ T lymphocytes during small intestinal inflammation. | lld:pubmed |
| pubmed-article:16299028 | pubmed:affiliation | Faculty of Life Sciences, University of Manchester, Manchester, UK. | lld:pubmed |
| pubmed-article:16299028 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16299028 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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