pubmed-article:7496909 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7496909 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
pubmed-article:7496909 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:7496909 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:7496909 | pubmed:dateCreated | 1996-1-16 | lld:pubmed |
pubmed-article:7496909 | pubmed:abstractText | Alzheimer's disease (AD) has been hypothesized to be an inflammatory condition. We hypothesized that anti-inflammatory cytokines, such as transforming growth factor beta (TGF-beta), counteract the inflammatory process. In the present study, we found that TGF-beta levels were elevated in both cerebrospinal fluid and serum samples obtained from AD patients < 6 h after death. Serum TGF-beta levels were also markedly elevated before death. These results suggest that elevated TGF-beta levels in AD may represent a protective host response to immunologically mediated neuronal injury. | lld:pubmed |
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pubmed-article:7496909 | pubmed:language | eng | lld:pubmed |
pubmed-article:7496909 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7496909 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7496909 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7496909 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7496909 | pubmed:month | Jan | lld:pubmed |
pubmed-article:7496909 | pubmed:issn | 1071-412X | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:FreyW HWH2nd | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:PetersonP KPK | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:TourtellotteW... | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:HoYY | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:ChaoC CCC | lld:pubmed |
pubmed-article:7496909 | pubmed:author | pubmed-author:AlaT ATA | lld:pubmed |
pubmed-article:7496909 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7496909 | pubmed:volume | 1 | lld:pubmed |
pubmed-article:7496909 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7496909 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7496909 | pubmed:pagination | 109-10 | lld:pubmed |
pubmed-article:7496909 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:7496909 | pubmed:meshHeading | pubmed-meshheading:7496909-... | lld:pubmed |
pubmed-article:7496909 | pubmed:meshHeading | pubmed-meshheading:7496909-... | lld:pubmed |
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pubmed-article:7496909 | pubmed:meshHeading | pubmed-meshheading:7496909-... | lld:pubmed |
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pubmed-article:7496909 | pubmed:meshHeading | pubmed-meshheading:7496909-... | lld:pubmed |
pubmed-article:7496909 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:7496909 | pubmed:articleTitle | Transforming growth factor beta in Alzheimer's disease. | lld:pubmed |
pubmed-article:7496909 | pubmed:affiliation | Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, MN 55404, USA. | lld:pubmed |
pubmed-article:7496909 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7496909 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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