pubmed-article:20403194 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C0014939 | lld:lifeskim |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C0442027 | lld:lifeskim |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C0015011 | lld:lifeskim |
pubmed-article:20403194 | lifeskim:mentions | umls-concept:C1415223 | lld:lifeskim |
pubmed-article:20403194 | pubmed:dateCreated | 2010-5-5 | lld:pubmed |
pubmed-article:20403194 | pubmed:abstractText | Remission of multiple sclerosis during periods of high ovarian hormone secretion (such as pregnancy) has led to a great deal of interest in the potential for estrogens to treat autoimmune disease. Previous work has established that 17beta-estradiol can inhibit onset of experimental autoimmune encephalomyelitis (EAE), while ethinyl estradiol (EE) can reduce the severity of established disease. In the current study, the influence of estrogen receptor-alpha (ERalpha) and the G-protein coupled estrogen receptor (GPR30 or GPER) on EE's ability to treat EAE was explored. | lld:pubmed |
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pubmed-article:20403194 | pubmed:language | eng | lld:pubmed |
pubmed-article:20403194 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20403194 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20403194 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20403194 | pubmed:issn | 1471-2172 | lld:pubmed |
pubmed-article:20403194 | pubmed:author | pubmed-author:OffnerHalinaH | lld:pubmed |
pubmed-article:20403194 | pubmed:author | pubmed-author:LiYuexinY | lld:pubmed |
pubmed-article:20403194 | pubmed:author | pubmed-author:YatesMelissa... | lld:pubmed |
pubmed-article:20403194 | pubmed:author | pubmed-author:ChlebeckPeter... | lld:pubmed |
pubmed-article:20403194 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20403194 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:20403194 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20403194 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20403194 | pubmed:pagination | 20 | lld:pubmed |
pubmed-article:20403194 | pubmed:dateRevised | 2010-9-30 | lld:pubmed |
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pubmed-article:20403194 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20403194 | pubmed:articleTitle | GPR30, but not estrogen receptor-alpha, is crucial in the treatment of experimental autoimmune encephalomyelitis by oral ethinyl estradiol. | lld:pubmed |
pubmed-article:20403194 | pubmed:affiliation | Neuroimmunology Research, Portland VA Medical Center, Portland, OR, USA. | lld:pubmed |
pubmed-article:20403194 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20403194 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:20403194 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20403194 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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