| pubmed-article:1747764 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1747764 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:1747764 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:1747764 | lifeskim:mentions | umls-concept:C0027912 | lld:lifeskim |
| pubmed-article:1747764 | lifeskim:mentions | umls-concept:C1522496 | lld:lifeskim |
| pubmed-article:1747764 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1747764 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:1747764 | pubmed:dateCreated | 1992-1-22 | lld:pubmed |
| pubmed-article:1747764 | pubmed:abstractText | Chronic administration of lipopolysaccharide (LPS) to mice markedly reduced activation of the neuroendocrine stress axis elicited by an acute challenge dose of LPS. LPS-induced elevation in norepinephrine turnover in the hypothalamus showed complete tolerance whereas elevation of plasma corticosterone showed only partial tolerance. Challenge-induced increased turnover of dopamine in hypothalamus persisted in LPS-tolerant animals. Neuroendocrine activation persisted following acute challenge with interleukin-1 and tumor necrosis factor following chronic LPS exposure. | lld:pubmed |
| pubmed-article:1747764 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1747764 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1747764 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1747764 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1747764 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:1747764 | pubmed:issn | 0006-8993 | lld:pubmed |
| pubmed-article:1747764 | pubmed:author | pubmed-author:EskayR LRL | lld:pubmed |
| pubmed-article:1747764 | pubmed:author | pubmed-author:MeffordI NIN | lld:pubmed |
| pubmed-article:1747764 | pubmed:author | pubmed-author:HeyesM PMP | lld:pubmed |
| pubmed-article:1747764 | pubmed:author | pubmed-author:MastersC FCF | lld:pubmed |
| pubmed-article:1747764 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1747764 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:1747764 | pubmed:volume | 557 | lld:pubmed |
| pubmed-article:1747764 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1747764 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1747764 | pubmed:pagination | 327-30 | lld:pubmed |
| pubmed-article:1747764 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:1747764 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1747764 | pubmed:articleTitle | Cytokine-induced activation of the neuroendocrine stress axis persists in endotoxin-tolerant mice. | lld:pubmed |
| pubmed-article:1747764 | pubmed:affiliation | Section of Clinical Pharmacology, National Institute of Mental Health, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:1747764 | pubmed:publicationType | Journal Article | lld:pubmed |
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