| pubmed-article:8132323 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8132323 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:8132323 | lifeskim:mentions | umls-concept:C0026794 | lld:lifeskim |
| pubmed-article:8132323 | lifeskim:mentions | umls-concept:C1167622 | lld:lifeskim |
| pubmed-article:8132323 | lifeskim:mentions | umls-concept:C1819464 | lld:lifeskim |
| pubmed-article:8132323 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:8132323 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8132323 | pubmed:dateCreated | 1994-4-21 | lld:pubmed |
| pubmed-article:8132323 | pubmed:abstractText | Endotoxin (lipopolysaccharide [LPS]) released during gram-negative bacterial infection induces varieties of cytokines which directly and/or indirectly cause shock, disseminated intravascular coagulation, and death. We previously showed that lysozyme (LZM) was an LPS-binding protein and inhibited various immunomodulating activities of LPS. In this study, we examined the effect of LZM on the LPS-triggered septic shock model induced by carrageenan treatment and assessed by tumor necrosis factor production. The data presented in this report strongly suggest that LZM-LPS complex formation completely abrogates tumor necrosis factor production and the mortality caused by LPS and that LZM may be useful for the treatment of endotoxin shock. | lld:pubmed |
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| pubmed-article:8132323 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8132323 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8132323 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8132323 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8132323 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8132323 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:8132323 | pubmed:author | pubmed-author:YadomaeTT | lld:pubmed |
| pubmed-article:8132323 | pubmed:author | pubmed-author:NAVAG CGC | lld:pubmed |
| pubmed-article:8132323 | pubmed:author | pubmed-author:TakadaKK | lld:pubmed |
| pubmed-article:8132323 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8132323 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:8132323 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8132323 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8132323 | pubmed:pagination | 1171-5 | lld:pubmed |
| pubmed-article:8132323 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8132323 | pubmed:meshHeading | pubmed-meshheading:8132323-... | lld:pubmed |
| pubmed-article:8132323 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8132323 | pubmed:articleTitle | Binding of lysozyme to lipopolysaccharide suppresses tumor necrosis factor production in vivo. | lld:pubmed |
| pubmed-article:8132323 | pubmed:affiliation | Laboratory of Immunopharmacology of Microbial Products, Tokyo College of Pharmacy, Japan. | lld:pubmed |
| pubmed-article:8132323 | pubmed:publicationType | Journal Article | lld:pubmed |
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