| pubmed-article:7705307 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7705307 | lifeskim:mentions | umls-concept:C0035222 | lld:lifeskim |
| pubmed-article:7705307 | lifeskim:mentions | umls-concept:C0016693 | lld:lifeskim |
| pubmed-article:7705307 | lifeskim:mentions | umls-concept:C0449413 | lld:lifeskim |
| pubmed-article:7705307 | pubmed:dateCreated | 1995-5-10 | lld:pubmed |
| pubmed-article:7705307 | pubmed:abstractText | The acute lung injury resulting from adult respiratory distress syndrome (ARDS) is thought to be largely mediated by activated neutrophils. Because activated neutrophils produce the superoxide radical, which is both bacterial and cytotoxic to host cells, this oxygen-derived free radical is likely responsible for at least part of the neutrophil-mediated lung injury. In a rat model of ARDS resulting from intratracheal instillation of interleukin-1, recombinant human manganous superoxide dismutase significantly decreased lung leak. One detrimental action of proteases released by adherent neutrophils may be the degradation of extracellular superoxide dismutase (ECSOD), which normally binds to the heparan sulfate on the surface the endothelium. We found that rabbit ECSOD incubated with either trypsin or activated neutrophils loses affinity for heparin. Furthermore, soluble ECSOD is elevated in the serum of patients with ARDS, consistent with this hypothesis. | lld:pubmed |
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| pubmed-article:7705307 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7705307 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7705307 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7705307 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7705307 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7705307 | pubmed:issn | 0091-6765 | lld:pubmed |
| pubmed-article:7705307 | pubmed:author | pubmed-author:GayHH | lld:pubmed |
| pubmed-article:7705307 | pubmed:author | pubmed-author:McCordJ MJM | lld:pubmed |
| pubmed-article:7705307 | pubmed:author | pubmed-author:LeffJJ | lld:pubmed |
| pubmed-article:7705307 | pubmed:author | pubmed-author:FloresS CSC | lld:pubmed |
| pubmed-article:7705307 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7705307 | pubmed:volume | 102 Suppl 10 | lld:pubmed |
| pubmed-article:7705307 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7705307 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7705307 | pubmed:pagination | 57-60 | lld:pubmed |
| pubmed-article:7705307 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7705307 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7705307 | pubmed:articleTitle | Neutrophil-generated free radicals: possible mechanisms of injury in adult respiratory distress syndrome. | lld:pubmed |
| pubmed-article:7705307 | pubmed:affiliation | Webb-Waring Institute for Biomedical Research, University of Colorado Health Sciences Center, Denver 80262. | lld:pubmed |
| pubmed-article:7705307 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7705307 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7705307 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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