| pubmed-article:2830072 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2830072 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:2830072 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:2830072 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:2830072 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:2830072 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:2830072 | pubmed:dateCreated | 1988-3-28 | lld:pubmed |
| pubmed-article:2830072 | pubmed:abstractText | Oxygen radical generation was measured using peritoneal exudate polymorphonuclear leucocytes (PMN) from a strain of beige mice, an animal model of the Chediak-Higashi syndrome. These PMN have been shown to exhibit delayed microbial killing and impaired phagosome-lysosome fusion. The amount of superoxide anion released by the PMN of the beige mice was similar to that released by the PMN of the control mice. The PMN of beige mice generated slightly less hydrogen peroxide than the control. Hydroxyl radical (.OH) generation and luminol-dependent chemiluminescence were significantly lowered in beige PMN stimulated with opsonized zymosan (OZ) or phorbol myristate acetate (PMA). Cytochalasin B-treated beige PMN showed a decreased ability to degranulate myeloperoxidase in response to OZ or PMA. We demonstrated the significant decrease in .OH generation and chemiluminescence in beige PMN, which might be one of the reasons to explain delayed microbial killing. | lld:pubmed |
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| pubmed-article:2830072 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2830072 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2830072 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2830072 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2830072 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:2830072 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:KuboAA | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:UchinoHH | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:NishimuraTT | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:YamamotoKK | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:SasadaMM | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:MoriguchiTT | lld:pubmed |
| pubmed-article:2830072 | pubmed:author | pubmed-author:KakitaTT | lld:pubmed |
| pubmed-article:2830072 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2830072 | pubmed:volume | 70 | lld:pubmed |
| pubmed-article:2830072 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2830072 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2830072 | pubmed:pagination | 658-63 | lld:pubmed |
| pubmed-article:2830072 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2830072 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:2830072 | pubmed:articleTitle | Oxygen radical generation by polymorphonuclear leucocytes of beige mice. | lld:pubmed |
| pubmed-article:2830072 | pubmed:affiliation | First Division of Internal Medicine, Faculty of Medicine, Kyoto University, Japan. | lld:pubmed |
| pubmed-article:2830072 | pubmed:publicationType | Journal Article | lld:pubmed |
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