| pubmed-article:17360462 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C0006434 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C0043250 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:17360462 | lifeskim:mentions | umls-concept:C0205125 | lld:lifeskim |
| pubmed-article:17360462 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:17360462 | pubmed:dateCreated | 2007-3-15 | lld:pubmed |
| pubmed-article:17360462 | pubmed:abstractText | A major component of burn injury is caused by additional local damage from acute inflammation. Using a scald burn model in mice, we find that this part of the injury is dependent on recognition of self-antigen by specific natural IgM, leading to activation of the complement system. We propose that the depth of a burn wound is a sum of the thermal energy applied and of the degree of host inflammatory response. | lld:pubmed |
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| pubmed-article:17360462 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17360462 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17360462 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17360462 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:17360462 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:17360462 | pubmed:author | pubmed-author:CarrollMichae... | lld:pubmed |
| pubmed-article:17360462 | pubmed:author | pubmed-author:MooreFrancis... | lld:pubmed |
| pubmed-article:17360462 | pubmed:author | pubmed-author:SuberFreemanF | lld:pubmed |
| pubmed-article:17360462 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17360462 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:17360462 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:17360462 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17360462 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17360462 | pubmed:pagination | 3973-7 | lld:pubmed |
| pubmed-article:17360462 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17360462 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17360462 | pubmed:articleTitle | Innate response to self-antigen significantly exacerbates burn wound depth. | lld:pubmed |
| pubmed-article:17360462 | pubmed:affiliation | Harvard Medical School, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:17360462 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17360462 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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