| pubmed-article:19149411 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0221014 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C1833334 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0040395 | lld:lifeskim |
| pubmed-article:19149411 | lifeskim:mentions | umls-concept:C0392762 | lld:lifeskim |
| pubmed-article:19149411 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:19149411 | pubmed:dateCreated | 2009-1-19 | lld:pubmed |
| pubmed-article:19149411 | pubmed:abstractText | Mice that constitutively express the human interleukin 6 (huIL6) protein from a heritable transgene (H2-L(d)-IL-6) express high levels of the acute-phase reactant, serum amyloid protein A, a liver-derived apoprotein of high-density lipoprotein that is the precursor of AA amyloid. Typically at approximately 5 mo of age B6(C)- Tg(H2-L(d)-IL-6)Kish (H2/huIL-6) animals begin to develop splenic deposits of AA amyloid, which progress to involve the liver, kidney, and vasculature, ultimately resulting in death due to severe systemic AA amyloidosis at 8 to 9 mo of age. These mice provide a robust model in which to study novel therapeutic and diagnostic imaging agents for AA amyloidosis. We recently have noted a change in onset of spontaneous disease, as evidenced by 2 female transgenic mice that were found moribund at only 5 mo of age. Extensive hepatosplenic amyloid deposits in both mice were identified and quantified by single-photon emission computed tomography, which further revealed heterogeneous distribution of radiotracer in the spleen indicating a distinction between amyloid-laden red pulp and the disease-free lymphoid follicles. The AA nature of the deposits was evidenced immunohistochemically and by mass spectrometric analyses of extracted amyloid fibrils. Our studies have documented the manifestation of early-onset, severe, spontaneous AA amyloidosis in 2- to 5-mo-old H2/ huIL-6 mice; we hypothesize that this disease is due to genetic rather than environmental factors. | lld:pubmed |
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| pubmed-article:19149411 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19149411 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19149411 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19149411 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19149411 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19149411 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:19149411 | pubmed:issn | 1532-0820 | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:SolomonAlanA | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:KennelSteve... | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:DonnellRobert... | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:WallJonathan... | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:AllenAmyA | lld:pubmed |
| pubmed-article:19149411 | pubmed:author | pubmed-author:RicheyTinaT | lld:pubmed |
| pubmed-article:19149411 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19149411 | pubmed:volume | 58 | lld:pubmed |
| pubmed-article:19149411 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19149411 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19149411 | pubmed:pagination | 542-50 | lld:pubmed |
| pubmed-article:19149411 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:19149411 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:19149411 | pubmed:articleTitle | Quantitative tomography of early-onset spontaneous AA amyloidosis in interleukin 6 transgenic mice. | lld:pubmed |
