pubmed-article:19582162 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C0599779 | lld:lifeskim |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C1948066 | lld:lifeskim |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C1707689 | lld:lifeskim |
pubmed-article:19582162 | lifeskim:mentions | umls-concept:C0597551 | lld:lifeskim |
pubmed-article:19582162 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:19582162 | pubmed:dateCreated | 2009-7-7 | lld:pubmed |
pubmed-article:19582162 | pubmed:abstractText | Mouse AA-amyloidosis is a transmissible disease by a prion-like mechanism where amyloid fibrils act by seeding. Synthetic peptides with no amyloid relationship can assemble into amyloid-like fibrils and these may have seeding capacity for amyloid proteins. | lld:pubmed |
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pubmed-article:19582162 | pubmed:language | eng | lld:pubmed |
pubmed-article:19582162 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19582162 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19582162 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19582162 | pubmed:issn | 1932-6203 | lld:pubmed |
pubmed-article:19582162 | pubmed:author | pubmed-author:WestermarkGun... | lld:pubmed |
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pubmed-article:19582162 | pubmed:author | pubmed-author:LundmarkKatar... | lld:pubmed |
pubmed-article:19582162 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19582162 | pubmed:volume | 4 | lld:pubmed |
pubmed-article:19582162 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19582162 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19582162 | pubmed:pagination | e6041 | lld:pubmed |
pubmed-article:19582162 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:19582162 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19582162 | pubmed:articleTitle | Fibrils from designed non-amyloid-related synthetic peptides induce AA-amyloidosis during inflammation in an animal model. | lld:pubmed |
pubmed-article:19582162 | pubmed:affiliation | Rudbeck Laboratory, Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden. | lld:pubmed |
pubmed-article:19582162 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19582162 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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