| pubmed-article:17367535 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0008109 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C1366645 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C0032149 | lld:lifeskim |
| pubmed-article:17367535 | lifeskim:mentions | umls-concept:C1554184 | lld:lifeskim |
| pubmed-article:17367535 | pubmed:dateCreated | 2007-3-27 | lld:pubmed |
| pubmed-article:17367535 | pubmed:abstractText | Adhesion of Plasmodium-infected red blood cells (iRBC) to different host cells, ranging from endothelial to red blood cells, is associated to malaria pathology. In vitro studies have shown the relevance of CD36 for adhesion phenotypes of Plasmodium falciparum iRBC such as sequestration, platelet mediated clumping and non-opsonic uptake of iRBC. Different adhesion phenotypes involve different host cells and are associated with different pathological outcomes of disease. Studies with different human populations with CD36 polymorphisms failed to attribute a clear role to CD36 expression in human malaria. Up to the present, no in vivo model has been available to study the relevance of different CD36 adhesion phenotypes to the pathological course of Plasmodium infection. | lld:pubmed |
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| pubmed-article:17367535 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17367535 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17367535 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17367535 | pubmed:issn | 1475-2875 | lld:pubmed |
| pubmed-article:17367535 | pubmed:author | pubmed-author:MotaMaria MMM | lld:pubmed |
| pubmed-article:17367535 | pubmed:author | pubmed-author:FebbraioMaria... | lld:pubmed |
| pubmed-article:17367535 | pubmed:author | pubmed-author:Cunha-Rodrigu... | lld:pubmed |
| pubmed-article:17367535 | pubmed:author | pubmed-author:PortugalSílvi... | lld:pubmed |
| pubmed-article:17367535 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17367535 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:17367535 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17367535 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17367535 | pubmed:pagination | 32 | lld:pubmed |
| pubmed-article:17367535 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17367535 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17367535 | pubmed:articleTitle | Bone marrow chimeric mice reveal a dual role for CD36 in Plasmodium berghei ANKA infection. | lld:pubmed |
| pubmed-article:17367535 | pubmed:affiliation | Unidade de Malária, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal. margaridacunha@fm.ul.pt <margaridacunha@fm.ul.pt> | lld:pubmed |
| pubmed-article:17367535 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17367535 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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