| pubmed-article:8648541 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C0008059 | lld:lifeskim |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C0002895 | lld:lifeskim |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C0034805 | lld:lifeskim |
| pubmed-article:8648541 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:8648541 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8648541 | pubmed:dateCreated | 1996-7-24 | lld:pubmed |
| pubmed-article:8648541 | pubmed:abstractText | Despite penicillin prophylaxis and vaccination, infection with encapsulated organisms remains a leading cause of morbidity and death in children with sickle cell disease. The role of Fc receptors in the clearance of encapsulated organisms is well documented. The His(H)-Arg(R) polymorphism at amino acid 131 of the Fc gamma RIIA receptor alters binding affinity for human IgG2 and influences infection with encapsulated organisms in children without sickle cell disease. We hypothesized that the genotype for high-affinity human IgG2 binding (H/H131) is underrepresented in children with sickle cell disease who had encapsulated organism infection. | lld:pubmed |
| pubmed-article:8648541 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8648541 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8648541 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8648541 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8648541 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8648541 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8648541 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8648541 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8648541 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8648541 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:8648541 | pubmed:issn | 0022-3476 | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:SchwartzEE | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:SurreySS | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:BuchananG RGR | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:McKenzieS ESE | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:BuninG RGR | lld:pubmed |
| pubmed-article:8648541 | pubmed:author | pubmed-author:NorrisC FCF | lld:pubmed |
| pubmed-article:8648541 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8648541 | pubmed:volume | 128 | lld:pubmed |
| pubmed-article:8648541 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8648541 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8648541 | pubmed:pagination | 813-9 | lld:pubmed |
| pubmed-article:8648541 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:8648541 | pubmed:meshHeading | pubmed-meshheading:8648541-... | lld:pubmed |
| pubmed-article:8648541 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8648541 | pubmed:articleTitle | Relationship between Fc receptor IIA polymorphism and infection in children with sickle cell disease. | lld:pubmed |
| pubmed-article:8648541 | pubmed:affiliation | Department of Pedlatrics, Children's Hospital of Philadelphia, Pennsylvania 19104, USA. | lld:pubmed |
| pubmed-article:8648541 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8648541 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8648541 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8648541 | lld:pubmed |
