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| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C1956346 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0229671 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0332835 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0282554 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C1332822 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:12695288 | lifeskim:mentions | umls-concept:C0205250 | lld:lifeskim |
| pubmed-article:12695288 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:12695288 | pubmed:dateCreated | 2003-4-22 | lld:pubmed |
| pubmed-article:12695288 | pubmed:abstractText | Human and animal studies of acute allograft rejection have implicated CCR5 and CXCR3 chemokines as causative factors. However these chemokines have not been assessed in transplant coronary artery disease (TCAD). | lld:pubmed |
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| pubmed-article:12695288 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12695288 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12695288 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12695288 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:12695288 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:12695288 | pubmed:author | pubmed-author:StrieterRober... | lld:pubmed |
| pubmed-article:12695288 | pubmed:author | pubmed-author:KaoJohnJ | lld:pubmed |
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| pubmed-article:12695288 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12695288 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:12695288 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:12695288 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12695288 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12695288 | pubmed:pagination | 1958-61 | lld:pubmed |
| pubmed-article:12695288 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:12695288 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12695288 | pubmed:articleTitle | Elevated serum levels of the CXCR3 chemokine ITAC are associated with the development of transplant coronary artery disease. | lld:pubmed |
| pubmed-article:12695288 | pubmed:affiliation | Department of Medicine, Division of Cardiology, David Geffen School of Medicine at University of California, Los Angeles 90024-1922, USA. | lld:pubmed |
| pubmed-article:12695288 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12695288 | pubmed:publicationType | Clinical Trial | lld:pubmed |
| pubmed-article:12695288 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12695288 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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