pubmed-article:12693661 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12693661 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
pubmed-article:12693661 | lifeskim:mentions | umls-concept:C0006110 | lld:lifeskim |
pubmed-article:12693661 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:12693661 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:12693661 | pubmed:dateCreated | 2003-4-15 | lld:pubmed |
pubmed-article:12693661 | pubmed:abstractText | Islet transplantation is now established as an optional treatment for type I diabetes. However, rates of insulin independence in islet transplant recipients are still low. Although the major source of allograft is derived from brain-dead patient, the nonphysiologic state of brain death (BD) deteriorates organs such as liver and kidney. To determine the effects of BD on islets, a rodent model of BD has been used. Histologically, islets of BD rats showed decreased permeability and impaired integrity of the cell membranes. Flow cytometric analysis showed that CD11b/c-positive cells within islets were slightly increased in BD. This result suggests that BD induces macrophage infiltration into the islets. Moreover, RT-PCR revealed significant augmentation of macrophages-associated inflammatory molecules (IL-1beta, IL-6, TNF-alpha, and MCP-1) in islets from a BD donor. Inducible nitric oxide synthase (iNOS) was weakly expressed, although not reaching statistical significance compared with control. Our results indicate that islets from a BD donor are immunologically activated and have a potential risk factor for early graft loss and a poor long-term function of grafts in clinical setting of islet transplantation. Immunomodulation, to eliminate intraislet immunocytes and/or activated macro phage-associated molecules, might be necessary for the better outcome after islet graft from BD donors. | lld:pubmed |
pubmed-article:12693661 | pubmed:language | eng | lld:pubmed |
pubmed-article:12693661 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12693661 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12693661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12693661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12693661 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12693661 | pubmed:issn | 0963-6897 | lld:pubmed |
pubmed-article:12693661 | pubmed:author | pubmed-author:KurodaYoshika... | lld:pubmed |
pubmed-article:12693661 | pubmed:author | pubmed-author:SuzukiYasuyuk... | lld:pubmed |
pubmed-article:12693661 | pubmed:author | pubmed-author:ToyamaHirochi... | lld:pubmed |
pubmed-article:12693661 | pubmed:author | pubmed-author:TakadaMoriats... | lld:pubmed |
pubmed-article:12693661 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12693661 | pubmed:volume | 12 | lld:pubmed |
pubmed-article:12693661 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12693661 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12693661 | pubmed:pagination | 27-32 | lld:pubmed |
pubmed-article:12693661 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
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pubmed-article:12693661 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12693661 | pubmed:articleTitle | Activation of macrophage-associated molecules after brain death in islets. | lld:pubmed |
pubmed-article:12693661 | pubmed:affiliation | Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kobe University, Kobe, Japan. | lld:pubmed |
pubmed-article:12693661 | pubmed:publicationType | Journal Article | lld:pubmed |
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