Source:http://linkedlifedata.com/resource/pubmed/id/12693661
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2003-4-15
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| 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0963-6897
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
12
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
27-32
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading |
pubmed-meshheading:12693661-Adjuvants, Immunologic,
pubmed-meshheading:12693661-Animals,
pubmed-meshheading:12693661-Antigens, CD11,
pubmed-meshheading:12693661-Brain Death,
pubmed-meshheading:12693661-Cell Membrane Permeability,
pubmed-meshheading:12693661-Chemotaxis, Leukocyte,
pubmed-meshheading:12693661-Cytokines,
pubmed-meshheading:12693661-Diabetes Mellitus, Type 1,
pubmed-meshheading:12693661-Disease Models, Animal,
pubmed-meshheading:12693661-Flow Cytometry,
pubmed-meshheading:12693661-Graft Survival,
pubmed-meshheading:12693661-Islets of Langerhans,
pubmed-meshheading:12693661-Islets of Langerhans Transplantation,
pubmed-meshheading:12693661-Macrophages,
pubmed-meshheading:12693661-Male,
pubmed-meshheading:12693661-Nitric Oxide,
pubmed-meshheading:12693661-Rats,
pubmed-meshheading:12693661-Rats, Inbred Lew,
pubmed-meshheading:12693661-Regional Blood Flow,
pubmed-meshheading:12693661-Tissue Donors
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| pubmed:year |
2003
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| pubmed:articleTitle |
Activation of macrophage-associated molecules after brain death in islets.
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| pubmed:affiliation |
Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kobe University, Kobe, Japan.
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| pubmed:publicationType |
Journal Article
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