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- W4313353984 startingPage "180.12" @default.
- W4313353984 abstract "Abstract Surgery necessitating cardiopulmonary bypass (snCPB) is associated with systemic inflammation which can be severe. Systemic inflammation is common in the critically ill, is linked to adverse outcome and currently has no specific therapy. Insight into the pathogenesis of systemic inflammation may lead to therapies. The receptor for advanced glycation end-products (RAGE) is an ubiquitous receptor that is up-regulated in the presence of its ligands which are glycated proteins, S100 proteins and high mobility group box 1 (HMGB1). It causes a pro-inflammatory response via NF-κB and the MAP kinases. RAGE inhibition has been associated with improved outcomes in animal models of inflammation and may represent a novel target for intervention. In this study, blood was obtained pre- and post-operation from patients having cardiac surgery involving CPB. The surface and intracellular expression levels of RAGE in neutrophils and monocytes were assessed by flow cytometry and mRNA was obtained for RT-PCR. Preliminary results showed that although snCPB made little difference to intracellular RAGE, cellular RAGE decreased significantly, suggesting that the operative procedure could have initiated shedding of the receptor. There was no significant difference in the RAGE mRNA levels pre- and post-operation. This study provides a better understanding of the involvement of RAGE in systemic inflammation suggesting that shedding of the surface RAGE might contribute to the inflammation process." @default.
- W4313353984 created "2023-01-06" @default.
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- W4313353984 date "2013-05-01" @default.
- W4313353984 modified "2023-09-25" @default.
- W4313353984 title "Decreased expression of receptor for advanced glycation end-products (RAGE) on neutrophils following surgery necessitating cardiopulmonary bypass (snCPB) (P5058)" @default.
- W4313353984 doi "https://doi.org/10.4049/jimmunol.190.supp.180.12" @default.
- W4313353984 hasPublicationYear "2013" @default.
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