Annals of medicine
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The multiligand receptor RAGE (receptor for advanced glycation end-products) is emerging as a central mediator in the immune/inflammatory response. Epidemiological evidence accruing in the human suggests upregulation of RAGE's ligands (AGEs, S100/calgranulins, high mobility group box-1 (HMGB1), and amyloid beta-peptide and beta-sheet fibrils) and the receptor itself at sites of inflammation and in chronic diseases such as diabetes and neurodegeneration. ⋯ Lastly, we consider findings from animal model studies suggesting that although tissue-damaging effects ensue from recruitment of the ligand-RAGE interaction, in distinct settings, adaptive and repair/regeneration outcomes appear to override detrimental effects of RAGE. As RAGE blockade moves further into clinical development, clarifying the biology of RAGE garners ever-increasing importance.
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Review
Vascular endothelial responses to altered shear stress: pathologic implications for atherosclerosis.
Atherosclerosis preferentially develops at branches and curvatures of the arterial tree, where blood flow is disturbed from a laminar pattern, and wall shear stress is non-uniform and has an irregular distribution. Vascular endothelial cells (ECs), which form an interface between the flowing blood and the vessel wall, are exposed to blood flow-induced shear stress. ⋯ The aim of this review article is to summarize current findings on the effects of shear stress on ECs, in terms of their signal transduction, gene expression, structure, and function. These endothelial cellular responses have important relevance to understanding the pathophysiological effects of altered shear stress associated with atherosclerosis and thrombosis and their complications.
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Chromogranin A (CGA), a stress marker released with catecholamines by the adrenal medulla, has never been associated with acute inflammation in critically ill patients. ⋯ Patients with CGA concentration superior to 71 microg/L have a significantly shorter survival. A Cox model confirmed that CGA and SAPS were independent predictors of outcome.
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Preptin is a novel hormone that is co-secreted with insulin and amylin from the pancreatic beta-cells. Preptin increases glucose-mediated insulin secretion, while the binding of endogenous preptin by antipreptin antibodies decreases glucose-mediated insulin secretion. Thus, it appears to act as a physiological amplifier of glucose-mediated insulin secretion. Aim. In this study, we investigate whether plasma preptin levels are different in non-diabetic subjects and patients with impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM). ⋯ The present work suggests a potential role of preptin in the pathogenesis of T2DM.
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Bleeding is a serious adverse drug reaction associated with warfarin therapy, often induced by interacting co-medication. ⋯ We conclude that co-medication in warfarin-treated in-patients is common and should be carefully evaluated to decrease the bleeding risk associated with warfarin therapy.