Showing papers by "Richard D. Griffiths published in 2015"
Université libre de Bruxelles1, University of Trieste2, Katholieke Universiteit Leuven3, University of Sydney4, University of Liverpool5, Kingston General Hospital6, University of Milan7, Sapienza University of Rome8, Geneva College9, Karolinska University Hospital10, University of Colorado Denver11
TL;DR: An update in understanding of the metabolic response to stress and the most appropriate means of managing nutrition in critically ill patients is presented, identifying and discussing a number of areas for which consensus has been reached and others where controversy remains.
Abstract: The results of recent large-scale clinical trials have led us to review our understanding of the metabolic response to stress and the most appropriate means of managing nutrition in critically ill patients. This review presents an update in this field, identifying and discussing a number of areas for which consensus has been reached and others where controversy remains and presenting areas for future research. We discuss optimal calorie and protein intake, the incidence and management of re-feeding syndrome, the role of gastric residual volume monitoring, the place of supplemental parenteral nutrition when enteral feeding is deemed insufficient, the role of indirect calorimetry, and potential indications for several pharmaconutrients.
305 citations
TL;DR: Enhanced rehabilitation combined with GEAA supplement may enhance physical recovery and reduce anxiety and depression.
60 citations
TL;DR: The changes in superoxide, activation of NF-kB and release of myokines were attenuated following pre-treatment with SS-31 peptide indicating that the ability of TNF-α to induce myokine release may be mediated through mitochondrialsuperoxide, which is, at least in part, associated with activation of the redox sensitive transcription factor NF-MB.
Abstract: TNF-α is a key inflammatory mediator and is proposed to induce transcriptional responses via the mitochondrial generation of Reactive Oxygen Species (ROS). The aim of this study was to determine the effect of TNF-α on the production of myokines by skeletal muscle. Significant increases were seen in the release of IL-6, MCP-1/CCL2, RANTES/CCL5 and KC/CXCL1 and this release was inhibited by treatment with Brefeldin A, suggesting a golgi-mediated release of cytokines by muscle cells. An increase was also seen in superoxide in response to treatment with TNF-α, which was localised to the mitochondria and this was also associated with activation of NF-κB. The changes in superoxide, activation of NF-kB and release of myokines were attenuated following pre-treatment with SS-31 peptide indicating that the ability of TNF-α to induce myokine release may be mediated through mitochondrial superoxide, which is, at least in part, associated with activation of the redox sensitive transcription factor NF-kB.
33 citations