Copyright (c) 2009 John Wiley & Sons, Ltd “
“Context: Major

Copyright (c) 2009 John Wiley & Sons, Ltd.”
“Context: Major surgery induces a catabolic state resulting in a net loss of body protein.\n\nObjectives: Our objective was to compare protein metabolism before and after surgery in nondiabetic FG-4592 manufacturer patients with and without preoperative insulin resistance

(IR). It was hypothesized that the anabolic response to feeding would be significantly impaired in those patients with preoperative insulin resistance.\n\nDesign: A hyperinsulinemic-euglycemic clamp has been used to identify two groups of patients: IR and insulin sensitive (IS). A tracer kinetics technique has been used to evaluate the metabolic response to food intake in both groups.\n\nSetting: Patients undergoing cardiopulmonary BEZ235 datasheet bypass participated.\n\nPatients or Other Participants: Ten IS patients and 10 IR patients were enrolled in the study.\n\nIntervention: After an overnight fasting, a 3-h infusion of a solution composed of 20% glucose and of amino acids at

a rate of 0.67 and 0.44 kcal/kg . h, respectively, was started in each group. Phenylalanine kinetics were studied at the end of fasting and feeding.\n\nMain Outcome Measure: Effect of feeding on protein balance before and after surgery was evaluated. Protein balance has been measured as the net difference of protein breakdown minus protein synthesis.\n\nResults: Protein balance increase after postoperative feeding was blunted only in the IR group. In contrast, in the IS group, the postoperative anabolic effect of feeding was the same as before surgery.\n\nConclusions: These findings propose a link between insulin resistance and protein metabolism. When non-IR patients are fed, a significant anabolic effect in the postoperative period is demonstrated. In contrast, IR patients are less able to use feeding for synthetic purposes. (J Clin Endocrinol Metab 96: E1789-E1797, 2011)”
“Background: Tumors of the head and neck present aggressive pathological behavior

in patients due to high expression of CDK/CCND1 proteins. P276-00, a novel CDK inhibitor currently being tested in clinic, inhibits growth of several cancers in vitro and in vivo. The pre clinical activity of P276-00 in head and neck cancer and its potential mechanisms of action at molecular level are the focus of the current studies.\n\nMethod: We have investigated the anti-cancer activity of P276-00 in head and neck tumors in vitro and in vivo. Candidate gene expression profiling and cell based proteomic approaches were taken to understand the pathways affected by P276-00 treatment.\n\nResults: It was observed that P276-00 is cytotoxic across various HNSCC cell lines with an IC50 ranging from 1.0-1.5 mu moles/L and culminated in significant cell-cycle arrest in G1/S phase followed by apoptosis.

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