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“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 https://www.selleckchem.com/products/pf-03084014-pf-3084014.html 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.