Patient and procedure characteristics as well as outcome were col

Patient and procedure characteristics as well as outcome were collected prospectively. From October 2006 to June 2010, 51 patients with a failed prior bariatic procedure (VBG or LAGB) were converted to (L)SG. The conversion

rate was zero. The median procedure time was 99 min (range 54-221) and hospital stay was 3 days (range 2-38). There was no mortality after 30 days. Complications included bleeding (six) and leakage of the staple line (seven). Mean follow-up was 13.8 (2-46) months. LSG as revision surgery for insufficient weight loss resulted in extra weight loss of 52.7%, and the overall extra weight loss was 49.3%. When LSG was performed because of vomiting, 82% was able to AZD6094 eat solid food at follow-up. Of the 65 pre-existent co-morbidities, 21 were resolved and

18 improved. LSG as a revision procedure is feasible. An additional weight loss and further resolution of co-morbidity seem achievable, however, at the cost of a high number of complications. Therefore, check details revision bariatric surgery should be limited to expert tertiary bariatric centers.”
“Leukotrienes, divided into cysteinyl leukotrienes (CysLTs), which are important mediators of asthmatic responses, and leukotriene B-4 (LTB4), a chemotactic and chemokinetic agent for leukocytes, are potent lipid mediators generated from arachidonic acid by 5-lipoxygenase JNK-IN-8 solubility dmso (5-LO). Leukotrienes are also considered to have immunoregulatory and pro-inflammatory actions. Propofol is an intravenous anesthetic widely used for anesthesia and sedation that is alleged to possess anti-inflammatory properties. The present study examined the effect of propofol on leukotriene production by dendritic cells (DC). In murine bone marrow-derived DC, propofol significantly suppressed CysLT and LTB4 production after short-term stimulation with zymosan. The protein levels of cytosolic phospholipase A(2) and 5-LO,

or arachidonic acid release from plasma membranes, were not affected by the presence of propofol. Although zymosan treatment induced or enhanced the phosphorylation of ERK1/2, p-38 MAPK, and JNK, which presumably up-regulates the activity of 5-LO, the presence of propofol had no additional effect on the phosphorylation status of any of these MAPKs. Similarly, zymosan significantly increased the concentration of intracellular calcium, which is the most crucial activator of 5-LO, but no additional concentration changes were observed with the addition of propofol. Lastly, in an in-vitro cell-free ferrous oxidation-xylenol orange assay, propofol significantly inhibited the 5-LO activity of purified human recombinant 5-LO enzyme with an IC50 of similar to 7.5 mu M.

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