Dor versus Toupet fundoplication after Laparoscopic Heller Myotomy: Systematic review and Bayesian meta-analysis of randomized controlled trials

Laparoscopic Heller Myotomy (LHM) with partial fundoplication has become the treatment of choice for esophageal achalasia. However, the choice of the partial fundoplication is debated. The aim of this study was to compare outcomes for Dor and Toupet fundoplication after LHM. A systematic search of randomized controlled trials comparing Dor and Toupet fundoplication was performed using PubMed, EMBASE and Web of Science. Three studies met the inclusion criteria. Overall, 174 patients were included in the analysis. The postoperative abnormal acid reflux [pooled Risk Ratio 0.98 (95% HPD 0.54-1.80)] and dysphagia [pooled Risk Ratio 1.03 (95% HPD 0.51-2.05)] were similar comparing Dor and Toupet fundoplication. The % total time pH  64 4 [estimated pooled mean difference -0.08 (95% HPD -1.04-0.90)] and DeMeester score [estimated pooled mean difference 0.51 (95% HPD -0.90-1.94)] were comparable. Additionally, the operative time [estimated pooled mean difference 0.02 (95% HPD -0.53-0.52)] and iatrogenic esophageal perforation [pooled Risk Ratio 1.05 (95% HPD 0.52-2.10)] were similar in the two groups. Dor and Toupet fundoplication after laparoscopic Heller myotomy seem comparable in term of postoperative abnormal acid exposure and dysphagia. The choice of the partial fundoplication should be left to surgeon experience and tailored on each patient

Diverse Beliefs and Time Variability of Risk Premia

Why do risk premia vary over time? We examine this problem theoretically and empirically by studying the effect of market belief on risk premia. Individual belief is taken as a fundamental primitive state variable. Market belief is observable; it is central to the empirical evaluation and we show how to measure it. Our asset pricing model is familiar from the noisy REE literature but we adapt it to an economy with diverse beliefs. We derive equilibrium asset prices and implied risk premium. Our approach permits a closed form solution of prices; hence we trace the exact effect of market belief on the time variability of asset prices and risk premia. We test empirically the theoretical conclusions. Our main result is that, above the effect of business cycles on risk premia, fluctuations in market belief have significant independent effect on the time variability of risk premia. We study the premia on long positions in Federal Funds Futures, 3- and 6-month Treasury Bills (T-Bills). The annual mean risk premium on holding such assets for 1-12 months is about 40-60 basis points and we find that, on average, the component of market belief in the risk premium exceeds 50% of the mean. Since time variability of market belief is large, this component frequently exceeds 50% of the mean premium. This component is larger the shorter is the holding period of an asset and it dominates the premium for very short holding returns of less than 2 months. As to the structure of the premium we show that when the market holds abnormally favorable belief about the future payoff of an asset the market views the long position as less risky hence the risk premium on that asset declines. More generally, periods of market optimism (i.e. "bull" markets) are shown to be periods when the market risk premium is low while in periods of pessimism (i.e. "bear" markets) the market's risk premium is high. Fluctuations in risk premia are thus inversely related to the degree of market optimism about future prospects of asset payoffs. This effect is strong and economically very significant

Kupffer Cells Hasten Resolution of Liver Immunopathology in Mouse Models of Viral Hepatitis

Kupffer cells (KCs) are widely considered important contributors to liver injury during viral hepatitis due to their pro-inflammatory activity. Herein we utilized hepatitis B virus (HBV)-replication competent transgenic mice and wild-type mice infected with a hepatotropic adenovirus to demonstrate that KCs do not directly induce hepatocellular injury nor do they affect the pathogenic potential of virus-specific CD8 T cells. Instead, KCs limit the severity of liver immunopathology. Mechanistically, our results are most compatible with the hypothesis that KCs contain liver immunopathology by removing apoptotic hepatocytes in a manner largely dependent on scavenger receptors. Apoptotic hepatocytes not readily removed by KCs become secondarily necrotic and release high-mobility group box 1 (HMGB-1) protein, promoting organ infiltration by inflammatory cells, particularly neutrophils. Overall, these results indicate that KCs resolve rather than worsen liver immunopathology