No abstract

The hENT1 expression in pancreatic adenocarcinoma strongly influences the outcome of preoperative Gem-CRT treatment. This biomarker could become a useful predictor of therapeutic effect for gemcitabine-based therapy in pancreatic cancer patients.

Previous clinical study has demonstrated that 30-40% of patients undergoing pancreaticoduodenectomy (PD) developed hepatic steatosis. However, nonalcoholic steatohepatitis (NASH) is a little-known complication after PD. Recently we encountered two patients with PD who later developed NASH diagnosed by liver biopsy. Case 1 was a 79-year-old woman who underwent PD for intraductal papillary mucinous neoplasm (IPMN). She had postoperative severe diarrhea due to pseudomembranous enterocolitis. Severe liver dysfunction was observed on the 31st postoperative day. Abdominal computed tomography (CT) on the 32nd day showed remarkably decreased hepatic CT value of 6 HU. Immediate liver biopsy revealed NASH (Brunt criteria: grade 2, stage 2). Case 2 was a 71-year-old woman who underwent PD for IPMN. Liver biopsy on 70th postoperative day, which was performed for assessment of moderate liver dysfunction and decreased hepatic CT value of 44 HU, demonstrated simple steatosis. In the 21st postoperative month, she developed severe urinary tract infection together with marked liver dysfunction. Immediate liver biopsy revealed NASH (Brunt criteria: grade 1, stage 1). For each patient, treatment of infection and high-dose pancreatic enzyme supplements improved liver dysfunction and liver steatosis. Clinical features of our cases seem to support the current leading hypothesis of the pathogenesis of NASH, i.e., the two-hit theory.

Abstract:We recorded evoked potentials (EPs) induced by intra-epidermal electrical stimulation using a needle electrode with specific parameters. We identified the fibers activated by this specific stimulation by assessing the conduction velocity (CV) of the peripheral nerve. The EPs were recorded from the Cz electrode (vertex) of the International 10-20 system in ten healthy male subjects. The dorsum of the left hand and forearm were stimulated with an intensity of 0.01 mA above the sensory threshold. The mean P1 latency of EPs for the hand and forearm were 1007 ± 88 and 783 ± 80 ms, respectively, and the CV estimated from the latency of P1 was 1.5 ± 0.7 m/s. The CV indicated that the fibers activated by the stimulation were C fibers. Since the method of stimulation is convenient and non-invasive, it should be useful for investigating the functions of small fibers.

The problems associated with small-for-size liver grafts (ie, high mortality rates, postoperative complications, and acute rejection) remain critical issues in partial orthotopic liver transplantation (OLT). In association with partial OLT, splenectomy (SP) is a procedure used to reduce the portal pressure. However, the precise effects of SP on partial OLT have been unclear. In this study, using small-for-size liver grafts in rats, we examined the cytoprotective effects of SP on OLT. Liver grafts were assigned to 2 groups: a control group (OLT alone) and an SP group (OLT after SP). SP significantly increased animal survival and decreased liver damage. SP exerted the following cytoprotective effects: (1) it improved hepatic microcirculation and prevented increases in the portal pressure after OLT, (2) it suppressed the hepatic infiltration of neutrophils and macrophages through the direct elimination of splenic inflammatory cells before OLT, (3) it decreased the hepatic expression of tumor necrosis factor a and interleukin-6, (4) it attenuated sinusoidal endothelial injury, (5) it decreased plasma endothelin 1 levels and increased hepatic heme oxygenase 1 expression, (6) it suppressed hepatocellular apoptosis through the down-regulation of hepatic caspase-3 and caspase-8 activity, and (7) it increased hepatic regeneration. In conclusion, SP for small-for-size grafts exerts dual cytoprotective effects by preventing excessive portal vein hepatic inflow and eliminating splenic inflammatory cell recruitment into the liver; this in turn inhibits hepatocellular apoptosis and improves liver regeneration. Liver Transpl 18:1361-1370, 2012. V C 2012 AASLD.Received January 23, 2012; accepted July 15, 2012.Because of the shortage of deceased liver grafts, the demand for partial liver grafts from living donors and for the splitting of deceased donor grafts has been increasing worldwide. Such measures are necessary because liver transplantation is the only curative therapy for many patients with end-stage liver disease and/or acute liver failure.1,2 However, the problems associated with small-for-size liver graft injuries remain major obstacles: small-for-size liver graft injuries are associated not only with high mortality rates and postoperative complications but also with acute rejection. 3-5The precise mechanisms of small-for-size liver graft injuries have not been completely clarified. A critical mechanism is associated with the severe shear stress due to transient portal hypertension just after reperfusion.6 Therefore, therapeutic treatments depend on portal decompression to protect small-for-size liver grafts. Various therapeutic strategies focusing on portal decompression have been reported for animal models.7,8 Using a small-for-size liver graft model in rats, our previous study showed that a preservation solution including activated protein C significantly increased hepatic microcirculation and decreased portal pressure caused by an increased hepatic level of nitric oxide via up-regulated endothelial nitric oxide syn...