Additional vascular involvement and location of the lesion at or above the bifurcation of the hepatic duct have a major impact on the extent of surgical intervention required and should be reflected in any classification of bile duct injuries.

Salinomycin raised hope to be effective in anti-cancer therapies due to its capability to overcome apoptosis-resistance in several types of cancer cells. Recently, its effectiveness against human hepatocellular carcinoma (HCC) cells both in vitro and in vivo was demonstrated. However, the mechanism of action remained unclear. Latest studies implicated interference with the degradation pathway of autophagy. This study aimed to determine the impact of Salinomycin on HCC-autophagy and whether primary human hepatocytes (PHH) likewise are affected. Following exposure of HCC cell lines HepG2 and Huh7 to varying concentrations of Salinomycin (0–10 µM), comprehensive analysis of autophagic activity using western-blotting and flow-cytometry was performed. Drug effects were analyzed in the settings of autophagy stimulation by starvation or PP242-treatment and correlated with cell viability, proliferation, apoptosis induction, mitochondrial mass accumulation and reactive oxygen species (ROS) formation. Impact on apoptosis induction and cell function of PHH was analyzed.Constitutive and stimulated autophagic activities both were effectively suppressed in HCC by Salinomycin. This inhibition was associated with dysfunctional mitochondria accumulation, increased apoptosis and decreased proliferation and cell viability. Effects of Salinomycin were dose and time dependent and could readily be replicated by pharmacological and genetic inhibition of HCC-autophagy alone. Salinomycin exposure to PHH resulted in transient impairment of synthesis function and cell viability without apoptosis induction. In conclusion, our data suggest that Salinomycin suppresses late stages of HCC-autophagy, leading to impaired recycling and accumulation of dysfunctional mitochondria with increased ROS-production all of which are associated with induction of apoptosis.

Regardless of bleeding severity or surface area, the Veriset™ haemostatic patch achieved haemostasis in this setting significantly faster than the control device in patients undergoing hepatic resection. It was safe and easy to handle in open hepatic surgery.

Nonalcoholic fatty liver disease (NAFLD) is highly prevalent in patients with acute coronary syndrome (ACS). We assessed the association between NAFLD and SYNTAX Score (SS) in patients with ACS. Eighty consecutive patients with ACS were enrolled. Patients were evaluated using ultrasound to detect NAFLD and hepatosteatosis stage. The prevalence of NAFLD was 81.2%; median SS was 15. The SS was significantly higher in patients with NAFLD (18 ± 8 vs. 11 ± 5, P = .001). Univariate analysis showed that the stage of NAFLD correlated with SS (r = .6, P < .001). In multivariate binary logistic analysis, increased age (odds ratio [OR], 1.05; 95% confidence interval [CI],1.00-1.10) and presence of NAFLD (OR, 13.20; 95% CI, 2.52-69.15) were independent factors associated with supramedian SS. In conclusion, among patients with ACS, those with NAFLD have more complex CAD as assessed by SS.