The established miRNA profile of the steatotic L02 cell model and the novel effect of miRNA-10b in regulating hepatocyte steatosis may provide a new explanation of the pathogenesis of NAFLD.

ObjectiveWe investigated whether red cell distribution width (RDW) was associated with mortality in patients with acute pancreatitis (AP).DesignA cross-sectional study.SettingPatients with AP were recruited in the emergency department and healthy individuals were recruited in healthcare centre in the First Affiliated Hospital of Zhejiang University.ParticipantsA total of 106 patients with AP and 204 healthy individuals were enrolled.Primary and secondary outcome measuresHaematology and biochemistry results of the first test after admission were collected. The significance of the differences in RDW values among healthy individuals, non-survivors of patients with AP, and survivors of patients with AP was determined using one-way analysis of variance. Patients with AP were divided into three groups according to RDW tertiles. All patients with AP were followed up for at least 3 months. Receiver-operating characteristic (ROC) curve analysis and Kaplan-Meier analysis were used to evaluate RDW values to predict mortality of patients with AP.ResultsThe RDW values were non-survivors of patients with AP>healthy individuals>survivors of patients with AP. Patients with AP with the highest RDW tertiles had the lowest levels of Ca, total protein, albumin, haemoglobin, white and red blood cell count, but the highest mortality. The area under the ROC curve of RDW was 0.846 (95% CI 0.727 to 0.964, p<0.001). With a cut-off value of 14.2 for RDW, sensitivity and specificity of RDW to predict mortality were 75.0% and 89.8%, and Kaplan-Meier analysis showed an increase in probability of death with high RDW values.ConclusionsThere is significant association between RDW and mortality of patients with AP.

We demonstrate that a storage time interval up to 24 h for D-dimers, Fbg, PT, and TT, and 8 h for APTT at either RT or 4 °C is acceptable.

Bioartificial liver (BAL) support system has been proposed as potential treatment method for end-stage liver diseases. We described an improved BAL system based on a choanoid fluidized bed bioreactor containing alginate-chitosan encapsulated primary porcine hepatocytes. The feasibility, safety, and efficiency of this device were estimated using an allogeneic fulminant hepatic failure (FHF) model. FHF was induced with intravenous administration of D-galactosamine. Thirty FHF pigs were divided into three groups: (1) an FHF group which was only given intensive care; (2) a sham BAL group which was treated with the BAL system with empty encapsulation, and (3) a BAL group which was treated with the BAL system containing encapsulated freshly isolated primary porcine hepatocytes. The survival times and biochemical parameters of these animals were measured, and properties of the encapsulations and hepatocytes before and after perfusion were also evaluated. Compared to the two control groups, the BAL-treated group had prolonged the survival time and decreased the blood lactate levels, blood glucose, and amino acids remained stable. No obvious ruptured beads or statistical decline in viability or function of encapsulated hepatocytes were observed. This new fluidized bed BAL system is safe and efficient. It may represent a feasible alternative in the treatment of liver failure.

Increased expression of HOXB7 has been reported to correlate with the progression in many cancers. However, the specific mechanism by which it promotes the evolution of gastric cancer (GC) is poorly understood.In this study, we sought to investigate the role of HOXB7 in GC by assessing HOXB7 expression in patient tissue and its correlation to clinical characteristics. We found that GC tissues showed increased expression of HOXB7 and that the HOXB7 expression was significantly associated with Lauren classification, invasion depth, lymphatic metastasis and poor prognosis, and could serve as an independent prognostic factor. To further investigate the role of HOXB7 in GC, we generated stable GC cell lines and both over-expressed and knocked down HOXB7 expression. Over-expression of HOXB7 in GC cell lines enhanced cell proliferation, colony formation, migration and invasion ability, whereas the opposite trends were observed upon reduction of HOXB7 expression by knockdown. These findings were further supported by our in vivo studies which show that HOXB7 expression can affect the GC cells' subcutaneous growth and lung metastases. A Phospho-MAPK Array Kit was used to explore the possible mechanism of HOXB7-induced cell proliferation and invasion. We found that the AKT signaling pathway and the two members of the MAPK pathway, were involved in those promoting effects. In conclusion, our results showed that increased expression of HOXB7 might play an important role in promoting GC proliferation, migration and invasion by inducing both AKT and MAPK pathways, thus resulting in progression of, and poor prognosis in GC patients.