Objective To study the efficacy and safety of sedation in gastroscopy with a combined use of rimifentani and propofol compared to a control,non-sedative group.Methods 120 cases in sedative group were given intravenous rimifentani and propofol.Patients'feeling and discomfort,operator's satisfaction and operative duration were compared with the controI group(n=120,without sedation).The changes of blood pressure,heat rate and blood oxygen saturation were recorded and analysed.Results 118 patients(98.3%)in sedative group and 0 patient(0)in control group did not complain any discomfort and pain duing gastroscopy(P＜0.01).The incidence of cough,restlessness,nausea and vomiting,and guttural discomfort in sedative group(1.7%,3.3%,1.7%,and 0,respectively)was lower as compared with the control group(9.2%,26.7%,48.3%and 100%,respectively,P＜0.01).The blood pressure in sedative group was decreased duing the procedure and recovered after the procedure.Conclusion With intravenous use of rimifentani and propofol,gastroscopy can be performed effectively and safely.

Aim To investigate the effect of salvianolic acid B (Sal B)on c-Jun N-terminal kinase (JNK)ac-tivation and apoptosis of INS-1 cells induced by inter-mittent high glucose.Methods INS-1 cells were pre-incubated with Sal B for 24 h,followed by exposure to intermittent high glucose (IHG,11.1 mmol·L-1 12 h,33. 3 mmol·L-1 12 h)for 72 h.Cell viability was assessed by MTT assay and cell apoptosis was evalua-ted by flow cytometry.Glucose induced insulin secre-tion capacity and intracellular reactive oxygen species (ROS)contents were measured by enzyme linked im-munosorbent assay (ELISA)and a fluorescent probe DCFH-DA,respectively.Levels of JNK activation and PDX-1 protein expression were determined by Western blot analysis.Results Sal B significantly alleviated IHG-induced cell injury and apoptosis,with glucose induced insulin secretion capacity improved evidently (P<0.05 or P<0.01).Preincubation with Sal B no-tably decreased intracellular ROS and JNK activation in INS-1 cells,while the level of PDX-1 protein was in-creased markedly (P<0.05 or P<0.01 ).Conclu-sion Sal B is capable of ameliorating IHG-induced cell injury and apoptosis in INS-1 cells,which might be derived from suppression of JNK activation and up-regulation of PDX-1 protein expression.

Background/Aims: Acute-on-chronic liver failure (ACLF) is a catastrophic illness. Few studies investigated the prognostic value of vitamin D-binding protein (VDBP) for hepatitis B virus (HBV)-related ACLF (HBV-ACLF) resulted in conflicting results. Methods: Two prospective HBV-ACLF cohorts (n=287 and n=119) were enrolled to assess and validate the prognostic performance of VDBP. Results: VDBP levels in the non-survivors were significantly lower than in the survivors (P<0.001). Multivariate Cox regression demonstrated that VDBP was an independent prognostic factor for HBV-ACLF. The VDBP level at admission gradually decreased as the number of failed organs increased (P<0.001), and it was closely related to coagulation failure. The areas under the receiver operating characteristic curve (AUCs) of the Child-Pugh-VDBP and chronic liver failuresequential organ failure assessment (CLIF–SOFA)-VDBP scores were significantly higher than those of Child-Pugh (P<0.001) and CLIF-SOFA (P=0.0013). The AUCs of model for end-stage liver disease (MELD)-VDBP were significantly higher than those of MELD (P= 0.0384) only in the case of cirrhotic HBV-ACLF patients. Similar results were validated using an external multicenter HBV-ACLF cohort. By longitudinal observation, the VDBP levels gradually increased in survivors (P=0.026) and gradually decreased in non-survivors (P<0.001). Additionally, the VDBP levels were found to be significantly decreased in the deterioration group (P=0.012) and tended to be decreased in the fluctuation group (P=0.055). In contrast, they showed a significant increase in the improvement group (P=0.036). Conclusions The VDBP was a promising prognostic biomarker for HBV-ACLF. Sequential measurement of circulating VDBP shows value for the monitoring of ACLF progression.

Ferroptosis is a novel type of oxidatively regulated cell death driven by iron-dependent lipid peroxidation.As the main site of iron utilization and oxidative metabolism,mitochondria are the main source of intracellular reactive oxy-gen species.Ferroptosis is associated with the severe impairment of mitochondrial structure and function,bioenergetics,and metabolism.Alzheimer disease(AD)is a devastating progressive neurodegenerative disease with the main clinical manifestation of decline in memory and cognitive function.Emerging evidence suggests that mitochondrial dysfunction plays a significant role in the process of ferroptosis in AD.This article elaborates on the mechanism of ferroptosis,mito-chondrial dysfunction and its role in ferroptosis in AD,and the treatment of AD,in order to provide a new perspective for exploring new strategies for the prevention and treatment of AD.