Hepatic encephalopathy (HE) is caused by severe liver disease or portal shunt. Metabolic disorders and central nervous system dysfunctions are the main symptoms of this syndrome. Ammonia is considered to play a central role in the pathogenesis of HE. Helicobacter pylori (H. pylori) have been suggested as a possible source of ammonia production because of its high urease content. However, the relationship between H.pylori and blood ammonia and HE, as well as the therapeutic effect of H.pylori eradication on HE, is inconclusive, and the results are full of contradictions. The aim of this review is to summarize current knowledge on the association of H. pylori with HE and to address the question of whether H. pylori eradication may be beneficial in the management of HE.

Objective To evaluate the effect of mefformin on the human keratinocyte line HaCaT,and to explore its molecular mechanism.Methods HaCaT cells were divided into several groups to be treated with mefformin at different concentrations of 1,2,5,10,20,50 mmol/L for 24,48 and 72 hours.Cell counting kit-8 (CCK-8) assay was performed to evaluate the effect of metformin on the survival rate of HaCaT cells.After 48-hour treatment with metformin at concentrations of 0 (control group),0.5,1,2,5,10 mmol/L,flow cytometry was conducted to evaluate the effect of metformin on cell cycle and apoptosis.Western blot analysis was performed to determine the expression of cell proliferation-and differentiation-related proteins (keratin-16 [K16],K17,K1,involucrin),apoptosis-related proteins (Bax,Bcl-2) and AKT/mTOR/STAT3 pathway proteins.Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the levels of interleukin (IL)-8,tumor necrosis factor (TNF)-α and IL-23 (inflammatory factors) in the culture supernatant of HaCaT cells.Statistical analysis was carried out with SPSS19.0 software using one-way analysis of variance for comparison of the above indices among the 0.5-,1-,2-,5-,10-mmol/L metformin groups and control group,repeated measures analysis of variance for comparisons among different time points or different metformin groups,least significant difference (LSD)-t test for multiple comparisons.Results CCK-8 assay showed that mefformin had inhibitory effects on the proliferation of HaCaT cells (F =116.87,P ＜ 0.05),and the cell survival rates gradually decreased along with the increase in the concentrations of mefformin.After 48-hour treatment with mefformin at concentrations of 0,0.5,1,2,5,10mmol/L,the proportion of HaCaT cells in G2/M phase gradually increased (5.55％ ± 1.03％,6.37％ ±0.93％,8.57％ ± 1.18％,10.05％ ± 0.60％,10.76％ ± 0.87％,13.63％ ± 1.41％,respectively,F =24.98,P ＜0.05),and the early apoptosis rate also gradually increased (0.78％ ± 0.71％,19.18％ ± 1.41％,25.67％ ±1.34％,28.45％ ± 0.92％,34.97％ ± 2.12％,40.41％ ± 1.49％,respectively,F =296.08,P ＜ 0.05).Along with the increase in the concentrations of metformin,there were increasing trends in the expression of K1 and the pro-apoptotic protein Bax (F =8.86,5.38 respectively,both P ＜ 0.05),while there were decreasing trends in the expression of K16,K17 and the apoptotic protein Bcl-2 (F =8.02,4.82,12.10 respectively,all P ＜ 0.05).There was no significant difference in the expression of involucrin among different metformin groups (F =0.57,P ＞ 0.05).After 48-hour treatment with mefformin at different concentrations,the levels of IL-8 and TNF-α in HaCaT cells significantly decreased (F =33.89,14.99 respectively,both P ＜0.05),while there was no significant change in the IL-23 level (F =2.12,P ＞ 0.05).Along with the increase in the concentrations of metformin,the expression of p-AKT,p-mTOR and p-STAT3 significantly decreased (F =11.38,0.35,4.38 respectively,all P ＜ 0.05),but there were no significant changes in the protein expression of AKT,mTOR and STAT3 (F =0.66,0.35,4.24 respectively,all P ＞ 0.05).Conclusion Metformin can inhibit the proliferation,promote the differentiation and apoptosis of HaCaT cells,and inhibit the secretion of inflammatory factors by regulating the AKT/mTOR/STAT3 signaling pathway.

Autoimmune atrophic gastritis (AAG) is a slowly progressive, immune‐mediated disorder with unspecific and subtle clinical manifestations. With the widespread use of endoscopy, especially the progression of early gastric cancer screening, it has increased awareness that AAG is a pre‐neoplastic condition, predisposing to the development of both type 1 neuroendocrine tumors and gastric adenocarcinoma. The diagnosis of AAG is based on distinctive endoscopic and histological features and serum intrinsic factor and/or parietal cell autoantibody positivity, which is challenging due to its wide clinical spectrum-ranging from a symptomless to a disabling disease course. This article summarizes the research progress of AAG in recent years, analyzes the reasons for delayed diagnosis of AAG, and proposes coping strategies.

Objective: To investigate the efficacy and safety of lobaplatin (LBP) plus S-1 for advanced gastric cancer (AGC) and determine the potential role of circulating tumor cells (CTC) for predicting the therapeutic response and prognosis. Methods: From January 2014 to February 2015, 64 consecutive patients with AGC received lobaplatin plus S-1 chemotherapy in Liaocheng People′s Hospital. The clinical features, clinical response, adverse effects, prognosis and CTC pre- and post-treatment were retrospectively analyzed. The correlation between CTC and patients′ disease control rate (DCR), objective response rate (ORR), progression free survival (PFS) as well as overall survival (OS) were investigated. Results: All 64 patients completed 2 cycles of chemotherapy.The number of patients who achieved complete regression, partial regression, stable and progression were 0, 24 (37.5%), 18 (28.1%) and 22 (34.4%), respectively. ORR was 37.5% and DCR was 65.6%. The median PFS was 10.8 months(95%CI 7.1-12.0) and the median OS was 16.1 months(95%CI 12.4-18.8). The ORR and PFS were not significantly different between patients with baseline CTC≥2 and CTC<2 (25.0% vs 53.6%, P=0.150; 6.2 months vs 7.5 months, P=0.780), while the DCR and OS were significantly different (45.9% vs 90.0%, P=0.008; 10.5 months vs 17.2 months, P<0.001). After 2 cycles of chemotherapy, the ORR and DCR in patients with CTC≥2 were 16.7% and 45.9%, respectively, which were significantly lower than those observed in patients with CTC<2 (50.0% and 90.0%, respectively). The former also had shorter median PFS and OS (6.6 months vs 8.9 months, 8.4 months vs 15.0 months, respectively). Patients with persistently CTC<2 or those exhibiting an conversion to CTC<2 following chemotherapy had an improved PFS and OS, while patients with persistently CTC≥2 or those exhibiting an conversion to CTC≥2 following therapy had shorter PFS and OS.The most frequent adverse effects were grade 1 or 2 gastrointestinal discomfort and myelosuppression. No patients discontinued chemotherapy because of adverse events. Conclusions Lobaplatin plus S-1 had manageable safety profile and promising antitumor activity in patients with AGC. CTC could be used as a biomarker in evaluating therapeutic response and predicting their prognosis.