Cholelithiasis was the main etiology in Jiangxi, China, and hyperlipidemia ranked second. There were different etiological proportion according to age, sex, and severity. Furthermore, the higher mortality rate occurred in severe idiopathic and hyperlipidemic pancreatitis, although there was no clear association between mortality and age.

No abstract

Background The eradication of Helicobacter pylori (H pylori) has been suggested to reduce the risk of gastric cancer, but its impact on the gut microbiota has attracted public attention. This study aimed to investigate the short‐term and long‐term effects of bismuth quadruple therapy on both gastric and fecal microbiota. Methods Ten asymptomatic young adults with H pylori‐related gastritis were treated with bismuth quadruple therapy for 14 days, and 7 age‐matched adults without H pylori infection were enrolled as healthy controls. Both fecal and gastric mucosa samples were collected from H pylori‐positive patients at weeks 0, 6, and 26, while fecal samples were collected from healthy controls. The gastric and gut microbiota were analyzed by 16S rRNA gene sequencing. Results The structure of the gastric microbiota was significantly changed after the eradication of H pylori with increased alpha diversity over time. The relative abundance of H pylori sharply decreased from more than 70% to nearly 0% after treatment, while some beneficial bacteria, such as Lactobacillus and Bifidobacterium, were increased. The microbial diversity of gut microbiota was higher in H pylori‐infected patients than in healthy controls, which tended to decrease after eradication. The potentially beneficial gut bacteria Blautia and Lachnoclostridium were enriched at week 26 compared to week 0, while the pathogenic Alistipes were depleted to a level close to that of the healthy controls. Conclusions Bismuth quadruple therapy for H pylori eradication can restore the diversity of gastric microbiota with enrichment of beneficial bacteria. The composition of gut microbiota after H pylori eradication trends toward healthy status instead of becoming dysbiotic.

BackgroundHelicobacter pylori (H. pylori) delivers oncoprotein CagA into gastric epithelial cells via the T4SS and drives activation of multiple oncogenic signalling pathways. YAP, a core effector of the Hippo tumour suppressor pathway, is frequently overexpressed in human cancers, suggesting its potential tumor-promoting role. Although CagA is a casual factor in H. pylori induced gastric carcinogenesis, the link between CagA and YAP pathway has not been identified. In this work, we investigated the regulation of oncogenic YAP pathway by H. pylori CagA.MethodsExpression of YAP and E-cadherin protein in human gastric biopsies were assessed by immunohistochemistry. H. pylori PMSS1 cagA− isogenic mutant strains were generated. Gastric epithelial cells were co-cultured with H. pylori wild-type cagA+ strains or isogenic mutants and were also treated by recombinant CagA expression. Immunofluorescence was performed for YAP localization. Immunoblot and quantitative PCR were performed for examining levels of YAP, downstream effectors and markers of epithelial-mesenchymal transition. Verteporfin and siRNA silencing were used to inhibit YAP activity.ResultsYAP is significantly upregulated in human gastric carcinogenesis. We generated PMSS1 CagA isogenic mutant strains with chloramphenicol resistance successfully. Our analysis indicated that H. pylori infection induced YAP and downstream effectors in gastric epithelial cells. Importantly, knockout of CagA in 7.13 and PMSS1 strains reduced the expression of YAP by H. pylori infection. Moreover, Inhibition of YAP suppressed H. pylori infection-induced Epithelial-mesenchymal transition (EMT).ConclusionOur results indicated that H. pylori CagA as a pathogenic protein promotes oncogenic YAP pathway, which contributes to EMT and gastric tumorigenesis. This study provided a novel mechanistic insight into why cagA+ H. pylori infection is associated with a higher risk for the development of gastric cancer.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0962-5) contains supplementary material, which is available to authorized users.

PurposeAcute pancreatitis in pregnancy (APIP) is a rare condition; however, it markedly affects maternal and fetal health. This study aimed to describe the types, clinical characteristics, mortality, and the safety and necessity of gestation termination of acute pancreatitis in pregnancy (APIP).MethodsWe retrospectively reviewed 121 APIP cases in the Gastroenterology Department of The First Affiliated Hospital of Nanchang University. APIP diagnosis were based on 2012 Atlanta Criteria. The correlation between APIP types, severity, biochemical parameters and mortality was analyzed.ResultsThe most common symptoms for APIP were abdominal pain (86.8%) and vomiting (73.6%). The most common causes for APIP were gallstone (36.4%) and hypertriglyceridemia (32.2%) and hypertriglyceridemic APIP was correlated with a higher rate for local complication (P = 0.012). Serum calcium level was negatively correlated with the severity of APIP (P < 0.01). The overall maternal and fetal mortality rate were 3.3% (4/121) and 11.6% (14/121), respectively. The severity of APIP was significantly correlated with higher risks for maternal and fetal death (P < 0.01). 72.7% of moderate-to-severe APIP patients underwent Cesarean section to terminate gestation safely.ConclusionThe most common causes of APIP were gallstone and hypertriglyceridemia. Lower level of serum calcium could be used as an indicator for the severity of the APIP. The severity of APIP was associated with higher risk for neonate asphyxia, and maternal and fetal death.

Accumulating evidence suggests that high-fat diet (HFD) induced metabolic disorders are associated with dysbiosis of gut microbiota. However, no study has explored the effect of HFD on the gastric microbiota. This study established the HFD animal model to determine the impact of HFD on the gastric microbiota and its relationship with the alterations of gut microbiota. A total of 40 male C57BL/6 mice were randomly allocated to receive a standard chow diet (CD) or HFD for 12 weeks (12CD group and 12HFD group) and 24 weeks (24CD group and 24HFD group) (n = 10 mice per group). Body weight and length were measured and Lee’s index was calculated at different time points. The insulin sensitivity and serum levels of metabolic parameters including blood glucose, insulin and lipid were also evaluated. The gastric mucosa and fecal microbiota of mice were characterized by 16S rRNA gene sequencing. The body weight was much heavier and the Lee’s index was higher in 24HFD group than 12HFD. The insulin resistance and serum level of lipid were increased in 24HFD group compared to 12HFD, indicating the aggravation of metabolic disorders as HFD went on. 16S rRNA gene sequencing showed dysbiosis of gastric microbiota with decreased community diversity while no significant alteration in gut microbiota after 12 weeks of HFD. The phyla Firmicutes and Proteobacteria tended to increase whereas Bacteroidetes and Verrucomicrobia decrease in the gastric microbiota of 12HFD mice compared to 12CD. Moreover, a remarkable reduction of bacteria especially Akkermansia muciniphila, which has beneficial effects on host metabolism, was observed firstly in the stomach of 12HFD group and then in the gut of 24HFD group, indicating the earlier alterations of microbiota in stomach than gut after HFD. We also found structural segregation of microbiota in the stomach as well as gut between 12HFD and 24HFD group, which is accompanied by the aggregation of metabolic disorders. These data suggest that HFD affects not only gut microbiota but also gastric microbiota and the disruption of microbial ecosystem in the digestive tract may play a part in the development and progression of metabolic diseases although molecular mechanism requires further investigation.

No abstract

Phosphorylation of PTEN at residues Ser380/Thr382/383 leads to loss of phosphatase activity and tumor suppressor function. Here, we found that phosphorylation of PTEN at residues Ser380/Thr382/383 was increased with gastric carcinogenesis, and more importantly, Helicobacter pylori was a trigger of this modification in chronic non-atrophic gastritis. H. pylori could phosphorylate and inactivate PTEN in vivo and in vitro, resulting in survival of gastric epithelial cells. Furthermore, stable expression of dominant-negative mutant PTEN or inhibition of Akt prevented the enhanced survival induced by H. pylori. These results indicate that PTEN phosphorylation at residues Ser380/Thr382/383 is a novel mechanism of PTEN inactivation in gastric carcinogenesis, and H. pylori triggers this modification, resulting in activation of the PI3K/Akt pathway and promotion of cell survival.