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Background Helicobacter pylori is an important carcinogenic factor in gastric cancer. Studies have shown that Helicobacter pylori infection is inversely associated with certain diseases such as esophageal cancer and whose infection appears to have a “protective effect.” At present, the relationship between Helicobacter pylori infection and esophageal cancer remains controversial. This study was designed to investigate the relationship between Helicobacter pylori infection and the risk of esophageal cancer in different regions and ethnicities. Methods Systematic search of the articles on the relationship between Helicobacter pylori infection and esophageal cancer from the database with the duration time up to December 2018. This systematic review was performed under the MOOSE guidelines. Results This meta-analysis included 35 studies with 345,886 patients enrolled. There was no significant correlation between Helicobacter pylori infection and esophageal squamous cell carcinoma in the general population (OR: 0.84; 95% CI: 0.64-1.09/OR: 0.74; 95% CI: 0.54-0.97). However, a significant correlation was found in the Middle East (OR: 0.34; 95% CI: 0.22-0.52/95% CI: 0.26-0.44). There was no significant difference in the prevalence of Helicobacter pylori between the case group and the control group in esophageal adenocarcinoma (8.87% vs. 9.67%). The pooled OR was 0.55 (95% CI: 0.43-0.70) or 0.23 (95% CI: 0.15-0.36). When grouped by match or not, the pooled OR of the nonmatching group and the matching group was 0.48/0.21 (95% CI: 0.36-0.65/95% CI: 0.13-0.36) and 0.73/0.71 (95% CI: 0.57-0.92/95% CI: 0.60-0.84), respectively. Conclusion In the general populations, no significant association was found between Helicobacter pylori infection and the risk of esophageal squamous cell carcinoma. However, lower risk was found in the Middle East. Helicobacter pylori infection may reduce the risk of esophageal adenocarcinoma, but such “protection effect” may be overestimated.

A common problem that arises in the meta-analysis of several studies, each with independent treatment and control groups, is to test for the homogeneity of effect sizes without the assumptions of equal variances of the treatment and the control groups and of equal variances among the separate studies. A commonly used test statistic, frequently denoted as Q, is the weighted sum of squares of the differences of the individual effect sizes from the mean effect size, with weights inversely proportional to the variances of the effect sizes. The primary contributions of this article are the presentation of improved and very accurate approximations to the distributions of the Q statistic when the effect size is a linear contrast such as the difference between the treatment and control means. Our improved approximation to the distribution of Q under the null hypothesis is based on a multiple of an F-distribution; its use yields a substantial reduction in the type I error rate of the homogeneity test. Our improved approximation to the distribution of Q under an alternative hypothesis is based on a shift of a chi-square distribution; its use allows for much greater accuracy in the computation of the power of the homogeneity test. These two improved approximate distributions are developed using the Welch methodology of approximating the moments of Q by the use of multivariate Taylor expansions. The quality of these approximations is studied by simulation. A secondary contribution of this article is a study of how best to combine the variances of the treatment and control groups (needed for the calculation of weights in the Q statistic). Our conclusion, based on simulations, is that use of pooled variances can result in substantially erroneous conclusions.

Aims: To profile and characterize the circular RNA (circRNA) expression pattern in poorly differentiated gastric adenocarcinoma (PDGA). Methods & materials: CircRNA expression profiles in PDGA and adjacent nontumor tissues were analyzed by microarray. Five randomly selected differentiated expressed circRNAs (DECs) were validated by real-time quantitative PCR. m6A qualification of the top 20 DECs was conducted by m6A-immunoprecipitation and real-time quantitative PCR. Results: A total of 65 DECs were found in PDGA compared with the control. Hsa_circRNA_0077837 had the largest area under the curve. Most DECs had m6A modifications, the trend of m6A modification alteration was mainly consistent with the circRNA expression level. Conclusion: Our study revealed a set of DECs and their m6A modification alterations, which may provide new insight for their potential function in PDGA.

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Background and AimHiatal hernia (HH) has been found in a large number of people, but there has been no unified way to diagnose it. The aim of this study was to compare the diagnostic efficiency of X‐ray, endoscopy, and high‐resolution manometry (HRM) in the diagnosis of HH using surgical diagnosis of HH as the gold standard.MethodsTwo biomedical databases (PubMed and EMBASE) were systematically searched through January 26, 2019. The pooled sensitivity, specificity, and area under the SROC curve (AUC) were calculated, and the AUC statistical significance was compared by Tukey's multiple comparisons test.ResultsA total of 5337 patients in seven articles were included. The pooled sensitivity, specificity, and AUC for X‐ray were 0.63 (0.46–0.77), 0.85 (0.69–0.94), and 0.80 (0.77–0.84), respectively, for diagnosing HH. The pooled estimates for endoscopy in diagnosing HH were as follows: sensitivity, 0.72 (0.39–0.91); specificity, 0.80 (0.70–0.87); and AUC, 0.82 (0.78–0.85). Similarly, the corresponding values for HRM were 0.77 (0.70–0.83); 0.92 (0.85–0.96), and 0.9527. Tukey's multiple comparisons tests were used to compare the AUCs of the three diagnostic methods: No significant differences were found between X‐ray and endoscopy (P = 0.7293), and HRM was superior to X‐ray (P = 0.0127) and endoscopy (P = 0.0442).ConclusionsHigh‐resolution manometry may exhibit a better diagnostic performance for hiatal hernia. In contrast, X‐ray and endoscopy may not be the best methods, and there was no significant difference in diagnostic efficiency between the X‐ray and endoscopy.

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Background: This study aimed to systematically analyze the association between long-term use of proton pump inhibitors (PPIs) and the risk of gastric cancer (GC).Methods: We performed a systematic search of articles on the relationship between long-term use of PPIs and the risk of GC from PubMed and EMBASE. We calculated the pooled odds ratio of GC in PPI users compared to non-PPI users using randomeffects models.Results: This meta-analysis included 18 studies from 20 different databases with 4348,905 patients enrolled. In the random effects model, we found that an increased risk of GC among PPI users (OR = 1.94; 95% CI [1.43, 2.64]). The long-term use of PPIs compared with histamine-2 receptor antagonist users did not increase the risk of GC (OR = 1.65; 95% CI [0.92, 2.97]). Stratified analysis showed that PPI users had a significantly increased risk of noncardia GC (OR = 2.53; 95% CI [2.03, 3.15]), but had a relatively small relationship with the risk of gastric cardia cancer. (OR = 1.79; 95% CI [1.06, 3.03]). With the extension of PPI use time, the estimated risk value decreases (<1 year: OR = 6.33, 95% CI [3.76, 10.65]; 1-3 years: OR = 1.82, 95% CI [1.30, 2.55]; >3 years: OR = 1.25, 95% CI [1.00, 1.56]). Despite Helicobacter pylori eradication, the long-term use of PPIs did not alter the increased risk of GC (OR = 2.29; 95% CI [1.57, 3.33]). Conclusion:Our meta-analysis found that PPI use may be associated with an increased risk of GC. Further research on the causal relationship between these factors is necessary.