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Aim: Investigate the prevalence of irritable bowel syndrome (IBS) after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and assess the association between IBS and SARS-CoV-2 infection. Methods: A systematic literature search for PubMed, Web of Science, Embase, Scopus, and the Cochrane Library was performed to identify all reports published before 31 December 2022. The confidence interval (CI), estimation effect (ES) of prevalence, and risk ratios (RR) were calculated to evaluate the prevalence of IBS after SARS-CoV-2 infection and their association. Individual results were pooled by the random-effects (RE) model. Subgroup analyses conducted a further investigation of the results. We employed funnel plots, Egger’s test, and Begg’s test to evaluate publication bias. Sensitivity analysis was performed for the assessment of the robustness of the result. Results: The data on IBS prevalence after SARS-CoV-2 infection were extracted from two cross-sectional studies and ten longitudinal studies from nineteen countries with 3950 individuals. The IBS prevalence after SARS-CoV-2 infection ranges from 3% to 91% in different countries, and the overall pooled prevalence of IBS following SARS-CoV-2 infection is 15% (ES: 0.15; 95% CI, 0.11–0.20; p = 0.000). The data on the association between IBS and SARS-CoV-2 infection were extracted from six cohort studies from fifteen countries with 3595 individuals. The risk of IBS increased following SARS-CoV-2 infection but was not significant (RR: 1.82; 95% CI, 0.90–3.69; p = 0.096). Conclusions: In conclusion, the overall pooled prevalence of IBS following SARS-CoV-2 infection was 15%, and SARS-CoV-2 infection increased the overall risk of IBS but was not statistically significant. Further extra high-quality epidemiological evidence and studies to clarify the underlying mechanism of IBS following SARS-CoV-2 infection are needed.

Nowadays, the relationship between Helicobacter pylori infection (HPI) and irritable bowel syndrome (IBS) remains controversial. Objective: The aim of this study is to investigate the relationship between HPI and IBS through a systematic review and meta-analysis based on the current evidence. Methods: We performed a systematic literature search in electronic databases (PubMed, EMBASE, and the Cochrane library) by computer to identify all reports published before 8 August 2021. The odds ratio (OR) and confidence interval (CI) were calculated to evaluate the association between HPI and IBS. Subgroup analyses were conducted for further assessment and exploration of heterogeneity sources. In addition, we assessed publication bias through funnel plots, Egger’s test, and Begg’s test. Finally, we conducted a sensitivity analysis to evaluate the robustness of the results. Results: Thirteen studies with 13,173 participants were included in the meta-analysis. The pooled OR of the association between HPI and IBS was 1.03 (95% CI [0.80,1.31]; p = 0.84). The adjusted OR of the association between HPI and IBS after excluding the studies with confounding factors defined by our team was 1.29 (95% CI [1.03,1.62]; p = 0.03). We found a positive association between HPI and IBS-D (diarrhea subtype) (OR: 1.54; 95% CI [1.22,1.95]; p = 0.0003). The OR of the relationship between cytotoxin-associated gene A (Cag A) positive HPI and IBS was 4.3 (95% CI [0.51,36.17]; p = 0.18). Conclusions: The likelihood of HPI in IBS patients is relatively higher than that of non-IBS participants but not statistically significant, implying that HPI is not significantly associated with IBS, albeit we may underestimate this association. Moreover, we found a positive association between HPI and IBS-D. We also observed an increased likelihood of Cag-A positive HPI in IBS patients than that of non-IBS participants but not statistically significant.

Background: Low-frequency noise may cause changes in cognitive function. However, there is no established consensus on the effect of low-frequency noise on cognitive function. Therefore, this systematic review and meta-analysis aimed to explore the relationship between low-frequency noise exposure and cognitive function. Methods: We conducted a systematic review and identified original studies written in English on low-frequency noise and cognition published before December 2022 using the PsycINFO, PubMed, Medline, and Web of Science databases. The risk of bias was evaluated according to established guidelines. A random-effects meta-analysis was performed where appropriate. To explore the association between low-frequency noise exposure and cognitive function, we reviewed eight relevant studies. These studies covered cognitive functions grouped into four domains: attention, executive function, memory, and higher-order cognitive functions. The data extraction process was followed by a random-effects meta-analysis for each domain, which allowed us to quantify the overall effect. Results: Our analysis of the selected studies suggested that interventions involving low-frequency noise only had a negative impact on higher-order cognitive functions (Z = 2.42, p = 0.02), with a standardized mean difference of -0.37 (95% confidence interval: -0.67, -0.07). A moderate level of heterogeneity was observed among studies (p = 0.24, I2 = 29%, Tau2 = 0.03). Conclusions: Our study findings suggest that low-frequency noise can negatively impact higher-order cognitive functions, such as logical reasoning, mathematical calculation, and data processing. Therefore, it becomes important to consider the potential negative consequences of low-frequency noise in everyday situations, and proactive measures should be taken to address this issue and mitigate the associated potential adverse outcomes. [ABSTRACT FROM AUTHOR]

Methylenetetrahydrofolate reductase (MTHFR) is a critical rate-limiting enzyme in the homocysteine/methionine metabolism pathway that is implicated in the pathogenesis and progression of autoimmune diseases. Previous association studies have been performed to investigate the effect of polymorphisms in MTHFR on the risk of autoimmune diseases with inconsistent results. Therefore, this meta-analysis was designed to assess the association between the MTHFR 677 C/T and 1298 A/C polymorphisms and the susceptibility to autoimmune diseases. We identified reports by a literature search in the following electronic databases: PubMed, Ovid, Web of science, and China National Knowledge Infrastructure. Statistical analyses of the summary odds ratios (ORs) and 95% confidence intervals (CIs) were done using STATA software. In a recessive genetic model, the MTHFR 677 C/T polymorphism was associated with an increased risk of Behcet's disease (OR = 1.97 , 95% CI, 1.31-2.97), multiple sclerosis (OR = 1.57 , 95% CI, 1.03-2.38), and ankylosing spondylitis (OR = 2.90 , 95% CI, 1.92-4.38). The MTHFR 1298 A/C polymorphism was associated an increased risk of multiple sclerosis in a heterozygote comparison (OR = 2.36 , 95% CI, 1.29-4.30) and in a dominant model (OR = 2.31 , 95% CI, 1.24-4.29). This meta-analysis demonstrated that the MTHFR 677 C/T was a risk factor for Behcet's disease, multiple sclerosis, and ankylosing spondylitis, and the 1298 A/C was a risk factor for multiple sclerosis. [ABSTRACT FROM AUTHOR]