Cholelithiasis increased prostate cancer risk: evidence from a case-control study and a meta-analysis.

INTRODUCTION: Cholelithiasis represents a known risk factor for digestive system neoplasm. Few studies reported the association between cholelithiasis and the risk of prostate cancer (PCa), and the results were controversial. METHODS: We reviewed the medical records of the Second Affiliated Hospital of Chongqing Medical University Hospital to perform a retrospective matched case-control study, which included newly diagnosed 221 PCa patients and 219 matched controls. Logistic regression was applied to compare cholelithiasis exposure and adjusted for confounding factors. Additionally, we conducted a meta-analysis pooling this and published studies further to evaluate the association between cholelithiasis and PCa risk. Related ratio (RR) and 95% confidence interval (95%CI) were used to assess the strength of associations. RESULTS: Our case-control study showed that cholelithiasis was associated with a higher incidence of PCa (OR = 1.87, 95% CI: 1.06-3.31) after multivariable adjustment for covariates. The incidence of PCa was increased in patients with gallstones but not cholecystectomy. 7 studies involving 80,403 individuals were included in the meta-analysis. Similarly, the results demonstrated that cholelithiasis was associated with an increased risk of PCa (RR = 1.35, 95%CI: 1.17-1.56) with moderate-quality evidence. Cholelithiasis patients with low BMI increased the PCa incidence. Moreover, Subgroup analysis based on region showed that cholelithiasis was associated with PCa in Europe (RR = 1.24, 95%CI 1.03-1.51) and Asia (RR = 1.32, 95%CI 1.24-1.41). CONCLUSIONS: The results suggested an association between cholelithiasis and the risk of PCa. There was no significant relationship between cholecystectomy therapy and PCa risk. Further cohort studies should be conducted to demonstrate the results better.

Association between male infertility and the risk of hypertension: A meta-analysis and literature review.

To explore the association between male infertility and hypertension risk, a meta-analysis and systematic review was conducted. Observational studies were sought in Medline, PubMed, EMBASE, Web of Science, and China National Knowledge Infrastructure up to April 30, 2021. Two independent reviewers selected available studies and extracted the data. The association between male infertility and hypertension risk was estimated by calculating the relative risk (RR) and 95% confidence interval (95% CI) using Stata12.0 statistical software. A total of seven studies were included in this meta-analysis, including 102,152 patients and 636,645 healthy individuals. The results demonstrated that male infertility was significantly associated with increased hypertension incidence (RR = 1.08; 95% CI 1.02-1.14; p = 0.004), with moderate-quality evidence. A subgroup analysis based on region showed that a positive association was observed in Europe but not the United States or Asia. This positive association was further confirmed in a cohort study, but not in a case-control study. After adjusting for potential confounders, male infertility was still significantly associated with hypertension risk (RR = 1.06, 95% CI 1.03-1.09). In conclusion, our findings suggest that male infertility increases the risk of hypertension incidence. However, further studies are needed to provide more conclusive evidence.

Expression of LASS2 controlled by LAG1 or ADH1 promoters cannot functionally complement Lag1p.

LAG1 contributes to the substrate specificity and catalytic activity of ceramide synthases in Saccharomyces cerevisiae. Double deletion of LAG1 and its yeast homologue LAC1 results in the slow growth defect of the cell under certain genetic backgrounds. LASS2, containing the conserved TLC domain and the specific HOX domain, is a human homologue of Lag1p. In this study, shuffling tests and tetrad analyses were carried out to examine the complementation between Lag1p and LASS2 or its fragment containing the TLC domain but lacking the HOX domain (LASS2DeltaHOX). Controlled by either the natural weak LAG1 promoter or the strong yeast ADH1 promoter, LASS2 and LASS2DeltaHOX could not rescue the slow growth defect of double mutant. The results indicated that LASS2 or LASS2DeltaHOX could not functionally complement Lag1p.