Prophylactic transanal drainage tube placement for preventing anastomotic leakage after anterior resection for rectal cancer: A meta-analysis.

AIM: The aim was to evaluate the efficacy of transanal drainage tube (TDT) placement for preventing anastomotic leakage after low anterior resection for rectal cancer. METHOD: PubMed, the Cochrane Central Register of Controlled Trials, Embase and ClinicalTrials.gov databases were searched up to October 2021. Studies comparing outcomes following low anterior resection with or without TDT were included. The primary outcomes measured were anastomotic leakage rate, reoperation rate and anastomotic bleed rate. RESULTS: Three randomized controlled trials (RCTs) and 16 observational studies (prospective or retrospective) involving 4560 patients satisfied the basic inclusion criteria. In RCTs, a TDT was associated with no statistically significant differences in anastomotic leakage (OR = 0.67, 95% CI 0.42-1.05, P = 0.08), reduction in reoperation (OR = 0.11, 95% CI 0.03-0.51, P = 0.004) and increased anastomotic bleeding rate (OR = 2.36, 95% CI 1.11-5.01, P = 0.03). In observational studies, a TDT was associated with significant reduction in anastomotic leak (OR = 0.44, 95% CI 0.30-0.64, P < 0.0001) and reoperation (OR = 0.47, 95% CI 0.33-0.69, P < 0.0001), with no statistically significant differences in anastomotic bleeding (OR = 1.30, 95% CI 0.20-8.30, P = 0.78). CONCLUSION: In RCTs, a TDT for rectal cancer was correlated with no detectable differences in anastomotic leakage and with an increased risk of anastomotic bleeding. In observational studies, a TDT was correlated with reduction in anastomotic leakage and no detectable differences in anastomotic bleeding. Both RCTs and observational studies demonstrated a comparable reduction in reoperation rate with TDT. These data in aggregate indicated that TDTs may not show superiority but emphasized differences between RCT and observational data.

TRIM38 protects H9c2 cells from hypoxia/reoxygenation injury via the TRAF6/TAK1/NF-κB signalling pathway.

Tripartite motif (TRIM) 38 is a ubiquitin E3 protein ligase that is involved in various intracellular physiological processes. However, the role of TRIM38 in myocardial ischaemia/reperfusion (I/R) injury remains to be elucidated. We aimed to establish an in vitro cellular hypoxia/reperfusion (H/R) model to explore the role and potential mechanisms of TRIM38 in H9c2, a rat cardiomyoblast cell line. Recombinant adenoviruses for silencing or overexpressing TRIM38 were constructed and transfected into H9c2 cells. Western blotanalysisshowed that TRIM38 expression was significantly decreased after H/R injury. Functionally, TRIM38 expression relieved inflammatory responses and oxidative stress, and inhibited H/R-induced apoptosis in H9c2 cells. Mechanistically, TRIM38 overexpression inhibited H/R-induced transforming growth factor beta-activated kinase 1 (TAK1)/nuclear factor-kappa B (NF-κB) pathway activity in H9c2 cells. The opposite results were observed after TRIM38 knockdown. Furthermore, H/R-induced injury aggravated by TRIM38 deficiency in H9c2 cells was reversed upon treatment with 5Z-7-oxozeaenol, a TAK1 inhibitor. Therefore, TRIM38 reduction attenuated the anti-apoptotic capacity and anti-inflammatory potential of H/R-stimulated H9c2 cells by activating the TAK1/NF-κB signalling pathway. Specifically, TRIM38 alleviated H/R-induced H9c2 cell injury by promoting TNF receptor-associated factor 6 degradation, which led to the inactivation of the TAK1/NF-κB signalling pathway. Thus, our study provides new insights into the molecular mechanisms underlying H/R-induced myocardial injuries.