A Janus adhesive hydrogel sheet for preventing postoperative tissue adhesion of intestinal injuries.

Although adhesive hydrogels represent an alternative to surgical sutures for non-invasive tissue wound sealing, those with indiscriminate adhesion fail to hold wounds while inhibiting postoperative tissue adhesion, thus limiting their application in intestinal repair. In this study, an asymmetric adhesive hydrogel sheet composed mainly of polyacrylic acid (PAA) and gelatin (GA) that can be wet-adhered to the surface of intestinal tissue was developed. One side of the GA-PAA hydrogel sheet was complexed with polyvinyl alcohol (PVA), which shielded the excess adhesion based on a physical barrier. Both sides of the PVA/GA-PAA hydrogel showed distinct adhesive and antiadhesive properties. Intriguingly, the anti-adhesive side showed significant anti-adhesion toward specific proteins. The results of animal experiments showed that the PVA/GA-PAA hydrogel could firmly adhere to the intestine to stop leakage and prevent post-operative tissue adhesion two weeks after surgery. The hematoxylin and eosin (H&E) staining results showed that the damaged intestinal serosa was repaired without tissue adhesion. It is believed that the controllable adhesion of the adhesive hydrogel offers better prospects for intestinal repair.

Causal analysis between gastroesophageal reflux disease and chronic rhinosinusitis.

BACKGROUND: Gastroesophageal reflux disease (GERD) and chronic rhinosinusitis (CRS) have been shown to be potentially closely related, but the relationship between these conditions, particularly the possibility of a causal link, is not fully understood. This study used Mendelian randomization (MR) to assess the causal relationship between these two disorders. METHODS: We extracted genome-wide association study data sets for GERD and CRS from publicly available gene summaries, and used MR to conduct a causal inference analysis. The main robustness test used in this study included MR-Egger regression, a leave-one-out sensitivity test, and multivariate MR (MVMR). RESULTS: GERD increased the risk of developing CRS by 36%, based on the inverse-variance weighted method, a statistically significant association (odds ratio [OR] 1.360, 95% confidence interval [CI] 1.179-1.568, P < 0.001). Other MR assessment methods, such as weighted median, simple mode, and weighted mode, similarly observed a significant increase in the risk of CRS occurrence (OR 1.434, 95% CI 1.186-1.734, P < 0.001; OR 1.927, 95% CI 1.166-3.184, P = 0.013; and OR 1.910, 95% CI 1.222-2.983, P = 0.006, respectively). No significant bias was found in the heterogeneity or pleiotropy tests (P = 0.071 and P = 0.700, respectively). Even after excluding possible mediators using MVMR, GERD appeared to significantly increase the risk of developing CRS (OR 1.013, 95% CI 1.008-1.023, P = 0.002). CONCLUSIONS: This study provides new, significant evidence that GERD is genetically associated with a higher incidence rate of CRS. However, further research is needed to elucidate the potential underlying biological mechanisms of this relationship.

Causal analysis between gastro-oesophageal reflux disease and obstructive sleep apnoea.

Background: Based on evidence from existing observational research, clarifying the causal relationship between gastro-oesophageal reflux disease (GORD) and obstructive sleep apnoea (OSA) is challenging. Here, Mendelian randomisation, a method based on genetics, was used to provide new evidence for causality. Methods: Summary statistics from two publicly available genome-wide association studies were used to evaluate the causal relationship between GORD and OSA (the GORD database was used as an exposure variable and the OSA database as an outcome). Inverse variance weighting was used as the main analytical tool in Mendelian randomisation to estimate causal effects. The robustness of the results was evaluated by sensitivity analysis. Possible mediators were evaluated using multivariate Mendelian randomisation. Results: A statistically significant causal relationship was observed between GORD and OSA (OR 1.597, 95% CI 1.401-1.821, p<0.001), and similar results were observed in weighted median and Mendelian randomisation-Egger regression analyses. No bias was found in the sensitivity analysis of Mendelian randomisation estimation. Multivariate Mendelian randomisation showed that GORD significantly increased the risk of developing OSA, even when the possible mediator was excluded (OR 1.107, 95% CI 1.101-1.212, p<0.001). Conclusion: Our study confirmed a causal relationship between GORD and OSA and suggests that intervention measures should be taken for patients with GORD to prevent the occurrence of OSA.