BACKGROUND:Few studies have investigated the association between diabetes mellitus and risk of anal cancer and the results to date have been inconsistent. We analysed the relation between a history of diabetes and diabetic retinopathy and risk of anal cancer in a nationwide cohort in Taiwan. METHODS:Data from a retrospective cohort study of 5.9 million Taiwanese men and women aged 18-90 years were used for the analysis. Multivariable proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between diabetes diagnosis and diabetic retinopathy and risk of anal cancer. RESULTS:During a mean of 7.8 years follow-up, 2315 anal cancer cases occurred. The HRs (95% CIs) of anal cancer among persons with compared to those without a history of diabetes mellitus was 1.04 (0.95-1.13), and for persons with diabetic retinopathy vs. no diabetic retinopathy was 1.52 (1.20-1.92) and proliferative diabetic retinopathy vs. no proliferative diabetic retinopathy was 1.78 (1.27-2.50), respectively. CONCLUSION:This large-scale cohort study provides evidence of no clear association between diabetes mellitus and anal cancer risk overall, however, there was indication of increased risk among persons with diabetic retinopathy and proliferative diabetic retinopathy. Additional large-scale cohort studies with more comprehensive risk factor data are needed to further clarify these findings.
Background and Objectives: Sclerostin or dickkopf-1 (DKK1) inhibits the canonical Wnt/β-catenin signaling pathway, which regulates vascular calcification and may contribute to the development of arterial stiffness. The brachial–ankle pulse wave velocity (baPWV) measures peripheral arterial stiffness (PAS). This study aimed to investigate the correlation between sclerostin and DKK1 levels and PAS in patients with type 2 diabetes mellitus (T2DM). Materials and Methods: Biochemical data and sclerostin and DKK1 levels were analyzed in the fasting blood samples of 125 patients with T2DM. baPWV measurements using the VaSera VS-1000 automatic pulse wave analyzer classified patients with values > 18.0 m/s on either side into the PAS group. Results: Among patients with T2DM, 47 (37.6%) were classified as having PAS. These patients exhibited higher hypertension prevalence (p = 0.002); greater age (p < 0.001); elevated systolic (p < 0.001) and diastolic blood (p = 0.012) pressures; and increased fasting glucose (p = 0.001), glycated hemoglobin (p = 0.008), triglyceride (p = 0.001), blood urea nitrogen (p < 0.001), and creatinine (p = 0.001) levels, urine albumin-to-creatinine ratio (p = 0.039), and C-reactive protein (p = 0.024) and serum sclerostin (p < 0.001) levels, but decreased estimated glomerular filtration rate (p < 0.001). Multivariate logistic regression analysis identified serum sclerostin level (odds ratio, 1.127; 95% confidence interval, 1.058–1.200; p < 0.001) as an independent PAS predictor in patients with T2DM. Serum log-transformed sclerostin levels were positively correlated with left (p = 0.005) and right (p = 0.001) baPWV via Spearman’s rank-order correlation coefficient analysis. Conclusions: Serum sclerostin levels, but not DKK1 levels, are positively correlated with PAS in patients with T2DM.
PURPOSE:To evaluate the longitudinal changes in corneal epithelial thickness after FS-LASIK, keratorefractive lenticule extraction (KLEx), and transepithelial photorefractive keratectomy (tPRK). SETTING:Multicenter, international. DESIGN:Systematic review and meta-analysis. METHODS:This study was registered with International Platform of Registered Systematic Review and Meta-Analysis Protocols (INPLASY202510085). A systematic search of electronic databases was conducted through January 2025 in accordance with PRISMA guidelines. Studies reporting both baseline and postoperative corneal epithelial thickness in myopic eyes treated with FS-LASIK, KLEx, or tPRK were included. Data from 33 studies (n = 2579 eyes) were extracted, with 23 studies incorporated into the meta-analysis. Meta-regressions were performed to identify predictors of epithelial thickness changes. RESULTS:FS-LASIK-treated eyes exhibited a central epithelial thickness increase of 3.31 ± 0.75 μm at 1 month, further increasing to 4.58 ± 0.72 μm at 6 months. KLEx resulted in central thickening of 2.51 ± 0.28 μm at 1 month and 3.82 ± 0.35 μm at 6 months. By contrast, tPRK eyes initially demonstrated epithelial thinning, followed by central thickening reaching 3.89 ± 0.38 μm at 6 months. Meta-regression analyses indicated that each additional diopter of myopic correction was associated with 1.05 μm greater central epithelial thickening in FS-LASIK and 1.04 μm in KLEx at 3 months postoperatively. In addition, an increase in the programmed optical zone (OZ) corresponded to a reduction in postoperative epithelial thickness. CONCLUSIONS:Distinct epithelial remodeling patterns were observed: rapid, early thickening and stabilization with FS-LASIK and KLEx vs delayed regeneration with tPRK. Baseline spherical equivalent and programmed OZ were predictors of corneal epithelial thickness changes, suggesting procedure-specific remodeling profiles that may support future refinement of refractive planning.
Titanium dioxide nanoparticles (TiO2-NPs) are widely produced and persist in aquatic ecosystems, yet their indirect effects on host-microbe interactions remain poorly defined. By using zebrafish (Danio rerio) as a sentinel species, this study investigated the effects of subchronic 5 mg/L TiO2-NP exposure. Dynamic light scattering was utilized to characterize the bimodal aggregates (peaks at 917 and 46,841 nm; surface charge: +22.08 mV) that define the environmental state of TiO2-NPs. Parallel 16S rRNA metagenomic profiling on Day 6, prior to mortality, revealed profound gut dysbiosis. A marked increase in Chao1 richness (p < 0.01), alongside a catastrophic 333-fold reduction in beneficial Cetobacterium and an 856-fold enrichment of pathogenic Mycobacterium, was observed. Beta-diversity and hierarchical clustering analyses revealed a striking convergence between gut and gill microbial signatures, supporting a gut-to-gill translocation model. These results suggest that TiO2-NPs exposure induces intestinal dysbiosis, facilitating opportunistic bacterial migration via internal (gut-blood-gill) or external (fecal-water-gill) pathways. This study identifies dysbiosis-driven secondary infection as a novel, overlooked mechanism of nanoparticle toxicity, necessitating a shift in ecological risk assessments toward host-microbe interactions.
Abstract Background Although diabetes mellitus has been associated with increased risk of several cancers, evidence in relation to vulvar and vaginal cancers has been limited and inconsistent. We investigated the association between diabetes and the risk of vulvar and vaginal cancer risk in a nationwide cohort of 2.8 million women in Taiwan. Methods A retrospective cohort study of 2.8 million women with and without diabetes mellitus aged 18–90 years was conducted. Multivariable proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between diabetes diagnosis and the risk of vulvar and vaginal cancer. Results During 7.8 years follow-up, 553 vulvar and 506 vaginal cancer cases occurred. A history of diabetes mellitus was associated with higher risk of vulvar cancer with a HR (95% CIs) of 1.34 (1.12–1.60), but not vaginal cancer (1.09, 0.91–1.31). The HR was 1.97 (0.95–4.11) for early-onset and 1.34 (1.12–1.61) for later-onset vulvar cancer and 1.81 (0.76–4.32) for early-onset and 1.09 (0.90–1.31) for later-onset vaginal cancer. The associations were similar when restricted to type 2 diabetes cases, and when excluding the first 5 years of follow-up. Conclusion These findings suggest diabetes mellitus is associated with increased risk of vulvar, but not vaginal cancer. Further studies are needed to clarify these findings.
