Effective therapies for erectile dysfunction (ED) associated with diabetes mellitus (DM) are needed. In this study, the effects of stromal cell-derived factor-1 (SDF-1)-expressing engineered mesenchymal stem cells (SDF-1 eMSCs) and the relevant mechanisms in the corpus cavernosum of a streptozotocin (STZ)-induced DM ED rat model were evaluated. In a randomized controlled trial, Sprague–Dawley (SD) rats (n = 48) were divided into four groups (n = 12/group): Normal (control), DM ED (diabetes induced by STZ), DM ED + BM-MSC (treated with bone marrow [BM]-derived MSCs), and DM ED + SDF-1 eMSC (treated with SDF-1-expressing BM-MSCs). After four weeks, intracavernosal pressure (ICP), an indicator of erectile function, was 0.75 ± 0.07 in the normal group, 0.27 ± 0.08 in the DM ED group, 0.42 ± 0.11 in the DM ED + BM-MSC group, and 0.58 ± 0.11 in the DM ED + SDF-1 eMSC group. BM-MSCs, especially SDF-1 eMSCs, improved ED (p < 0.05). SDF-1 eMSC treatment improved the smooth muscle content in the corpus cavernosum (p < 0.05). As SDF-1 expression increased, ED recovery improved. In the SDF-1 eMSC group, levels of neuronal nitric oxide synthase (nNOS) and phosphorylated endothelial NOS (p-eNOS) were higher than those in other groups (p < 0.05). In addition, high stromal cell-derived factor-1 (SDF-1) expression was associated with increased vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in DM ED rats (p < 0.05). Higher levels of phosphorylated protein kinase B (p-AKT)/protein kinase B (AKT) (p < 0.05) and B-cell lymphoma-2 (Bcl-2) and lower levels of the apoptosis factors Bcl2-associated x (Bax) and caspase-3 were observed in the MSC-treated group than in the DM ED group (p < 0.05). SDF-1 eMSCs showed beneficial effects on recovery from erectile function.

Kim KS, et al. World J Mens Health. 2019 Jan;37:e59. https://doi.org/10.5534/wjmh.190130

We estimated the impact of obesity on bladder cancer with stratification by smoking status using nationally representative data on the Korean population from the National Health Insurance System (NHIS). Of the 45,850,458 people who underwent at last one health examination from 2009 to 2012, 23,378,895 without bladder cancer were followed from the January 2009 to the December 2015. First, the HR for bladder cancer was lowest in people with a BMI < 18.5 (HR = 0.92) and highest for those with BMI ≥ 30 (HR = 1.17) in multiple Cox regression analyses. The positive association between bladder cancer and BMI showed an increasing trend beyond the reference BMI. Second, an analysis of HR for bladder cancer stratified by obesity across smoking status strata showed a significant trend of increasing HR for bladder cancer across obesity and smoking status in multivariate-adjusted models. Conclusively, this population-based study showed that increasing BMI was a risk factor for bladder cancer independent of confounding variables. When stratified by smoking status, there was still a positive association between bladder cancer and BMI (P for trend < 0.01).