Association of short-term nitrogen dioxide exposure with hospitalization for urolithiasis in Xinxiang, China: a time series study.

Urolithiasis accounts for the highest incidence of all urologic-associated hospitalizations. However, few studies have explored the effect of nitrogen dioxide (NO2) on hospitalizations for urolithiasis. We included 5956 patients with urolithiasis, collected daily meteorological and air pollution data between 2016 and 2021, and analyzed the associations between air pollutants and hospitalization, length of the hospital stay, and hospitalization costs attributable to urolithiasis. NO2 exposure was associated with an increased risk of hospitalization for urinary tract stones. For each 10-µg/m3 increase and 1-day lag of NO2, the maximum daily effect on the risk of hospitalization for urolithiasis was 1.020 (95% confidence interval [CI]: 1.001-1.039), and the cumulative effect peaked on lag day 4 (relative risk [RR]: 1.061; 95% CI: 1.003-1.122). Attribution scores and quantitative analysis revealed that the mean number of hospital days and mean hospital costs were 16 days and 21,164.39 RMB, respectively. Up to 5.75% of all urolithiasis hospitalizations were estimated to be attributable to NO2, and the cost of NO2-related urolithiasis hospitalizations reached approximately 3,430,000 RMB. Stratified analysis showed that NO2 had a more sensitive impact on urolithiasis hospitalizations in women and in those aged ≥65 years. Notably, men and those younger than 65 years of age (exclude people aged 65) incurred more costs for urolithiasis hospitalizations. In the population level, the association between NO2 and risk of urolithiasis hospitalization was more pronounced during the warm season. NO2 can increase hospitalizations for urolithiasis for Xinxiang City residents, and there is a cumulative lag effect. Focusing on air pollution may have practical significance in terms of the prevention and control of urolithiasis.

microRNA-218 inhibits prostate cancer cell growth and promotes apoptosis by repressing TPD52 expression.

The tumor protein D52 (TPD52) is an oncogene overexpressed in prostate cancer (PC) due to gene amplification. Although the oncogenic effect of TPD52 is well recognized, how its expression is regulated is still not clear. This study tried to explore the regulative role of miR-218, a tumor suppressing miRNA on TPD52 expression and prostate cancer cell proliferation. We found the expression of miR-218 was significantly lower in PC specimens. Based on gain and loss of function analysis, we found miR-218 significantly inhibit cancer cell proliferation by inducing apoptosis. These results strongly suggest that miR-218 plays a tumor suppressor role in PC cells. In addition, our data firstly demonstrated that miR-218 directly regulates oncogenic TPD52 in PC3 cells and the miR-218-TPD52 axis can regulate growth of this prostate cancer cell line. Knockdown of TPD52 resulted in significantly increased cancer cell apoptosis. Clearly understanding of oncogenic TPD52 pathways regulated by miR-218 might be helpful to reveal new therapeutic targets for PC.