BackgroundWe investigated whether the effect of air pollution on daily mortality is enhanced by high temperatures in Wuhan, China, using data from 2001 to 2004. Wuhan has been called an “oven” city because of its hot summers. Approximately 4.5 million permanent residents live in the 201-km2 core area of the city.MethodWe used a generalized additive model to analyze pollution, mortality, and covariate data. The estimates of the interaction between high temperature and air pollution were obtained from the main effects and pollutant–temperature interaction models.ResultsWe observed effects of consistently and statistically significant interactions between particulate matter ≤ 10 μm (PM10) and temperature on daily nonaccidental (p = 0.014), cardiovascular (p = 0.007), and cardiopulmonary (p = 0.014) mortality. The PM10 effects were strongest on extremely high-temperature days (daily average temperature, 33.1°C), less strong on extremely low-temperature days (2.2°C), and weakest on normal-temperature days (18.0°C). The estimates of the mean percentage of change in daily mortality per 10-μg/m3 increase in PM10 concentrations at the average of lags 0 and 1 day during hot temperature were 2.20% (95% confidence interval), 0.74–3.68) for nonaccidental, 3.28% (1.24–5.37) for cardiovascular, 2.35% (−0.03 to 4.78) for stroke, 3.31% (−0.22 to 6.97) for cardiac, 1.15% (−3.54% to 6.07) for respiratory, and 3.02% (1.03–5.04) for cardiopulmonary mortality.ConclusionsWe found synergistic effects of PM10 and high temperatures on daily nonaccidental, cardiovascular, and cardiopulmonary mortality in Wuhan.

Osteoarthritis (OA) is a serious disease of the articular cartilage, and inflammation has been implicated in its pathogenesis. Previously, microRNAs (miRNAs) have been proposed as novel regulators of inflammation, however, the functional role of microRNAs in regulating inflammation in OA remains to be fully elucidated. The aim of the present study was to investigate the roles of miRNAs in OA inflammation and the underlying molecular mechanism. Firstly, the miRNA expression patterns were analyzed in the articular cartilage tissues from experimental OA mice using an miRNA microarray. miRNA (miR)-93 was identified with particular interest due to its reported effects on apoptosis and inflammation suppression. Subsequently, the expression of miR-93 was further validated in the articular cartilage tissues of OA mice and lipopolysaccharide (LPS)-stimulated primary chondrocytes. Using this LPS-induced chondrocyte injury model, the overexpression of miR-93 enhanced cell viability, improved cell apoptosis and attenuated the inflammatory response, as reflected by reductions in pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. In addition, Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor-κB (NF-κB) signaling pathway, was identified as a direct target of miR-93 in chondrocytes. Furthermore, the restoration of TLR4 markedly abrogated the inhibitory effects of miR-93 on the chondrocyte apoptosis and inflammation induced by LPS. In addition, the overexpression of miR-93 by agomir-miR-93 significantly inhibited the levels of pro-inflammatory cytokines and cell apoptosis, whereas antagomir-93 exacerbated apoptosis and inflammation in vivo. Taken together, the results of the study suggested that miR-93 may be a promising therapeutic target for the treatment of human OA.

No abstract

No abstract

No abstract