This study first tested and verified the ability of the Weather Research and Forecasting (WRF) model to simulate the near-surface temperature in the North China Plain. Then the static land cover data in the WRF were replaced, and thereafter the modified WRF model was used to explore the impacts of land cover change on the near-surface temperature in the North China Plain in year 1992 and year 2005. The results indicated that the land cover change in the North China Plain, which was characterized by the regional urbanization, had led to significant changes in the near-surface temperature, increasing the regional near-surface temperature by 0.03°C/year on average. The spatial pattern of the climate change basically corresponded to that of the land cover change; for example, the temperature increased most significantly in the regions mainly consisting of cities and built-up area. Besides, there were some variations in the degree and range of influence of the land cover change on the temperature among seasons. The result can provide important theoretical support for the adaptation to climate change, scientific land cover change management, and land use planning.

Inorganic arsenic is a well-known environmental toxicant and carcinogen, and there is overwhelming evidence for an association between this metalloid poisoning and hepatic diseases. However, the biological mechanism involved is not well characterized. In the present study, we probed how inorganic arsenic modulates the hepatic polarization of macrophages, as well as roles of PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy participates in regulating the metalloid-mediated macrophage polarization. Our results indicate that acute arsenic exposure induced macrophage polarization with up-regulated gene expression of inducible nitric oxide synthase (Inos) and arginase-1 (Arg1), monocyte chemotactic protein-1 (Mcp-1) and macrophage inflammatory protein-2 (Mip-2), tumor necrosis factor (Tnf)-α, interleukin (Il)-1β and Il-6, as well as anti-inflammatory factors Il-4 and Il-10. In parallel, we demonstrated the disrupted hepatic redox balance typically characterized by the up-regulation of hydrogen peroxide (H2O2) and glutathione (GSH), and activation of PINK1/Parkin-mediated mitophagy in the livers of acute arsenic-exposed mice. In addition, our results demonstrate that it might be the PINK1/Parkin-mediated mitophagy that renders hepatic macrophage refractory to arsenic-induced up-regulation of the genes Inos, Mcp-1, Mip-2, Tnf-α, Il-1β, Il-6 and Il-4. In this regard, this is the first time the protective effects of PINK1/Parkin-mediated mitophagy in inorganic arsenic-induced hepatic macrophage polarization in vivo have been reported. These findings add novel insights into the arsenical immunotoxicity and provide a basis for the preve.ntive and therapeutic potential of PINK1/Parkin-mediated mitophagy in arsenic poisoning.

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