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China is regarded as the largest contributor of mercury (Hg) to the global atmospheric Hg budget. However, concentration levels and depositions of atmospheric Hg in China are poorly known. Continuous measurements of atmospheric total gaseous mercury (TGM) were carried out from May 2008 to May 2009 at the summit of Mt. Leigong in south China. Wet and dry deposition fluxes of Hg were also calculated following collection of precipitation, throughfall and litterfall. Atmospheric TGM concentrations averaged 2.80±1.51 ngm-3, which was highly elevated compared to global background values but much lower than semi-rural and industrial/urban areas in China, indicating great emissions of Hg in central, south and southwest China. Seasonal and diurnal variations of TGM were observed, which reflected variations in source intensity, deposition processes and meteorological factors. Wet deposition of Hg was quite low, while its dry deposition of Hg (litterfall+throughfall-direct wet deposition) constituted a major portion of total deposition (∼88% for total mercury (THg) and 84% for methyl mercury (MeHg)). This highlights the importance of vegetation to Hg atmospheric cycling. In a remote forest ecosystem of China, dry deposition of TGM, especially gaseous elemental mercury (GEM), was very important for the depletion of atmospheric Hg. Elevated TGM level in ambient air may accelerate the foliar uptake of Hg through air which may partly explain the elevated Hg dry deposition fluxes observed in Mt. Leigong. [ABSTRACT FROM AUTHOR]

In our study, the impact of miR-16-1-3p on cell proliferation and invasion in NSCLC was explored. miR-16-1-3p mimics were transfected to A549 cells for miR-16-1-3p overexpression. qRT- PCR and Western blot were applied to explore the relative expression of mRNA and protein in A549 cells. Furthermore, the cell proliferation capability was determined by MTT assay. Additionally, cell migration and invasion were measured using a scratch assay and transwell assay, respectively. Moreover, TargetScan and luciferase reporter assay was utilized to investigate the target of miR-16-1-3p. The results indicated that miR-16-1-3p was downregulated in NSCLC cells and upregulation of miR-16-1-3p was able to inhibit the expression of TWIST1. In addition, the reduced cell proliferation, inhibited cell migration and invasion were observed in miR-16-1-3p mimic group compared to the negative control group. The luciferase reporter gene showed that TWIST1 was a target of miR-16-1-3p. Therefore, the present study demonstrated that miR-16-1-3p may suppress A549 cell proliferation, migration and invasion by targeting TWIST1. Thus, miR-16-1-3p might play important roles in NSCLC development, which provides a novel aspect for NSCLC investigation (Fig. 6, Ref. 26).