[1] To understand the seasonality of methane flux from alpine wetlands in Zoige Plateau, 30 plots were set to measure the methane emissions in the growing and nongrowing seasons in three environmental types: dry hummock (DH), Carex muliensis (CM), and Eleocharis valleculosa (EV) sites. There were clearly seasonal patterns of methane flux in different environmental types in the growing and nongrowing seasons. In the growing season, the main maximum values of methane flux were found in July and August, except for a peak value in September in CM sites. In the nongrowing season, the similar seasonal variation pattern was shared among all the three sites, in which the methane emissions increased from February to April. In the growing season, the determining factors were surface temperatures (r 2 = 0.55, P < 0.05), standing water depths (r 2 = 0.32, P < 0.01) and plant community heights (r 2 = 0.61, P < 0.01), while in the nongrowing season, ice thickness (r 2 = 0.27, P < 0.05; in CM and EV sites) was found most related to flux. In our understanding, the seasonality of methane emissions in our study areas was temperature-and-plant-growth-dependent, and the water table position was also very important to shape the temperature-and-plantgrowth-dependent seasonal variation of flux with its vigorous variations in alpine wetland ecosystems. Different environmental types within the wetland also influenced the seasonal pattern of methane flux. For an accurate estimate of the global methane source strength of alpine wetlands, the pronounced seasonal or even temporal variability in methane emission from alpine wetlands should be taken into consideration.

No abstract

EGFR-targeted cancer therapy is a breakthrough in non-small cell carcinoma. miRNAs have been proved to play important roles in cancer. Currently, for the role of miRNAs in EGFR-targeted cancer therapy is unclear. In this study, first we found that erlotinib reduced the expression of miR-9. MiR-9 expression was increased in human lung cancer tissues compared with peripheral normal tissues, and miR-9 promoted the growth of NSCLC cells. Overexpression of miR-9 decreased the growth inhibitory effect of erlotinib. Second, miR-9 decreased FoxO1 expression by directly inhibition of its mRNA translation. Adenovirus-mediated overexpression of FoxO1 or siRNA-mediated downregulation of FoxO1 negatively regulated cell growth. And exogenous overexpression FoxO1 reduced the pro-growth effect of miR-9. Finally, we found that erlotinib upregulated FoxO1 protein expression. Moreover, overexpression of miR-9 decreased erlotinib-induced FoxO1 expression, and overexpression of FoxO1 enhanced the growth inhibitory effects of erlotinib. Additionally, we found that erlotinib downregulates miR-9 expression through suppressing the transcrption of miR-9-1 and enhanced DNA methylation maybe involved. These findings suggest that oncogenic miR-9 targeted FoxO1 to promote cell growth, and downregulation of this axis was involved in erlotinib’s growth inhibitory effects. Clarifying the regulation of miRNAs by erlotinib may indicate novel strategies for enhancing EGFR-targeted cancer therapy.