Increasing impacts of the relative contributions of regional transport on air pollution in Beijing: Observational evidence.

Benefiting from the pollution controls implemented by the Chinese government, the concentrations of PM2.5, SO2, NO2 and CO showed a significant decrease in Beijing during 2013-2017. In this study, an observation-based method was employed to estimate the relative contributions of regional transport (MaxRTC) and local emissions (MinLEC) to air pollutant levels during 2013-2017 in Beijing. The results showed that the MaxRTC to SO2 and PM2.5 increased significantly over the five years, while those to CO and NO2 changed little. Furthermore, the difference in the emissions control efficiency (ΔECE) between Beijing (receptor region) and Shijiazhuang (source region), which refers to the concentration changes corresponding to unit emission changes of a certain air pollutant between the two regions, was introduced to verify the estimated variation in MaxRTC and MinLEC over 2013-2017. The negative value of ΔECE found for PM2.5 and SO2 supports the conclusion of an increasing effect of regional transport. This implies that local emissions control alone is not adequate for mitigating Beijing's air pollution, especially with the demand for continuously improving air quality. Joint prevention and control with regard to air quality on a regional scale is more important and urgent in the next Five-Year Plan.

Long intergenic non-protein coding RNA 324 prevents breast cancer progression by modulating miR-10b-5p.

Mounting evidence suggests that long noncoding RNAs serve as specific biomarkers and potent modulators of multiple cancers. Long intergenic non-protein coding RNA 324 (LINC00324) is ubiquitously expressed in various tissues, including breast cancer. The biological function of LINC00324 in the development and progression of breast cancer remains unknown. Here, we fully elucidate the relation between LINC00324 expression and breast cancer, and suggest a potential mechanism of action. We found that decreased expression of LINC00324 was dramatically correlated with malignancy of breast cancer, both in breast cancer tissues and in cell lines. Overexpression of LINC00324 in MDA-MB-231 cells resulted in a decrease in cell proliferation, invasion, and migration, while increasing cells apoptosis. On the other hand, loss-of-function experiments indicated that deficiency of LINC00324 promoted malignant phenotypes in breast cancer cells. Mechanically, we found that LINC00324 is mainly distributed in the cytoplasm, fostering the expression of E-cadherin by sponging miR-10b-5p. Taken together, these findings suggest that LINC00324 plays a critical role in breast cancer progression by directly interacting with miR-10b-5p. LINC00324 can thus potentially act as an early diagnostic marker and a novel therapeutic agent for breast cancer.