Spatial-temporal evolution characteristics of PM2.5 and its driving mechanism: spatially explicit insights from Shanxi Province, China.

In China, despite the fact that the atmospheric environment quality has continued to improve in recent years, the PM2.5 pollution still had not been controlled fundamentally and its driving mechanism was complex which remained to be explored. Based on the 1-km ground-level PM2.5 datasets of China from 2000 to 2020, this study combined spatial autocorrelation, trend analysis, geographical detector, and multi-scale geographically weighted regression (MGWR) model to explore the spatial-temporal evolution of PM2.5 in Shanxi Province and revealed its complex driving mechanism behind this process. The results reflected that (1) there was a pronounced spatial clustering of PM2.5 concentration within Shanxi Province, with PM2.5 concentrations decreasing from southwest to northeast. From 2000 to 2020, the levels of PM2.5 pollution demonstrated a decline over time, with its concentrations decreasing by 9.15 µg/m3 overall. The Hurst exponent indicated a projected decrease in PM2.5 concentrations in the central and northern areas of Shanxi Province, contrasting with an anticipated increase in other regions. (2) The geographical detector indicated that all drivers had significant influences on PM2.5 concentrations, with meteorological factors exerting the greatest effects then followed by human activity and vegetation cover showing the least effects. (3) Both gross domestic product and population density exhibited positive correlations with PM2.5 concentration, while vegetation fractional cover, wind speed, precipitation, and elevation exerted negative influences on PM2.5 concentration all over the space. This study enriched the research content and ideas on the driving mechanism of PM2.5 and provided a reference for similar studies.

Modeling the spatially heterogeneous relationships between tradeoffs and synergies among ecosystem services and potential drivers considering geographic scale in Bairin Left Banner, China.

Understanding the complex relationships of tradeoffs and synergies among ecosystem services (ESs) is essential to achieve a comprehensive, coordinated, and sustainable development for human well-being. However, the quantitative measurement for the properties and intensities within these relationships as well as the deeper exploration of its formation mechanism from a spatial-explicit perspective is still a challenge. In this study, a comprehensive and general methodology was developed to quantitatively illustrate the intensities of tradeoffs/synergies among pairwise ESs and explore the spatially heterogeneous relationships between these relations and several socio-ecological drivers, integrating InVEST, geographical detector and multi-scale geographically weighted regression (MGWR) methods. The results indicated that (1) the properties and intensities of tradeoffs/synergies among various ESs varied greatly over space and presented significant clustered distribution patterns; (2) different relations between ESs were dominated by diverse drivers and the combined effects from multiple factors were stronger than any single one within this process. The tradeoffs/synergies between soil conservation and other ESs were mainly affected by geomorphological drivers including elevation and slope, while relations involved habitat quality could be attributed to vegetation and climate drivers such as precipitation and vegetation fractional cover. The relationships among ESs were more susceptible to topographic and anthropogenic drivers when concerning the carbon storage service; (3) compared to global ordinary least squares and local geographically weighted regression (GWR), the MGWR obtained better performance in explaining relationships between tradeoffs/synergies among ESs and potential drivers by operating different spatial scales. Accordingly, several spatially targeted ecological measures were proposed and recommended to reduce ESs tradeoffs and ultimately achieve better synergies. This research could enrich the methods in revealing the complex evolvement mechanism behind the tradeoffs/synergies among ESs and the proposed framework also provided a new perspective in the field of ESs tradeoffs/synergies studies and might be valuable guidance for other regions worldwide.

CXCL12/CXCR4 axis triggers the activation of EGF receptor and ERK signaling pathway in CsA-induced proliferation of human trophoblast cells.

INTRODUCTION: Our previous study has demonstrated Cyclosporin A (CsA) promotes the proliferation of human trophoblast cells. Therefore, we further investigate the intracellular signaling pathway involved in the CsA-induced proliferation of human trophoblast cells. METHODS: Enzyme-linked immunosorbent assay (ELISA) was performed to evaluate the regulation of CsA on CXCL12 secretion in human trophoblast cells. Immunofluorescence analysis and western blotting analysis were used to investigate the role of CXCL12/CXCR4 axis in the CsA-induced epidermal growth factor receptor (EGFR) phosphorylation in human trophoblast cells. 5-Bromo-2'-deoxyuridine (BrdU) cell proliferation assay was performed to analyze the involvement of EGFR and its downstream extracellular signal-regulated protein kinase (ERK) signaling pathway in the CsA-induced proliferation of human trophoblast cells. RESULTS: Low concentration of CsA promoted the secretion of CXCL12, and recombinant human CXCL12 promoted the phosphorylation of EGFR in primary human trophoblast cells and choriocarcinoma cell line JEG-3. The inhibition of CXCL12 or CXCR4 by either neutralizing antibodies or small interfering RNA (siRNA) could completely block the CsA-induced EGFR phosphorylation. The CsA-induced proliferation of human trophoblast cells was effectively abrogated by the EGFR inhibitor AG1478 as well as the ERK inhibitor U0126, but not by the PI3K/PKB inhibitor LY294002. CsA promoted the activation of ERK in JEG-3 cells, which was markedly abrogated in the presence of CXCL12 siRNA, or CXCR4 siRNA, or AG1478. CONCLUSIONS: CsA may promote EGFR activation via CXCL12/CXCR4 axis, and EGFR downstream ERK signaling pathway may be involved in the CsA-induced proliferation of human trophoblast cells.