Evaluating net primary productivity dynamics and their response to land-use change in the loess plateau after the 'Grain for Green' program.

Assessing net primary productivity (NPP) dynamics and the contribution of land-use change (LUC) to NPP can help guide scientific policy to better restore and control the ecological environment. Since 1999, the "Green for Grain" Program (GGP) has strongly affected the spatial and temporal pattern of NPP on the Loess Plateau (LP); however, the multifaceted impact of phased vegetation engineering measures on NPP dynamics remains unclear. In this study, the Carnegie-Ames-Stanford Approach (CASA) model was used to simulate NPP dynamics and quantify the relative contributions of LUC and climate change (CC) to NPP under two different scenarios. The results showed that the average NPP on the LP increased from 240.7 gC·m-2 to 422.5 gC·m-2 from 2001 to 2020, with 67.43% of the areas showing a significant increasing trend. LUC was the main contributor to NPP increases during the study period, and precipitation was the most important climatic factor affecting NPP dynamics. The cumulative amount of NPP change caused by LUC (ΔNPPLUC) showed a fluctuating growth trend (from 46.23 gC·m-2 to 127.25 gC·m-2), with a higher growth rate in period ΙΙ (2010-2020) than in period Ι (2001-2010), which may be related to the accumulation of vegetation biomass and the delayed effect of the GGP on NPP. The contribution rate of LUC to increased NPP in periods Ι and ΙΙ was 101.2% and 51.2%, respectively. Regarding the transformation mode, the transformation of grassland to forest had the greatest influence on ΔNPPLUC. Regarding land-use type, the increased efficiency of NPP was improved in cropland, grassland, and forest. This study provides a scientific basis for the scientific management and development of vegetation engineering measures and regional sustainable development.

Rechargeable Multifunctional Anti-Bacterial AEMs for Electrodialysis: Improving Anti-Biological Performance via Synergistic Antibacterial Mechanism.

Constructing a functional layer on the surface of commercial membrane (as a substrate) to inhibit the formation of biofilms is an efficient strategy to prepare an antibacterial anion exchange membrane (AEM). Herein, a rechargeable multifunctional anti-biological system is reported by utilizing the mussel-inspired L-dopa connection function on commercial AEMs. Cobalt nanoparticles (Co NPs) and N-chloramine compounds are deposited on the AEM surface by a two-step modification procedure. The anti-biofouling abilities of the membranes are qualitatively and quantitatively analyzed by adopting common Gram-negative (E. coli) and Gram-positive (S. aureus & Bacillus) bacteria as model biofouling organisms. The optimized membrane exhibits a high stability concerning the NaCl solution separation performance within 240 min. Meantime, the mechanism of the anti-adhesion is un-veiled at an atomic level and molecular dynamics (MD) simulation are conducted to measure the interaction, adsorption energy and average loading by using lipopolysaccharide (LPS) of E. coli. In view of the superior performance of antibacterial surfaces, it is believed that this work could provide a valuable guideline for the design of membrane materials with resistance to biological contamination.

Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.

Excessive production of inflammatory mediators is an important feature of inflammatory lung disease. In macrophages, mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) are crucial mediators for the production of proinflammatory cytokines. In the present study, the role of MAPK and STAT3 on tumor necrosis factor (TNF)-α and interleukin (IL)-10 production was investigated in mouse alveolar macrophages. The levels of TNF-α and IL-10 in lipopolysaccharide (LPS; 100 ng/ml)-stimulated MH-S cell lines were measured by an enzyme-linked immunosorbent assay, with or without p38 inhibitor (SB203580; 5, 10 or 15 µM) intervention. Phosphorylated STAT3 (p-STAT3) expression was examined by western blot analysis and immunocytochemistry following LPS stimulation for 15 or 30 min. Antibodies against STAT3 were used to verify comparable sample loading. Cells stimulated with LPS showed significantly increased levels of p-STAT3 protein (P<0.05) when compared with the baseline levels. TNF-α and IL-10 protein levels also increased following LPS stimulation (P<0.05). By contrast, treatment with the p38 inhibitor, SB203580, decreased the levels of p-STAT3, TNF-α and IL-10 (P<0.05) following LPS stimulation. SB203580 was shown to inhibit LPS-stimulated TNF-α expression (P<0.05) in a concentration-dependent manner, reaching significance at a concentration of 10 µM. However, the inhibition of IL-10 expression was not concentration-dependent. Therefore, LPS-stimulated overproduction of TNF-α and IL-10 is mediated at least partially by the MAPK pathway. Inhibition of p38 prevented LPS-induced STAT3 phosphorylation, indicating an interaction between the STAT3 and MAPK signaling pathways.