Detecting the effects of opencast mining on ecosystem services value in arid and semi-arid areas based on time-series remote sensing images and Google Earth Engine (GEE).

Ecosystem Services Value (ESV) are the various beneficial functions and products that natural ecosystems provide to humans, and are important indicators for evaluating ecosystem conditions and human well-being. Opencast mining is one of the human activities that severely damage the surface environment, but its long-term impact on ecosystem services lacks systematic assessment. This study takes the Ordos opencast mining area as an example, and calculates the value of ESV from 1990 to 2020 based on the Google Earth Engine platform. Mann-Kendall Tau-b with Sen's Method (Sen + mk test) and Joinpoint regression model were used to analyzes its spatiotemporal variation characteristics. Further revealed the impacts of opencast mining on ESV as well as the trend of ESV changes. The results show that: (1) The dynamic ESV levels in the study area fluctuated considerably from 1990 to 2020 with an overall decreasing trend of 89.45%. (2) Among nine types ecosystem services, most of them were significantly different (p < 0.001) between mining areas and control areas, with biodiversity protection (BP), climate regulation (CR), gas regulation (GR), soil formation and retention (SFR), water supply (WS) and waste treatment (WT) showed a significant decrease between 1990 and 2020. (3) In the past 30 years, the ESV of the study area showed an overall improvement trend, where the improved area accounted for 48.45% of the total area of the study area. However, the degraded area also accounted for 21.28, and 17.19% of the area belonged to severe degradation. With 67% of the significantly degraded areas distributed within mining concessions. (4) The trend of ESV changes in the mining impact areas and the control area showed significant differences. The ESV of the control area increased continuously, with an average annual percentage change (AAPC) of 0.7(95%CI:0.50 ~ 0.9, P < 0.001) from 1990 to 2020; while the ESV of the mining impact areas first stabilized and then decreased significantly, with an AAPC of - 0.2(95%CI:- 0.3 ~ - 0.1,P < 0.001) from 1990 to 2020. This study provides scientific support for formulating ecosystem management, restoration plans, and payment for ecosystem service policies, which is conducive to achieving regional sustainable development and improving human well-being.

Will attitudes corrected by social norms have a more powerful impact on pro-environmental behavior? Evidence from a process model moderated by self-construal.

Residents' pro-environmental behaviors are considered important for reducing carbon emissions and achieving carbon neutrality. However, optimizing the implementation of pro-environmental behavior need to be further studied. To this end, we placed residents' recycling behavior within a socialized situation. Explored the "Attitude-Behavior intention-Behavior" intermediary path regulated by self-construal, whether and how it can more effectively promote residents to transfer recycling behavior intention as recycling behavior after joining the influence of social norms. The results showed that after considering the influence of social norms, the transformation of residents' Habit adjustment recycling behavior (HAB) was significantly improved. Further, the masking effect of "Behavioral intention-Interpersonal facilitation recycling behavior (IFB)" in the mediation model was effectively reduced. HAB and IFB had stronger dependence on independent self-construal (IDSC) and interdependent self-construal (ITSC), respectively. In addition, when the self-construal level was low, the overall effect of the chain mediation model was stronger, highlighting the advantage of the role played by social norms.

Epigenetic modulation of Drp1-mediated mitochondrial fission by inhibition of S-adenosylhomocysteine hydrolase promotes vascular senescence and atherosclerosis.

AIMS: Vascular senescence, which is closely related to epigenetic regulation, is an early pathological condition in cardiovascular diseases including atherosclerosis. Inhibition of S-adenosylhomocysteine hydrolase (SAHH) and the consequent increase of S-adenosylhomocysteine (SAH), a potent inhibitor of DNA methyltransferase, has been associated with an elevated risk of cardiovascular diseases. This study aimed to investigate whether the inhibition of SAHH accelerates vascular senescence and the development of atherosclerosis. METHODS AND RESULTS: The case-control study related to vascular aging showed that increased levels of plasma SAH were positively associated with the risk of vascular aging, with an odds ratio (OR) of 3.90 (95% CI, 1.17-13.02). Elevated pulse wave velocity, impaired endothelium-dependent relaxation response, and increased senescence-associated ß-galactosidase staining were observed in the artery of SAHH+/- mice at 32 weeks of age. Additionally, elevated expression of p16, p21, and p53, fission morphology of mitochondria, and over-upregulated expression of Drp1 were observed in vascular endothelial cells with SAHH inhibition in vitro and in vivo. Further downregulation of Drp1 using siRNA or its specific inhibitor, mdivi-1, restored the abnormal mitochondrial morphology and rescued the phenotypes of vascular senescence. Furthermore, inhibition of SAHH in APOE-/- mice promoted vascular senescence and atherosclerosis progression, which was attenuated by mdivi-1 treatment. Mechanistically, hypomethylation over the promoter region of DRP1 and downregulation of DNMT1 were demonstrated with SAHH inhibition in HUVECs. CONCLUSIONS: SAHH inhibition epigenetically upregulates Drp1 expression through repressing DNA methylation in endothelial cells, leading to vascular senescence and atherosclerosis. These results identify SAHH or SAH as a potential therapeutic target for vascular senescence and cardiovascular diseases.

Inhibition of S-adenosylhomocysteine hydrolase induces endothelial senescence via hTERT downregulation.

BACKGROUND AND AIMS: It has been established that endothelial senescence plays a critical role in the development of atherosclerosis. Elevated S-adenosylhomocysteine (SAH) level induced by inhibition of S-adenosylhomocysteine hydrolase (SAHH) is one of the risk factors of atherosclerosis; however, the interplay between endothelial senescence and inhibition of SAHH is largely unknown. METHODS: Human umbilical vein endothelial cells (HUVECs) after serial passage were used. SAHH-specific inhibitor adenosine dialdehyde (ADA) and SAHH siRNA treated HUVECs and SAHH+/-mice were used to investigate the effect of SAHH inhibition on endothelial senescence. RESULTS: HUVECs exhibited distinct senescence morphology as HUVECs were passaged, together with a decrease in intracellular SAHH expression and an increase in intracellular SAH levels. SAHH inhibition by ADA or SAHH siRNA elevated SA ß-gal activity, arrested proliferation, and increased the expression of p16, p21 and p53 in HUVECs and the aortas of mice. In addition, decreased expression of hTERT and reduced occupancy of H3K4me3 over the hTERT promoter region were observed following SAHH inhibition treatment. To further verify the role of hTERT in the endothelial senescence induced by SAHH inhibition, hTERT was overexpressed with a plasmid vector under CMV promoter. hTERT overexpression rescued the senescence phenotypes in endothelial cells induced by SAHH inhibition. CONCLUSIONS: SAHH inhibition induces endothelial senescence via downregulation of hTERT expression, which is associated with attenuated histone methylation over the hTERT promoter region.

S-adenosylhomocysteine induces cellular senescence in rat aorta vascular smooth muscle cells via NF-κB-SASP pathway.

Vascular aging plays an important role in the development and progression of atherosclerosis (AS) , and one-carbon metabolism dysfunction will lead to Vascular Smooth Muscle Cells (VSMCs) senescence, which contributes to vascular senescence. However, the mechanisms underlying the role of VSMCs senescence in AS remain unclear. This study aimed to evaluate S-adenosyl-homocysteine (SAH) as a one-carbon metabolite that affects VSMCs senescence. We treated Rat Aorta Smooth Muscle Cells (RASMCs) with S-adenosylhomocysteine Hydrolase (SAHH) inhibitor, adenosine-2,3-dialdehyde (ADA) and SAHH siRNA to examine the effect of elevated SAH levels on RASMCs phenotypes. SAHH inhibition induced RASMCs senescence, as demonstrated by the manifestation of senescence-associated secretory phenotype in cells and induction of senescence in pre-senescent RASMCs. Furthermore, we found that SAHH inhibition induced CpG island demethylation in the promoter of NF-κB, a molecule that drives the pro-inflammatory response of the cells manifesting the senescence-associated secretory phenotype (SASP). Overall, these findings indicate that the elevated intracellular SAH levels could be targeted to ameliorate vascular aging.

Association of serum methionine metabolites with non-alcoholic fatty liver disease: a cross-sectional study.

BACKGROUND AND PROJECT: Non-alcoholic fatty liver disease (NAFLD) is viewed as the hepatic manifestation of metabolic syndrome. Methionine metabolites have been linked to metabolic syndrome and its related diseases. Whether serum methionine metabolites levels are associated with NAFLD remains unclear. The study aimed to assess the association between methionine metabolites and NAFLD. METHODS: This cross-sectional study included a total of 2814 individuals aged 40-75 years old. All participants underwent anthropometric measurements, laboratory tests, dietary assessment and abdominal ultrasonography. Multivariable logistic regression analysis was performed to estimate the association of methionine metabolites with NAFLD. RESULTS: Overall, 1446 with and 1368 without NAFLD were enrolled in this study. Participants with NAFLD had significantly higher serum S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH) and homocysteine (Hcy) levels, and a lower S-adenosylmethionine/S-adenosylhomocysteine (SAM/SAH) ratio than those without NAFLD (all P < 0.001). After adjusting multiple confounders, odds ratios (95% confidence interval) for quartile 4 versus quartile 1 of SAH, Hcy and SAM/SAH ratio were 1.65 (1.27-2.14), 1.63 (1.26-2.12) and 0.63 (0.49-0.83), respectively (all P for trend < 0.01). In addition, serum SAH, Hcy levels and SAM/SAH ratio were significantly correlated with the degree of hepatic steatosis (all P for trend < 0.001). CONCLUSION: Elevated serum SAH, Hcy levels and lower SAM/SAH ratio may be independently associated with the presence of NAFLD in middle-aged and elder Chinese.

Lower adropin expression is associated with oxidative stress and severity of nonalcoholic fatty liver disease.

BACKGROUND & AIMS: Adropin has been reported to be involved in metabolic disorders, including nonalcoholic fatty liver disease (NAFLD). However, the clinical relevance of adropin expression to the histological severity of NAFLD is unclear. This study aimed to investigate adropin expression in biopsy-proven NAFLD patients. METHODS: This case-control study enrolled a total of 109 participants, including 15 normal histological controls, 26 nonalcoholic fatty liver (NAFL), 21 nonalcoholic steatohepatitis (NASH) subjects and B-ultrasound NAFLD-free normal controls matched to the cases based on age and sex (the case:control ratio was 1:1). Liver biopsies were obtained and histological characteristics were assessed. Primary murine hepatocytes were isolated from C57BL/6J mice and incubated with doses of palmitate to induce oxidative stress. RESULTS: The serum adropin level in NASH patients was 9.99 ± 5.51 ng/ml, significantly lower than that in B-ultrasound normal controls (22.70 ± 6.32 ng/ml), histological normal controls (21.93 ± 6.63 ng/ml) and NAFL patients (17.82 ± 6.90 ng/ml). Serum adropin levels were negatively correlated with the histological severity of NAFLD. The lower serum adropin level predicted NASH (area under the ROC curve: 87.1%). Adropin expression in serum and liver was also negatively associated with hepatic MDA and serum 8-iso-PGF2α levels. Furthermore, palmitate rather than oleate induced oxidative stress in a dose-dependent manner with a gradient decrease in adropin expression in primary murine hepatocytes. Adropin overexpression or treatment ameliorated palmitate-induced oxidative stress in hepatocytes. CONCLUSIONS: Circulating adropin was inversely associated with the oxidative stress and histological severity of NAFLD. It may play an important role in the development of NAFLD.

Effect of crop cultivation on the soil carbon stock in mine dumps of the Loess Plateau, China.

In the ecological restoration of mine dumps, soil carbon stock (SCS) improvement is an important issue. The type of land use and management approach taken can have a great influence on this issue. On the Loess Plateau, different crops have been cultivated on reclaimed land; however, the effect of long-term crop cultivation on SCS is poorly understood. To address this issue, a field investigation of mine dumps was performed at the Kee Open Pit Mine in Shanxi Province, China. Four sites utilizing different land management methods were analyzed: no reclamation (NR), reclamation with no crop cultivation (NC), and reclamation followed by 11 or 27 years crop cultivation (RC-11 and RC-27, respectively). SCS, associated soil properties (total nitrogen (TN), total phosphorus (TP), total potassium (TK), moisture content (MoiC), and pH), plant community (species composition, plant diversity, and traits), and microbial community operational taxonomic units (OTUs) of fungi and bacteria were determined by field investigation and laboratory analysis. Redundancy analysis was used to show the relationship between SCS and other environmental variables. Results varied by soil depth. At the depth range of 0-20 cm, the SCS of RC-11 was significantly greater compared to that in NR and NC, by 14.64- and 2.25-fold, respectively; whereas compared to RC-27, it was higher by 52.78%. At the depth of 20-40 cm, NC has the largest SCS; the SCS of RC-27 was the lowest, which was less compared to that in NC by 43.64%. Redundancy analysis showed a positive relationship between the SCS and TN, TP, MoiC, as well as average plant coverage, while the bacterial OTUs were negatively related with the SCS. This research suggests the potential of mine dumps for crop cultivation, which could improve the SCS of the mining area on the Loess Plateau.

Adropin regulates hepatic glucose production via PP2A/AMPK pathway in insulin-resistant hepatocytes.

Adropin as a secretory peptide has shown a protective role on the disorders of glucose and lipid metabolism. However, the role and mechanism of this peptide on the hepatic glucose production has remained unclear. Adropin knockout (KO) mice were generated to explore its effects on the enhanced hepatic glucose production in obesity. We found that compared to wild-type (WT) mice, adropin-KO mice developed the unbalanced enhanced hepatic glucose production in advance of the whole-body insulin resistance (IR) by high-fat diet (HFD). Mechanistically, adropin dissociated CREB-CRTC2 and FoxO1-PGC1α complex and reduced their binding to the promoters of G6Pase and PEPCK to decrease glucose production in IR. However, these effects were not observed in insulin-sensitive hepatocytes. Furthermore, in IR hepatocytes, dampened AMPK signaling was re-activated by adropin treatment via inhibition of PP2A. To further authenticate AMPK role in vivo, we administrated HFD-fed mice with AAV8-CA AMPKα and found that AMPK activation functionally restored the aberrant glucose production and IR induced by adropin-deficiency. This study provides evidence that adropin activates the AMPK pathway via inhibition of PP2A and decreases the liver glucose production in IR context. Therefore, adropin may represent a novel target for the prevention and treatment of diabetes.