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Long-term stability is crucial in cropland for maintaining stable agricultural production and ensuring national food security. However, relatively few studies have been conducted on the long-term stability of cropland at the national level. This study assessed the long-term stability of cropland in China from 1990 to 2018 using a fine-resolution land use dataset. The experimental results indicated that the average area of unstable cropland in China from 1990 to 2018 amounted to 2.08 ×   10 6 km2, 47.31% of the total. The Qinghai–Tibet Plateau exhibited the highest average proportion of unstable cropland at 65.9%, followed by the northern arid and semiarid region, Southern China, and the Yunnan–Guizhou Plateau. The quantity of unstable cropland in China initially declined before increasing, reaching a final growth rate of 5.09%. Furthermore, this study explored the relevant driving factors of cropland's long-term stability from both natural factors and human activities based on artificial neural networks. The relative importance of distance to vegetation reached a value of 0.30, indicating that it had the most significant influence on the long-term stability of cropland, followed by relief amplitude and soil type. This phenomenon may be attributed to the inadequate execution of the Grain for Green Policy and the requisition–compensation balance of cropland policy, along with the depletion of young and middle-aged laborers due to urban migration from rural areas. Local governments should focus on addressing the unsustainable exploitation of sloped land in rural mountainous or hilly regions while preventing urban developers from appropriating fertile cropland to compensate for less fertile areas. [ABSTRACT FROM AUTHOR]

Using the principle of antibody-drug conjugates that deliver highly potent cytotoxic agents to cancer cells for cancer therapy, we here report the synthesis of antisense-oligonucleotides (ASO) and thyroid hormone T3 conjugates for obesity treatment. ASOs primarily target fat and liver with poor penetrance to other organs. Pharmacological T3 treatment increases energy expenditure and causes weight loss, but is contraindicated for obesity treatment due to systemic effects on multiple organs. We hypothesize that ASO-T3 conjugates may knock down target genes and enrich T3 action in fat and liver. Two established ASOs are tested. Nicotinamide N-methyltransferase (NNMT)-ASO prevents diet-induced obesity in mice. Apolipoprotein B (ApoB)-ASO is an FDA approved drug for treating familial hypercholesterolemia. NNMT-ASO and ApoB-ASO are chemically conjugated with T3 using a non-cleavable sulfo-SMCC linker. Both NNMT-ASO-T3 (NAT3) and ApoB-ASO-T3 (AAT3) enhance thyroid hormone receptor activity. Treating obese mice with NAT3 or AAT3 decreases adiposity and increases lean mass. ASO-T3 enhances white fat browning, decreases genes for fatty acid synthesis in liver, and shows limited effects on T3 target genes in heart and muscle. Furthermore, AAT3 augments LDL cholesterol-lowering effects of ApoB-ASO. Therefore, ASO and hormone/drug conjugation may provide a novel strategy for obesity and hyperlipidemia treatment.

Background: Nanoplastics (NPs) are now a new class of pollutants widely present in the soil, atmosphere, freshwater and marine environments. Nanoplastics can rapidly penetrate cell membranes and accumulate in human tissues and organs, thus posing a potential threat to human health. The heart is the main power source of the body. But up to now, the toxicological effects of long-term exposure to nanoplastics on the heart has not been revealed yet. Results: We evaluated the effects of long term exposure of nanoplastics on cardiac cell/tissue in vitro and in vivo model. Furthermore, we explored the molecular mechanism by which nanoplastics exposure causes myocardial cell senescence. Immunohistochemistry, indirect immunofluorescence and ELISA were performed to detect the effects of nanoplastics on heart aging. We found that nanoplastics were able to induce significant cardiac aging through a series of biochemical assays in vivo. In vitro, the effects of nanoplastics on cardiac cell were investigated, and found that nanoplastics were able to internalize into cardiomyocytes in time and dose-dependant manner. Further biochemical analysis showed that nanoplastics induces cardiomyocytes senescence by detecting a series of senescence marker molecules. Molecular mechanism research shows that nanoplastics may cause mitochondrial destabilization by inducing oxidative stress, which leads to the leakage of mtDNA from mitochondria into the cytoplasm, and then cytoplasm-localized mt-DNA activates the cGAS-STING signaling pathway and promotes inflammation response, ultimately inducing cardiomyocytes senescence. Conclusions: In this work, we found that nanoplastics exposure induces premature aging of heart. Current research also reveals the molecular mechanism by which nanoplastics induces cardiomyocyte senescence. This study laid the foundation for further studying the potential harm of nanoplastics exposure on heart. [ABSTRACT FROM AUTHOR]

Wind energy is an important clean energy, according to China's carbon peak and carbon neutral strategy, the policy of replacing small with large wind turbine blades and replacing old with new is imperative. The main material of wind turbine blades is glass fiber reinforced polymer, which has problems of difficult recycling technology and high recycling cost. Nowadays, there is no ideal large-scale recycling method. Therefore, the systematic and high-value utilization of waste wind turbine blades is imminent. In this paper, the material type, recycling methods and their respective characteristics of wind turbine blades are summarized. The recent developments of waste wind turbine blades in cement-based materials and thermoplastic polymer materials are thoroughly discussed. Overall, this paper can provide reference for the subsequent development and research on the recycling waste wind turbine blades. [ABSTRACT FROM AUTHOR]