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China is among the top nitrous oxide (N2O)-emitting countries, but existing national inventories do not provide full-scale emissions including both natural and anthropogenic sources. We conducted a four-decade (1980 – 2020) of comprehensive quantification of Chinese N2O inventory using empirical emission factor method for anthropogenic sources and two up-to-date process-based models for natural sources. Total N2O emissions peaked at 2287.4 (1774.8 – 2799.9) Gg N2O yr−1 in 2018, and agriculture-developed regions, like the East, Northeast, and Central, were the top N2O-emitting regions. Agricultural N2O emissions have started to decrease after 2016 due to the decline of nitrogen fertilization applications, while, industrial and energetic sources have been dramatically increasing after 2005. N2O emissions from agriculture, industry, energy, and waste represented 49.3%, 26.4%, 17.5%, and 6.7% of the anthropogenic emissions in 2020, respectively, which revealed that it is imperative to prioritize N2O emission mitigation in agriculture, industry, and energy. Natural N2O sources, dominated by forests, have been steadily growing from 317.3 (290.3 – 344.1) Gg N2O yr−1 in 1980 to 376.2 (335.5 – 407.2) Gg N2O yr−1 in 2020. Our study produces a Full-scale Annual N2O dataset in China (FAN2020), providing emergent counting to refine the current national N2O inventories. [ABSTRACT FROM AUTHOR]

Emissions of nitrous oxide (N2O) from aquatic ecosystems are on the rise due to the dramatic increase in global reactive nitrogen input by anthropogenic activities (e.g., agricultural nitrogen fertilizer use). However, uncertainties exist in the estimation of aquatic N2O budgets due to limited knowledge of mechanisms involved in aquatic N2O emissions, as well as the N2O flux measurements and modelling. To give a full picture of aquatic N2O emissions, this review discusses the biotic and abiotic mechanisms involved in aquatic N2O emissions, common methods used in aquatic N2O flux measurements (including field measurement methods and formula simulation methods), and alternatives for aquatic N2O budget estimation. In addition, this review also suggests that stable isotope technology is promising in the application of aquatic N2O source partitioning. [ABSTRACT FROM AUTHOR]

Hydroxylamine (NH 2 OH) is a critical precursor of nitrous oxide (N 2 O) and key intermediate in the nitrogen cycle. However, the conversion of NH 2 OH is very fast, and the lack of real-time 15 N analytical methods for NH 2 OH hinders the on-time capture of its biochemical signals in the N cycle. To bridge this gap, we developed a novel approach for real-time determination of 15 N-enriched NH 2 OH. In this approach, an automated sample inlet unit was coupled to a membrane-inlet mass spectrometer, and NH 2 OH was converted to N 2 O by sodium hypochlorite for analysis. The interference of carbon dioxide was successfully removed by an ascarite trap, and the N 2 O signal showed good linearity over the targeted NH 2 OH concentrations. The limit of detection and limit of quantification of this approach were 0.38 and 1.28 μM, respectively, and 15 N enrichment can be accurately detected when the 15 N enrichment is higher than 5 atom %. This approach provides a first online analytical tool to capture real-time NH 2 OH transforming signals using the 15 N tracing technique, which will advance mechanism studies of the N cycle.

Background: Diabetic foot ulcers (DFUs) pose a substantial healthcare challenge due to their high rates of morbidity, recurrence, disability, and mortality. Current DFU therapeutics continue to grapple with multiple limitations. Senescent cells (SnCs) have been found to have a beneficial effect on acute wound healing, however, their roles in chronic wounds, such as DFU, remain unclear. Methods and results: We collected skin, fat, and muscle samples from clinical patients with DFU and lower limb fractures. RNA-sequencing combined with qPCR analyses on these samples demonstrate a significant accumulation of SnCs at DFU, as indicated by higher senescence markers (e.g., p16 and p21) and a senescence-associated secretory phenotype (SASP). We constructed a type 2 diabetic model of db/db mice, fed with a high-fat diet (Db-HFD), which were wounded using a 6 mm punch to the dorsal skin. HFD slightly affected wound healing in wild-type (WT) mice, but high glucose significantly delayed wound healing in the Db-HFD mice. We injected the mice with a previously developed fluorescent probe (XZ1208), which allows the detection of SnCs in vivo , and observed a strong senescence signal at the wound site of the Db-HFD mice. Contrary to the beneficial effects of SnCs in acute wound healing, our results demonstrated that clearance of SnCs using the senolytic compound ABT263 significantly accelerated wound healing in Db-HFD mice. Conclusion: Collectively, these findings suggest that SnCs critically accumulate at wound sites, delaying the healing process in DFUs. Thus, targeting SnCs with senolytic therapy represents a promising approach for DFU treatment, potentially improving the quality of life for patients with DFUs., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Background: Currently, a significant number of miners are involved in mining operations at the Gejiu tin mine in Yunnan. This occupational setting is associated with exposure to dust particles, heavy metals, polycyclic aromatic hydrocarbons, and radioactive radon, thereby significantly elevating the risk of lung cancer. This study aims to investigate the involvement of leptin-mediated extracellular regulated protein kinase (ERK) signaling pathway in the malignant transformation of rat alveolar type II epithelial cells induced by Yunnan tin mine dust., Methods: Immortalized rat alveolar cells type II (RLE-6TN) cells were infected with Yunnan tin mine dust at a concentration of 200 μg/mL for nine consecutive generations to establish the infected cell model, which was named R₂₀₀ cells. The cells were cultured normally, named as R cells. The expression of leptin receptor in both cell groups was detected using the Western blot method. The optimal concentration of leptin and mitogen-activated protein kinase kinase (MEK) inhibitor (U0126) on R₂₀₀ cells was determined using the MTT method. Starting from the 20th generation, the cells in the R group were co-cultured with leptin, while the cells in the R₂₀₀ group were co-cultured with the MEK inhibitor U0126. The morphological alterations of the cells in each group were visualized utilizing hematoxylin-eosin staining. Additionally, concanavalin A (ConA) was utilized to detect any morphological differences, and an anchorage-independent growth assay was conducted to assess the malignant transformation of the cells. The changes in the ERK signaling pathway in epithelial cells after the action of leptin were detected using the Western blot method., Results: Both the cells in the R group and R₂₀₀ group express leptin receptor OB-R. Compared to the R₂₀₀ group, the concentration of leptin at 100 ng/mL shows the most significant pro-proliferation effect. The proliferation of R₂₀₀ cells infected with the virus is inhibited by 30 μmol/L U0126, and a statistically significant divergence was seen when compared to the control group (P<0.05). Starting from the 25th generation, the cell morphology of the leptin-induced R₂₀₀ group (R₂₀₀L group) underwent changes, leading to malignant transformation observed at the 30th generation. The characteristics of malignant transformation became evident by the 40th generation in the R₂₀₀L group. In contrast, the other groups showed agglutination of P40 cells, and the speed of cell aggregation increased with an increase in ConA concentration. Notably, the R₂₀₀L group exhibited faster cell aggregation compared to the U0126-induced R₂₀₀ (R₂₀₀LU) group. Additionally, the cells in the R₂₀₀L group were capable of forming clones starting from P30, with a colony formation rate of 2.25‰±0.5‰. However, no clonal colonies were observed in the R₂₀₀LU group and R₂₀₀ group. The expression of phosphorylated extracellular signal-regulated kinase (pERK) was enhanced in cells of the R₂₀₀L group. However, when the cells in the R₂₀₀L group were treated with U0126, a blocking agent, the phosphorylation level of pERK decreased., Conclusions: Leptin can promote the malignant transformation of lung epithelial cells infected by mine dust, and the ERK signaling pathway may be necessary for the transformation of alveolar type II epithelial cells induced by Yunnan tin mine dust.