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Combined treatment with potassium chloride (KCl) and N fertilizer produced lower N2O emissions than combined treatment with potassium sulfate (K2SO4) and N fertilizer during 15-d incubation periods. Our results imply that there are significant interaction effects between N fertilizers and K fertilizers on N2O emissions. In particular, combining N fertilizers with fertilizers that reduce soil acidity or contain Cl or K ions may significantly affect agricultural N2O emissions.Antibiotic resistance genes (ARGs) in the environment are an exposure risk to humans and animals and is emerging as a global public health concern. In this study, mercury (Hg) driven co-selection of ARGs was investigated under controlled conditions in two Australian non-agricultural soils with differing pH. Soils were spiked with increasing concentrations of inorganic Hg and left to age for 5 years. Both soils contained ARGs conferring resistance to tetracycline (tetA, tetB), sulphonamides (sul1), trimethoprim (dfrA1) and the ARG indicator class 1 integron-integrase gene, intI1, as measured by qPCR. The last resort antibiotic vancomycin resistance gene, vanB and quinolone resistance gene, qnrS were not detected. Hg driven co-selection of several ARGs namely intI1, tetA and tetB were observed in the alkaline soil within the tested Hg concentrations. No co-selection of the experimental ARGs was observed in the neutral pH soil. 16S rRNA sequencing revealed proliferation of Proteobacteria and Bacteriodetes in Hg contaminated neutral and alkaline soils respectively. Multivariate analyses revealed a strong effect of Hg, soil pH and organic carbon content on the co-selection of ARGs in the experimental soils. Additionally, although aging caused a significant reduction in Hg content, agriculturally important bacterial phyla such as Nitrospirae did not regrow in the contaminated soils. The results suggest that mercury can drive co-selection of ARGs in contaminated non-agricultural soils over five years of aging which is linked to soil microbiota shift and metal chemistry in the soil.To date, there have been no well-organized clinical studies evaluating which air pollutants affect dry eye disease (DED). In this study, we investigated changes in the clinical parameters of DED according to exposure to outdoor air pollutants, including PM2.5 (particulate matter with an aerodynamic diameter of less than 2.5 μm), PM10 (less than 10 μm), and ozone. A prospective observational study was conducted on 43 DED patients who had used the same topical eye drop treatment between 2016 and 2018 in South Korea. Ocular surface discomfort index (OSDI) score, tear film break-up time (TBUT), corneal fluorescein staining score (CFSS), and tear secretion were measured during each visit. Air pollution data of ambient PM10, PM2.5, and ozone, based on the patients' address, were obtained, and mean concentrations were computed for one day, one week, and one month before the examination. The relationships between air pollutants and DED were analyzed in single- and multi-pollutant models adjusted for demographic and clutant may aggravate DED via different mechanisms of action.We investigated the levels and distribution patterns of α- and β-endosulfan and endosulfan sulfate in air, soil, water, and sediment samples collected from the South Korean persistent organic pollutants (POPs) monitoring networks. In the air samples, the highest concentrations of the total (Σ3) endosulfan (50.3-611 pg/m3, mean 274 pg/m3) were observed during summer. Spearman analysis revealed a good correlation between agricultural land area and atmospheric concentrations of Σ3 endosulfan except during winter. Regardless of the season, the ratio of the two isomers (α/β) was 3.6-4.9 in the air samples, higher than that observed in technical mixtures (2.0-2.3), possibly due to the higher volatility of α-endosulfan, compared to β-endosulfan. Concentrations of Σ3 endosulfan in the soil samples (n.d.-13.4 ng/g, mean 0.8 ng/g) were not significantly different except at some stations adjacent to large areas of farmland. The average levels of Σ3 endosulfan in the water and sediment samples were 2.1 ng/L and 0.1 ng/g dw, respectively. In analyzing the four largest rivers, it was observed that a few water stations during spring and fall and sediment stations in fall had high concentrations of the two isomers and endosulfan sulfate, particularly around the Yeoungsan and Nakdong Rivers near large areas of agricultural land. Endosulfan sulfate was dominant at most water and sediment sampling stations. This study demonstrates that the endosulfan found in most environmental compartments most probably derives from agricultural areas despite its ban as a pesticide. On the other hand, given that it was also detected in industrial and urban areas, in which pesticide application does not occur, it can be conjectured that endosulfan is aerially transported at higher temperatures and continuously circulates within the environment.Thifluzamide is widely used in treatment of rice diseases and has potential toxicity on aquatic organism. Although previous studies have focused on the toxic effect of thifluzamide in zebrafish, no consistent conclusions have been reached. To help to elucidate the toxic mechanism, qualities of liver and mitochondria were evaluated. The global changes in the transcriptome of zebrafish after exposure to thifluzamide were measured. Based on this, the expression and activities of chitinase and succinate dehydrogenase (SDH) were further assayed. And the targeted site of thifluzamide in zebrafish was confirmed by dock study and co-exposure study. Here we report that developmental inhibition was observed along with presence of liver and mitochondrial damage. The expression of SDHa-d and genes related to mitochondrial DNA (mtDNA) replicate and mitochondrial complexes were significantly altered. And, as the top differentially expressed genes, the expression of chia.1-6 did show apparent changes, but differences of chitinase activity between exposure groups and the controls did not reach significance. In line with that, dock study showed that the binding potentials of thifluzamide toward zebrafish chitinase and SDH exhibited in the following order SDH> chitinase. And sdhb-sdhc-sdhd (Qp site) showed the highest binding activity toward thifluzamide. learn more The joint exposure (thifluzamide + Q10) significantly improved the survival of zebrafish compared with single thifluzamide exposure. These results indicate that SDH, especially Qp-site, may be the target of thifluzamide in zebrafish and inhibition of SDH activity may be at least in partial responsible for the toxicity of thifluzamide in zebrafish. In addition, the antagonistic effect of Q10 on thifluzamide toxicity in zebrafish suggests that Q10 may be a useful adjunct to detoxification.
Here's my website: https://www.selleckchem.com/ALK.html
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