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Sökning: WFRF:(Dong Huixian)

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1.
  • Kang, Ying, et al. (författare)
  • Weak Bonds Joint Effects Catalyze the Cleavage of Strong C−C Bond of Lignin‐Inspired Compounds and Lignin in Air by Ionic Liquids
  • 2020
  • Ingår i: ChemSusChem. - : John Wiley & Sons. - 1864-5631 .- 1864-564X. ; 13:22, s. 5945-5953
  • Tidskriftsartikel (refereegranskat)abstract
    • Oxidation of lignin to value‐added aromatics through selective C−C bond cleavage via metal‐free and mild strategies is promising but challenging. It was discovered that the cations of ionic liquids (ILs) could effectively catalyze this kind of strong bond cleavage by forming multiple weak hydrogen bonds, enabling the reaction conducted in air at temperature lower than 373 K without metal‐containing catalysts. The cation [CPMim]+ (1‐propylronitrile‐3‐methylimidazolium) afforded the highest efficiency in C−C bond cleavage, in which high yields (>90 %) of oxidative products were achieved. [CPMim]+ could form three ipsilateral hydrogen bonds with the oxygen atom of C=O and ether bonds at both sides of the C−C bond. The weak bonds joint effects could promote adjacent C−H bond cleave to form free radicals and thereby catalyze the fragmentation of the strong C−C. This work opens up an eco‐friendly and energy‐efficient route for direct valorization of lignin by enhancing IL properties via tuning the cation.
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2.
  • Li, Shenpan, et al. (författare)
  • Hepatic injury and ileitis associated with gut microbiota dysbiosis in mice upon F–53B exposure
  • 2024
  • Ingår i: Environmental Research. - : Elsevier. - 0013-9351 .- 1096-0953. ; 248
  • Tidskriftsartikel (refereegranskat)abstract
    • Chlorinated polyfluorinated ether sulfonate (F–53B), a substitute of perfluorooctane sulfonic acid (PFOS), has attracted significant attention for its link to hepatotoxicity and enterotoxicity. Nevertheless, the underlying mechanisms of F–53B-induced enterohepatic toxicity remain incompletely understood. This study aimed to explore the role of F–53B exposure on enterohepatic injury based on the gut microbiota, pathological and molecular analysis in mice. Here, we exposed C57BL/6 mice to F–53B (0, 4, 40, and 400 μg/L) for 28 days. Our findings revealed a significant accumulation of F–53B in the liver, followed by small intestines, and feces. In addition, F–53B induced pathological collagen fiber deposition and lipoid degeneration, up-regulated the expression of fatty acid β-oxidation-related genes (PPARα and PPARγ, etc), while simultaneously down-regulating pro-inflammatory genes (Nlrp3, IL-1β, and Mcp1) in the liver. Meanwhile, F–53B induced ileal mucosal barrier damage, and an up-regulation of pro-inflammatory genes and mucosal barrier-related genes (Muc1, Muc2, Claudin1, Occludin, Mct1, and ZO-1) in the ileum. Importantly, F–53B distinctly altered gut microbiota compositions by increasing the abundance of Akkermansia and decreasing the abundance of Prevotellaceae_NK3B31_group in the feces. F–53B-altered microbiota compositions were significantly associated with genes related to fatty acid β-oxidation, inflammation, and mucosal barrier. In summary, our results demonstrate that F–53B is capable of inducing hepatic injury, ileitis, and gut microbiota dysbiosis in mice, and the gut microbiota dysbiosis may play an important role in the F–53B-induced enterohepatic toxicity.
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