A simple and environmentally friendly self-assembly process of oppositely charged polymer PEI and inorganic oxide SiO2 was demonstrated for the construction of an ultrathin layer on the surface of PE separator. The XPS, FT-IR, SEM, and EDS characterizations give clear evidence of the successful self-assembly of PEI and SiO2 without significantly increasing the thickness and sacrificing the pristine porous structure of PE separator. This process improves a variety of crucial properties of PE separator such as the electrolyte wetting, the electrolyte uptake, the thermal stability, the ionic conductivity, Li+ transference number, the electrochemical stability and the compatibility with lithium electrode, endowing lithium-ion battery (Li as anode and LiCoO2 as cathode) with excellent capacity retention at high C-rates and superior cycling performance. At the current density of 5 C, the cell with PE separator almost loses all the capacity. In contrast, the cell with (PEI/SiO2)-modified PE separator still holds 45.2% of the discharge capacity at 0.2 C. The stabilized SEI formation and high Li+ transference number of (PEI/SiO2)-modified PE separator were interpreted to be the substantial reasons leading to the remarkably enhanced battery performance, rendering some new insights into the role of the separator in lithium-ion batteries.

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Background and Purpose Intrahepatic cholestasis is mainly caused by dysfunction of bile secretion and has limited effective treatment. Rosiglitazone is a synthetic agonist of PPARγ, whose endogenous agonist is 15‐deoxy‐Δ12,14‐PGJ2 (15d‐PGJ2). Reticulon 4B (Nogo‐B) is the detectable Nogo protein family member in the liver and secreted into circulation. Here, we determined if rosiglitazone can alleviate intrahepatic cholestasis in mice. Experimental Approach Wild‐type, hepatocyte‐specific PPARγ or Nogo‐B knockout mice received intragastric administration of α‐naphthylisothiocyanate (ANIT) and/or rosiglitazone, followed by determination of intrahepatic cholestasis and the involved mechanisms. Serum samples from primary biliary cholangitis (PBC) patients and non‐PBC controls were analysed for cholestasis‐related parameters. Key Results Rosiglitazone prevented wild type, but not hepatocyte‐specific PPARγ deficient mice from developing ANIT‐induced intrahepatic cholestasis by increasing expression of bile homeostatic proteins, reducing hepatic necrosis, and correcting abnormal serum parameters and enterohepatic circulation of bile. Nogo‐B knockout provided protection similar to that of rosiglitazone treatment. ANIT‐induced intrahepatic cholestasis decreased 15d‐PGJ2 but increased Nogo‐B in serum, and both were corrected by rosiglitazone. Nogo‐B deficiency in the liver increased 15d‐PGJ2 production, thereby activating expression of PPARγ and bile homeostatic proteins. Rosiglitazone and Nogo‐B deficiency also alleviated cholestasis‐associated dyslipidemia. In addition, rosiglitazone reduced symptoms of established intrahepatic cholestasis in mice. In serum from PBC patients, the decreased 15d‐PGJ2 and increased Nogo‐B levels were significantly correlated with classical cholestatic markers. Conclusions and Implications Levels of 15d‐PGJ2 and Nogo are important biomarkers for intrahepatic cholestasis. Synthetic agonists of PPARγ could be used for treatment of intrahepatic cholestasis and cholestasis‐associated dyslipidemia.

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