Single-Step Topochemical Synthesis of NiFe Layered Double Hydroxides for Superior Anion Removal from Aquatic Systems.

Layered double hydroxides (LDHs) have attracted significant attention as adsorbents for the removal of anions from wastewater. However, it is challenging to develop a simple, economical, and environmentally friendly method for fabricating efficient LDH adsorbents. In this paper, we present an alternative approach for preparing a superb NiFe LDH adsorbent via a single-step topochemical synthesis method based on density functional theory (DFT) calculation. The NiFe LDH adsorbent [Ni0.75Fe0.25(OH)2]·(CO3)0.125·0.25H2O was obtained via the topotactic transformation of an oxide precursor (NaNi0.75Fe0.25O2), which was prepared by utilizing the high-temperature flux method, in ultrapure water. When the oxide precursor was soaked in ultrapure water, the host layer valence state changed from Ni3+ and Fe3+ to Ni2+ and Fe3+, and carbonate (CO32-) ions were simultaneously intercalated in the interlayer. Thereafter, the CO32- ions were deintercalated by Cl- ions to increase the adsorption capacity. The adsorbent exhibited high crystallinity, cation state, and porosity, and unique particle shape. In addition, it showed superior adsorption capacities of approximately 194.92, 176.15, and 146.28 mg g-1 toward phosphate, fluoride, and nitrate ions, respectively. The adsorption capacity toward all the anions reached over 70% within 10 min. The adsorption behavior was investigated by performing from adsorption kinetics, isotherm, and thermodynamics studies. The results showed that the anions were endothermically and spontaneously chemisorbed through an ion exchange process onto the adsorbent in a monolayer. In addition, the as-prepared NiFe LDH adsorbent showed high stability after multicycle testing.

Very low-density lipoprotein receptor increases in a liver-specific manner due to protein deficiency but does not affect fatty liver in mice.

Very low-density lipoprotein receptor (VLDLR) is a member of the LDL receptor family that is involved in the uptake of VLDL into cells. Increased hepatic VLDLR under endoplasmic reticulum (ER) stress has been shown to cause fatty liver. In this study, the effect of dietary protein restriction on hepatic VLDLR and the role of VLDLR in fatty liver were investigated using Vldlr knockout (KO) mice. Growing wild-type (WT) and KO mice were fed a control diet containing 20% ​​protein or a low protein diet containing 3% protein for 11 days. In WT mice, the amount of hepatic Vldlr mRNA and VLDLR protein increased by approximately 8- and 7-fold, respectively, due to protein restriction. Vldlr mRNA and protein levels increased in both type 1 and type 2 VLDLR. However, neither Vldlr mRNA nor protein levels were significantly increased in heart, muscle, and adipose tissue, demonstrating that VLDLR increase due to protein restriction occurred in a liver-specific manner. Increased liver triglyceride levels during protein restriction occurred in KO mice to the same extent as in WT mice, indicating that increased VLDLR during protein restriction was not the main cause of fatty liver, which was different from the case of ER stress.