Surface Lattice Modulation Enables Stable Cycling of High-Loading All-solid-state Batteries at High Voltages.

Halide solid electrolytes, known for their high ionic conductivity at room temperature and good oxidative stability, face notable challenges in all-solid-state Li-ion batteries (ASSBs), especially with unstable cathode/solid electrolyte (SE) interface and increasing interfacial resistance during cycling. In this work, we have developed an Al3+-doped, cation-disordered epitaxial nanolayer on the LiCoO2 surface by reacting it with an artificially constructed AlPO4 nanoshell; this lithium-deficient layer featuring a rock-salt-like phase effectively suppresses oxidative decomposition of Li3InCl6 electrolyte and stabilizes the cathode/SE interface at 4.5 V. The ASSBs with the halide electrolyte Li3InCl6 and a high-loading LiCoO2 cathode demonstrated high discharge capacity and long cycling life from 3 to 4.5 V. Our findings emphasize the importance of specialized cathode surface modification in preventing SE degradation and achieving stable cycling of halide-based ASSBs at high voltages.

Facile Construction of Nanofilms from a Dip-Coating Process to Enable High-Performance Solid-State Batteries.

The use of solid-state electrolytes (SSEs) instead of those liquid ones has found promising potential to achieve both high energy density and high safety for their applications in the next-generation energy storage devices. Unfortunately, SSEs also bring forth challenges related to solid-to-solid contact, making the stability of the electrode/electrolyte interface a formidable concern. Herein, using a garnet-type Li6.5La3Zr1.5Ta0.5O12 (LLZT) electrolyte as an example, we demonstrated a facile treatment based on the dip-coating technique, which is highly efficient in modifying the LLZT/Li interface by forming a MgO interlayer. Using polyvinyl pyrrolidone (PVP) as a coordination polymer, uniform and crack-free nanofilms are fabricated on the LLZT pellet with good control of the morphological parameters. We found that the MgO interlayer was highly effective to reduce the interfacial resistance to 6 Ω cm2 as compared to 1652 Ω cm2 of the unmodified interface. The assembled Li symmetrical cell was able to achieve a high critical current density of 1.2 mA cm-2 at room temperature, and it has a long cycling capability for over 4000 h. Using the commercialized materials of LiFePO4 and LiNi0.83Co0.07Mn0.1O2 as the cathode materials, the full cells based on the LLZT@MgO electrolyte showed excellent cyclability and high rate performance at 25 °C. Our study shows the feasibility of precise and controllable surface modification based on a simple liquid phase method and highlights the essential importance of interface control for the future application of high-performance solid-state batteries.

miR-381-3p inhibits high glucose-induced vascular smooth muscle cell proliferation and migration by targeting HMGB1.

BACKGROUND: Hyperglycemia increases the risk of many cardiovascular diseases (CVD), and the dysregulation of proliferation and migration in vascular smooth muscle cells (VSMCs) also participates in the pathogenesis of CVD. miR-381-3p is known to suppress the proliferation and migration of multiple human cell types. Nevertheless, the function of miR-381-3p in VSMCs remains largely indistinct. METHODS: A quantitative real-time polymerase chain reaction (qRT-PCR) was employed to investigate miR-381-3p expression in high-glucose-induced VSMCs. Inflammatory cytokines tumor necrosis factor-α, interleukin-1ß and interleukin-6, as well as oxidative stress markers SOD and MDA, were determined by an enzyme-linked immunosorbent assay. Reactive oxygen species generation was examined using a 2,7'-dichlorofluorescein kit. The proliferation, migration and apoptosis of VSMCs were monitored by 3-(4,5-dimethylthiazl2-yl)-2,5-diphenyltetazolium bromide (MTT), transwell and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assays. The TargetScan database (http://www.targetscan.org) was employed to seek the potential target gene of miR-381-3p. Interaction between miR-381-3p and HMGB1 was determined by a qRT-PCR, western blotting and a luciferase reporter assay. RESULTS: miR-381-3p expression was significantly reduced in a VSMCs dysfunction model induced by high-glucose in a dose- and time-dependent manner. Transfection of miR-381-3p mimics suppressed the inflammation, oxidative stress, proliferation and migration of VSMCs, whereas apoptosis of VSMCs was promoted, and the transfection of miR-381-3p inhibitors had the opposite effect. Mechanistically, HMGB1, an important factor in inflammation response, was confirmed as a target gene of miR-381-3p. CONCLUSIONS: miR-381-3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high-glucose-induced VSMCs by targeting HMGB1.