Dual redox catalysis of VN/nitrogen-doped graphene nanocomposites for high-performance lithium-sulfur batteries

Lithium-sulfur(Li-S)batteries are regarded as one of the promising candidates for the next-generation energy storage system owing to their high capacity and energy density.However,the durable operation for the batteries is blocked by the shuttle behavior of soluble lithium polysulfides and the sluggish kinetics in the redox process.Here,VN nanoparticles on nitrogen-doped graphene(VN/NG)composite is synthesized by simple calcining method to modify the separators,which can not only chemically trap polysulfides,but also catalyze the conversion reaction between the polysulfides and the insoluble Li2S during the charge/discharge process.The catalytic effects of VN/NG are verified by the calculated activation energy(E_(a)),which is smaller than the counterpart with NG toward both directions of redox.Because of the synergistic adsorption-catalysis of VN/NG,the cells with VN/NG-modified separators deliver a superior rate performance(791 mAh g^(-1) at 5C)and cycling stability(863 mAh g^(-1) after 300 cycles with a low decaying rate of 0.068%per loop at 1C).This work provides a simple preparation strategy and fundamental understanding of the bifunctional catalyst for high-performance Li-S batteries.

Effect of specifically-adsorbed polysulfides on the electron transfer kinetics of sodium metal anodes

Room-temperature sodium-sulfur(RT Na-S)batteries hold great promise for large-scale energy storage applications owing to the high energy density and earth-abundance of Na and S.However,the dissolution and migration of sodium polysulfides,uncontrollable Na dendrite growth,and the lack of studies on Na electrodeposition kinetics have hindered the development of these batteries.Herein,we reveal the mechanism of sodium polysulfides on the Na plating/stripping kinetics using a three-electrode system.First,the kinetic behavior deviates from the commonly supposed Butler-Volmer model,which is well described by the Marcus model.In addition,the specific adsorption of polysulfides on the sodium electrode surface is a key factor influencing the kinetics.Higher-order polysulfides(S_(8)^(2-)and S_(6)^(2-))exhibit distinct specific adsorption behaviors because of their high adsorption energies compared to lower-order polysulfides(S_(4)^(2-)and S_(2)^(2-)).The electrostatic effect caused by specific adsorption can accelerate the kinetics,whereas the blocking effect can slow the kinetics.Thus,this competitive relationship enables low concentrations of high-order polysulfides to stimulate kinetics.This implies that a weak shuttle effect is beneficial for obtaining a stable Na deposition in RT Na-S batteries.An in-depth understanding of the Na electrodeposition kinetics provides beneficial clues for future metal sodium/electrolyte interface designs.

Study on Cisplatin Aggravating DNA Damage and Causing a High Apoptosis Rate on Breast Cancer MCF-7 Cells

[Objectives] To investigate the mechanism of DNA damage of cisplatin( DDP),a broad spectrum anticancer drug on breast cancer MCF-7 cells,and to study the mechanism of apoptosis induced by DDP.[Methods]MCF-7 cells were treated by DDP( 0 mg/L,2 mg/L,4 mg/L,6 mg/L,6 mg/L,and 10 mg/L) for 48 hours. MTT assay was used to detect the inhibitory effect of DDP on MCF-7 cells and IC50 value was calculated. Western blot was adopted to detect the expression of γ-H2 AX,which was the marker of DNA double stranded breaks( DSBs) and ATM( sensory molecules of DSBs),the apoptotic signal transduction molecule cleaved caspase-3,and the proteins associated with apoptosis calpain.[Results]DDP inhibited MCF-7 cell activity in a concentration-dependent manner and IC50 was 7. 57 mg/L. In contrast to the control group( without DDP treatment),MCF-7 cells with DDP treatment expressed more γ-H2 AX,ATM,cleaved caspase-3 and calpain.[Conclusions] DDP could inhibit the activity of breast cancer MCF-7 cells. Its mechanisms may be associated with inhibition of MCF-7 cell apoptosis,induction of DNA double strand breaking and the expression of pro-apoptotic protein up-regulation.