High-Rate and Long-Cycle Cathode for Sodium-Ion Batteries: Enhanced Electrode Stability and Kinetics via Binder Adjustment.

Sodium-ion batteries (SIBs) are heralded as promising candidates for grid-scale energy storage systems due to their low cost and abundant sodium resources. Excellent rate capacity and outstanding cycling stability are always the goals for SIBs. Up to now, nearly all attention has been focused on the control of morphology and structure of electrode materials, but the influence of binders on their performance is neglected, especially in cathode materials. Herein, using Na3V2(PO4)2O2F (NVPOF) as a cathode material, the influence of four different binders (sodium alginate, SA; carboxymethylcellulose sodium, CMC; poly(vinylidene fluoride), PVDF; and poly(acrylic latex), LA133) on its electrochemical performance is studied. As a result, when using SA as the binder, the electrochemical performance of the NVPOF electrode is improved significantly, which is mainly because of the high water solubility, rich carboxyl and hydroxyl groups, and high adhesive and cohesive properties of the SA binder, leading to the uniform distribution of active materials NVPOF and carbon black in electrodes, good integrity, low polarization, and superior kinetic properties of the NVPOF electrodes, as demonstrated by scanning electron microscopy, cyclic voltammetry, electrochemical impedance spectroscopy, and galvanostatic intermittent titration technique. More importantly, when coupled with a hard carbon anode, the fabricated sodium-ion full cells also exhibit excellent rate performance, thus providing a preview of their practical application. This work shows that the battery performance can be improved by matching suitable binder systems, which is believed to have great importance for the further optimization of the electrochemical performance of SIBs.

Tim-3 expression in glioma cells is associated with drug resistance.

OBJECTIVE: T-cell immunoglobulin and mucin-domain containing-3 (Tim-3) has been widely recognized as a negative regulator of antitumor immunity. However, the mechanism by which Tim-3 suppresses antitumor treatment in gliomas remains unclear. This study aims to explore whether Tim-3 is expressed and to evaluate its effect in drug-fasted glioma cells. SUBJECTS AND METHODS: U87 and U251 glioma cell lines were tested. Cell proliferation activity, cell viability, and the protein and mRNA levels of Tim-3 were detected using CCK-8, flow cytometry, Western blotting, and reverse transcription-quantitative polymerase chain reaction, respectively. Enhancement of the sensitivity of glioma cells to chemotherapeutic agents was tested after inhibiting Tim-3 expression using Tim-3 small interfering RNAs (siRNA). RESULTS: As temozolomide (TMZ) concentration increased, the ratio of apoptotic cells also increased accordingly. However, the level of Tim-3 expression in living cells from the high-dose group was higher than in the low- and middle-dose groups. After interfering with the expression of Tim-3 using siRNA against Tim-3, the killing effect of TMZ rose through an increase in apoptosis. CONCLUSIONS: The presence of Tim-3 mRNA and protein in glioma cells was detected. Significantly, knocking down Tim-3 expression improved the potential of TMZ treatment.