TiNb 2 O 7 (TNO) is a competitive candidate of a fastcharging anode due to its high specific capacity. However, the insulator nature seriously hinders its rate performance. Herein, the La 3+ -doped mesoporous TiNb 2 O 7 materials (La−M−TNO) were first synthesized via a facile one-step solvothermal method with the assistance of polyvinyl pyrrolidone (PVP). The synergic effect of La 3+ doping and the mesoporous structure enables a dual improvement on the electronic conductivity and ionic diffusion coefficient, which delivers an impressive specific capacity of 213 mAh g −1 at 30 C. The capacity retention (@30C/@1C) increases from 33 to 53 and 74% for TNO, M−TNO, and La−M−TNO (0.03), respectively, demonstrating a step-by-step improvement of rate performance by making porous structures and intrinsic conductivity enhancement. DFT calculations verify that the enhancement in electronic conductivity due to La 3+ doping and oxygen vacancy, which induce localized energy levels via slight hybridization of O 2p, Ti 3d, and Nb 4d orbits. Meanwhile, the GITT result indicates that PVP-induced self-assembly of TNO accelerates the lithium ion diffusion rate by shortening the Li + diffusion path. This work verifies the effectiveness of the porous structure and highlights the significance of electronic conductivity to rate performance, especially at >30C. It provides a general approach to low-conductivity electrode materials for fast Li-ion storage.

Lithium−sulfur (Li−S) battery is a promising energy storage system due to its cost effectiveness and high energy density. However, formation of Li dendrites from Li metal anode and shuttle effect of lithium polysulfides (LiPSs) from S cathode impede its practical application. Herein, ultrafine ZnS nanodots are uniformly grown on 2D MXene nanosheets by a low‐temperature (60 °C) hydrothermal method for the first time. Distinctively, the ZnS nanodot‐decorated MXene nanosheets (ZnS/MXene) can be easily filtered to be a flexible and freestanding film in several minutes. The ZnS/MXene film can be used as a current collector for Li‐metal anode to promote uniform Li deposition due to the superior lithiophilicity of ZnS nanodots. ZnS/MXene powders obtained by freeze drying can be used as separator decorator to address the shuttle effect of LiPSs due to their excellent adsorbability. Theoretical calculation proves that the existence of ZnS nanodots on MXene can obviously improve the adsorption ability of ZnS/MXene with Li+ and LiPSs. Li−S full cells with composite Li‐metal anode and modified separator exhibit remarkable rate and cycling performance. Other transition metal sulfides (CdS, CuS, etc.) can be also grown on 2D MXene nanosheets by the low‐temperature hydrothermal strategy.

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BackgroundGNL3 has been reported to be up-regulated in cancers and function in tumor progression, whereas the role of GNL3 in the progression of osteosarcoma remains unclear.Materials and methodsIn this study, we blocked the expression of GNL3 by siRNA interference in osteosarcoma cell lines MG63 and U20S. CCK8, colony formation, wound-healing, Transwell, flow cytometry, and Hoechst/PI staining assays were used to examine the effects of GNL3 knockdown on cell proliferation, migration, invasion and apoptosis in MG63 and U20S cells. The relative activity of MMP9 was detected using Gelatin zymography assay. Western blot was performed to detect the expression of related proteins.ResultsWe found that silencing of GNL3 reduced the growth, migration, and invasion abilities of MG63 and U20S cells. Moreover, silencing GNL3 triggered cell cycle arrest in MG63 and U20S cells, as well as promoted cell apoptosis. In addition, depletion of GNL3 was observed to reduce the activity of MMP9 and suppress the process of epithelial–mesenchymal transition (EMT) through up-regulation of E-cadherin and down-regulation of N-cadherin. Furthermore, we found that X-box-binding protein 1 (XBP1) could bind to GNL3 using dual-luciferase reporter assay, and XBP1 overexpression could restore the inhibitory effects on proliferation, invasion, and EMT in MG63 and U20S cells caused by GNL3 knockdown.ConclusionThese data suggest that GNL3 functions as an oncogene in the progression of osteosarcoma by regulation of EMT, and XBP1 is also involved in its mechanism.