The uncontrolled zinc dendrite growth during plating leads to quick battery failure, which hinders the widespread applications of aqueous zinc-ion batteries. The growth of Zn dendrites is often promoted by the "tip effect". In this work, we propose a generate strategy to eliminate the "tip effect" by utilizing the electrostatic shielding effect, which is achieved by coating Zn anodes with magnetron sputtered Al-based alloy protective layers. The Al can form a surface insulating Al 2 O 3 layer and by manipulating the Al content of Zn−Al alloy films, we are able to control the strength of the electrostatic shield, therefore realizing a long lifespan of Zn anodes up to 3000 h at a practical operating condition of 1.0 mA cm −2 and 1.0 mAh cm −2 . In addition, the concept can be extended to other Al-based systems such as Ti−Al alloy and achieve enhanced stability of Zn anodes, demonstrating the generality and efficacy of our strategy.

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Rechargeable zinc-ion batteries (ZIBs) have shown great potential as an alternative to lithium-ion batteries. The ZIBs utilize Zn metal as the anode, which possesses many advantages such as low cost, high safety, eco-friendliness, and high capacity. However, on the other hand, the Zn anode also suffers from many issues, including dendritic growth, corrosion, and passivation. These issues are largely related to the surface and interface properties of the Zn anode. Many efforts have therefore been devoted to the modification of the Zn anode, aiming to eliminate the above-mentioned problems. This review gives a comprehensive summary on the mechanism behind these issues as well as the recent progress on Zn anode modification with focus on the strategies of surface and interface engineering, covering the design and application of both the Zn anode supports and surface protective layers, along with abundant examples. In addition, the promising research directions and perspective on these strategies are also presented.

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CrN thin films deposited on Si substrates show promising applications as electrode materials for high performance supercapacitors.

a b s t r a c tA series of graphitic-C 3 N 4 /ZnS (g-C 3 N 4 /ZnS) supercapacitor electrode materials have been prepared via a one-step calcination process of zinc acetate/thiourea with different mass ratios under nitrogen atmosphere. The optimized g-C 3 N 4 /ZnS composite shows a highest specific capacitance of 497.7 F/g at 1 A/g and good cycling stability with capacitance retention of 80.4% at 5 A/g after 10 0 0 cycles. Moreover, g-C 3 N 4 /ZnS composites display an improved supercapacitor performance in terms of specific capacitance compared to the pure g-C 3 N 4 and ZnS. In addition, our designed symmetric supercapacitor device based on g-C 3 N 4 /ZnS composite electrodes can exhibit an energy density of 10.4 Wh/kg at a power density of 187.3 W/kg. As a result, g-C 3 N 4 /ZnS composites are expected to be a prospective material for supercapacitors and other energy storage applications.

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Ovarian cancer stem cells (OCSCs) are sources of tumor chemoresistance and recurrence. A hypoxic microenvironment contributes to the chemoresistance of cancer stem cells (CSCs), but the underlying mechanism is not fully understood yet. Here, we show that increased HIF‐2α expression is associated with enhanced stemness of OCSCs and poor outcomes in ovarian cancer patients. OVCAR‐3 and CAOV‐3 sphere‐forming (OVCAR‐3 S and CAOV‐3 S) cells with OCSC‐like properties showed strong resistance to adriamycin (ADR). Hypoxia (1% O2) induced high expression of both HIF‐1α and especially HIF‐2α, and increased the resistance of OVCAR‐3 S and CAOV‐3 S cells to ADR. Notably, treatment with ADR further increased the expression of HIF‐2α, but not that of HIF‐1α. Knockdown of HIF‐2α expression substantially attenuated the resistance of OVCAR‐3 S and CAOV‐3 S cells to ADR, and the HIF‐2α overexpression had the opposite effect. Furthermore, in mouse models xenografted with OCSCs, HIF‐2α depletion significantly inhibited tumor growth and sensitized OCSCs to ADR in vivo. Mechanistically, HIF‐2α directly promotes transcription/expression of BCRP, a gene encoding a transporter protein responsible for pumping drugs (e.g., ADR) out of cells, which in turn increases drug resistance due to increased drug transportation. Collectively, our studies reveal a novel drug‐resistant mechanism in ovarian cancer by which hypoxia (and ADR treatment)‐induced HIF‐2α overexpression endows OCSCs with resistance to ADR by promoting BCRP expression and ADR transportation. Therefore, targeting the HIF‐2α/BCRP axis holds therapeutic potential for treating drug‐resistant ovarian cancer.