Zinc (Zn) holds great promise as a desirable anode material for next‐generation rechargeable batteries. However, the uncontrollable dendrite growth and low coulombic efficiency of the Zn plating/stripping process severely impede further practical applications of Zn‐based batteries. Here, these roadblocks are removed by using in situ grown zeolitic imidazolate framework‐8 (ZIF‐8) as the ion modulation layer to tune the diffusion behavior of Zn 2+ ions on Zn anodes. The well‐ordered nanochannels and N species of ZIF‐8 can effectively homogenize Zn 2+ flux distribution and modulate the plating/stripping rate, ensuring uniform Zn deposition without dendrite growth. The Zn corrosion and hydrogen evolution are also alleviated by the insulating nature of ZIF‐8, resulting in high coulombic efficiency. Therefore, the Zn@ZIF anode shows highly reversible, dendrite‐free Zn plating/stripping behavior under a broad range of current densities, and a symmetric cell using this anode can work correctly up to 1200 h with a low polarization at 2 mA cm −2 . Moreover, this ultrastable Zn@ZIF anode also enables a full Zn ion battery with outstanding cyclic stability (10 000 cycles).

We report the successful growth of high-quality single crystals of potassium intercalated iron selenide K x Fe 2−y Se 2 by Bridgeman method. The effect of iron vacancies on transport properties was investigated by electrical resistivity and magnetic susceptibility measurements. With varying iron content, the system passes from semiconducting/insulating to superconducting state. Comparing with superconductivity, the anomalous "hump" effect in the normal state resistivity is much more sensitive to the iron deficiency. The electrical resistivity exhibits a perfect metallic behavior (R 300K /R 35K ≈42) for the sample with little iron vacancies. Our results suggest that the anomalous "hump" effect in the normal state resistivity may be due to the ordering process of the cation vacancies in this non-stoichiometric compound rather than magnetic/structure transition. A trace of superconductivity extending up to near 44 K was also detected in some crystals of K x Fe 2−y Se 2 , which has the highest T c of the reported iron selenides.

We carried out high resolution angle-resolved photoemission measurements on the electronic structure and superconducting gap of K0.68Fe1.79Se2 (Tc=32 K) and (Tl0.45K0.34)Fe1.84Se2 (Tc=28 K) superconductors. In addition to the electron-like Fermi surface near M(π,π), two electronlike Fermi pockets are revealed around the zone center Γ(0,0) in K0.68Fe1.79Se2. This observation makes the Fermi surface topology of K0.68Fe1.79Se2 consistent with that of (Tl,Rb)xFe2−ySe2 and (Tl,K)xFe2−ySe2 compounds. A nearly isotropic superconducting gap (∆) is observed along the electron-like Fermi pocket near the M point in K0.68Fe1.79Se2 (∆∼ 9 meV) and (Tl0.45K0.34)Fe1.84Se2 (∆∼ 8 meV). The establishment of a universal picture on the Fermi surface topology and superconducting gap in the AxFe2−ySe2 (A=K, Tl, Cs, Rb and etc.) superconductors will provide important information in understanding the superconductivity mechanism of the iron-based superconductors.

Tumor cells preferentially adopt aerobic glycolysis for their energy supply, a phenomenon known as the Warburg effect. It remains a matter of debate as to how the Warburg effect is regulated during tumor progression. Here, we show that CHIP (carboxyl terminus of Hsc70-interacting protein), a U-box E3 ligase, suppresses tumor progression in ovarian carcinomas by inhibiting aerobic glycolysis. While CHIP is downregulated in ovarian carcinoma, induced expression of CHIP results in significant inhibition of the tumor growth examined by in vitro and in vivo experiments. Reciprocally, depletion of CHIP leads to promotion of tumor growth. By a SiLAD proteomics analysis, we identified pyruvate kinase isoenzyme M2 (PKM2), a critical regulator of glycolysis in tumors, as a target that CHIP mediated for degradation. Accordingly, we show that CHIP regulates PKM2 protein stability and thereafter the energy metabolic processes. Depletion or knockout of CHIP increased the glycolytic products in both tumor and mouse embryonic fibroblast cells. Simultaneously, we observed that CHIP expression inversely correlated with PKM2 levels in human ovarian carcinomas. This study reveals a mechanism that the Warburg effect is regulated by CHIP through its function as an E3 ligase, which mediates the degradation of PKM2 during tumor progression. Our findings shed new light into understanding of ovarian carcinomas and may provide a new therapeutic strategy for ovarian cancer.