A N-carbon coated P-modified W2C composite (P-W2C@NC), prepared by annealing a mixture of H3PW12O40and dicyandiamide, exhibits excellent HER electrocatalytic activity and durability over the whole pH range.

A rationally designed oxygen evolution reaction (OER) catalyst with advanced structural and compositional superiority is highly desirable to optimize electrocatalytic performance. Prussian blue analogues (PBAs) with adjustable element compositions and accessible porous structures represent a promising precursor for the preparation of OER catalysts. Herein, oxygen‐doped nickel iron phosphide nanocube arrays (Ni2P/(NiFe)2P(O) NAs) grown on Ni foam is rationally designed and fabricated from PBAs. The porous structure and the synergistic effect of Ni and Fe enable superior electrocatalytic performance and stability toward the OER in alkaline electrolytes. Density functional theory calculations reveal that Fe‐incorporated Ni2P can generate new active sites on the Fe atoms, and the energy barriers of the intermediates and products are decreased efficiently in the presence of surface doped oxygen, both processes are crucial factors for enhanced catalytic performances. In 1 m KOH, the Ni2P/(NiFe)2P(O) NAs afford current densities of 10 and 800 mA cm−2 at overpotentials of 150 and 530 mV, respectively, which outperform the commercial noble metal IrO2. Ni2P/(NiFe)2P(O) NAs also have long‐term stability over 100 h at a high current density. The present approach may provide a new avenue for the controlled assembly of nanoarrays for energy storage and conversion applications.

A carbon-coated ultrafine cable-like WC/W2C heterojunction nanowire electrocatalyst exhibits remarkable HER performance in a wide pH range.

Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated cancer vulnerabilities in TNBC and identified an interplay between oncogenic and tumor suppressor pathways. This study reveals tumor regulatory functions for essential components of the mTOR and Hippo pathways in TNBC. Using in vitro drug matrix synergy models and in vivo patient-derived xenografts, we further establish the therapeutic relevance of our findings and show that pharmacological inhibition of mTORC1/2 and oncoprotein YAP efficiently reduces tumorigenesis in TNBC. At the molecular level, we find that while verteporfin-induced YAP inhibition leads to apoptosis, torin1-mediated mTORC1/2 inhibition promotes macropinocytosis. Torin1-induced macropinocytosis further facilitates verteporfin uptake, thereby greatly enhancing its pro-apoptotic effects in cancer cells. Overall, our study underscores the power and robustness of in vivo CRISPR genome-wide screens in identifying clinically relevant and innovative therapeutic modalities in cancer.