Ultrahigh nickel cathode materials are widely utilized due to their outstanding energy and power densities. However, the presence of cobalt can cause significant lattice distortion during charge and discharge cycles, leading to the loss of active lithium, the formation of lattice cracks, and the emergence of a rock salt phase that hinders lithium-ion transport. Herein, we developed a novel cobalt-free, aluminum-doped cathode material, LiNiMnAlO (NMA), which effectively delays the harmful H2-H3 phase transition, reduces lattice distortion, alleviates stress release, and significantly enhances structural stability.
View Article and Find Full Text PDFEsophageal squamous cell carcinoma (ESCC) is prone to metastasis and is a leading cause of mortality. The cytoskeleton is closely related to cell morphology and movement; however, little research has been conducted on ESCC metastasis. In this study, we found that the anchoring filament protein ladinin 1 (LAD1) specifically binds to LINC01305 for co-regulating the level of modulating cortactin proteins (CTTN) and neuronal Wiskott-Aldrich syndrome protein (N-WASP) phosphorylation, which mediates cytoskeletal reorganization and affects the metastasis of ESCC cells.
View Article and Find Full Text PDFThe thermocatalytic hydrogenation of CO2 to ethanol has attracted significant interest because ethanol offers ease of transport and substantial value in chemical synthesis. Here, we present a state-of-the-art catalyst for the CO2 hydrogenation to ethanol achieved by precisely depositing single-atom Ir species on P cluster islands situated on the In2O3 nanosheets. The Ir1-Px/In2O3 catalyst achieves an impressive ethanol yield of 3.
View Article and Find Full Text PDFIn plants, sperm cell formation involves two rounds of pollen mitoses, in which the microspore initiates the first pollen mitosis (PMI) to produce a vegetative cell and a generative cell, then the generative cell continues the second mitosis (PMII) to produce two sperm cells. DUO1, a R2R3 Myb transcription factor, is activated in the generative cell to promote S-G2/M transition during PMII. Loss-of-function of DUO1 caused a complete arrest of PMII.
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