Hard-carbon is considered as one of the most promising anode materials for sodium-ion batteries (SIBs).

The discovery of proper ligands to simultaneously modulate the reactivity and effectively control the stereoselectivity is a central topic in the field of enantioselective C−H activation. Herein, we reported the synthesis of axially chiral biaryls by Pd‐catalyzed atroposelective C−H olefination. A novel chiral spiro phosphoric acid, STRIP, was identified as a superior ligand for this transformation. A broad range of axially chiral quinoline derivatives were synthesized in good yields with excellent enantioselectivities (up to 98 % ee). Density functional theory was used to gain a theoretical understanding of the enantioselectivities in this reaction.

P2-type Na 2/3 Ni 1/3 Mn 2/3 O 2 is an air-stable cathode material for sodium-ion batteries. However, it suffers irreversible P2-O2 phase transition in 4.2-V plateau and shows poor cycling stability and rate capability within this plateau. To evaluate the practicability of this material in 2.3-4.1 V voltage range, single-crystal micro-sized P2-type Na 2/3 Ni 1/3 Mn 2/3 O 2 with high rate capability and cycling stability is synthesized via polyvinylpyrrolidone (PVP)-combustion method. The electrochemical performance is evaluated by galvanostatic charge-discharge tests. The kinetics of Na + intercalation/ deintercalation is studied detailly with potential intermittent titration technique (PITT), galvanostatic intermittent titration technique (GITT) and cyclic voltammetry (CV). The discharge capacity at 0.1 C in 2.3-4.1 V is 87.6 mAh g-1. It can deliver 91.5% capacity at 40 C rate and keep 89% after 650 cycles at 5C. The calculated theoretical energy density of full cell with hard carbon anode is 210 Wh kg-1. The moderate energy density associated with high power density and long cycle life is acceptable for load adjustment of new-energy power, showing the prospect of practical application.

Cellular senescence is an initial barrier to tumor development that prevents the proliferation of premalignant cells. However, some of the features of senescent cells seem to promote tumor progression via senescence-associated secretory phenotype (SASP). Here, we demonstrated that the protein level of forkhead box Q1 (FOXQ1), which highly overexpresses in several kinds of tumors, was significantly downregulated during both replicative and oncogene-induced senescence. Moreover, overexpression of FOXQ1 delayed senescence, whereas FOXQ1 silence led to premature senescence in human fibroblasts. Furthermore, we identified that FOXQ1 upregulated SIRT1 expression through transcriptional regulation via directly binding to the SIRT1 promoter. Finally, we showed that FOXQ1 remarkably inhibited the replicative senescence through depressing the expression of the inflammatory cytokines interleukin-6 (IL-6) and IL-8 via modulation of SIRT1-NF-κB pathway. In addition, FOXQ1 overexpressed in human esophageal cancer cells and ablation of FOXQ1 restrained the tumourigenic ability of the esophageal cancer cells (EC109 and EC9706) in a mouse xenograft model in vivo. Taken together, these findings uncover a previously unidentified role of FOXQ1 regulating SASP and tumor development at same time.