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Lithium metal battery has great development potential because of its lowest electrochemical potential and highest theoretical capacity. However, the uneven deposition of Li+ flux in the process of deposition and stripping induces the vigorous growth of lithium dendrites, which results in severely battery performance degradation and serious safety hazards. Here, the tetragonal BaTiO3 polarized by high voltage corona was used to build an artificial protective layer with uniform positive polarization direction, which enables uniform Li+ flux. In contrast to traditional strategies of using protective layer, which can guide the uniform deposition of lithium metal. The ferroelectric protective layer can accurately anchor the Li+ and achieve bottom deposition of lithium due to the automatic adjustment of the electric field. Simultaneously, the huge volume changes caused by Li+ migration change of the lithium metal anode during charging and discharging is functioned to excite the piezoelectric effect of the protective layer, and achieve seamless dynamic tuning of lithium deposition/stripping. This dynamic effect can accurately anchor and capture Li+. Finally, the layer‐modified Li anode enables reversible Li plating/stripping over 1500 h at 1 mA cm−2 and 50 °C in symmetric cells. In addition, the assembled Li‐S full cell exhibits over 300 cycles with N/P ≈ 1.35. This work provides a new perspective on the uniform Li+ flux at the Li‐anode interface of the artificial protective layer. [ABSTRACT FROM AUTHOR]

Increasing the exposure of active crystal facets is an effective strategy to promote the transmission of Na+ through the electrolyte/cathode interface and is key to developing high-performance sodium-ion battery (SIB) cathodes. Here, Na3V2(PO4)2F3 (NVPFs) were synthesized with diverse (002) active facet exposure rates, in which the growth rate of the different crystal facets was regulated by adjusting the surface energy. The growth mechanism of the NVPF crystals was proposed using density functional theory calculations. The NVPFs with 82% (002) active facet exposure delivered a remarkable reversible capacity of 123 mA h g−1 and energy density of 431 W h kg−1 in a full cell. Theoretical investigations of the Na+ adsorption, diffusion, and storage clarified that the exposed (002) crystal facet had more stable Na+-storage sites, which resulted in a lower energy barrier during the Na+-diffusion process. The promoted Na+-transportation kinetics and related enhanced stability were further elucidated based on the combined analyses of synchrotron X-ray absorption spectroscopy and electrochemical measurements. This research aimed to develop a way to promote the transmission process of Na+ through the electrolyte/cathode interface from the perspective of crystal facet regulation, which is expected to promote the commercial application of SIB cathodes. [ABSTRACT FROM AUTHOR]

Sorafenib is the most widely used first-line drug for the treatment of the advanced hepatocellular carcinoma (HCC). Unfortunately, sorafenib resistance often limits its therapeutic efficacy. To evaluate the efficacy of artesunate against sorafenib-resistant HCC and to investigate its underlying pharmacological mechanisms, a "sorafenib resistance related gene-ART candidate target" interaction network was constructed, and a signaling axis consisting with artesunate candidate target AFAP1L2 and sorafenib target SRC, and the downstream FUNDC1-dependent mitophagy was identified as a major contributor to the sorafenib resistance and a potential way of artesunate to mitigate resistance. Notably, our clinical data demonstrated that AFAP1L2 expression in HCC tissues was markedly higher than that in adjacent non-cancerous liver tissues (P < 0.05), and high AFAP1L2 expression was also significantly associated with an unfavorable overall survival of HCC patients (P < 0.05). Experimentally, AFAP1L2 was overexpressed in sorafenib resistant cells, leading to the activation of downstream SRC-FUNDC1 signaling axis, further blocking the FUNDC1 recruitment of LC3B to mitochondria and inhibiting the activation of mitophagy, based on both in vitro and in vivo systems. Moreover, artesunate significantly enhanced the inhibitory effects of sorafenib on resistant cells and tumors by inducing excessive mitophagy. Mechanically, artesunate reduced the expression of AFAP1L2 protein, suppressed the phosphorylation levels of SRC and FUNDC1 proteins, promoted the FUNDC1 recruitment of massive LC3B to mitochondria, and further overactivated the mitophagy and subsequent cell apoptosis of sorafenib resistant cells. In conclusion, artesunate may be a promising strategy to mitigate sorafenib resistance in HCC via exacerbating AFAP1L2-SRC-FUNDC1 axis-dependent mitophagy. Abbreviations: AFAP1L2, actin filament associated protein 1 like 2; ANOVA, analysis of variance; ANXA5, annexin V; ART: artesunate; CETSA, cellular thermal shift assay; CI: combination index; CO-IP: co-immunoprecipitation; CQ: chloroquine; CT, computed tomography; [18F]-FDG, fluoro-2-D-deoxyglucose F18; FUNDC1: FUN14 domain containing 1; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HCC, hepatocellular carcinoma; H&E Staining: hematoxylin – eosin staining; HepG2R, sorafenib resistant HepG2; IF, immunofluorescence; IHC, immunohistochemistry; LAMP1: lysosomal associated membrane protein 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; miR, microRNA; mRNA: messenger RNA; OE, overexpression; OS, overall survival; PET, positron emission tomography; qRT-PCR: quantitative real-time PCR; sh, short hairpin; shNC: negative control shRNA; shAFAP1L2: short hairpin AFAP1L2; SORA, sorafenib; SPR, surface plasmon resonance; SRC, SRC proto-oncogene, non-receptor tyrosine kinase; SUV, standardized uptake value; TEM, transmission electron microscopy; TOMM20: translocase of outer mitochondrial membrane 20. [ABSTRACT FROM AUTHOR]