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Inevitable dissolution in aqueous electrolytes, intrinsically low electrical conductivity, and sluggish reaction kinetics have significantly hampered the zinc storage performance of vanadium oxide‐based cathode materials. Herein, core–shell N‐doped carbon‐encapsulated amorphous vanadium oxide arrays, prepared via a one‐step nitridation process followed by in situ electrochemical induction, as a highly stable and efficient cathode material for aqueous zinc‐ion batteries (AZIBs) are reported. In this design, the amorphous vanadium oxide core provides unobstructed ions diffusion routes and abundant active sites, while the N‐doped carbon shell can ensure efficient electron transfer and greatly stabilize the vanadium oxide core. The assembled AZIBs exhibit remarkable discharge capacity (0.92 mAh cm−2 at 0.5 mA cm−2), superior rate capability (0.51 mAh cm−2 at 20 mA cm−2), and ultra‐long cycling stability (≈100% capacity retention after 500 cycles at 0.5 mA cm−2 and 97% capacity retention after 10 000 cycles at 20 mA cm−2). The working mechanism is further validated by in situ X‐ray diffraction combined with ex situ tests. Moreover, the fabricated cathode is highly flexible, and the assembled quasi‐solid‐state AZIBs present stable electrochemical performance under large deformations. This work offers insights into the development of high‐performance amorphous vanadium oxide‐based cathodes for AZIBs. [ABSTRACT FROM AUTHOR]

Radiation enteritis (RE) is a prevalent complication of radiotherapy for pelvic malignant tumors, characterized by severe intestinal epithelial destruction and progressive submucosal fibrosis. However, little is known about the pathogenesis of this disease, and so far, there is no specific targeted therapy. Here, we report that CXCL16 is upregulated in the injured intestinal tissues of RE patients and in a mouse model. Genetic deletion of Cxcl16 mitigates fibrosis and promotes intestinal stem cell‐mediated epithelial regeneration after radiation injury in mice. Mechanistically, CXCL16 functions on myofibroblasts through its receptor CXCR6 and activates JAK3/STAT3 signaling to promote fibrosis and, at the same time, to transcriptionally modulate the levels of BMP4 and hepatocyte growth factor (HGF) in myofibroblasts. Moreover, we find that CXCL16 and CXCR6 auto‐ and cross‐regulate themselves in positive feedback loops. Treatment with CXCL16 neutralizing monoclonal antibody attenuates fibrosis and improves the epithelial repair in RE mouse model. Our findings emphasize the important role of CXCL16 in the progression of RE and suggest that CXCL16 signaling could be a potential therapeutic target for RE. © 2022 The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Most cancer‐related deaths result from the progressive growth of metastases. Patients with peritoneal metastatic (PM) colorectal cancer have reduced overall survival. Currently, it is still unclear why colorectal cancer (CRC) cells home to and proliferate inside the peritoneal cavity, and there is no effective consolidation therapy for improved survival. Using a proteomic approach, we found that key enzymes of fatty acid oxidation (FAO) were decreased in patients with PM colorectal cancer. Furthermore, we confirmed that carnitine palmitoyltransferase IA (CPT1A), a rate‐limiting enzyme of FAO, was expressed at significantly low levels in patients with PM colorectal cancer, as determined by RT‐qPCR, IHC, and GEO dataset analysis. However, lipidomics revealed no difference in FFA levels between PM and non‐PM primary tumors. Here, we showed that cancer‐associated fibroblasts (CAFs) promote the proliferation, migration, and invasion of colon cancer cells via upregulating CPT1A to actively oxidize FAs and conduct minimal glycolysis. In addition, coculture‐induced glycolysis increased in cancer cells while fatty acid catabolism decreased with lower adiponectin levels. Importantly, inhibition of glycolysis significantly reduced the survival of CRC cells after incubation with conditioned medium from CAFsCPT1A‐OEin vitro and impaired the survival and growth of organoids derived from CRC‐PM. Finally, we found that directly blocking FAO in CAFsCPT1A‐OE with etomoxir inhibits migration and invasion in vitro and decreases tumor growth and intraperitoneal dissemination in vivo, revealing a role for CAF CPT1A in promoting tumor growth and invasion. In conclusion, our results suggest the possibility of testing FAO inhibition as a novel approach and clinical strategy against CAF‐induced colorectal cancer with peritoneal dissemination/metastases. [ABSTRACT FROM AUTHOR]

A broadband rectangular waveguide TE10–TE20 mode converter with high mode purity and conversion efficiency is designed, fabricated and measured in this Letter. Based on the broadband characteristic of ridged twist waveguide and its characteristic of polarisation direction torsion of electromagnetic wave, this mode converter achieves broadband and high-efficiency TE10–TE20 mode conversion. Simulation results reveal that the return loss of the proposed mode converter is >20 dB and insertion loss is <0.04 dB in whole Ka-band. Two prototype TE20 mode converters were fabricated. Back-to-back millimeter-wave measurements by vector network analyser were performed to verify the design. The measured performances show return loss of the proposed mode converter is >20 dB and insertion loss is <0.1 dB in whole Ka-band, the corresponding mode conversion efficiency is >97.7%. [ABSTRACT FROM AUTHOR]