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As the core component of wearable electronic devices, flexible energy storage materials play an irreplaceable role. At present, it is still a challenge to prepare flexible electrode materials with high energy density. In this paper, a polyaniline‐based composite flexible conductive hydrogel (PPG‐P) with a two‐level conductive network is successfully prepared by a secondary induced assembly in situ polymerization method. The special conductive structure greatly promotes the efficiency of charge transfer and the utilization of electroactive substances, so that PPG‐P exhibits excellent electrochemical performance. In a three‐electrode system, PPG‐P has a mass‐specific capacitance as high as 989 F g−1 (0.5 A g−1). After 1000 charge and discharge cycles, the capacitance retention is 87%. Symmetrical flexible supercapacitors based on PPG‐P have high specific capacitance (176 F g−1/0.5 A g−1) and high energy density (15.6 Wh kg−1). After 1000 cycles of constant current charge and discharge, the capacitance maintains 78.1%. The preparation of PPG‐P with a hierarchical structure demonstrates the possibility of achieving high energy density in flexible electrode materials, which has great application potential in the development of energy storage elements in wearable devices. [ABSTRACT FROM AUTHOR]

Background and Aim: We comprehensively carry out a systematic review and meta‐analysis of previous studies to determine the association between intestinal Faecalibacterium prausnitzii (F. prausnitzii) and inflammatory bowel disease (IBD) in human studies. Methods: A systematic literature search of PubMed, Embase, and the Cochrane Library database was conducted until April 1, 2020. Inclusion criteria were studies involving patients with Crohn's disease (CD) or ulcerative colitis (UC) with abundance of F. prausnitzii. The quality of the studies was assessed by the modified Newcastle–Ottawa scale. Results: A total of 1669 subjects (427 CD patients, 560 UC patients, and 682 healthy controls) were enrolled from 16 studies. Both CD (standardized mean difference [SMD]: −1.36; 95% CI, −1.74 to −0.98; P < 0.00001) and UC patients (SMD: −0.81; 95% CI, −1.21 to −0.42; P < 0.0001) had a lower abundance of F. prausnitzii than the healthy controls. Compared with the IBD remission patients, the IBD active patients had lower levels of F. prausnitzii (SMD: ‐0.56; 95% CI, −0.91 to −0.21; P = 0.002). In the subgroup analyses, the abundance of F. prausnitzii was reduced in both active CD patients (SMD: −0.78; 95% CI, −1.51 to −0.04; P = 0.04) and active UC patients (SMD:−0.44; 95%CI, −0.81 to −0.07; P = 0.02) when compared with the patients with CD or UC in remission, respectively. Conclusion: A negative association between abundance of F. prausnitzii and IBD activity is observed, but a cut‐off level of F. prausnitzii to diagnose and/or to start treating IBD is not determined. [ABSTRACT FROM AUTHOR]

Background and Aim: Autophagy and gut microbiota correlates closely with the inflammatory bowel disease. Herein, we aimed to study the roles of rapamycin on the gut microbiota in inflammatory bowel disease. Methods: Acute colitis was induced with dextran sodium sulfate (DSS) and 2,4,6‐trinitrobenzenesulfonic acid solution in mice. Mice were administered with rapamycin or hydroxychloroquine. Weight loss, disease activity index scores, histopathological score, serum inflammatory cytokines, intestinal permeability, and colonic autophagy‐related proteins were detected. Cecal content was also preserved in liquid nitrogen and subsequently analyzed following the 16S DNA sequencing. The antibiotic cocktail‐induced microbiome depletion was performed to further investigate the relationship between autophagy activation and gut microbiota. Results: Compared with the control group, the colonic autophagy‐related proteins of P62, mTOR, and p‐mTOR increased significantly, while the levels of LC3B and ATG16L1 decreased (all P < 0.05) in the model group. After rapamycin intervention, the colonic pathology of mice improved, while the disease activity index score decreased substantially; the colon length increased, and the expression of IL‐6 and TNF‐α decreased. Following hydroxychloroquine treatment, some indicators suggested aggravation of colitis. Principal coordinates analysis showed that the DSS group was located on a separate branch from the rapamycin group but was closer to the hydroxychloroquine group. Compared with the DSS group, the rapamycin group was associated with higher abundances of f_Lactobacillaceae (P = 0.0151), f_Deferribacteraceae (P = 0.0290), g_Lactobacillus (P = 0.0151), g_Mucispirillum (P = 0.0137), s_Lactobacillus_reuteri (P = 0.0028), and s_Clostridium sp Culture_Jar‐13 (P = 0.0082) and a lower abundance of s_Bacteroides_sartorii (P = 0.0180). Linear discriminant analysis effect size showed that rapamycin increased the abundances of Lactobacillus‐reuteri, Prevotellaceae, Paraprevotella, Christensenella and Streptococcus and decreased those of Peptostreptococcaceae and Romboutsia Bacteroides‐sartorii. Besides, the improvement effect of autophagy activation on colitis disappears following gut microbiome depletion. Conclusion: The therapeutic effects of rapamycin on extenuating experimental colitis may be related to the gut microbiota. [ABSTRACT FROM AUTHOR]

Background and Aim: Mucosal healing has emerged as a desirable treatment goal for patients with ulcerative colitis (UC). Healing of mucosal wounds involves epithelial cell proliferation and differentiation, and Y‐box transcription factor ZONAB has recently been identified as the key modulator of intestinal epithelial restitution. Methods: We studied the characteristics of UXT‐V1 expression in UC patients using immunohistochemistry and qPCR. The functional role of UXT‐V1 in the colonic epithelium was investigated using lentivirus‐mediated shRNA in vitro and ex vivo. Through endogenous Co‐immunoprecipitation and LC–MS/MS, we identified ZONAB as a UXT‐V1‐interactive protein. Results: Herein, we report that UXT‐V1 promotes differentiation of intestinal epithelial cells by regulating the nuclear translocation of ZONAB. UXT‐V1 was upregulated in the intestinal epithelia of UC patients compared with that of healthy controls. Knocking down UXT‐V1 in NCM‐460 cells led to the enrichment of pathways associated with proliferation and differentiation. Furthermore, the absence of UXT‐V1 in cultured intestinal epithelial cells and colonic organoids inhibited differentiation to the goblet cell phenotype. Mechanistically, the loss of UXT‐V1 in the intestinal epithelial cells allowed nuclear translocation of ZONAB, wherein it regulated the transcription of differentiation‐related genes, including AML1 and KLF4. Conclusion: Taken together, our study reveals a potential role of UXT‐V1 in regulating epithelial cell differentiation, proving a molecular basis for mucosal healing in UC. [ABSTRACT FROM AUTHOR]