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A solid‐state electrolyte (SSE), which is a solid ionic conductor and electron‐insulating material, is known to play a crucial role in adapting a lithium metal anode to a high‐capacity cathode in a solid‐state battery. Among the various SSEs, the single Li‐ion conductor has advantages in terms of enhancing the ion conductivity, eliminating interfacial side reactions, and broadening the electrochemical window. Covalent organic frameworks (COFs) are optimal platforms for achieving single Li‐ion conduction behavior because of well‐ordered one‐dimensional channels and precise chemical modification features. Herein, we study in depth three types of Li‐carboxylate COFs (denoted LiOOC‐COFn, n = 1, 2, and 3) as single Li‐ion conducting SSEs. Benefiting from well‐ordered directional ion channels, the single Li‐ion conductor LiOOC‐COF3 shows an exceptional ion conductivity of 1.36 × 10−5 S cm−1 at room temperature and a high transference number of 0.91. Moreover, it shows excellent electrochemical performance with long‐term cycling, high‐capacity output, and no dendrites in the quasi‐solid‐state organic battery, with the organic small molecule cyclohexanehexone (C6O6) as the cathode and the Li metal as the anode, and enables effectively avoiding dissolution of the organic electrode by the liquid electrolyte. [ABSTRACT FROM AUTHOR]

Background: Realgar, a Chinese herbal decoction, has been used to treat various types of tumors with positive outcomes; however, there is a lack of convincing evidence on its use for the treatment of esophageal cancer (EC). In this study, the role of the p62-Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the regulation of EC cell proliferation, migration, and ferroptosis in response to realgar was assessed., Methods: Different concentrations of realgar (0, 10, 20, 40, 60, 80, and 100 μmol/L) were applied to the EC cell lines Eca109 and KYSE150. The inhibition rate and half-inhibitory concentration (IC 50 ) were determined using the Cell Counting Kit-8 (CCK-8) method. Subsequently, the cells were treated with realgar (1/2IC 50 , IC 50 , 2IC 50 ). Cell migration was measured using the scratch assay, and cell invasion was measured using the transwell assay. The mRNA expression of p62, Keap1, and Nrf2 was measured by quantitative real-time polymerase chain reaction (qRT-PCR), and the protein expression of p62, Keap1, Nrf2, matrix metalloproteinase (MMP)-2, MMP-9, E-cadherin, Slug, N-cadherin, and vimentin was measured by Western blot. The control, 2IC 50 , shRNA-NC, shRNA-p62, 2IC 50 + shRNA-NC, 2IC 50 + shRNA-p62, shRNA-Keap1, 2IC 50 + shRNA-Keap1, and 2IC 50 + shRNA-p62 + shRNA-Keap1 groups were defined. The CCK-8 method was used to measure the cell inhibition rate, and the clone formation assay was used to measure the clone formation ability. Moreover, the scratch assay was used to detect the cell migration ability, and the transwell assay was used to detect the cell invasion ability. Transmission electron microscopy was used to observe the mitochondrial morphology, Prussian blue staining was used to observe the intracellular iron particle distribution, and flow cytometry was used to detect changes in intracellular reactive oxygen species. In addition, qRT-PCR was performed to detect p62, Keap1, Nrf2, and glutathione peroxidase 4 (GPX4) mRNA expression, and Western blot was performed to detect p62, Keap1, Nrf2, E-cadherin, Slug, N-cadherin, and GPX4 protein expression., Results: Realgar inhibited Eca109 and KYSE150 cell proliferation in a time- and concentrationdependent manner. It also significantly inhibited the migration and invasion of Eca109 and KYSE150 cells and affected the mRNA and protein expression of p62, Keap1, and Nrf2. In response to realgar, low p62 expression inhibited the proliferation, migration, and invasion of Eca109 and KYSE150 cells, as well as ferroptosis induction., Conclusion: The findings demonstrate that inhibiting the p62-Keap1-Nrf2 signaling pathway promotes the inhibitory effects of realgar on EC cells., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Lithium-sulfur (Li-S) batteries stand out for their high theoretical specific capacity and cost-effectiveness. However, the practical implementation of Li-S batteries is hindered by issues such as the shuttle effect, tardy redox kinetics, and dendrite growth. Herein, an appealingly designed covalent organic framework (COF) with bi-functional active sites of cyanide groups and polysulfide chains (COF-CN-S) is developed as cooperative functional promoters to simultaneously address dendrites and shuttle effect issues. Combining in situ techniques and theoretical calculations, it can be demonstrated that the unique chemical architecture of COF-CN-S is capable of performing the following functions: 1) The COF-CN-S delivers significantly enhanced Li + transport capability due to abundant ion-hopping sites (cyano-groups); 2) it functions as a selective ion sieve by regulating the dynamic behavior of polysulfide anions and Li + , thus inhibiting shuttle effect and dendrite growth; 3) by acting as a redox mediator, the COF-CN-S can effectively control the electrochemical behavior of polysulfides and enhance their conversion kinetics. Based on the above advantages, the COF-CN-S endows Li-S batteries with excellent performance. This study highlights the significance of interface modification and offers novel insights into the rational design of organic materials in the Li-S realm., (© 2023 Wiley-VCH GmbH.)

Iron homeostasis plays an important role for the maintenance of human health. It is known that iron metabolism is tightly regulated by several key genes, including divalent metal transport-1( DMT1 ), transferrin receptor 1( TFR1 ), transferrin receptor 2( TFR2 ), ferroportin( FPN ), hepcidin( HAMP ), hemojuvelin( HJV ) and Ferritin H . Recently, it is reported that DNA methylation, histone acetylation, and microRNA (miRNA) epigenetically regulated iron homeostasis. Among these epigenetic regulators, DNA hypermethylation of the promoter region of FPN, TFR2, HAMP , HJV and bone morphogenetic protein 6 ( BMP6 ) genes result in inhibitory effect on the expression of these iron-related gene. In addition, histone deacetylase (HADC) suppresses HAMP gene expression. On the contrary, HADC inhibitor upregulates HAMP gene expression. Additional reports showed that miRNA can also modulate iron absorption, transport, storage and utilization via downregulation of DMT1, FPN, TFR1, TFR2, Ferritin H and other genes. It is noteworthy that some key epigenetic regulatory enzymes, such as DNA demethylase TET2 and histone lysine demethylase JmjC KDMs, require iron for the enzymatic activities. In this review, we summarize the recent progress of DNA methylation, histone acetylation and miRNA in regulating iron metabolism and also discuss the future research directions.