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Abstract The electrochemical conversion of CO2 into CO represents a promising strategy for mitigating excessive global greenhouse gas emissions. Nevertheless, achieving industrial‐scale electrochemical CO2‐to‐CO conversion with enhanced selectivity and reduced energy consumption presents significant challenges. In this study, a borate‐enhanced molten salt process for CO2 capture and electrochemical transformation is employed, achieving over 98% selectivity for CO and over 55% energy efficiency without the necessity for complex and costly electrocatalysts. Cathodic CO2 electro‐reduction (CO2ER) with the anodic oxygen evolution reaction (OER) at an overall current density of 500 mA cm−2 using non‐nanostructured transition‐metal plate electrodes at 650 °C is coupled. By regulating the electrolyte's oxo‐basicity with earth‐abundant borax (Na2B4O7), a borate‐enhanced electrolyte is established that accelerates the overall electrochemical reaction efficiently. This system involved a series of well‐designed target borate species (BO33−, BO2−, and B4O72−) that acted as mediators shuttling between the cathode and anode, favoring CO as the primary cathodic product. Manipulating the atmosphere above the anode facilitated a spontaneous transformation of borates, further enhancing OER performance with long‐term operational stability over a cumulative period of 50 h, while also reducing overall energy consumption. This work presents a cost‐effective strategy for the industrial‐scale production of CO derived from CO2, contributing to a lower carbon footprint by establishing a sustainable borate‐mediated closed loop.

ABSTRACT: Objectives: Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell possessing self-renewal and multilineage differentiation capabilities. The dysfunction of DPSCs is related to the pathologic process of pulpitis. The participation of circular RNAs (circRNAs) in DPSC differentiation has been identified. This work focussed on exploring the functions and mechanism of circFKBP5 in DPSC dysfunction evoked by lipopolysaccharide (LPS). Materials and methods: The viability and apoptosis of human DPSCs (hDPSCs) were determined using Cell Counting Kit-8 assay and flow cytometry. Inflammation was analysed by measuring the release of inflammatory cytokines. The osteogenic differentiation of hDPSCs was investigated by performing alkaline phosphatase (ALP) staining and alizarin red S staining and detecting the changes of ALP and runt-related transcription factor 2 (RUNX2) proteins. The dual-luciferase reporter, RNA immunoprecipitation (RIP), and pull-down assays were used to confirm the binding between miR-708-5p and circFKBP5 or G-protein-coupled receptor (GPCR)–kinase interacting protein 2 (GIT2). Results: CircFKBP5 expression was decreased in hDPSCs and, functionally, reexpression of circFKBP5 attenuated LPS-induced apoptosis, inflammation, and inhibition of proliferation ability and osteogenic differentiation in hDPSCs. Mechanistically, circFKBP5 acted as a sponge for miR-708-5p, which was verified to target GIT2. LPS induced miR-708-5p expression in hDPSCs, and knockdown of miR-708-5p protected against LPS-evoked hDPSC dysfunction. Besides, GIT2 expression was decreased in hDPSCs after LPS treatment. Rescue experiments showed that GIT2 could mediate the protective functions of circFKBP5 on hDPSCs under LPS treatment. Conclusions: CircFKBP5 could protect against LPS-induced apoptosis, inflammation, and osteogenic differentiation inhibition in hDPSCs via the miR-708-5p/GIT2 axis.

A low-cost and efficient high-temperature oxygen evolution reaction electrode is a big challenge. Here, the authors report an iron-base electrode with an in situ formed lithium ferrite for enhanced stability and catalytic activity in molten carbonate and chloride salts and achieve kiloampere-scale electrolysis.

Tuberculosis is a serious zoonotic disease caused by Mycobacterium tuberculosis (M.tb) and the M.tb complex. Mycolic acid is an extracellular carbohydrate polymer produced, secreted, and accumulated outside the cells of various Mycobacterium tuberculosis strains. Mycolic acid produced by Mycobacterium plays an important role in infection. However, there have been few reports on drugs that inhibit mycolic acid-induced cytotoxicity. The purpose of this study was to investigate the role of the panned peptide in Mycobacterium-derived mycolic acid (M.tb-MA)-induced cell injury. The heptapeptide (APTX4870) was isolated from various phage libraries using phage display (Ph.D-7, Ph.D-12, and Ph.D-C7C). The efficacy of APTX4870 against mycolic acid was demonstrated by evaluating clinical samples and conducting in vitro and Vivo. APTX4870 inhibited apoptosis, increased autophagy to decrease inflammation, and reduced M.tb-MA-induced lung damage. These findings suggest that this heptapeptide, which selectively targets M.tb-MA, might be exploited as a potential novel M.tb therapeutic treatment.

Abstract Objective Tourette syndrome (TS) is a childhood neurodevelopmental disorder caused by various genetic and environmental factors and presents with apparent genetic heterogeneity. As ASH1L potentially contributes to neurodevelopmental diseases, especially in TS, we aim to investigate the susceptibility of ASH1L on TS in the Chinese Han population. Methods Three tag single nucleotide polymorphisms (SNPs) (rs5005770, rs12734374, and rs35615695) in ASH1L were screened in 271 TS nuclear family trios and 337 healthy subjects by the TaqMan assays real time. A case–control study combined with family‐based analysis was applied to study the genetic susceptibility of common variants of ASH1L. Results The results revealed a significant over‐transmission of rs35615695 and rs5005770 (for rs35615695, transmission disequilibrium test, χ2 = 57.375, p = .000, HHRR, χ2 = 4.807, p = .028; for rs5005770, HRR, χ2 = 4.116, p = .042, HHRR, χ2 = 8.223, p = .004) in family‐based study. Furthermore, rs5005770 and rs35615695 still remained significant after Bonferroni correction (p