Nitrogen, sulfur co-coordinated iron single-atom catalysts with the optimized electronic structure for highly efficient oxygen reduction in Zn-air battery and fuel cell.

Atomically dispersed iron-nitrogen-carbon (FesbndNsbndC) materials have been considered ideal catalysts for the oxygen reduction. Unfortunately, designing and adjusting the electronic structure of single-atom Fe sites to boost the kinetics and activity still faces grand challenges. In this work, the coordination environment engineering is developed to synthesize the FeSA/NSC catalyst with the tailored N, S co-coordinated Fe atomic site (Fe-N3S site). The structural characterizations and theoretical calculations demonstrate that the incorporation of sulfur can optimize the charge distribution of Fe atoms to weaken the adsorption of OH* and facilitate the desorption of OH*, thus leading to enhanced kinetics process and intrinsic activity. As a result, the S-modified FeSA/NSC exhibits outstanding catalytic activity with the half-wave potentials (E1/2) of 0.915 V and 0.797 V, as well as good stability, in alkaline and acidic electrolytes, respectively. Impressively, the excellent performance of FeSA/NSC is further confirmed in Zn-air batteries (ZABs) and fuel cells, with high peak power densities (146 mW cm-2 and 0.259 W cm-2).

High selective electrocatalytic reduction of carbon dioxide to ethylene enabled by regulating the microenvironment over Cu-Ag nanowires.

Copper-based tandem catalysts are effective candidates for yielding multi-carbon (C2+) products in electrochemical reduction of carbon dioxide (CO2RR). However, these catalysts still face a significant challenge regarding in the low selectivity for the production of a specific product. In this study, we report a high selectivity of 77.8 %±2 % at -1.0 V (vs RHE) for the production of C2H4 by using a Cu88Ag12NW catalyst which is primarily prepared through a combined Cu-Ag co-deposition and wet chemical method, employing an attractive strategy focused on regulating the microenvironment over Cu-Ag nanowires. The experimental and computational studies show that the higher *CO coverage and lower intermediate adsorption energy are important reasons for achieving the high C2H4 selectivity of Cu88Ag12NW catalyst. Comsol simulation results indicate that dense nanowires exhibit a nano-limiting effect on OH- ions, thereby leading to an increase in local pH and promoting coupling reactions. The catalyst demonstrates no noticeable decrease in current density or selectivity even after 12 h of continuous operation. The Cu-Ag nanowire composite exhibits remarkable catalytic activity, superior faradaic efficiency, excellent stability, and easy synthesis, which highlights its significant potential for electro-reducing carbon dioxide into valuable products.

Bimetallic co-doping engineering over nickel-based oxy-hydroxide enables high-performance electrocatalytic oxygen evolution.

Enhancing the electrocatalytic oxygen evolution reaction (OER) performance is essential to realize practical energy-saving water electrolysis and CO2 electroreduction. Herein, we report a bimetallic co-doping engineering to design and fabricate nickel-cobalt-iron collaborative oxy-hydroxide on nickel foam that labeled as NiCoFeOxHy-NF. As expected, NiCoFeOxHy-NF exhibits an outstanding OER activity with current density of 10 mA cm-2 at 194 mV, Tafel slope of 53 mV dec-1, along with the robust long-term stability, which is significantly better than bimetallic NiCo and NiFe combinations. Comprehensive computational simulations and characterizations jointly unveil that the twisted ligand environment induced by heteroatoms ensures the balance strength between the metal-oxygen hybrid orbital states and the oxidized intermediates adsorption, thus lowering the oxygen cycling energy barriers for overcoming the sluggish OER kinetics. Moreover, a novel phase transition behavior is monitored by in-situ Raman spectra under OER operating conditions, which facilitates electron-mass transfer as well as boosts the exposure of activity sites. For practical applications, Ni2P-NF || NiCoFeOxHy-NF and Cu || NiCoFeOxHy-NF couples were constructed to realize high-efficiency water electrolysis and CO2 electrochemical reduction for the production of valuable H2 and C2H4, respectively. This work elucidates a novel mechanism by which bimetallic co-doping improves the electrocatalytic OER activity of nickel-based hydroxides.

miR­654­3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non­small­cell lung cancer.

Non­small­cell lung cancer (NSCLC) accounts for 80% of lung cancer cases, and is the leading cause of cancer­associated mortality worldwide. The present study aimed to investigate the roles of microRNA (miR)­654­3p in NSCLC. The expression levels of miR­654­3p and its target ras protein activator like 2 (RASAL2) mRNA were determined by reverse transcription­quantitative polymerase chain reaction; protein expression was analyzed by western blotting. Plasmids expressing miR­654­3p mimics were constructed and transfected into A549 cells. In addition, the viability and apoptotic rate of cells were analyzed by an MTT assay and flow cytometry, respectively. A luciferase reporter assay was performed to verify whether RASAL2 is a target of miR­654­3p. Downregulated miR­654­3p and upregulated RASAL2 expression were observed in tumor tissues and cells. Cell viability was suppressed and the apoptotic rate was increased in the miR­654­3p mimics­transfected cells compared with the control. Luciferase activity was decreased in the RASAL2­3' untranslated region­wild type group treated with miR­654­3p mimics. Furthermore, the present study revealed that overexpression of miR­654­3p could suppress the viability and induce the apoptosis of cells by targeting RASAL2 in NSCLC. The present findings may contribute to developments in the treatment of NSCLC.

STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/ß­catenin pathway and feedback regulation by c­myc.

Lung cancer, which is a leading cause of cancer­related deaths, is diagnosed at a male to female ratio of 2.1:1. Serine­threonine kinase 31 (STK31) is a novel cancer/testis (CT)­related gene that is highly expressed in several types of cancers, such as lung and colorectal cancer, and plays crucial roles in cancer. In the present study, increased expression of STK31 and ß­catenin was observed in lung cancer tissues and cell lines. Downregulation of STK31 expression in lung cancer cells significantly inhibited their proliferation by arresting the cell cycle in the G1 phase concurrent with decreased ß­catenin, c­myc and cyclin D1 protein levels, while upregulation of STK31 had the opposite effects. In addition, STK31­induced lung cancer cell viability, proliferation, cell cycle progression, and expression of related genes were completely attenuated by a Wnt/ß­catenin inhibitor (XAV939). Similar to XAV939, a c­myc inhibitor (10058­F4) also significantly attenuated STK31­induced proliferation and cell cycle progression in lung cancer cells. Inhibiting c­myc and TRRAP significantly decreased the expression of STK31, and a chromatin immunoprecipitation (ChIP) assay confirmed that c­myc directly bound to the STK31 promoter. These results indicated that STK31 may act as an oncogene in lung cancer and that c­myc may be the transcription factor that promotes STK31 expression. Moreover, the results suggested that c­myc can also regulate STK31 expression in a positive feedback loop, and the downregulation of STK31 in lung cancer cells had an inhibitory effect on cell viability, cell proliferation and cell cycle progression, likely by inactivating the Wnt/ß­catenin pathway and positive feedback regulation by c­myc.

miR­140­5p regulates cell migration and invasion of non­small cell lung cancer cells through targeting VEGFA.

Lung cancer is the most common type of cancer worldwide, the most prevalent form of which is non­small cell lung cancer (NSCLC). MicroRNAs (miRs) are involved in the progression of NSCLC; however, the specific function of miR­140­5p in NSCLC remains unclear. The present study demonstrated that miR­140­5p was downregulated in the tumor tissues of patients with NSCLC, and it was associated with a poor prognosis. Furthermore, miR­140­5p significantly suppressed cell migration and invasion of the NSCLC cell line A549. In addition, the direct regulatory effect of miR­140­5p on vascular endothelial growth factor­A (VEGFA) was predicted by TargetScan and verified using a luciferase reporter gene assay. The present study also hypothesized that miR­140­5p may inhibit the expression of phosphorylated­protein kinase B by targeting VEGFA. In conclusion, miR­140­5p may be a potential target for the development of anti­neoplastic therapies in lung cancer.