ABSTRACT
Developing highly active electrocatalysts for overall water splitting is of remarkable significance for industrial production of H2. Herein, exceptionally active Fe(OH)x modified ultra-small Ru nanoparticles on Ni(OH)2 nanosheets array (Fe(OH)x-Ru/Ni(OH)2) for both hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) are reported. The Fe(OH)x-Ru/Ni(OH)2 nanosheets array prepared with Fe/Ru molar ratio of 5 only requires extremely low overpotentials of 61, 127 and 170 mV to reach current densities of 100, 500 and 800 mA cm-2 in 1 M KOH, respectively, exceeding Pt/C catalyst (75, 160 and 177 mV). Meanwhile, the Fe(OH)x/Ni(OH)2 nanosheets array derived from Fe(OH)x-Ru/Ni(OH)2 exhibits excellent OER activity. It gains current densities of 100, 500 and 800 mA cm-2 at considerably low overpotentials of 265, 285 and 296 mV, respectively, much lower than those of RuO2 and most reported electrocatalysts. The introduction of Fe(OH)x significantly improves the HER activity of Ru nanoparticles by tunning the electronic structure and forming interfaces between Ru and Fe(OH)x. Dramatically, the integrated alkaline electrolyzer based on Fe(OH)x-Ru/Ni(OH)2 and Fe(OH)x/Ni(OH)2 nanosheets array pair just needs 1.649 V to yield a current density up to 500 mA cm-2, exceeding most reported water-splitting electrocatalysts. The strategy reported in this work can be facilely extended to prepare other similar Ru based materials and their derivatives with outstanding catalytic performance for water splitting.
ABSTRACT
In the central nervous system diseases, glioma is one of the most common malignancies around the world. Despite the recent improvements in therapies for glioma, the prognosis of some high-risk glioma remains poor. In glioma, isoliquiritigenin (ISL) is reported to have antioxidative and antitumor activities. However, the potential mechanisms between ISL and circle RNAs (circRNAs) in the glioma tumorigenesis process have not yet been reported. Here, we treated glioma cells with ISL, and circRNA expression levels were detected. Circ0030018 was found significantly downregulated by ISL. Therefore, we explored circ0030018 expression profiles and functions in glioma, finding that circ0030018 was evidently overexpressed in glioma cell lines. Colony formation, CCK-8, and transwell assay made clear that circ0030018 silencing dramatically cut down glioma growth and invasion. Moreover, ROS level was detected to find that circ0030018 silence remarkably enhanced cell oxidative stress in glioma. Mechanism studies were conducted to investigate the underlying basis of circ0030018 function in glioma, unveiling that circ0030018 realized its functions partially through the miR-1236/HER2 signaling in glioma. In conclusion, our study investigated the roles and mechanisms of the ISL on the circ0030018/miR-1236/HER2 pathway in glioma tumorigenesis and progression. Circ0030018 could act as the prospective biologic signature or therapeutic target for glioma.
