ABSTRACT
B, N co-doped carbon-supported small-sized Ru nanoparticles (RuBCN) were constructed by a facile ion exchange strategy using closo-[B12H12]2- and Ru(bpy)32+ as the precursors. Benefitting from strong metal-support interactions caused by the synergistic coupling effect of co-dopants B and N, RuBCN exhibits improved sintering resistance and the Ru nanoparticles are stabilized at sub-3 nm at 900 °C. Besides, introducing B doping further increases the electron deficiency of Ru in RuBCN, which could weaken the interaction between Ru and Had species or O2 adsorption. As a result, it exhibits impressive HER (η10 = 20 mV) and ORR (E1/2 = 0.76 V) catalytic performances, as well as outstanding stability, which are much higher than those of the single dopant counterpart.
ABSTRACT
As a promising dopant, electron deficient B atom not only tunes the electronic structure of electrocatalysts for improving their intrinsic catalytic activities, but also combines with hydroxy radical as strong adsorption sites for accelerating the water dissociation during the hydrogen evolution reaction (HER). In this paper, we report an electrocatalyst based on boron-modified Ru anchored on carbon nanotubes (B-Ru@CNT) that shows impressive HER activity in acidic and alkaline media. The boron-rich closo-[B12H12]2- borane was selected as a moderately strong reductant for the in situ reduction of a Ru salt, which yielded B-doped Ru nanoparticles. The experimental and theoretical results indicate that the incorporation of B not only weakens the Ru-H bond and downshifts the d-bond centre of Ru from the Fermi level by reducing the electron density at Ru but also accelerates the water dissociation reaction by providing B sites, which strongly adsorb OH* intermediates, and nearby Ru sites, which act as sites for the adsorption of the H* intermediate, thus boosting the HER performance and enhancing the HER kinetics. As a result of the tuning of the electronic structure via B doping, B-Ru@CNT showed excellent HER performance, yielding overpotentials of 17 and 62 mV at a current density of 10 mA cm-2 in alkaline and acidic solutions, respectively. These results indicate that our synthetic method is a promising route to B-doped metallic Ru with enhanced pH-independent HER performance.
ABSTRACT
Porous graphitic carbon nitride (p-C3N4) was fabricated via simple pyrolyzing treatment of graphitic carbon nitride (g-C3N4). The defects could be introduced into the structure of g-C3N4 by breakage of some bonds, which was beneficial for the generation of electron-hole pairs and inhibiting their recombination. Compared with g-C3N4, p-C3N4 showed a narrow band gap to promote the utilization of visible light. Furthermore, the porous structure also increased the specific surface area to maximize the exposure of active sites and promote mass transfer during photodegradation. As a result, the as-reported p-C3N4 exhibited considerably higher degradation efficiency for Rhodamine B (RhB) and Methyl Orange (MO) than that of the original g-C3N4. Moreover, the photocatalyst showed high durability and stability in recycling experiments.
Subject(s)
Light , Catalysis , Photolysis , PorosityABSTRACT
Antimetabolite drugs, including the adenosine deaminase inhibitor cladribine, have been shown to induce apoptosis in a variety of cancer cells, and have been widely used in clinical trials of various cancers in conjunction with tyrosine kinase inhibitors (TKIs). Combination treatment with cladribine and gefitinib or dasatinib is expected to have a synergistic inhibitory effect on breast cancer cell growth. Our results demonstrated that the combination treatment had synergistic activity against human breast cancer (MCF-7) cells, enhanced G2/M cell arrest and reactive oxygen species (ROS) generation, and increased the loss of mitochondrial membrane potential and cell apoptosis. In addition, the combination treatment decreased Bcl-2 expression. Our results demonstrated that cladribine in combination with gefitinib or dasatinib exerted synergistic anticancer effects on MCF-7 cells by inducing cell cycle arrest, ROS production and apoptosis through the mitochondria-mediated intrinsic pathway.
