RESUMEN
Methane-based nitridation was employed to produce wurtzite zinc-gallium oxynitride (ZnGaNO) photocatalyst particles using Zn/Ga/CO3 layered double hydroxides (LDHs) as precursor. Introduction of methane to nitridation would promote the formation of Zn-O bonding and suppress shallow acceptor complexes such as V(Zn)-Ga(Zn) and Ga-Oi in ZnGaNO particles. On the other hand, high flow rate of methane would induce breaking of Ga-N bonding and enhance surface deposition of metallic Ga atoms. After loading with Rh and RuO2, ZnGaNO particles had free electron density in an order of S50 > S20 > S90 > S0, which correlated well with their photocatalytic performance upon visible-light irradiation. The best performance of the loaded S50 was ascribed to the relatively flat surface band bending of the particle. Methane-based nitridation of Zn/Ga/CO3 LDHs would provide a new route to tune the surface chemistry of ZnGaNO and enhance the photocatalytic performance to its full potential.
RESUMEN
Background: Bath-type ultrasonic-assisted extraction (UAE) has been developed as one of the most important sample pretreatment methods, especially for batch-sample pretreatment. So far, however, requirements for the performance of bath-type UAE equipment have not been standardized, nor has a suitable evaluation method that can be used to judge the feasibility of ultrasonic equipment for extraction been presented in the available regulations or standards. Objective: A simple and efficient method that can be used to evaluate the performance of bath-type UAE equipment is necessary to be proposed and established. Methods: First, distribution of a sound field in ultrasonic equipment was measured by acoustimeter and the dyeing method, through which influencing factors including frequency, preheating time, and output power of the equipment, as well as the horizontal and vertical position for locating the sample in the equipment, were investigated, and optimized parameters for extraction were achieved. Then, through the aluminum foil lattice method, by calculating the perforated rate of the aluminum foil, cavitation intensity of the ultrasonic equipment can be quantitatively determined. Results: With the optimized working conditions and by selecting appropriate parameters for the aluminum foil, perforated holes formed on the foil displayed a good pattern. Further validation experiments indicated conformity between the established method and the actual extraction effect of the ultrasonic equipment, proposing a suitable requirement for the cavitation effect of the bath-type UAE equipment. Conclusions: The aluminum foil lattice method has been proved to be simple, convenient, inexpensive, and reliable for quickly evaluating the extraction performance of bath-type UAE equipment.
RESUMEN
NogoA is a myelinassociated protein, which is important in the inhibition of axonal fiber growth and in regeneration following injury of the mammalian central nervous system. A previous study suggested that NogoA may be key in the process of Parkinson's disease (PD), which is the second most common chronic neurodegenerative disorder worldwide. The regulatory mechanism underlying the effect of NogoA on the process of PD remains to be fully elucidated. The present study aimed to investigate the effect and underlying mechanism of NogoA on cellular viability, apoptosis and autophagy induced by 1-methyl-4-phenylpyridinium (MPP+) in PC12 cells, a commonly used in vitro PD model. PC12 cells were treated with 1 mM MPP+ for 24 h and the cells were harvested for western blotting. The results demonstrated that the protien expression levels of NogoA were increased in the PC12 cells treated with MPP+. Subsequently, NogoA small interfering RNA was synthesized and transfected into PC12 cells to silence the expression of NogoA. NogoA knockdown significantly reduced the MPP+induced decrease in cell viability and apoptosis, detected using a cell counting kit8 and flow cytometric analysis, respectively. Interference in the expression of NogoA increased the MPP+induced decrease in mitochondrial membrane potential, determined quantitatively by flow cytometry using JC-1 dye, and the protein levels of Beclin1. In addition, MPP+ treatment activated the mammalian target of rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Knockdown of NogoA significantly inhibited the expression levels of mTOR and STAT3. Furthermore, overexpression of NogoA had similar neurotoxic effects on the PC12 cells as MPP+ treatment. Treatment with rapamycin, an inhibitor of the mTOR/STAT3 signaling pathway had a similar effect to that of NogoA knockdown in the MPP+treated PC12 cells. Taken together, the results from the present study demonstrated that NogoA may regulate MPP+induced neurotoxicity in PC12 cells via the mTOR/STAT3 signaling pathway and provided an explanation regarding the regulatory mechanism of NogoA on the process of PD.