ABSTRACT
In this work, by employing field plate (FP) and N ion-implantation edge termination (NIET) structure, the electrical performance of the ß-Ga2O3 Schottky barrier diode (SBD) was greatly improved. Ten samples of vertical SBDs were fabricated to investigate the influence of the relative positions of field plates (FPs) and ion implantation on the device performance. The device with the FP of 15 µm and the ion implantation at the edge of the Schottky electrode exhibited a breakdown voltage (Vbr) of 1616 V, a specific on-resistance (Ron,sp) of 5.11 mΩ·cm2, a power figure of merit (PFOM) of 0.511 GW/cm2, and a reverse current density of 1.2 × 10-5 A/cm2 @ -1000 V. Compared to the control device, although the Ron,sp increased by 1 mΩ·cm2, the Vbr of the device increased by 183% and the PFOM increased by 546.8%. Moreover, the reverse leakage current of the device with the FP and NIET structure decreased by three orders of magnitude. The TCAD simulation revealed that the peak electric field at the interface decreased from 7 MV/cm @ -500 V to 4.18 MV/cm @ -1000 V. These results demonstrate the great potential for the ß-Ga2O3 SBD with a FP and NIET structure in power electronic applications.
ABSTRACT
Previous studies have demonstrated that sublethal metamifop exposures induce hepatic lipid metabolism disorder in zebrafish. Whether metamifop will cause adverse effects in zebrafish gut is unknown. In the present study, effects of metamifop on gut heath of zebrafish were investigated after sublethal concentration (0.025, 0.10 and 0.40 mg/L) exposure. Histopathology analysis showed that metamifop induced inflammation and reduction of goblet cells in the gut, indicating that gut health may be impaired. Metamifop exposure could reduce activities of digestive enzymes (lipase and alkaline phosphatase), indicating the capacity of lipid absorption were impaired. Meanwhile, the content of fatty acid-binding protein 2 (FABP2) and mRNA levels of related genes (apoa-1a, apoe-b, fatp4, lpl and fabp2) were reduced in zebrafish gut after exposure to metamifop, suggesting the lipid transportation were decreased. The transcripts of genes associated with inflammation (il-17c, tnf-α and nf-kb) were significantly increased in 0.40 mg/L metamifop treatment group, which were 1.90-, 1.53- and 2.77-fold of the control group, respectively, confirming that metamifop induced inflammatory response in zebrafish gut. Moreover, reduction of mRNA levels of cldn-15 and elevation of lipopolysaccharides (LPS) content were observed in metamifop-treated groups, which suggested that metamifop exposure increased the intestinal permeability. Furthermore, metamifop exposure decreased the relative abundance of beneficial bacteria (Psychrobacter and Aeromonas) and elevated the abundance of pathogenic bacteria (Rhodobacter and Ralstonia) in zebrafish intestine. These results indicated that metamifop exposure at sublethal concentrations would impair zebrafish gut health, via reduction of lipids absorption, inflammatory response, elevation of permeability and microbiota disorder.
Subject(s)
Gastrointestinal Microbiome , Zebrafish , Anilides , Animals , Benzoxazoles , Inflammation , Lipids , RNA, Messenger/metabolism , Zebrafish/metabolismABSTRACT
Metamifop (MET) is an effective herbicide that has been extensively used in paddy fields. Previous research demonstrated that MET was highly toxic to zebrafish embryos, and this threat has caused great concern; moreover, 0.40 mg/L MET elevated the hepatosomatic index (HSI) in adult zebrafish without lethal effect after 21 d of exposure. In this study, we further determined the detailed impacts of MET on adult zebrafish at sublethal concentrations (0.025, 0.10 and 0.40 mg/L). We found that 0.40 mg/L MET caused liver injury by increasing the activity of aspartate aminotransferase and alanine aminotransferase in plasma, the content of interleukin-1ß, IL-6, tumor necrosis factor-α, and mRNA expression level of genes associated with inflammatory response in liver of adult zebrafish. The hepatic triglyceride (TG), free fatty acid and fatty acid synthase levels were significantly elevated in 0.40 mg/L MET-treated group (1.55-, 2.20- and 2.30-fold, respectively), and the transcript of lipid accumulation-related genes (fabp10, fas, acc, chrebp, dagt2 and agpat4) were upregulated. Meanwhile, the total cholesterol content was decreased by 0.48-fold, bile acid level was increased by 2.44-fold, and levels of cholesterol metabolism-related genes (apoa-1a, hmgcra, cyp51, dhcr7 and cyp7a1) were increased, suggesting cholesterol metabolism disorder occurred in zebrafish. Furthermore, analysis of lipidomics revealed that 0.40 mg/L MET significantly increased the abundance of 91 lipids, which mainly belonged to TG lipid class and were enriched in pathways of glycerolipid metabolism, cholesterol metabolism, etc. These results suggested that MET exposure at sublethal concentrations would induce hepatic inflammation and lipid metabolism disorders in adult zebrafish.
