RESUMO
Low-dimensional electronic systems such as silicon nanowires exhibit weak screening which is detrimental to the performance and scalability of nanodevices, e.g., tunnel field-effect transistors. By atomistic quantum transport simulations, we show how bound charges can be engineered at interfaces of Si and low-κ oxides to strengthen screening. To avoid compromising gate control, low-κ and high-κ oxides are used in conjunction. In Si nanowire tunnel field-effect transistors, we demonstrate that bound charge engineering increases the on-state current by orders of magnitude, and the combination of oxides yields minimal subthreshold swing. We conclude that the proposed bound-charge engineering paves a way toward improved low-power transistors.
RESUMO
Suppression of α/ß-domain hydrolase-6 (ABHD6), a monoacylglycerol (MAG) hydrolase, promotes glucose-stimulated insulin secretion by pancreatic ß cells. We report here that high-fat-diet-fed ABHD6-KO mice show modestly reduced food intake, decreased body weight gain and glycemia, improved glucose tolerance and insulin sensitivity, and enhanced locomotor activity. ABHD6-KO mice also show increased energy expenditure, cold-induced thermogenesis, brown adipose UCP1 expression, fatty acid oxidation, and white adipose browning. Adipose browning and cold-induced thermogenesis are replicated by the ABHD6 inhibitor WWL70 and by antisense oligonucleotides targeting ABHD6. Our evidence suggests that one mechanism by which the lipolysis derived 1-MAG signals intrinsic and cell-autonomous adipose browning is via PPARα and PPARγ activation, and that ABHD6 regulates adipose browning by controlling signal competent 1-MAG levels. Thus, ABHD6 regulates energy homeostasis, brown adipose function, and white adipose browning and is a potential therapeutic target for obesity and type 2 diabetes.