MoTe2 p-n Homojunctions Defined by Ferroelectric Polarization.

Doped p-n junctions are fundamental electrical components in modern electronics and optoelectronics. Due to the development of device miniaturization, the emergence of two-dimensional (2D) materials may initiate the next technological leap toward the post-Moore era owing to their unique structures and physical properties. The purpose of fabricating 2D p-n junctions has fueled many carrier-type modulation methods, such as electrostatic doping, surface modification, and element intercalation. Here, by using the nonvolatile ferroelectric field polarized in the opposite direction, efficient carrier modulation in ambipolar molybdenum telluride (MoTe2 ) to form a p-n homojunction at the domain wall is demonstrated. The nonvolatile MoTe2 p-n junction can be converted to n-p, n-n, and p-p configurations by external gate voltage pulses. Both rectifier diodes exhibited excellent rectifying characteristics with a current on/off ratio of 5 × 105 . As a photodetector/photovoltaic, the device presents responsivity of 5 A W-1 , external quantum efficiency of 40%, specific detectivity of 3 × 1012 Jones, fast response time of 30 µs, and power conversion efficiency of 2.5% without any bias or gate voltages. The MoTe2 p-n junction presents an obvious short-wavelength infrared photoresponse at room temperature, complementing the current infrared photodetectors with the inadequacies of complementary metal-oxide-semiconductor incompatibility and cryogenic operation temperature.

Berberine activates thermogenesis in white and brown adipose tissue.

Obesity develops when energy intake exceeds energy expenditure. Promoting brown adipose tissue formation and function increases energy expenditure and hence may counteract obesity. Berberine (BBR) is a compound derived from the Chinese medicinal plant Coptis chinensis. Here we show that BBR increases energy expenditure, limits weight gain, improves cold tolerance and enhances brown adipose tissue (BAT) activity in obese db/db mice. BBR markedly induces the development of brown-like adipocytes in inguinal, but not epididymal adipose depots. BBR also increases expression of UCP1 and other thermogenic genes in white and BAT and primary adipocytes via a mechanism involving AMPK and PGC-1α. BBR treatment also inhibits AMPK activity in the hypothalamus, but genetic activation of AMPK in the ventromedial nucleus of the hypothalamus does not prevent BBR-induced weight loss and activation of the thermogenic programme. Our findings establish a role for BBR in regulating organismal energy balance, which may have potential therapeutic implications for the treatment of obesity.