Ultra-High Sensitive NO2 Gas Sensor Based on Tunable Polarity Transport in CVD-WS2/IGZO p-N Heterojunction.

In this work, a thin-film transistor gas sensor based on the p-N heterojunction is fabricated by stacking chemical vapor deposition-grown tungsten disulfide (WS2) with a sputtered indium-gallium-zinc-oxide (IGZO) film. To the best of our knowledge, the present device has the best NO2 gas sensor response compared to all the gas sensors based on transition-metal dichalcogenide materials. The gas-sensing response is investigated under different NO2 concentrations, adopting heterojunction device mode and transistor mode. High sensing response is obtained of p-N diode in the range of 1-300 ppm with values of 230% for 5 ppm and 18 170% for 300 ppm. On the transistor mode, the gas-sensing response can be modulated by the gate bias, and the transistor shows an ultrahigh response after exposure to NO2, with sensitivity values of 6820% for 5 ppm and 499 400% for 300 ppm. Interestingly, the transistor has a typical ambipolar behavior under dry air, while the transistor becomes p-type as the amount of NO2 increases. The assembly of these results demonstrates that the WS2/IGZO device is a promising platform for the NO2-gas detection, and its gas-modulated transistor properties show a potential application in tunable engineering for two-dimensional material heterojunction-based transistor device.

Mouse trefoil factor 3 ameliorated high-fat-diet-induced hepatic steatosis via increasing peroxisome proliferator-activated receptor-α-mediated fatty acid oxidation.

Hepatic trefoil factor 3 (Tff3) was identified as a potential protein for the treatment of diabetes, yet the effect of Tff3 on nonalcoholic fatty liver disease (NAFLD) has never been explored. Here, we found that the expression of hepatic Tff3 was significantly decreased in NAFLD mice models, suggesting that Tff3 was a potential marker gene for NAFLD. Restoring the expression of Tff3 in the liver of NAFLD mice, including diabetic (db), obese (ob/ob), and diet-induced obese mice, with adenovirus-mediated Tff3 (Ad-Tff3) apparently attenuates the fatty liver phenotype. In contrast, adenovirus-mediated knockdown of Tff3 (Ad-shTff3) in C57BL/6J mice results in an obvious fatty liver phenotype. Furthermore, our molecular experiments indicated that hepatic Tff3 could alleviate hepatic steatosis via upregulating the expression of peroxisome proliferator-activated receptor-α (PPARα) directly, thereby enhancing the fatty acid oxidation process in the liver. Notably, we found that Tff3 attenuates the fatty liver phenotype independent of modulation of lipogenesis and improves the capacity of anti-inflammation. Overall, our results suggested that hepatic Tff3 could be effectively used as a potential therapy target for the treatment of NAFLD.