Retrieving soil moisture using cosmic-ray neutron technology based on COSMIC model in the desert-oasis region.

Cosmic-ray neutron technology could estimate average soil moisture on scale of hectometers by monitoring the neutron intensity near the ground, which has been successfully applied in forest, grassland, farmland, and other ecosystems. To verify the reliability of Cosmic-ray Soil Moisture Interaction Code (COSMIC) model for retrieving mesoscale soil moisture in arid regions, we carried out soil moisture observation experiment by using the cosmic-ray neutron rover in the desert-oasis region of the middle reaches of Heihe River. The results showed that the fast neutron intensity in the desert-oasis region were 350-715 counts·(30 s)-1, and the calibrated high energy neutron intensity (Ncosmic) were (38.5±2.2) counts·(30 s)-1, which was affected by land surface characteristics. Both COSMIC model (root mean square error=0.019 g·g-1) and N0 equation (root mean square error=0.018 g·g-1) could well assess the mesoscale soil moisture, with the accuracy of soil moisture being higher considering soil lattice water. The average penetration depth was 19 cm in the oasis region and 36 cm in the desert region during the experiment. COSMIC model could be used to retrieve soil moisture by cosmic ray neutron in the desert-oasis regions, which had great potential to realize data assimilation of surface meteorological-hydrological-ecological variables by combining with land surface models.

Arecoline inhibits the growth of 3T3-L1 preadipocytes via AMP-activated protein kinase and reactive oxygen species pathways.

The present study was designed to investigate the pathways involved in the effect of betel nut arecoline on cell viability in 3T3-L1 preadipocytes. Arecoline, but not arecaidine or guvacine, inhibited preadipocyte viability in a concentration- and time-dependent manner. Arecoline arrested preadipocyte growth in the G2/M phase of the cell cycle; decreased the total levels of cyclin-dependent kinase 1 (CDK1), p21, and p27 proteins; increased p53 and cyclin B1 protein levels; and had no effect on CDK2 protein levels. These results suggested that arecoline selectively affected a particular CDK subfamily. Arecoline inhibited AMP-activated protein kinase (AMPK) activity; conversely, the AMPK activator, AICAR, blocked the arecoline-induced inhibition of cell viability. Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins. These AMPK- and ROS-dependent effects of arecoline on preadipocyte growth may be related to the mechanism underlying the modulatory effect of arecoline on body weight.