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The non-photosynthetic vegetation – soil separation index (NSSI) and normalized difference vegetation index (NDVI) can be used to simultaneously estimate the fractional cover of non-photosynthetic vegetation (fNPV), photosynthetic vegetation (fPV), and bare soil (fBS) in vegetation ecosystems. However, these estimates suffer from problems due to shading by dense vegetation or topography. Based on field-measured data and on hyperspectral data acquired by unmanned aerial vehicles, we analyse how shading affects the morphology of NDVI-NSSI and enhanced vegetation index – NSSI (EVI-NSSI). We also investigate the simultaneous estimation of fNPV, fPV, and fBS. The results show that the NDVI-NSSI normalized difference feature space mitigates the impact of shade. Shade causes the NDVI-NSSI and EVI-NSSI to shift rightward parallel to the BS axis and leftward parallel to the PV axis, respectively. Although such shifts may hinder the determination of NPV, PV, and BS endmembers, they do not affect the spectral separation of NPV. Overall, with the NDVI-NSSI and EVI-NSSI methods, the estimation error for fNPV under shaded conditions is approximately 5% greater than that under illuminated conditions. Shaded green vegetation more strongly affects the estimation error of fPV and fBS in EVI-NSSI than in NDVI-NSSI, whereas fBS and fPV depend more strongly on shade than fNPV. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D) is characterized by insulin resistance and increased hepatic glucose production, yet the molecular mechanisms underlying these abnormalities are poorly understood. MicroRNAs (miRs) are a class of small, noncoding RNAs that have been implicated in the regulation of human diseases, including T2D. miR-26a is known to play a critical role in tumorigenesis; however, its function in cellular metabolism remains unknown. Here, we determined that miR-26a regulates insulin signaling and metabolism of glucose and lipids. Compared with lean individuals, overweight humans had decreased expression of miR-26a in the liver. Moreover, miR-26 was downregulated in 2 obese mouse models compared with control animals. Global or liver-specific overexpression of miR-26a in mice fed a high-fat diet improved insulin sensitivity, decreased hepatic glucose production, and decreased fatty acid synthesis, thereby preventing obesity-induced metabolic complications. Conversely, silencing of endogenous miR-26a in conventional diet-fed mice impaired insulin sensitivity, enhanced glucose production, and increased fatty acid synthesis. miR-26a targeted several key regulators of hepatic metabolism and insulin signaling. These findings reveal miR-26a as a regulator of liver metabolism and suggest miR-26a should be further explored as a potential target for the treatment of T2D.