ABSTRACT
Machine learning (ML) techniques offer a promising avenue for improving the integration of remote sensing data into mathematical crop models, thereby enhancing crop growth prediction accuracy. A critical variable for this integration is the leaf area index (LAI), which can be accurately assessed using proximal or remote sensing data based on plant canopies. This study aimed to (1) develop a machine learning-based method for estimating the LAI in rice and soybean crops using proximal sensing data and (2) evaluate the performance of a Remote Sensing-Integrated Crop Model (RSCM) when integrated with the ML algorithms. To achieve these objectives, we analyzed rice and soybean datasets to identify the most effective ML algorithms for modeling the relationship between LAI and vegetation indices derived from canopy reflectance measurements. Our analyses employed a variety of ML regression models, including ridge, lasso, support vector machine, random forest, and extra trees. Among these, the extra trees regression model demonstrated the best performance, achieving test scores of 0.86 and 0.89 for rice and soybean crops, respectively. This model closely replicated observed LAI values under different nitrogen treatments, achieving Nash-Sutcliffe efficiencies of 0.93 for rice and 0.97 for soybean. Our findings show that incorporating ML techniques into RSCM effectively captures seasonal LAI variations across diverse field management practices, offering significant potential for improving crop growth and productivity monitoring.
ABSTRACT
Little is known about the role of non-coding regions in the etiology of autism spectrum disorder (ASD). We examined three classes of non-coding regions: human accelerated regions (HARs), which show signatures of positive selection in humans; experimentally validated neural VISTA enhancers (VEs); and conserved regions predicted to act as neural enhancers (CNEs). Targeted and whole-genome analysis of >16,600 samples and >4,900 ASD probands revealed that likely recessive, rare, inherited variants in HARs, VEs, and CNEs substantially contribute to ASD risk in probands whose parents share ancestry, which enriches for recessive contributions, but modestly contribute, if at all, in simplex family structures. We identified multiple patient variants in HARs near IL1RAPL1 and in VEs near OTX1 and SIM1 and showed that they change enhancer activity. Our results implicate both human-evolved and evolutionarily conserved non-coding regions in ASD risk and suggest potential mechanisms of how regulatory changes can modulate social behavior.