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Abstract The most dynamic electromagnetic coupling between the magnetosphere and ionosphere occurs in the polar upper atmosphere. It is critical to quantify the electromagnetic energy and momentum input associated with this coupling as its impacts on the ionosphere and thermosphere system are global and major, often leading to considerable disturbances in near‐Earth space environments. The current general circulation models of the upper atmosphere exhibit systematic biases that can be attributed to an inadequate representation of the Joule heating rate resulting from unaccounted stochastic fluctuations of electric fields associated with the magnetosphere‐ionosphere coupling. These biases exist regardless of geomagnetic activity levels. To overcome this limitation, a new multiresolution random field modeling approach is developed, and the efficacy of the approach is demonstrated using Super Dual Auroral Radar Network (SuperDARN) data carefully curated for the study during a largely quiet 4‐hour period on February 29, 2012. Regional small‐scale electrostatic fields sampled at different resolutions from a probabilistic distribution of electric field variability conditioned on actual SuperDARN LOS observations exhibit considerably more localized fine‐scale features in comparison to global large‐scale fields modeled using the SuperDARN Assimilative Mapping procedure. The overall hemispherically integrated Joule heating rate is increased by a factor of about 1.5 due to the effect of random regional small‐scale electric fields, which is close to the lower end of arbitrarily adjusted Joule heating multiplicative factor of 1.5 and 2.5 typically used in upper atmosphere general circulation models. The study represents an important step toward a data‐driven ensemble modeling of magnetosphere‐ionosphere‐atmosphere coupling processes. 

Abstract The evolution of the COVID-19 pandemic is described through a time-dependent stochastic dynamic model in discrete time. The proposed multi-compartment model is expressed through a system of difference equations. Information on the social distancing measures and diagnostic testing rates are incorporated to characterize the dynamics of the various compartments of the model. In contrast with conventional epidemiological models, the proposed model involves interpretable temporally static and dynamic epidemiological rate parameters. A model fitting strategy built upon nonparametric smoothing is employed for estimating the time-varying parameters, while profiling over the time-independent parameters. Confidence bands of the parameters are obtained through a residual bootstrap procedure. A key feature of the methodology is its ability to estimate latent unobservable compartments such as the number of asymptomatic but infected individuals who are known to be the key vectors of COVID-19 spread. The nature of the disease dynamics is further quantified by relevant epidemiological markers that make use of the estimates of latent compartments. The methodology is applied to understand the true extent and dynamics of the pandemic in various states within the United States (US). 

Background: Both lifestyle and genetic factors confer risk for cardiovascular diseases, type 2 diabetes, and dyslipidemia. However, the interactions between these 2 groups of risk factors were not comprehensively understood due to previous poor estimation of genetic risk. Here we set out to develop enhanced polygenic risk scores (PRS) and systematically investigate multiplicative and additive interactions between PRS and lifestyle for coronary artery disease, atrial fibrillation, type 2 diabetes, total cholesterol, triglyceride, and LDL-cholesterol. Methods: Our study included 276 096 unrelated White British participants from the UK Biobank. We investigated several PRS methods (P+T, LDpred, PRS continuous shrinkage, and AnnoPred) and showed that AnnoPred achieved consistently improved prediction accuracy for all 6 diseases/traits. With enhanced PRS and combined lifestyle status categorized by smoking, body mass index, physical activity, and diet, we investigated both multiplicative and additive interactions between PRS and lifestyle using regression models. Results: We observed that healthy lifestyle reduced disease incidence by similar multiplicative magnitude across different PRS groups. The absolute risk reduction from lifestyle adherence was, however, significantly greater in individuals with higher PRS. Specifically, for type 2 diabetes, the absolute risk reduction from lifestyle adherence was 12.4% (95% CI, 10.0%–14.9%) in the top 1% PRS versus 2.8% (95% CI, 2.3%–3.3%) in the bottom PRS decile, leading to a ratio of >4.4. We also observed a significant interaction effect between PRS and lifestyle on triglyceride level. Conclusions: By leveraging functional annotations, AnnoPred outperforms state-of-the-art methods on quantifying genetic risk through PRS. Our analyses based on enhanced PRS suggest that individuals with high genetic risk may derive similar relative but greater absolute benefit from lifestyle adherence. 

We are interested in testing general linear hypotheses in a high-dimensional multivariate linear regression model. The framework includes many well-studied problems such as two-sample tests for equality of population means, MANOVA and others as special cases. A family of rotation-invariant tests is proposed that involves a flexible spectral shrinkage scheme applied to the sample error covariance matrix. The asymptotic normality of the test statistic under the null hypothesis is derived in the setting where dimensionality is comparable to sample sizes, assuming the existence of certain moments for the observations. The asymptotic power of the proposed test is studied under various local alternatives. The power characteristics are then utilized to propose a data-driven selection of the spectral shrinkage function. As an illustration of the general theory, we construct a family of tests involving ridge-type regularization and suggest possible extensions to more complex regularizers. A simulation study is carried out to examine the numerical performance of the proposed tests. 

Since the initial success of genome-wide association studies (GWAS) in 2005, tens of thousands of genetic variants have been identified for hundreds of human diseases and traits. In a GWAS, genotype information at up to millions of genetic markers is collected from up to hundreds of thousands of individuals, together with their phenotype information. Several scientific goals can be accomplished through the analysis of GWAS data, including the identification of variants, genes, and pathways associated with diseases and traits of interest; the inference of the genetic architecture of these traits; and the development of genetic risk prediction models. In this review, we provide an overview of the statistical challenges in achieving these goals and recent progress in statistical methodology to address these challenges.