We propose a semiparametric latent Gaussian copula model for modelling mixed multivariate data, which contain a combination of both continuous and binary variables. The model assumes that the observed binary variables are obtained by dichotomizing latent variables that satisfy the Gaussian copula distribution. The goal is to infer the conditional independence relationship between the latent random variables, based on the observed mixed data. Our work has two main contributions: we propose a unified rankbased approach to estimate the correlation matrix of latent variables; we establish the concentration inequality of the proposed rankbased estimator. Consequently, our methods achieve the same rates of convergence for precision matrix estimation and graph recovery, as if the latent variables were observed. The methods proposed are numerically assessed through extensive simulation studies, and real

This article studies estimation of partially linear hazard regression models for multivariate survival data. A profile pseudopartial likelihood estimation method is proposed under the marginal hazard model framework. The estimation on the parameters for the linear part is accomplished by maximization of a pseudopartial likelihood profiled over the nonparametric part. This enables us to obtain-consistent estimators of the parametric component. Asymptotic normality is obtained for the estimates of both the linear and nonlinear parts. The new technical challenge is that the nonparametric component is indirectly estimated through its integrated derivative function from a local polynomial fit. An algorithm of fast implementation of our proposed method is presented. Consistent standard error estimates using sandwich-type ideas are also developed, which facilitates inferences for the model. It is shown that the

Recovering low-rank structures via eigenvector perturbation analysis is a common problem in statistical machine learning, such as in factor analysis, community detection, ranking, matrix completion, among others. While a large variety of results provide tight bounds on the average errors between empirical and population statistics of eigenvectors, fewer results are tight for entrywise analyses, which are critical for a number of problems such as community detection and ranking.

We propose a novel technique to boost the power of testing a highdimensional vector <i>H</i>:<i><b></b></i>=<b>0</b> against sparse alternatives where the null hypothesis is violated by only a few components. Existing tests based on quadratic forms such as the Wald statistic often suffer from low powers due to the accumulation of errors in estimating highdimensional parameters. More powerful tests for sparse alternatives such as thresholding and extreme value tests, on the other hand, require either stringent conditions or bootstrap to derive the null distribution and often suffer from size distortions due to the slow convergence. Based on a screening technique, we introduce a power enhancement component, which is zero under the null hypothesis with high probability, but diverges quickly under sparse alternatives. The proposed test statistic combines the power enhancement component with an asymptotically pivotal statistic, and

Severe acute respiratory syndrome (SARS) is a new infectious disease with a global impact. Understanding its pathogenesis and developing specific diagnostic methods for its early diagnosis are crucial for the effective management and control of this disease. By using proteomic technology, truncated forms of ₁antitrypsin (TF₁AT) were found to increase significantly and consistently in sera of SARS patients compared to control subjects. The result showed a sensitivity of 100% for SARS patients and a specificity of 92.8% for controls. Furthermore, the levels of these proteins significantly correlated with certain clinicopathological parameters. The dramatic increase in TF₁AT may be the result of degradation of ₁AT. As ₁AT plays an important role in the protection of lung function, its degradation may be an important factor in the pathogenesis of SARS. These findings indicate that increased TF₁AT