The process of diagnosis involves learning about the state of a system from various observations of symptoms or findings about the system. Sophisticated Bayesian (and other) algorithms have been developed to revise and maintain beliefs about the system as observations are made. Nonetheless, diagnostic models have tended to ignore some common sense reasoning exploited by human diagnosticians; In particular, one can learn from which observations have not been made, in the spirit of conversational implicature. There are two concepts that we describe to extract information from the observations not made. First, some symptoms, if present, are more likely to be reported before others. Second, most human diagnosticians and expert systems are economical in their data-gathering, searching first where they are more likely to find symptoms present. Thus, there is a desirable bias toward reporting symptoms that are present. We develop a simple model for these concepts that can significantly improve diagnostic inference.
Most real-world networks are too large to be measured or studied directly and there is substantial interest in estimating global network properties from smaller sub-samples. One of the most important global properties is the number of vertices/nodes in the network. Estimating the number of vertices in a large network is a major challenge in computer science, epidemiology, demography, and intelligence analysis. In this paper we consider a population random graph G = (V;E) from the stochastic block model (SBM) with K communities/blocks. A sample is obtained by randomly choosing a subset W and letting G(W) be the induced subgraph in G of the vertices in W. In addition to G(W), we observe the total degree of each sampled vertex and its block membership. Given this partial information, we propose an efficient PopULation Size Estimation algorithm, called PULSE, that accurately estimates the size of the whole population as well as the size of each community. To support our theoretical analysis, we perform an exhaustive set of experiments to study the effects of sample size, K, and SBM model parameters on the accuracy of the estimates. The experimental results also demonstrate that PULSE significantly outperforms a widely-used method called the network scale-up estimator in a wide variety of scenarios.
Predicated on the increasing abundance of electronic health records, we investigate the problem of inferring individualized treatment effects using observational data. Stemming from the potential outcomes model, we propose a novel multi-task learning framework in which factual and counterfactual outcomes are modeled as the outputs of a function in a vector-valued reproducing kernel Hilbert space (vvRKHS). We develop a nonparametric Bayesian method for learning the treatment effects using a multi-task Gaussian process (GP) with a linear coregionalization kernel as a prior over the vvRKHS. The Bayesian approach allows us to compute individualized measures of confidence in our estimates via pointwise credible intervals, which are crucial for realizing the full potential of precision medicine. The impact of selection bias is alleviated via a risk-based empirical Bayes method for adapting the multi-task GP prior, which jointly minimizes the empirical error in factual outcomes and the uncertainty in (unobserved) counterfactual outcomes. We conduct experiments on observational datasets for an interventional social program applied to premature infants, and a left ventricular assist device applied to cardiac patients wait-listed for a heart transplant. In both experiments, we show that our method significantly outperforms the state-of-the-art.
It is the main purpose of this paper to introduce a graph-valued stochastic process in order to model the spread of a communicable infectious disease. The major novelty of the SIR model we promote lies in the fact that the social network on which the epidemics is taking place is not specified in advance but evolves through time, accounting for the temporal evolution of the interactions involving infective individuals. Without assuming the existence of a fixed underlying network model, the stochastic process introduced describes, in a flexible and realistic manner, epidemic spread in non-uniformly mixing and possibly heterogeneous populations. It is shown how to fit such a (parametrised) model by means of Approximate Bayesian Computation methods based on graph-valued statistics. The concepts and statistical methods described in this paper are finally applied to a real epidemic dataset, related to the spread of HIV in Cuba in presence of a contact tracing system, which permits one to reconstruct partly the evolution of the graph of sexual partners diagnosed HIV positive between 1986 and 2006.
This paper describes a probabilistic framework for studying associations between multiple genotypes, biomarkers, and phenotypic traits in the presence of noise and unobserved confounders for large genetic studies. The framework builds on sparse linear methods developed for regression and modified here for inferring causal structures of richer networks with latent variables. The method is motivated by the use of genotypes as ``instruments'' to infer causal associations between phenotypic biomarkers and outcomes, without making the common restrictive assumptions of instrumental variable methods. The method may be used for an effective screening of potentially interesting genotype phenotype and biomarker-phenotype associations in genome-wide studies, which may have important implications for validating biomarkers as possible proxy endpoints for early stage clinical trials. Where the biomarkers are gene transcripts, the method can be used for fine mapping of quantitative trait loci (QTLs) detected in genetic linkage studies. The method is applied for examining effects of gene transcript levels in the liver on plasma HDL cholesterol levels for a sample of sequenced mice from a heterogeneous stock, with $\sim 10^5$ genetic instruments and $\sim 47 \times 10^3$ gene transcripts.