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Abstract Survey questionnaires are commonly used by psychologists and social scientists to measure various latent traits of study subjects. Various causal inference methods such as the potential outcome framework and structural equation models have been used to infer causal effects. However, the majority of these methods assume the knowledge of true causal structure, which is unknown for many applications in psychological and social sciences. This calls for alternative causal approaches for analyzing such questionnaire data. Bayesian networks are a promising option as they do not require causal structure to be knowna prioribut learn it objectively from data. Although we have seen some recent successes of using Bayesian networks to discover causality for psychological questionnaire data, their techniques tend to suffer from causal non-identifiability with observational data. In this paper, we propose the use of a state-of-the-art Bayesian network that is proven to be fully identifiable for observational ordinal data. We develop a causal structure learning algorithm based on an asymptotically justified BIC score function, a hill-climbing search strategy, and the bootstrapping technique, which is able to not only identify a unique causal structure but also quantify the associated uncertainty. Using simulation studies, we demonstrate the power of the proposed learning algorithm by comparing it with alternative Bayesian network methods. For illustration, we consider a dataset from a psychological study of the functional relationships among the symptoms of obsessive-compulsive disorder and depression. Without any prior knowledge, the proposed algorithm reveals some plausible causal relationships. This paper is accompanied by a user-friendly open-source R package OrdCD on CRAN. 

Abstract MotivationMendelian randomization (MR) infers causal relationships between exposures and outcomes using genetic variants as instrumental variables. Typically, MR considers only a pair of exposure and outcome at a time, limiting its capability of capturing the entire causal network. We overcome this limitation by developing MR.RGM (Mendelian randomization via reciprocal graphical model), a fast R-package that implements the Bayesian reciprocal graphical model and enables practitioners to construct holistic causal networks with possibly cyclic/reciprocal causation and proper uncertainty quantifications, offering a comprehensive understanding of complex biological systems and their interconnections. ResultsWe developed MR.RGM, an open-source R package that applies bidirectional MR using a network-based strategy, enabling the exploration of causal relationships among multiple variables in complex biological systems. MR.RGM holds the promise of unveiling intricate interactions and advancing our understanding of genetic networks, disease risks, and phenotypic complexities. Availability and implementationMR.RGM is available at CRAN (https://CRAN.R-project.org/package=MR.RGM, DOI: 10.32614/CRAN.package.MR.RGM) and https://github.com/bitansa/MR.RGM. 

With the increasing integration of machine learning into IoT devices, managing energy consumption and data transmission has become a critical challenge. Many IoT applications depend on complex computations performed on server-side infrastructure, necessitating efficient methods to reduce unnecessary data transmission. One promising solution involves deploying compact machine learning models near sensors, enabling intelligent identification and transmission of only relevant data frames. However, existing near-sensor models lack adaptability, as they require extensive pre-training and are often rigidly configured prior to deployment. This paper proposes a novel framework that fuses online learning, active learning, and knowledge distillation to enable adaptive, resource-efficient near-sensor intelligence. Our approach allows near-sensor models to dynamically fine-tune their parameters post-deployment using online learning, eliminating the need for extensive pre-labeling and training. Through a sequential training and execution process, the framework achieves continuous adaptability without prior knowledge of the deployment environment. To enhance performance while preserving model efficiency, we integrate knowledge distillation, enabling the transfer of critical insights from a larger teacher model to a compact student model. Additionally, active learning reduces the required training data while maintaining competitive performance. We validated our framework on both benchmark data from the MS COCO dataset and in a simulated IoT environment. The results demonstrate significant improvements in energy efficiency and data transmission optimization, highlighting the practical applicability of our method in real-world IoT scenarios. 

ABSTRACT Graphical models are powerful tools to investigate complex dependency structures in high-throughput datasets. However, most existing graphical models make one of two canonical assumptions: (i) a homogeneous graph with a common network for all subjects or (ii) an assumption of normality, especially in the context of Gaussian graphical models. Both assumptions are restrictive and can fail to hold in certain applications such as proteomic networks in cancer. To this end, we propose an approach termed robust Bayesian graphical regression (rBGR) to estimate heterogeneous graphs for non-normally distributed data. rBGR is a flexible framework that accommodates non-normality through random marginal transformations and constructs covariate-dependent graphs to accommodate heterogeneity through graphical regression techniques. We formulate a new characterization of edge dependencies in such models called conditional sign independence with covariates, along with an efficient posterior sampling algorithm. In simulation studies, we demonstrate that rBGR outperforms existing graphical regression models for data generated under various levels of non-normality in both edge and covariate selection. We use rBGR to assess proteomic networks in lung and ovarian cancers to systematically investigate the effects of immunogenic heterogeneity within tumors. Our analyses reveal several important protein–protein interactions that are differentially associated with the immune cell abundance; some corroborate existing biological knowledge, whereas others are novel findings. 

Abstract Recent technologies such asspatial transcriptomics, enable the measurement of gene expressions at the single-cell level along with the spatial locations of these cells in the tissue. Spatial clustering of the cells provides valuable insights into the understanding of the functional organization of the tissue. However, most such clustering methods involve some dimension reduction that leads to a loss of the inherent dependency structure among genes at any spatial location in the tissue. This destroys valuable insights of gene co-expression patterns apart from possibly impacting spatial clustering performance. In spatial transcriptomics, the matrix-variate gene expression data, along with spatial coordinates of the single cells, provides information on both gene expression dependencies and cell spatial dependencies through its row and column covariances. In this work, we propose a joint Bayesian approach to simultaneously estimate these gene and spatial cell correlations. These estimates provide data summaries for downstream analyses. We illustrate our method with simulations and analysis of several real spatial transcriptomic datasets. Our work elucidates gene co-expression networks as well as clear spatial clustering patterns of the cells. Furthermore, our analysis reveals that downstream spatial-differential analysis may aid in the discovery of unknown cell types from known marker genes.