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Reconstructing missing information in epidemic spreading on contact networks can be essential in prevention and containment strategies. For instance, identifying and warning infective but asymptomatic individuals (e.g., manual contact tracing) helped contain outbreaks in the COVID-19 pandemic. The number of possible epidemic cascades typically grows exponentially with the number of individuals involved. The challenge posed by inference problems in the epidemics processes originates from the difficulty of identifying the almost negligible subset of those compatible with the evidence (for instance, medical tests). Here we present a new generative neural networks framework that can sample the most probable infection cascades compatible with observations. Moreover, the framework can infer the parameters governing the spreading of infections. The proposed method obtains better or comparable results with existing methods on the patient zero problem, risk assessment, and inference of infectious parameters in synthetic and real case scenarios like spreading infections in workplaces and hospitals.

We propose kernel ridge regression estimators for mediation analysis and dynamic treatment effects over short horizons. We allow treatments, covariates, and mediators to be discrete or continuous, and low, high, or infinite dimensional. We propose estimators of means, increments, and distributions of counterfactual outcomes with closed form solutions in terms of kernel matrix operations. For the continuous treatment case, we prove uniform consistency with finite sample rates. For the discrete treatment case, we prove root-n consistency, Gaussian approximation, and semiparametric efficiency. We conduct simulations then estimate mediated and dynamic treatment effects of the US Job Corps program for disadvantaged youth.

Tech companies (e.g., Google or Facebook) often use randomized online experiments and/or A/B testing primarily based on the average treatment effects to compare their new product with an old one. However, it is also critically important to detect qualitative treatment effects such that the new one may significantly outperform the existing one only under some specific circumstances. The aim of this paper is to develop a powerful testing procedure to efficiently detect such qualitative treatment effects. We propose a scalable online updating algorithm to implement our test procedure. It has three novelties including adaptive randomization, sequential monitoring, and online updating with guaranteed type-I error control. We also thoroughly examine the theoretical properties of our testing procedure including the limiting distribution of test statistics and the justification of an efficient bootstrap method. Extensive empirical studies are conducted to examine the finite sample performance of our test procedure.

Linear regression on a set of observations linked by a network has been an essential tool in modeling the relationship between response and covariates with additional network data. Despite its wide range of applications in many areas, such as in social sciences and health-related research, the problem has not been well-studied in statistics so far. Previous methods either lack inference tools or rely on restrictive assumptions on social effects and usually assume that networks are observed without errors, which is unrealistic in many problems. This paper proposes a linear regression model with nonparametric network effects. The model does not assume that the relational data or network structure is exactly observed; thus, the method can be provably robust to a certain network perturbation level. A set of asymptotic inference results is established under a general requirement of the network observational errors, and the robustness of this method is studied in the specific setting when the errors come from random network models. We discover a phase-transition phenomenon of the inference validity concerning the network density when no prior knowledge of the network model is available while also showing a significant improvement achieved by knowing the network model. As a by-product of this analysis, we derive a rate-optimal concentration bound for random subspace projection that may be of independent interest. Extensive simulation studies are conducted to verify these theoretical results and demonstrate the advantage of the proposed method over existing work in terms of accuracy and computational efficiency under different data-generating models. The method is then applied to middle school students' network data to study the effectiveness of educational workshops in reducing school conflicts.

We propose a doubly robust approach to characterizing treatment effect heterogeneity in observational studies. We utilize posterior distributions for both the propensity score and outcome regression models to provide valid inference on the conditional average treatment effect even when high-dimensional or nonparametric models are used. We show that our approach leads to conservative inference in finite samples or under model misspecification, and provides a consistent variance estimator when both models are correctly specified. In simulations, we illustrate the utility of these results in difficult settings such as high-dimensional covariate spaces or highly flexible models for the propensity score and outcome regression. Lastly, we analyze environmental exposure data from NHANES to identify how the effects of these exposures vary by subject-level characteristics.

Measurement error is a pervasive issue which renders the results of an analysis unreliable. The measurement error literature contains numerous correction techniques, which can be broadly divided into those which aim to produce exactly consistent estimators, and those which are only approximately consistent. While consistency is a desirable property, it is typically attained only under specific model assumptions. Two techniques, regression calibration and simulation extrapolation, are used frequently in a wide variety of parametric and semiparametric settings. However, in many settings these methods are only approximately consistent. We generalize these corrections, relaxing assumptions placed on replicate measurements. Under regularity conditions, the estimators are shown to be asymptotically normal, with a sandwich estimator for the asymptotic variance. Through simulation, we demonstrate the improved performance of the modified estimators, over the standard techniques, when these assumptions are violated. We motivate these corrections using the Framingham Heart Study, and apply the generalized techniques to an analysis of these data.

This paper presents a topological learning-theoretic perspective on causal inference by introducing a series of topologies defined on general spaces of structural causal models (SCMs). As an illustration of the framework we prove a topological causal hierarchy theorem, showing that substantive assumption-free causal inference is possible only in a meager set of SCMs. Thanks to a known correspondence between open sets in the weak topology and statistically verifiable hypotheses, our results show that inductive assumptions sufficient to license valid causal inferences are statistically unverifiable in principle. Similar to no-free-lunch theorems for statistical inference, the present results clarify the inevitability of substantial assumptions for causal inference. An additional benefit of our topological approach is that it easily accommodates SCMs with infinitely many variables. We finally suggest that the framework may be helpful for the positive project of exploring and assessing alternative causal-inductive assumptions.

Clinical studies often encounter with truncation-by-death problems, which may render the outcomes undefined. Statistical analysis based only on observed survivors may lead to biased results because the characters of survivors may differ greatly between treatment groups. Under the principal stratification framework, a meaningful causal parameter, the survivor average causal effect, in the always-survivor group can be defined. This causal parameter may not be identifiable in observational studies where the treatment assignment and the survival or outcome process are confounded by unmeasured features. In this paper, we propose a new method to deal with unmeasured confounding when the outcome is truncated by death. First, a new method is proposed to identify the heterogeneous conditional survivor average causal effect based on a substitutional variable under monotonicity. Second, under additional assumptions, the survivor average causal effect on the overall population is also identified. Furthermore, we consider estimation and inference for the conditional survivor average causal effect based on parametric and nonparametric methods with good asymptotic properties. Good finite-sample properties are demonstrated by simulation and sensitivity analysis. The proposed method is applied to investigate the effect of allogeneic stem cell transplantation types on leukemia relapse.

Proximal causal inference was recently proposed as a framework to identify causal effects from observational data in the presence of hidden confounders for which proxies are available. In this paper, we extend the proximal causal approach to settings where identification of causal effects hinges upon a set of mediators which unfortunately are not directly observed, however proxies of the hidden mediators are measured. Specifically, we establish (i) a new hidden front-door criterion which extends the classical front-door result to allow for hidden mediators for which proxies are available; (ii) We extend causal mediation analysis to identify direct and indirect causal effects under unconfoundedness conditions in a setting where the mediator in view is hidden, but error prone proxies of the latter are available. We view (i) and (ii) as important steps towards the practical application of front-door criteria and mediation analysis as mediators are almost always error prone and thus, the most one can hope for in practice is that our measurements are at best proxies of mediating mechanisms. Finally, we show that identification of certain causal effects remains possible even in settings where challenges in (i) and (ii) might co-exist.

Causality can be described in terms of a structural causal model (SCM) that carries information on the variables of interest and their mechanistic relations. For most processes of interest the underlying SCM will only be partially observable, thus causal inference tries to leverage any exposed information. Graph neural networks (GNN) as universal approximators on structured input pose a viable candidate for causal learning, suggesting a tighter integration with SCM. To this effect we present a theoretical analysis from first principles that establishes a novel connection between GNN and SCM while providing an extended view on general neural-causal models. We then establish a new model class for GNN-based causal inference that is necessary and sufficient for causal effect identification. Our empirical illustration on simulations and standard benchmarks validate our theoretical proofs.