Sparse signal recovery addresses the problem of solving underdetermined linear inverse problems subject to a sparsity constraint. We propose a novel prior formulation, the structured spike and slab prior, which allows to incorporate a priori knowledge of the sparsity pattern by imposing a spatial Gaussian process on the spike and slab probabilities. Thus, prior information on the structure of the sparsity pattern can be encoded using generic covariance functions. Furthermore, we provide a Bayesian inference scheme for the proposed model based on the expectation propagation framework. Using numerical experiments on synthetic data, we demonstrate the benefits of the model.

The learning with privileged information setting has recently attracted a lot of attention within the machine learning community, as it allows the integration of additional knowledge into the training process of a classifier, even when this comes in the form of a data modality that is not available at test time. Here, we show that privileged information can naturally be treated as noise in the latent function of a Gaussian process classifier (GPC). That is, in contrast to the standard GPC setting, the latent function is not just a nuisance but a feature: it becomes a natural measure of confidence about the training data by modulating the slope of the GPC probit likelihood function. Extensive experiments on public datasets show that the proposed GPC method using privileged noise, called GPC+, improves over a standard GPC without privileged knowledge, and also over the current state-of-the-art SVM-based method, SVM+. Moreover, we show that advanced neural networks and deep learning methods can be compressed as privileged information.

We present an inference method for Gaussian graphical models when only pairwise distances of n objects are observed.

One of the most fundamental problems in causal inference is the estimation of a causal effect when variables are confounded. This is difficult in an observational study because one has no direct evidence that all confounders have been adjusted for. We introduce a novel approach for estimating causal effects that exploits observational conditional independencies to suggest "weak" paths in a unknown causal graph. The widely used faithfulness condition of Spirtes et al. is relaxed to allow for varying degrees of "path cancellations" that will imply conditional independencies but do not rule out the existence of confounding causal paths. The outcome is a posterior distribution over bounds on the average causal effect via a linear programming approach and Bayesian inference. We claim this approach should be used in regular practice to complement other default tools in observational studies.

It has been long argued that, because of inherent ambiguity and noise, the brain needs to represent uncertainty in the form of probability distributions. The neural encoding of such distributions remains however highly controversial. Here we present a novel circuit model for representing multidimensional real-valued distributions using a spike based spatio-temporal code. Our model combines the computational advantages of the currently competing models for probabilistic codes and exhibits realistic neural responses along a variety of classic measures. Furthermore, the model highlights the challenges associated with interpreting neural activity in relation to behavioral uncertainty and points to alternative populationlevel approaches for the experimental validation of distributed representations. Core brain computations, such as sensory perception, have been successfully characterized as probabilistic inference, whereby sensory stimuli are interpreted in terms of the objects or features that gave rise to them [1, 2].

We develop a model by choosing the maximum entropy distribution from the set of models satisfying certain smoothness and independence criteria; we show that inference on this model generalizes local kernel estimation to the context of Bayesian inference on stochastic processes. Our model enables Bayesian inference in contexts when standard techniques like Gaussian process inference are too expensive to apply. Exact inference on our model is possible for any likelihood function from the exponential family. Inference is then highly efficient, requiring only O (log N) time and O (N) space at run time. We demonstrate our algorithm on several problems and show quantifiable improvement in both speed and performance relative to models based on the Gaussian process.

Learning and memory in the brain are implemented by complex, time-varying changes in neural circuitry. The computational rules according to which synaptic weights change over time are the subject of much research, and are not precisely understood. Until recently, limitations in experimental methods have made it challenging to test hypotheses about synaptic plasticity on a large scale. However, as such data become available and these barriers are lifted, it becomes necessary to develop analysis techniques to validate plasticity models. Here, we present a highly extensible framework for modeling arbitrary synaptic plasticity rules on spike train data in populations of interconnected neurons. We treat synaptic weights as a (potentially nonlinear) dynamical system embedded in a fully-Bayesian generalized linear model (GLM). In addition, we provide an algorithm for inferring synaptic weight trajectories alongside the parameters of the GLM and of the learning rules. Using this method, we perform model comparison of two proposed variants of the well-known spike-timing-dependent plasticity (STDP) rule, where nonlinear effects play a substantial role. On synthetic data generated from the biophysical simulator NEURON, we show that we can recover the weight trajectories, the pattern of connectivity, and the underlying learning rules.

We address the problem of deciding whether a causal or probabilistic query is estimable from data corrupted by missing entries, given a model of missingness process. We extend the results of Mohan et al. [2013] by presenting more general conditions for recovering probabilistic queries of the form P(y|x) and P(y,x) as well as causal queries of the form P(y|do(x)). We show that causal queries may be recoverable even when the factors in their identifying estimands are not recoverable. Specifically, we derive graphical conditions for recovering causal effects of the form P(y|do(x)) when Y and its missingness mechanism are not d-separable. Finally, we apply our results to problems of attrition and characterize the recovery of causal effects from data corrupted by attrition.

Many single-channel signal decomposition techniques rely on a low-rank factorization of a time-frequency transform. In particular, nonnegative matrix factorization (NMF) of the spectrogram - the (power) magnitude of the short-time Fourier transform (STFT) - has been considered in many audio applications. In this setting, NMF with the Itakura-Saito divergence was shown to underly a generative Gaussian composite model (GCM) of the STFT, a step forward from more empirical approaches based on ad-hoc transform and divergence specifications. Still, the GCM is not yet a generative model of the raw signal itself, but only of its STFT. The work presented in this paper fills in this ultimate gap by proposing a novel signal synthesis model with low-rank time-frequency structure. In particular, our new approach opens doors to multi-resolution representations, that were not possible in the traditional NMF setting. We describe two expectation-maximization algorithms for estimation in the new model and report audio signal processing results with music decomposition and speech enhancement.

We introduce a model where the rate of an inhomogeneous Poisson process is modified by a Chinese restaurant process. Applying a MCMC sampler to this model allows us to do posterior Bayesian inference about the number of states in Poisson-like data. Our sampler is shown to get accurate results for synthetic data and we apply it to V1 neuron spike data to find discrete firing rate states depending on the orientation of a stimulus.