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  1. We introduce the isoperimetric loss as a regularization criterion for learning the map from a visual representation to a semantic embedding, to be used to transfer knowledge to unknown classes in a zero-shot learning setting. We use a pretrained deep neural network model as a visual representation of image data, a Word2Vec embedding of class labels, and linear maps between the visual and semantic embedding spaces. However, the spaces themselves are not linear, and we postulate the sample embedding to be populated by noisy samples near otherwise smooth manifolds. We exploit the graph structure defined by the sample points to regularize the estimates of the manifolds by inferring the graph connectivity using a generalization of the isoperimetric inequalities from Riemannian geometry to graphs. Surprisingly, this regularization alone, paired with the simplest baseline model, outperforms the state-of-the-art among fully automated methods in zeroshot learning benchmarks such as AwA and CUB. This improvement is achieved solely by learning the structure of the underlying spaces by imposing regularity 
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  2. Abstract Background

    Network propagation has been widely used for nearly 20 years to predict gene functions and phenotypes. Despite the popularity of this approach, little attention has been paid to the question of provenance tracing in this context, e.g., determining how much any experimental observation in the input contributes to the score of every prediction.

    Results

    We design a network propagation framework with 2 novel components and apply it to predict human proteins that directly or indirectly interact with SARS-CoV-2 proteins. First, we trace the provenance of each prediction to its experimentally validated sources, which in our case are human proteins experimentally determined to interact with viral proteins. Second, we design a technique that helps to reduce the manual adjustment of parameters by users. We find that for every top-ranking prediction, the highest contribution to its score arises from a direct neighbor in a human protein-protein interaction network. We further analyze these results to develop functional insights on SARS-CoV-2 that expand on known biology such as the connection between endoplasmic reticulum stress, HSPA5, and anti-clotting agents.

    Conclusions

    We examine how our provenance-tracing method can be generalized to a broad class of network-based algorithms. We provide a useful resource for the SARS-CoV-2 community that implicates many previously undocumented proteins with putative functional relationships to viral infection. This resource includes potential drugs that can be opportunistically repositioned to target these proteins. We also discuss how our overall framework can be extended to other, newly emerging viruses.

     
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