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The collective operation of robots, such as unmanned aerial vehicles (UAVs) operating as a team or swarm, is affected by their individual capabilities, which in turn is dependent on their physical design, aka morphology. However, with the exception of a few (albeit ad hoc) evolutionary robotics methods, there has been very little work on understanding the interplay of morphology and collective behavior. There is especially a lack of computational frameworks to concurrently search for the robot morphology and the hyper-parameters of their behavior model that jointly optimize the collective (team) performance. To address this gap, this paper proposes a new co-design framework. Here the exploding computational cost of an otherwise nested morphology/behavior co-design is effectively alleviated through the novel concept of “talent” metrics; while also allowing significantly better solutions compared to the typically sub-optimal sequential morphology → behavior design approach. This framework comprises four major steps: talent metrics selection, talent Pareto exploration (a multi-objective morphology optimization process), behavior optimization, and morphology finalization. This co-design concept is demonstrated by applying it to design UAVs that operate as a team to localize signal sources, e.g., in victim search and hazard localization. Here, the collective behavior is driven by a recently reported batch Bayesian search algorithm called Bayes-Swarm. Our case studies show that the outcome of co-design provides significantly higher success rates in signal source localization compared to a baseline design, across a variety of signal environments and teams with 6 to 15 UAVs. Moreover, this co-design process provides two orders of magnitude reduction in computing time compared to a projected nested design approach. 

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies predominantly to nuclear material. Many aspects of disease pathology are mediated by the deposition of nucleic acid containing immune complexes, which also induce the type 1interferon response, a characteristic feature of SLE. Notably, SLE is remarkably heterogeneous, with a variety of organs involved in different individuals, who also show variation in disease severity related to their ancestries. Here, we probed one potential contribution to disease heterogeneity as well as a possible source of immunoreactive nucleic acids by exploring the expression of human endogenous retroviruses (HERVs). We investigated the expression of HERVs in SLE and their potential relationship to SLE features and the expression of biochemical pathways, including the interferon gene signature (IGS). Towards this goal, we analyzed available and new RNA-Seq data from two independent whole blood studies using Telescope. We identified 481 locus specific HERV encoding regions that are differentially expressed between case and control individuals with only 14% overlap of differentially expressed HERVs between these two datasets. We identified significant differences between differentially expressed HERVs and non-differentially expressed HERVs between the two datasets. We also characterized the host differentially expressed genes and tested their association with the differentially expressed HERVs. We found that differentially expressed HERVs were significantly more physically proximal to host differentially expressed genes than non-differentially expressed HERVs. Finally, we capitalized on locus specific resolution of HERV mapping to identify key molecular pathways impacted by differential HERV expression in people with SLE.