Search for: All records

Algorithmic systems are often called upon to assist in high-stakes decision making. In light of this, algorithmic recourse, the principle wherein individuals should be able to take action against an undesirable outcome made by an algorithmic system, is receiving growing attention. The bulk of the literature on algorithmic recourse to-date focuses primarily on how to provide recourse to a single individual, overlooking a critical element: the effects of a continuously changing context. Disregarding these effects on recourse is a significant oversight, since, in almost all cases, recourse consists of an individual making a first, unfavorable attempt, and then being given an opportunity to make one or several attempts at a later date — when the context might have changed. This can create false expectations, as initial recourse recommendations may become less reliable over time due to model drift and competition for access to the favorable outcome between individuals. In this work we propose an agent-based simulation framework for studying the effects of a continuously changing environment on algorithmic recourse. In particular, we identify two main effects that can alter the reliability of recourse for individuals represented by the agents: (1) competition with other agents acting upon recourse, and (2) competition with new agents entering the environment. Our findings highlight that only a small set of specific parameterizations result in algorithmic recourse that is reliable for agents over time. Consequently, we argue that substantial additional work is needed to understand recourse reliability over time, and to develop recourse methods that reward agents’ effort. 

Beyond natural stimuli such as growth factors and stresses, the ability to experimentally modulate at will the levels or activity of specific intracellular signaling molecule(s) in specified cells within a tissue can be a powerful tool for uncovering new regulation and tissue behaviors. Here we perturb the levels of cAMP within specific cells of an epithelial monolayer to probe the time-dynamic behavior of cell-cell communication protocols implemented by the cAMP/PKA pathway and its coupling to the ERK pathway. The time-dependent ERK responses we observe in the perturbed cells for spatially uniform cAMP perturbations (all cells) can be very different from those due to spatially localized perturbations (a few cells). Through a combination of pharmacological and genetic perturbations, signal analysis, and computational modeling, we infer how intracellular regulation and regulated cell-cell coupling each impact the intracellular ERK response in single cells. Our approach reveals how a dynamic gap junction state helps sculpt the intracellular ERK response over time in locally perturbed cells.