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The unfavorable treatment of people with physical disfigurements is well-documented, yet little is known about basic perceptual and cognitive responses to disfigurement. Here, we identify a specialized pattern of cognitive processing consistent with the hypothesis that disfigurements act as heuristic cues to contagious disease. Disfigurements are often invariant across time and difficult to conceal, and thus observers can detect the presence of such cues without necessarily remembering the particular individuals bearing these cues. Indeed, despite the fact that disfigured faces were especially likely to hold disease-sensitive perceivers' attention (Study 1), disfigured individuals were often confused with one another and thus not well remembered later (Study 2), revealing a disjunction of the typical relationship between elevated attention and elevated memory. We discuss the implications of our results for stigmatization of people with and without physical abnormalities and suggest the possibility that cognitive mechanisms for processing social information may be functionally tuned to the variant nature of important cues.

The field of collective animal behaviour examines how relatively simple, local interactions between individuals in groups combine to produce global-level outcomes. Existing mathematical models and empirical work have identified candidate mechanisms for numerous collective phenomena but have typically focused on one-off or short-term performance. We argue that feedback between collective performance and learning - giving the former the capacity to become an adaptive, and potentially cumulative, process - is a currently poorly explored but crucial mechanism in understanding collective systems. We synthesise material ranging from swarm intelligence in social insects through collective movements in vertebrates to collective decision making in animal and human groups, to propose avenues for future research to identify the potential for changes in these systems to accumulate over time.

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Pulmonary HO-1 expression is increased in silicosis. HO-1 suppresses reactive oxygen species activity, and subsequent pathologic changes, thereby attenuating disease progression.