SummaryDisorders of human skin manifest themselves with patterns of lesions ranging from simple scattered spots to complex rings and spirals. These patterns are an essential characteristic of skin disease, yet the mechanisms through which they arise remain unknown. Here we show that all known patterns of psoriasis, a common inflammatory skin disease, can be explained in terms of reaction-diffusion. We constructed a computational model based on the known interactions between the main pathogenic cytokines: interleukins IL-17 and IL-23, and tumor necrosis factor TNF-α. Simulations revealed that the parameter space of the model contained all classes of psoriatic lesion patterns. They also faithfully reproduced the growth and evolution of the plaques and the response to treatment by cytokine targeting. Thus the pathogenesis of inflammatory diseases, such as psoriasis, may be readily understood in the framework of the stimulatory and inhibitory interactions between a few diffusing mediators.
Although many simulation models of natural phenomena have been developed to date, little attention was given to a major contributor to the beauty of nature: the colorful patterns of flowers. We survey typical patterns and propose methods for simulating them inspired by the current understanding of the biology of floral patterning. The patterns are generated directly on geometric models of flowers, using different combinations of key mathematical models of morphogenesis: vascular patterning, positional information, reaction-diffusion, and random pattern generation. The integration of these models makes it possible to capture a wide range of the flower pigmentation patterns observed in nature.
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