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An activator-inhibitor-substrate model of side-branching used in the context of pulmonary vascular and lung development is considered on the supposition that spatially localized concentrations of the activator trigger local side-branching. The model consists of four coupled reaction-diffusion equations and its steady localized solutions therefore obey an eight-dimensional spatial dynamical system in one dimension (1D). Stationary localized structures within the model are found to be associated with a subcritical Turing instability and organized within a distinct type of foliated snaking bifurcation structure. This behavior is in turn associated with the presence of an exchange point in parameter space at which the complex leading spatial eigenvalues of the uniform concentration state are overtaken by a pair of real eigenvalues; this point plays the role of a Belyakov-Devaney point in this system. The primary foliated snaking structure consists of periodic spike or peak trains with $N$ identical equidistant peaks, $N=1,2,dots ,$, together with cross-links consisting of nonidentical, nonequidistant peaks. The structure is complicated by a multitude of multipulse states, some of which are also computed, and spans the parameter range from the primary Turing bifurcation all the way to the fold of the $N=1$ state. These states form a complex template from which localized physical structures develop in the transverse direction in 2D.
An understanding of the underlying mechanism of side--branching is paramount in controlling and/or therapeutically treating mammalian organs, such as lungs, kidneys, and glands. Motivated by an activator-inhibitor-substrate approach that is conjectur
We derive a full 3-dimensional (3-D) model of inhomogeneous -- anisotropic diffusion in a tumor region coupled to a binary population model. The diffusion tensors are acquired using Diffusion Tensor Magnetic Resonance Imaging (DTI) from a patient dia
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