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- W4377042103 abstract "A plethora of computational models have been developed in recent decades to account for the morphogenesis of complex biological fluid networks, such as capillary beds. Contemporary adaptation models are based on optimization schemes where networks react and adapt vessel conductance toward given flow patterns. Recent numeric studies on network morphogenesis, incorporating uptake of metabolites by the embedding tissue, have indicated this conventional approach to be insufficient. Here, we systematically study a hybrid model intended to generate space-filling perfusion as well as optimal filtration of metabolites. As a result, we find hydrodynamic stimuli (wall-shear stress) and filtration based stimuli (uptake of metabolites) to be antagonistic as hydrodynamically optimized systems have suboptimal uptake qualities and vice versa. We show that a switch between optimization regimes is typically accompanied with a transition between topologically redundant meshes and spanning trees. Depending on the metabolite demand and uptake capabilities of the adapting networks, we further demonstrate the existence of nullity reentrance as a function of dissipation and the development of compromised phenotypes such as dangling nonperfused vessels and bottlenecks." @default.
- W4377042103 created "2023-05-19" @default.
- W4377042103 creator A5015816161 @default.
- W4377042103 creator A5061610546 @default.
- W4377042103 date "2023-05-17" @default.
- W4377042103 modified "2023-10-17" @default.
- W4377042103 title "Biological flow networks: Antagonism between hydrodynamic and metabolic stimuli as driver of topological transitions" @default.
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- W4377042103 doi "https://doi.org/10.1103/physrevresearch.5.023106" @default.
- W4377042103 hasPublicationYear "2023" @default.
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