Response to disease occurs over many scales ranging from individual gene expression to whole organ physiology. We employed the supertoroidal model of the diffusion tensor to study the interaction between gene expression and microstructure of the heart. Left ventricular hypertrophy (LVH) was induced in C57Bl6 mice through aortic banding, and characterization of the cardiac microstructure was performed in vivo with DTI. The supertoroidal model was constrained by both diffusion information and gene expression data related to cardiomyocyte hypertrophy and myofiber orientation. Our model enabled further characterization of LVH by unifying information at different scales and across domains.
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