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Pilot & Feasibility Program Application Abstract
Monitoring Diabetic Retinopathy Progression in Mice using Hyperspectral Imaging
Karl Zuzak
(Arlington, TX)
Pilot & Feasibility Program
Diabetic retinopathy is the leading cause of irreversible blindness caused by vascular dysfunction. The long term goal is for creating a Hyperspectral Mouse Imaging Center (HMIC) within the Advanced Imaging Research Center (AIRC) at UT Southwestern supported by the National Mouse Metabolic Phenotyping Center (MMPC). HMIC will provide a service for phenotyping and monitoring diabitic retinopathy in mice by providing (1) a diabetic retinopathy mouse model, the double-knock-out apoE-/-db/db mouse, and (2) hyperspectral imaging, chemometric deconvolution and statistical analysis for monitoring vascular changes in the retina of the mouse non-invasively and in-vivo at regular intervals over months. To that end the specific aims for this project are (1) develop and characterize a hyperspectral imaging dissection microscope for visualizing vascular dysfunction in the retina of the mouse, in vivo and non-invasively, (2) monitor retinal vascular changes over 6 months in diabetic mice (the apoE-/-db/db mouse) having a predisposition for developing diabetic retinopathy. The diabetic retinopathy mouse will be provided by The Jackson Laboratory (Bar harbor, ME) in a newly characterized murine model of nonproliferative diabetic retinopathy, which has been observed that hyperlipidemia accelerates structural vascular changes in diabetic retinas leading to diabetic retinopathy. The clinical hyperspectral imaging method developed by the PI while serving an NIH tenure for detecting vascular dysfunction, and recently while at UT Arlington applied toward visualizing retinal vascular changes, clinically, will be augmented for imaging the retinas of live mice over 6 months to monitor the vascular progression of diabetic retinopathy. Testing the hypothesis that the hyperspectral dissection microscope and chemometric deconvolution will visualize vascular changes while monitoring the development of diabetic retinopathy in the apoE-/-db/db mouse, which will not be present in the control groups, mice with apoe tm1Unc and Lepr db mutation, mice that are bred to generate the apoE-/-db/db mouse.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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