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dc.contributor.authorVick, Sarah
dc.date.accessioned2019-02-13T20:07:19Z
dc.date.available2019-02-13T20:07:19Z
dc.date.issued2019-02-13
dc.identifier.urihttp://hdl.handle.net/10675.2/622129
dc.descriptionPresentation given at the 20th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractIt is estimated that 41.6% of the US population suffers from vitamin D deficiency, with Blacks (82.1%) and Hispanics (69.2%) at even greater risk�Vitamin D deficiency can be caused by a variety of sources and given the wide range of causes, it is important to understand what measures this population might take to proactively prevent greater harm, or to reverse harm that might have already occurred. This project is designed to test the general hypothesis that Vitamin D deficiency exacerbates preexisting primary corneal pathologies. Previous research has established that the corneal epithelium in diabetic mice heals at a faster rate than the epithelium in diabetic vitamin D receptor (VDR) knockout (KO) mice. It is known that within diabetic mice, the corneal nerve density is decreased. However, it is unknown how VDR KO mice or vitamin D deficient with diabetes will affect corneal nerve density. In order to identify variabilities within the nerves that indicate slow wound healing, the mouse corneas will be collected, stained for confocal microscope observation, and analyzed through image processing to determine nerve density.
dc.subjectcorneaen
dc.subjectnerve densityen
dc.titleEFFECTS OF VITAMIN D3 DEFICIENCY, VITAMIN D RECEPTOR KNOCKOUT, AND DIABETES ON CORNEAL EPITHELIAL NERVE DENSITYen
dc.typePoster Presentationen
dc.contributor.departmentDepartment of Biological Sciencesen
dc.contributor.departmentDepartment of Cellular Biology and Anatomyen
cr.funding.sourceNIH National Eye Institute Grant R01EY021747en
dc.contributor.sponsorLu, Xiaowenen
dc.contributor.sponsorWatsky, Mitchellen
dc.contributor.affiliationAugusta Universityen
html.description.abstractIt is estimated that 41.6% of the US population suffers from vitamin D deficiency, with Blacks (82.1%) and Hispanics (69.2%) at even greater risk�Vitamin D deficiency can be caused by a variety of sources and given the wide range of causes, it is important to understand what measures this population might take to proactively prevent greater harm, or to reverse harm that might have already occurred. This project is designed to test the general hypothesis that Vitamin D deficiency exacerbates preexisting primary corneal pathologies. Previous research has established that the corneal epithelium in diabetic mice heals at a faster rate than the epithelium in diabetic vitamin D receptor (VDR) knockout (KO) mice. It is known that within diabetic mice, the corneal nerve density is decreased. However, it is unknown how VDR KO mice or vitamin D deficient with diabetes will affect corneal nerve density. In order to identify variabilities within the nerves that indicate slow wound healing, the mouse corneas will be collected, stained for confocal microscope observation, and analyzed through image processing to determine nerve density.


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