By Chi-Chao Chan
This booklet describes experimental animal versions that mimic universal human ocular illnesses: herpetic keratitis, cataract, glaucoma, age-related macular degeneration, diabetic retinopathy, uveitis, retinitis pigmentosa, Graves’ illness, and intraocular tumors. In conjunction, those versions replicate the range and application of instruments used to check human ailment. global professional clinicians speak about each one version in line with their scientific event and the textual content is supported by means of quite a few photographs and diagrams. In describing the main pertinent animal types of ophthalmic ailments, this ebook can be of curiosity to ophthalmologists, imaginative and prescient researchers, fellows, citizens and scientific students.
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Additional resources for Animal Models of Ophthalmic Diseases
Many of the rabbit studies investigate the preventive effect of contact lenses containing UV-blocking materials. These findings show that contact lenses are beneficial in protecting ocular tissues of the rabbit against harmful effects of UV light, including photokeratitis and anterior subcapsular cataract (Giblin et al. 2012). 3 Steroid-Induced Cataracts The use of steroid therapy in recent years has contributed to an increase in the incidence of cataracts (Gupta and Wagner 2009; Watanabe et al.
Pathologies Oculaires Liees a l’Age. Am J Epidemiol 151(5):497–504 DeRosa AM, Xia CH, Gong X, White TW (2007) The cataract-inducing S50P mutation in Cx50 dominantly alters the channel gating of wild-type lens connexins. J Cell Sci 120(Pt 23):4107–4116. 012237 DeRosa AM, Mese G, Li L, Sellitto C, Brink PR, Gong X, White TW (2009) The cataract causing Cx50-S50P mutant inhibits Cx43 and intercellular communication in the lens epithelium. Exp Cell Res 315(6):1063– 1075. 017 Devi RR, Yao W, Vijayalakshmi P, Sergeev YV, Sundaresan P, Hejtmancik JF (2008) Crystallin gene mutations in Indian families with inherited pediatric cataract.
Homozygous Cx46-null mice developed nuclear cataracts that formed due to aggregation 2 Animal Models of Cataracts of lens protein, facilitated by the degradation of crystallins (Gong et al. 1997). This mouse model showed normal early lens development, but with small opacities forming 2–3 weeks after birth that continued into full nuclear cataracts by 2 months, with 100 % penetrance of cataracts reported, indicating Cx46 is required for proper lens function (Gong et al. 1997). Interestingly, the severity of the cataracts on the Cx46-null model varied depending on the breeding background of the mouse, with milder cataracts observed in C57B16 mice when compared with mice bred from the 129 strain (Gong et al.