Background: Pterygium is a sun-related ocular surface disease secondary to ultraviolet (UV) radiation exposure. Outdoor occupational UV exposure is known to occur secondary to sun exposure. We present a unique case of pterygium associated with indoor occupational light-emitting diode (LED) exposure not previously described in the literature.
Case Description: A mobile phone repairer presented with blurred vision and a superotemporal pterygium of his dominant left eye associated with a magnifying glass LED work lamp was diagnosed. This was excised routinely with conjunctival autografting to the defect. Histopathology confirmed benign pterygium and recovery was uncomplicated with resolution of blur.
Conclusions: The development of pterygium in our patient may have arisen due to the LED lamp’s wavelengths possibly falling within the UV as well as the upper end of the visible light radiation spectrum. Given the increasing reliance on LED light sources in modern life, ocular conditions arising from exposure to these radiation sources may now need to be listed in the differential diagnoses of patients with pterygium. Appropriate UV protection counselling for these types of lights may also now need to be considered.
Objective: In this review, non-transgenic models of age-related macular degeneration (AMD) are discussed, with focuses on murine retinal degeneration induced by sodium iodate and lipid peroxide (HpODE) as preclinical study platforms.
Background: AMD is the most common cause of vision loss in a world with an increasingly aging population. The major phenotypes of early and intermediate AMD are increased drusen and autofluorescence, Müller glia activation, infiltrated subretinal microglia and inward moving retinal pigment epithelium (RPE) cells. Intermediate AMD may progress to advanced AMD, characterized by geography atrophy and/or choroidal neovascularization (CNV). Various transgenic and non-transgenic animal models related to retinal degeneration have been generated to investigate AMD pathogenesis and pathobiology, and have been widely used as potential therapeutic evaluation platforms.
Methods: Two retinal degeneration murine models induced by sodium iodate and HpODE are described. Distinct pathological features and procedures of these two models are compared. In addition, practical protocol and material preparation and assessment methods are elaborated.
Conclusions: Retina degeneration induced by sodium iodate and HpODE in mouse eye resembles many clinical aspects of human AMD and complimentary to the existent other animal models. However, standardization of procedure and assessment protocols is needed for preclinical studies. Further studies of HpODE on different routes, doses and species will be valuable for the future extensive use. Despite many merits of murine studies, differences between murine and human should be always considered.
