RESUMO
Corneal endothelium is a single cell layer that is mainly responsible for maintaining corneal clarity. Endothelial damage secondary to toxicity, stress, or genetic predisposition are common and in conjunction with the low regenerative ability of the cells, making their preservation critical for maintaining visual acuity. Patients with glaucoma, who are estimated to be close to 80 million worldwide, have a plethora of reasons for developing endothelial damage, being exposed to a spectrum that extends from various medical and surgical interventions to the disease itself. The wide spectrum of glaucoma pharmacotherapy that has been recently extended by addition of newer classes of medications has been the focus of extensive research on its effects on corneal endothelium. Both basic and clinical research have attempted to shine a light on the complex mechanisms associated with the effects of glaucoma medication on corneal endothelium and to answer the important question as to whether these findings are clinically significant. The aim of this review is to summarize and present current literature of the various findings, both from in vivo and in vitro studies that have focused on the complex relationship between different classes of glaucoma medication and their effect on corneal endothelium.
RESUMO
The purpose of this work was to evaluate peripheral image quality in the pseudophakic eye using computational, physical, and psychophysical methods. We designed and constructed a physical model of the pseudophakic human eye with realistic dimensions using a corneal phantom and a board-only camera that was pivoted around an axis that matched the anatomical center of a human retina, assuming a radius of curvature of 12â mm, while it was submersed in a 23.4â mm long water filled chamber to emulate human ocular axial length. We used this optical setup to perform direct recording of the point spread function (PSF) and the associated retinal images for a commercial intraocular lens (IOL). Additionally, psychophysical tests were carried out to investigate the impact of the off-axis astigmatism in peripheral visual performance, where spectacle-induced astigmatism simulated the pseudophakic conditions in healthy subjects. Our findings using the physical eye model confirm the existence of large amounts of astigmatism in the periphery of the pseudophakic eye. The psychophysical tests revealed a significant reduction of detection sensitivity in the peripheral visual field. The latter suggests that off-axis astigmatism in patients implanted with IOLs may have performance and safety implications for activities requiring efficient peripheral vision.
RESUMO
Currently, no pharmacotherapy has been proven effective in treating photoreceptor degeneration in patients. Discovering readily available and safe neuroprotectants is therefore highly sought after. Here, we investigated nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD+), in a retinal detachment (RD) induced photoreceptor degeneration. NMN administration after RD resulted in a significant reduction of TUNEL+ photoreceptors, CD11b+ macrophages, and GFAP labeled glial activation; a normalization of protein carbonyl content (PCC), and a preservation of the outer nuclear layer (ONL) thickness. NMN administration significantly increased NAD+ levels, SIRT1 protein expression, and heme oxygenase-1 (HO-1) expression. Delayed NMN administration still exerted protective effects after RD. Mechanistic in vitro studies using 661W cells revealed a SIRT1/HO-1 signaling as a downstream effector of NMN-mediated protection under oxidative stress and LPS stimulation. In conclusion, NMN administration exerts neuroprotective effects on photoreceptors after RD and oxidative injury, suggesting a therapeutic avenue to treating photoreceptor degeneration.