Vision starts with the absorption of light by the retinal photoreceptors-cones and rods. However, due to the 'inverted' structure of the retina, the incident light must propagate through reflecting and scattering cellular layers before reaching the photoreceptors. It has been recently suggested that Müller cells function as optical fibres in the retina, transferring light illuminating the retinal surface onto the cone photoreceptors. Here we show that Müller cells are wavelength-dependent wave-guides, concentrating the green-red part of the visible spectrum onto cones and allowing the blue-purple part to leak onto nearby rods. This phenomenon is observed in the isolated retina and explained by a computational model, for the guinea pig and the human parafoveal retina. Therefore, light propagation by Müller cells through the retina can be considered as an integral part of the first step in the visual process, increasing photon absorption by cones while minimally affecting rod-mediated vision.
Amyloid-β (Aβ), reported as a significant constituent of drusen, was implicated in the pathophysiology of age-related macular degeneration (AMD), yet the identity of the major pathogenic Aβ species in the retina has remained hitherto unclear. Here, we examined the in-vivo retinal impact of distinct supramolecular assemblies of Aβ. Fibrillar (Aβ40, Aβ42) and oligomeric (Aβ42) preparations showed clear biophysical hallmarks of amyloid assemblies. Measures of retinal structure and function were studied longitudinally following intravitreal administration of the various Aβ assemblies in rats. Electroretinography (ERG) delineated differential retinal neurotoxicity of Aβ species. Oligomeric Aβ42 inflicted the major toxic effect, exerting diminished ERG responses through 30 days post injection. A lesser degree of retinal dysfunction was noted following treatment with fibrillar Aβ42, whereas no retinal compromise was recorded in response to Aβ40 fibrils. The toxic effect of Aβ42 architectures was further reflected by retinal glial response. Fluorescence labelling of Aβ42 species was used to detect their accumulation into the retinal tissue. These results provide conceptual evidence of the differential toxicity of particular Aβ species in-vivo, and promote the mechanistic understanding of their retinal pathogenicity. Stratifying the impact of pathological Aβ aggregation in the retina may merit further investigation to decipher the pathophysiological relevance of processes of molecular self-assembly in retinal disorders.
Purpose: Subtle folds can be seen in the anterior cornea in eyes with hypotony using fluorescein and blue light. We aim to assess their extent and grade with respect to the level of intraocular pressure (IOP). Patients and Methods: Patients who presented to the department of ophthalmology at Rambam Health Care Campus with IOP<10 mm Hg during the period between July 2016 and June 2017. Corneal folds were evaluated after instilling an anesthetic drop and fluorescein staining. Outcome measures included: IOP, presence of anterior corneal folds, and the percentage of corneal surface containing folds. Results: Overall, 100 eyes of 100 patients were included. The mean age±SD was 63.6±16.7 years (range, 19 to 96 y); 56% (n=56) were of male sex. Mean IOP was 5.3±2.7 mm Hg (range, 0 to 9 mm Hg). Subjects with and without anterior corneal folds were of similar age (P=0.25) and sex (P=0.69). Those with anterior corneal folds had a significantly lower IOP than the control group (4.0±2.4 vs. 7.4±1.7; P<0.001). Eyes with IOP of 0 to 2, 3 to 4, 5 to 6, 7 to 9 mm Hg demonstrated anterior corneal folds in 95%, 91%, 67%, and 18.4%, respectively. At an IOP≤5 mm Hg cut-off, the sensitivity and specificity of corneal folds as a predictor of hypotony was 89.8% and 70.6%, respectively. A significant inverse correlation between the relative area of the cornea covered by folds and the IOP was found (r=−0.7; P<0.001). Conclusions: Folds observed in the anterior corneal surface appear to be a robust sign of severe hypotony.
Background This study describes a simple technique for the treatment of kissing choroidal detachment. In contrast to the commonly used technique, this technique is minimally invasive, fast, sutureless, and does not require access to the vitreous space. Methods A maintainer is inserted into the anterior chamber. A 25G trocar is inserted at the pars plana into the suprachoroidal space. Drainage is evident by the clear yellowish fluid freely emerging through the trocar, accompanied with deepening of the anterior chamber and an increase in the red reflex. Results Follow-up ultrasound 1 week after the surgery demonstrated resolution of the choroidal detachment. Net surgery time is about 10 minutes. No complications were noted. Discussion This is the first report of the technique performed in phakic eye, with video description of the steps and real-time clues for successful drainage even with reduced posterior segment visibility due to lens opacities.
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