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retinal degeneration/edema

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Müller cells as players in retinal degeneration and edema.

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BACKGROUND Under normal conditions, Müller cells support neuronal activity and the integrity of the blood-retinal barrier, whereas gliotic alterations of Müller cells under pathological conditions may contribute to retinal degeneration and edema formation. A major function of Müller cells is the

High-resolution Imaging in Male Germ Cell-Associated Kinase (MAK)-related Retinal Degeneration.

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OBJECTIVE To describe the characteristics of MAK-related retinal degeneration using optical coherence tomography angiography (OCTA) and adaptive optics scanning laser ophthalmoscopy (AOSLO). METHODS Cross-sectional study. METHODS Six patients with rod-cone degeneration and disease-causing mutations

Macular edema and cystoid macular edema.

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We examined the foveomacular regions from three eyes in which fluorescein angiography had demonstrated the characteristic appearance of cystoid macular edema by light and electron microscopy. Cystoid macular edema was present in two eyes (one of which was from a 63-year-old diabetic man) that

Bilateral disc edema in retinitis pigmentosa.

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Retinitis pigmentosa (RP), one of the most common forms of hereditary retinal degeneration, is characterized by night blindness and constricted visual fields. In addition to bone spicule pigmentation, other ocular findings may include posterior subcapsular cataracts, cystoid macular edema, and

Cystoid edema, neovascularization and inflammatory processes in the murine Norrin-deficient retina.

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Mutations in the Norrin (NDP) gene cause severe developmental blood vessel defects in the retina leading to congenital blindness. In the retina of Ndph-knockout mice only the superficial capillary network develops. Here, a detailed characterization of this mouse model at late stages of the disease

Severe retinal degeneration at an early age in Usher syndrome type 1B associated with homozygous splice site mutations in MYO7A gene.

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UNASSIGNED Usher syndrome is the most common cause of deafness associated with visual loss of a genetic origin. The purpose of this paper is to report very severe phenotypic features of type 1B Usher syndrome in a Saudi family affected by positive homozygous splice site mutation in MYO7A

AUTOIMMUNE RETINOPATHY MIMICKING HERITABLE RETINAL DEGENERATION IN A PATIENT WITH COMMON VARIABLE IMMUNE DEFICIENCY.

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1) To describe a case of autoimmune retinopathy mimicking heritable photoreceptor degeneration in a patient with common variable immune deficiency and 2) to investigate the humoral and cell-mediated branches of the immune system in this patient to better understand the mechanism of

Short-term outcomes of intravitreal dexamethasone in relation to biomarkers in diabetic macular edema

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Purpose: The purpose of this study was to determine the effects of dexamethasone implant (0.7 mg) on biomarkers such as hyper-reflective dots, external limiting membrane integrity and disorganization of retinal inner layers in treatment-naïve patients, patients who

Macular edema-like change and pseudopapilledema in a case of Scheie syndrome.

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We reported a case of Scheie syndrome in which diffuse fine corneal deposits, pigmentary retinal degeneration, pseudopapilledema, and macular edema-like change were observed bilaterally. This is the first report describing macular change in Scheie syndrome.

Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions.

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Breakdown of the inner endothelial blood-retinal barrier (BRB), as occurs in diabetic retinopathy, age-related macular degeneration, retinal vein occlusions, uveitis and other chronic retinal diseases, results in vasogenic edema and neural tissue damage, causing loss of vision. The central mechanism

TEMPOL, a superoxide dismutase mimic, ameliorates light-induced retinal degeneration.

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The efficacy of 4-hydroxy-2,2,6,6-tetramethylpiperidine-l-oxyl (TEMPOL), a metal independent superoxide dismutase (SOD) mimic, in ameliorating light-induced retinal degeneration was investigated. Thirty-six Lewis albino rats were exposed to green fluorescent light (490-580 nm, 160-180 foot-candles)

[Pharmacological concepts to treat hereditary retinal degenerations].

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This article reviews the current pharmacological strategies to treat inherited retinal degeneration. To date there is no causal therapy despite growing knowledge of the particular pathomechanisms. However, treatment is available for complications, such as cystic macular changes and cystoid macular

Detailed Clinical Phenotype and Molecular Genetic Findings in CLN3-Associated Isolated Retinal Degeneration.

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UNASSIGNED Mutations in genes traditionally associated with syndromic retinal disease are increasingly found to cause nonsyndromic inherited retinal degenerations. Mutations in CLN3 are classically associated with juvenile neuronal ceroid lipofuscinosis, a rare neurodegenerative disease with early

Retinal Reflectivity Measurement for Cone Impairment Estimation and Visual Assessment After Diabetic Macular Edema Resolution (RECOVER-DME).

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Photoreceptor loss has been suspected of being involved in incomplete visual recovery after diabetic macular edema (DME) resolution. Recent studies have shown that cone density in the perifoveal area could be estimated by in vivo measurements of the outer retinal reflectivity on optical coherence

Glial cell-mediated spread of retinal degeneration during detachment: a hypothesis based upon studies in rabbits.

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In human subjects with peripheral retinal detachments, visual deficits are not restricted to the detached retina but are also present in the non-detached tissue. Based upon studies on a rabbit model of rhegmatogenous retinal detachment, we propose a glial cell-mediated mechanism of spread of retinal
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