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Purpose: The aim of this study was to compare noncycloplegic refraction performed in school camp with that performed in eye clinic in children aged 6-16 years.Methods: A prospective study of children with unaided vision <0.2 LogMAR who underwent noncycloplegic retinoscopy (NCR) and subjective refraction (SR) in camp and subsequently in eye clinic between February and March 2017 was performed. A masked optometrist performed refractions in both settings. The agreement between refraction values obtained at both settings was compared using the Bland-Altman analysis.Results: A total of 217 eyes were included in this study. Between the school camp and eye clinic, the mean absolute error ± standard deviation in spherical equivalent (SE) of NCR was 0.33 ± 0.4D and that of SR was 0.26 ± 0.5D. The limits of agreement for NCR were +0.91D to - 1.09D and for SR was +1.15D to -1.06D. The mean absolute error in SE was ≤0.5D in 92.62% eyes (95% confidence interval 88%-95%).Conclusion: A certain degree of variability exists between noncycloplegic refraction done in school camps and eye clinic. It was found to be accurate within 0.5D of SE in 92.62% eyes for refractive errors up to 4.5D of myopia, 3D of cylinder, and 1.5D of hyperopia. [ABSTRACT FROM AUTHOR]

Genetic changes and epigenetic modifications are associated with neuronal dysfunction in the pathogenesis of neurodegenerative disorders. However, the mechanism behind genetic mutations in the non-coding region of genes that affect epigenetic modifications remains unclear. Here, we identified an ALS-associated SNP located in the intronic region of MEF2C (rs304152), residing in a putative enhancer element, using convolutional neural network. The enhancer mutation of MEF2C reduces own gene expression and consequently impairs mitochondrial function in motor neurons. MEF2C localizes and binds to the mitochondria DNA, and directly modulates mitochondria-encoded gene expression. CRISPR/Cas-9-induced mutation of the MEF2C enhancer decreases expression of mitochondria-encoded genes. Moreover, MEF2C mutant cells show reduction of mitochondrial membrane potential, ATP level but elevation of oxidative stress. MEF2C deficiency in the upper and lower motor neurons of mice impairs mitochondria-encoded genes, and leads to mitochondrial metabolic disruption and progressive motor behavioral deficits. Together, MEF2C dysregulation by the enhancer mutation leads to mitochondrial dysfunction and oxidative stress, which are prevalent features in motor neuronal damage and ALS pathogenesis. This genetic and epigenetic crosstalk mechanism provides insights for advancing our understanding of motor neuron disease and developing effective treatments.