Correlation between ocular residual astigmatism and anterior corneal astigmatism in children with low and moderate myopia.

BACKGROUND: To assess the correlation between ocular residual astigmatism and anterior corneal astigmatism in children with low and moderate myopia. METHODS: Refractive astigmatism was determined by subjective manifest refraction. Anterior corneal astigmatism was determined by IOL Master. Thibos vector analysis was used to calculate ocular residual astigmatism. Correlation analysis was used to assess the relationship between the amounts of ocular residual astigmatism and anterior corneal astigmatism. The relationship between the vectors of ocular residual astigmatism and anterior corneal astigmatism was evaluated by a physical method. RESULTS: The study analysed 241 right eyes of 241 children aged 8 to 18 years old. In this study, the median magnitude of ocular residual astigmatism was 1.02 D, with an interquartile range was of 0.58 D. Against-the-rule ocular residual astigmatism was seen in 232 eyes (96.3%). There was a significant and moderate correlation between ocular residual astigmatism and anterior corneal astigmatism (r = 0.50, P < 0.001). Ocular residual astigmatism compensated for anterior corneal astigmatism in 240 eyes (99.6%). The mean compensation value was 1.00 ± 0.41 D (range 0.02 D to 2.34 D). Based on this effect, 37 eyes had a different axial classification of anterior corneal astigmatism and refractive astigmatism. In contrast, one eye (0.4%) had oblique ocular residual astigmatism and the ocular residual astigmatism superimposed with-the-rule anterior corneal astigmatism. CONCLUSIONS: The magnitude of ocular residual astigmatism was relatively large in myopic children and predominantly compensated for anterior corneal astigmatism. Ocular residual astigmatism should be assessed in patients before fitting them with orthokeratology lenses.

circRNF20 aggravates the malignancy of retinoblastoma depending on the regulation of miR-132-3p/PAX6 axis.

Circular RNAs (circRNAs) serve as essential players in diverse human cancers, including retinoblastoma (RB). In this study, the function of circRNA Ring Finger Protein 20 (circRNF20) in RB progression was investigated. Quantitative real-time polymerase chain reaction, western blot assay or immunohistochemistry assay was performed to determine the expression of circRNF20, miR-132-3p and Paired Box 6 (PAX6). Dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay were utilized to verify the relationships among circRNF20, miR-132-3p and PAX6. In vivo experiment was done for circRNF20 function in tumor formation. It was found that ircRNF20 level was increased in RB tissues and linked to advanced tumor, nodes, metastases (TNM) stage and poor overall survival rate. Deficiency of circRNF20 suppressed cell proliferation, migration and invasion and induced apoptosis in vitro, as well as blocked tumor growth in vivo. circRNF20 directly targeted miR-132-3p and miR-132-3p overexpression inhibited RB cell progression. PAX6 was the target gene of miR-132-3p. Moreover, miR-132-3p inhibition or PAX6 overexpression reversed circRNF20 deficiency-mediated effects on RB cell malignant behaviors. In addition, exosomal circRNF20 was able to promote RB cell progression. Thus, we concluded that circRNF20 served as an oncogene in RB progression through the circRNF20/miR-132-3p/PAX6 pathway.