A Comparison of the Effects of Orthokeratology Lens, Medcall Lens, and Ordinary Frame Glasses on the Accommodative Response in Myopic Children.

OBJECTIVE: To observe and compare changes in accommodative response between myopic children wearing ordinary frame glasses (OFG), Mouldway orthokeratology lenses (M-OK), and medcall lenses (ML). METHODS: A total of 240 myopic children were divided into three groups: OFG [n=90]; M-OK [n=90]; and ML [n=60]). The diopter, accommodative lag, and binocular accommodative facility before wearing glasses (T0) and 1-year after wearing glasses (T1) were compared among the three groups. RESULTS: Commercially available software was used to perform statistical analysis, and the data were expressed as mean±SD. There were no significant differences among the three groups at T0. The accommodative lags in M-OK and ML at T1 were significantly lower than those at T0; this finding was most evident in M-OK. Although accommodative facility increased in all three groups, the increase was most evident in M-OK and ML. CONCLUSION: Mouldway orthokeratology lenses and ML can reduce the accommodative lag and increase the accommodative facility in myopic children. Compared with ML, M-OK showed considerably more marked effects to myopia progression in children.

miR-26a-5p Attenuates Oxidative Stress and Inflammation in Diabetic Retinopathy through the USP14/NF-κB Signaling Pathway.

Purpose: Diabetic retinopathy (DR) is an ocular disease caused by diabetes and may lead to vision impairment and even blindness. Oxidative stress and inflammation are two key pathogenic factors of DR. Recently, regulatory roles of different microRNAs (miRNAs) in DR have been widely verified. miR-26a-5p has been confirmed to be a potential biomarker of DR. Nevertheless, the specific functions of miR-26a-5p in DR are still unclear. Methods: Primary cultured mouse retinal Müller cells in exposure to high glucose (HG) were used to establish an in vitro DR model. Müller cells were identified via morphology observation under phase contrast microscope and fluorescence staining for glutamine synthetase. The in vivo animal models for DR were constructed using streptozotocin-induced diabetic C57BL/6 mice. Western blotting was performed to quantify cytochrome c protein level in the cytoplasm and mitochondria of Müller cells and to measure protein levels of glial fibrillary acidic protein (GFAP), ubiquitin-specific peptidase 14 (USP14), as well as factors associated with NF-κB signaling (p-IκBα, IκBα, p-p65, and p65) in Müller cells or murine retinal tissues. ROS production was detected by CM-H2DCFDA staining, and the concentration of oxidative stress markers (MDA, SOD, and CAT) was estimated by using corresponding commercial kits. Quantification of mRNA expression was conducted by RT-qPCR analysis. The concentration of proinflammatory factors (TNF-α, IL-1ß, and IL-6) was evaluated by ELISA. Hematoxylin-eosin staining for murine retinal tissues was performed for histopathological analysis. Immunofluorescence staining was conducted to determine NF-κB p65 nuclear translocation in Müller cells. Furthermore, the interaction between miR-26a-5p and USP14 was verified via the luciferase reporter assays. Results: HG stimulation contributed to Müller cell dysfunction by inducing inflammation, oxidative injury, and mitochondrial damage to Müller cells. miR-26a-5p was downregulated in Müller cells under HG condition, and overexpression of miR-26a-5p relieved HG-induced Müller cell dysfunction. Moreover, miR-26a-5p targeted USP14 and inversely regulated USP14 expression. Additionally, HG-evoked activation of NF-κB signaling was suppressed by USP14 knockdown or miR-26a-5p upregulation. Rescue assays showed that the protective impact of miR-26a-5p upregulation against HG-induced Müller cell dysfunction was reversed by USP14 overexpression. Furthermore, USP14 upregulation and activation of NF-κB signaling in the retinas of DR mice were detected in animal experiments. Injection with miR-26a-5p agomir improved retinal histopathological injury and weakened the concentration of proinflammatory cytokines and oxidative stress markers in the retinas of DR mice. Conclusion: miR-26a-5p inhibits oxidative stress and inflammation in DR progression by targeting USP14 and inactivating the NF-κB signaling pathway.

Spironolactone versus observation in the treatment of acute central serous chorioretinopathy.

PURPOSE: To evaluate the efficacy of oral spironolactone in patients with acute central serous chorioretinopathy (CSC). METHODS: This is a prospective, randomised controlled clinical study. Thirty patients with acute CSC were the participants, including 18 patients who were treated with spironolactone (40 mg orally, twice daily) for 2 months in the experimental group and 12 patients who received observation in the control group. Main outcome measures included the proportion of eyes achieving complete resolution of subretinal fluid (SRF), changes in central macular thickness (CMT), the height of SRF (SRFH), best corrected visual acuity (BCVA) and subfoveal choroidal thickness (SFCT). The follow-up period was 2 months. RESULTS: Complete resolution of SRF was achieved in 55.6% (10/18) and 8.3% (1/12) of the eyes in the treatment group and the control group, respectively, at 2 months (p=0.018). The mean CMT and SRFH decreased significantly at each visit in both groups (p<0.05), and there was significant difference between the two groups at 2 months (p<0.05 and p<0.05, respectively). BCVA (in logarithm of the minimum angle of resolution; mean) improved in both groups at 2 months (p<0.05). In the treatment group, the mean baseline SFCT significantly decreased from 502.50±87.38 µm to 427.44±74.37 µm at 2 months (p<0.01), while the change from baseline (from 480.33±102.38 µm to 463.75±100.63 µm) was not significant in the control group (p=0.195). But the differences between the two groups in BCVA and SFCT were not significant. CONCLUSIONS: Oral spironolactone is more effective with a faster absorption of SRF than observations. It is a promising treatment for acute CSC. TRIAL REGISTRATION NUMBER: ChiCTR-IPR-16008428, Results.

Focal choroidal excavation and a traumatic macular hole secondary to accidental Q-switched Nd:YAG laser.

Today, the widespread use of laser instruments in various fields has resulted in many accidental retinal injuries. Here we describe a rare clinical case of full-thickness macular hole (MH) and focal choroidal excavation (FCE) caused by a 1064-nm Q-switched Nd:YAG laser. After pars plana vitrectomy and the following 14 months, consecutive optical coherence tomography imagings showed closure of the MH. Visual acuity improved even in the absence of the outer retina and in the presence of FCE. We speculate that different focusing effects of the unexpected Nd:YAG lasers which target different levels of retinal tissue generate diverse prognosis.