Relative peripheral refraction and its role in myopia onset in teenage students.

AIM: To characterize peripheral refraction and its relationship with myopia development in a selected group of male teenage Chinese students. METHODS: This 2-year prospective cohort study randomly enrolled 85 non-myopic boys (age, 14-16y) from the Experimental Class of Air Force in China. Cycloplegic peripheral refraction was examined at 0°, ±10°, and ±20° along the horizontal visual field in the right eye at the baseline and 2-year follow-up. RESULTS: The incidence of myopia at the 2-year follow-up was 15.29% (13/85). The baseline central refraction (CR) and peripheral refraction at ±10° were significantly lower in students who developed myopia than in those who did not (P<0.05). Relative peripheral refraction (RPR) did not differ between students with and without myopia (P>0.05). At the 2-year follow-up, the RPR at ±10° and 20° nasal was significantly more hyperopic in the myopic group than in the non-myopic group. Multiple linear regression analysis indicated that the change in CR was significantly correlated with the changes in RPR at 20° nasal, 10° nasal, and 20° temporal. Multivariate Logistic regression analysis indicated that the baseline CR [odds ratio (OR): 0.092, 95% confidence interval (CI): 0.012-0.688, P=0.020] and the baseline RPR at 10° nasal (OR: 0.182, 95%CI: 0.042-0.799, P=0.024) were significantly correlated with incident myopia (Omnibus test, χ 2=10.20, P=0.006). CONCLUSION: CR change is significantly correlated with changes in RPR, and students who develop myopia have more relative peripheral hyperopia. More baseline CR and relative peripheral hyperopia at 10° nasal are protective of myopia onset.

Risk Factors for Incident Myopia among Teenaged Students of the Experimental Class of the Air Force in China.

BACKGROUND: In recent decades, the prevalence rate of myopia has markedly increased, especially among teenagers. Our purpose was to determine the incidence of myopia and identify the related risk factors among schoolchildren in the experimental classes of the Air Force in China. METHODS: In May 2015, this 3-year prospective cohort study enrolled 522 boys (age, 14-16 years) attending grade 10 in 16 high schools in 15 cities in China. Cycloplegic refraction was examined using retinoscopy in both eyes at the baseline and follow-up (3 years). A detailed questionnaire was completed by the students at the 3-year follow-up and included questions on parental myopia and on the total time spent doing near work and outdoor activities each week. RESULTS: The incidence of myopia at the 3-year follow-up was 27.01% (141/522, 95% confidence interval (CI): 23.38% to 30.98%). The refractive change was -0.46 D (95% CI: -0.49 to -0.42 D). More hyperopic or less myopic baseline refraction, outdoor activity time per week ≥14 h (odds ratio (OR) = 0.464, 95% CI: 0.227 to 0.950), and reading/writing distance ≥ 30 cm (OR = 0.505, 95% CI: 0.270 to 0.944) were significant protective factors against incident myopia. Near-work time ≥28 h per week was a significant risk factor (OR = 2.579, 95% CI: 1.314 to 5.061). Parental myopia, age at the start of primary school, continuous reading/writing for ≥1 h, sleep duration per week <49 h, and one or more dietary biases were not significant risk factors (P > 0.05). CONCLUSION: A more hyperopic baseline refraction, more time spent outdoors, and longer writing/reading distance were protected against myopia onset, while more near-work time was a risk factor.

Refractive Change and Incidence of Myopia Among A Group of Highly Selected Senior High School Students in China: A Prospective Study in An Aviation Cadet Prerecruitment Class.

Purpose: To assess the incidence rate of myopia, refractive change, and the effects of influencing factors on a group of highly selected senior high school students in an Aviation Cadet prerecruitment class in China. Methods: A total of 800 nonmyopic, male, Grade 9 students aged 14- to 16-years old with cycloplegic refraction of -0.25 or greater diopters (D) to 1.75 D or less in both eyes were enrolled in May 2016. During their senior high school studies, students had one 20-minute physical training period a day, and they were encouraged to participate in outdoor activities during class recess without any time limits. The first follow-up was 8 months after enrollment when they were in Grade 10, and the second follow-up was 1 year after the first follow-up when they were in Grade 11. Comprehensive ocular examinations and a detailed questionnaire, which included questions about outdoor activity time, parental myopia, and near work, were completed at each follow-up. Results: The average spherical equivalent refraction (SER) of the right eyes was 0.39 ± 0.44 D at baseline, 0.16 ± 0.41 D at the first follow-up, and -0.10 ± 0.38 D at the second follow-up. The cumulative refractive change was -0.50 D (95% confidence interval [CI], -0.53 to -0.47). The cumulative incidence rate of myopia was 15.5% (124/800). Incident myopia was significantly associated with outdoor activity for more than 1 versus less than 0.5 hr/d (odds ratio [OR] = 0.272, 95% CI, 0.132-0.560), baseline refraction (OR = 0.079, 95% CI, 0.041-0.153), maternal myopia (OR = 2.251, 95% CI, 1.160-4.368), longer class time (OR =3.215, 95% CI, 1.088-9.499), frequent, continuous, and long time reading/writing (OR = 1.620, 95% CI, 1.022-2.570), and shorter reading/writing distance (OR = 1.828, 95% CI, 1.065-3.140). In multiple linear regression model, having outdoor activity for more than 1 hr/d was protective from cumulative SER decrease. A higher baseline refraction together with longer reading/writing time, frequent, continuous, and longtime reading/writing, and shorter reading/writing distance were risk factors for SER decrease. Conclusions: In this cohort of highly selected, nonmyopic students, longer outdoor activity time was a protective factor for both incident myopia and refractive change of myopic shift. The risk factors for incident myopia included lower hyperopic baseline refraction, more near work, and maternal myopia. The risk factors for refractive change of myopic shift included more hyperopic baseline refraction and more near work.

The reason for the amelioration of N-methyl-N-nitrosourea-induced retinitis pigmentosa in rats by hydrogen-rich saline.

AIM: To investigate the effects of hydrogen-rich saline (HRS) on microglia activation and Sirtuin type 1 (Sirt1) in rats with N-methyl-N-nitrosourea (MNU)-induced retinitis pigmentosa (RP). METHODS: Rats were divided into norm (N) group, model (M) group and HRS (H) group. Rats in M and H groups were given saline and HRS respectively prior to and after administration of MNU. At one day (d1) and d3 afterwards, electroretinogram and histological examination were performed to confirm the effects of HRS on retinal function and structure of MNU-induced RP. Immunofluorescence staining of anti-ionized calcium-binding adapter molecule 1 (Iba1), a maker of microglia cells, was performed, with quantitative real-time polymerase chain reaction (qRT-PCR) for its mRNA quantification. Moreover, Sirt1 mRNA and protein expression in the retinas were detected by Western blot and qRT-PCR. RESULTS: HRS preserved the retinal function and mitigated the reduction of photoreceptor degeneration in MNU-treated retinas. The presence of microglia cells was somewhat more obvious in H group than that in M group at d1. HRS suppressed the further activation of microglia cells, with the number of microglia cells less than that of M group at d3. Results of qRT-PCR of Iba1 were consistent with those of immunofluorescence staining, with the mRNA expression of Iba1 in H group more intensive than that of M group at d1 (P<0.05), while less than that of M group at d3 (P<0.05). Furthermore, the Sirt1 mRNA and protein expression decreased after MNU administration, while HRS mitigated the MNU-induced downregulation of Sirt1. CONCLUSION: HRS can effectively keep microglia activation induced by MNU to an appropriate extent, while upregulate Sirt1 in MNU-induced RP.

The Time Course of Deafness and Retinal Degeneration in a Kunming Mouse Model for Usher Syndrome.

Usher syndrome is a group of autosomal recessive diseases characterized by congenital deafness and retinitis pigmentosa. In a mouse model for Usher syndrome, KMush/ush, discovered in our laboratory, we measured the phenotypes, characterized the architecture and morphology of the retina, and quantified the level of expression of pde6b and ush2a between postnatal (P) days 7, and 56. Electroretinograms and auditory brainstem response were used to measure visual and auditory phenotypes. Fundus photography and light microscopy were used to measure the architecture and morphology of the retina. Quantitative real-time PCR was used to measure the expression levels of mRNA. KMush/ush mice had low amplitudes and no obvious waveforms of Electroretinograms after P14 compared with controls. Thresholds of auditory brainstem response in our model were higher than those of controls after P14. By P21, the retinal vessels of KMush/ush mice were attenuated and their optic discs had a waxy pallor. The retinas of KMush/ush mice atrophied and the choroidal vessels were clearly visible. Notably, the architecture of each retinal layer was not different as compared with control mice at P7, while the outer nuclear layer (ONL) and other retinal layers of KMush/ush mice were attenuated significantly between P14 and P21. ONL cells were barely seen in KMush/ush mice at P56. As compared with control mice, the expression of pde6b and ush2a in KMush/ush mice declined significantly after P7. This study is a first step toward characterizing the progression of disease in our mouse model. Future studies using this model may provide insights about the etiology of the disease and the relationships between genotypes and phenotypes providing a valuable resource that could contribute to the foundation of knowledge necessary to develop therapies to prevent the retinal degeneration in patients with Usher Syndrome.

Ginsenoside Rd attenuates Aß25-35-induced oxidative stress and apoptosis in primary cultured hippocampal neurons.

One of the most common pathological changes in Alzheimer's disease (AD) brain is the large number of amyloid ß (Aß) peptides accumulating in lesion areas. Ginsenosides are the most active components extracted from ginseng. Ginsenoside Rd (GRd) is a newly discovered saponin that has a stronger pharmacological activity than other ginsenosides, especially in neuroprotection. Here we examined the neuroprotective effects of GRd against neuronal insults induced by Aß25-35 in primary cultured hippocampal neurons. A 10µM GRd treatment significantly prevented the loss of hippocampal neurons induced by Aß25-35. In addition, GRd significantly ameliorated Aß25-35-induced oxidative stress by decreasing the reactive oxygen species (ROS) production and malondialdehyde (MDA) level, and increasing the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); which is similar in treatments with 10µM of probucol (PB) and 100µM of edaravone (EDA). Moreover, our present study demonstrated that GRd significantly enhanced the expression of Bcl-2 mRNA, and decreased the expressions of Bax mRNA and Cyt c mRNA. GRd also downregulated the protein level of cleaved Caspase-3 compared to controls. These results highlighted the neuroprotective effects of GRd against Aß25-35-induced oxidative stress and neuronal apoptosis, suggesting that this may be a promising therapeutics against AD.

Sirtuin Type 1 Mediates the Retinal Protective Effect of Hydrogen-Rich Saline Against Light-Induced Damage in Rats.

PURPOSE: Molecular hydrogen has been used as an antioxidant to treat many diseases in clinical and animal studies. However, the therapeutic mechanism of molecular hydrogen remains unclear. We previously reported mitigation of light-induced damage in the rat retina by intraperitoneal injection of hydrogen-rich saline (HRS). In the present study, we investigated whether Sirtuin Type 1 (Sirt1), a class III histone deacetylase, mediates the retinal protective effect of HRS in rats with light-induced retinal damage. METHODS: Rats were treated with HRS for 5 days after intense light exposure, and then ERGs were performed and retinas were collected to evaluate the effect of HRS on Sirt1 expression. The necessity of Sirt1 for the retinal protective effect of HRS was investigated using the Sirt1 activator resveratrol, the Sirt1 inhibitor EX-527, and short interfering RNAs. RESULTS: In light-damaged retinas, 5 days of HRS treatment increased Sirt1 expression, mitigated a- and b-wave amplitude reduction, and decreased the reduction of outer nuclear cell layers. The Sirt1 activator resveratrol mimicked the effect of HRS in light-damaged retinas. This result supported our hypothesis that Sirt1 mediates the protective effect of HRS. Additionally, the retinal protective effect of HRS was inhibited by both the Sirt1 inhibitor EX-527 and Sirt1 targeted short interfering RNAs. Hydrogen-rich saline also increased B-cell lymphoma 2 (Bcl-2) expression and the activity of the antioxidant enzyme superoxide dismutase (SOD). Conversely, HRS decreased Bcl2-associated X protein expression, cleaved caspase-3, and oxidant-stress product malondialdehyde (MDA) in a Sirt1-dependent manner. CONCLUSIONS: Sirt1 mediates light-induced damage mitigation by HRS through inhibition of apoptosis and oxidant-stress.