Low vision aids and age are associated with Müller-Lyer illusion in congenital visually impaired children

BackgroundThe correlation between visual impairment and Müller-Lyer illusion is not yet elucidated. This study aimed to explore the connection between visual status, age, and the intensity of Müller-Lyer illusion in congenitally visually impaired and visually healthy children aged 4–17 years. Additionally, the developmental trends were compared.MethodsThis cross-sectional study included 125 visually impaired children (age: 10.59 ± 4.05 years), among them, 53 had utilized low vision aids (LVAs) and 133 healthy controls (age: 11.33 ± 3.39 years). The participants were presented with Müller-Lyer illusion stimuli via binocular and engaged in a two-alternative forced choice task to quantify the illusion intensity. Pertinent factors including age, gender, residence, binocular distant best-corrected visual acuity and LVAs usage history, were assessed.ResultsThe visually impaired group exhibited significantly elevated illusion intensity compared to the healthy group (9.74 ± 2.89% vs. 5.42 ± 3.81%, p < 0.001), and visually impaired participants who had used LVAs exhibited significantly lower intensity compared to those had not (9.13 ± 3.00% vs. 10.19 ± 2.74%, p = 0.043). Multivariate generalized estimation equations revealed that visual impairment [odds ratio (OR) = 2.75, p < 0.001] and age (OR = 0.60, p < 0.001) were associated with illusion intensity in all participants, while history of LVAs usage (OR = 0.49, p = 0.045) and age (OR = 0.61, p < 0.001) were negatively correlated in visually impaired group. A significantly negative correlation was found between illusion intensity and age 4–17 years in the subgroups of visually impaired who had used LVAs (Y = −0.54X + 15.06, R2 = 0.56), who had not used (Y = −0.49X + 15.24, R2 = 0.51), and healthy controls (Y = −0.50X + 11.18, R2 = 0.21); all p-values were < 0.001.ConclusionChildren aged 4–17 years afflicted with congenital visual impairment exhibited a heightened intensity of Müller-Lyer illusion compared to visually normal counterparts, LVAs usage experience could reduce this higher intensity. The developmental trajectory of illusion intensity declined consistently with age across all three groups. The abnormal visual experiences during early-life may adversely affect integration in congenitally visually impaired children, and LVAs could facilitate this functional development

Prevalence and determinants of asthenopia among ophthalmologists in China: a national cross-sectional survey

IntroductionThe role of ophthalmologists is defined by tasks requiring visual effort, emphasizing the importance of examining their condition within the realm of occupational visual health. Our goal was to explore the occurrence of asthenopia among Chinese ophthalmologists and identify contributing factors through the use of a reliable and validated survey instrument.MethodsA national cross-sectional online survey was carried out in June 2017, involving 6,220 practicing ophthalmologists in China. Utilizing an 11-item Asthenopia Survey Questionnaire with established reliability and validity. Prevalence rates of asthenopia among subgroups categorized by age, gender, hospital classification, physician level, daily near vision activity duration, sleep duration, sleep quality, presbyopia status, and history of eye surgery were determined using the independent t-test, chi-square test and bonferroni test. Multiple logistic regression analysis was employed to pinpoint independent factors linked to asthenopia.ResultsOut of the 5,009 ophthalmologists who completed the survey, a 40.7% prevalence of asthenopia was identified. Multivariate analysis revealed that good sleep quality (OR: 0.24, 95%CI: 0.20–0.30), moderate sleep quality (OR: 0.47, 95%CI: 0.38–0.59), engaging in daily near vision activities for less than 7 h (OR: 0.76, 95%CI: 0.68–0.86), having daily sleep duration exceeding 7 h (OR: 0.87, 95%CI: 0.77–0.98), and working in tertiary hospitals (OR: 0.88, 95%CI: 0.78–0.99) were protective factors against asthenopia. Conversely, presbyopia was identified as a risk factor (OR: 1.33, 95%CI: 1.04–1.70). All calculated p values were below 0.05. Age, gender, physician level, and eye surgery history were not related factors.ConclusionAsthenopia is prevalent among Chinese ophthalmologists, with employment in tertiary hospitals providing a protective effect and presbyopia is a risk factor. Preventive strategies include improving sleep quality, restricting daily near vision activity to under 7 h, and extending daily sleep duration to over 7 h. Further investigation is needed to explore the protective implications of working in tertiary hospitals

Whole-genome resequencing of 472 Vitis accessions for grapevine diversity and demographic history analyses

Despite the importance of grapevine cultivation in human history and the economic values of cultivar improvement, large-scale genomic variation data are lacking. Here the authors resequence 472 Vitis accessions and use the identified genetic variations for domestication history, demography, and GWAS analyses

Macular Microvasculature Density Changes in Anisometropic Amblyopic Eyes after Successful Treatment

Purpose. To determine if the abnormal macular microvasculature in hyperopic anisometropic amblyopia changes after occlusion therapy, and to discover if the macular microvasculature influences the efficacy of amblyopic treatment. Materials and Methods. Twenty-two children with hyperopic anisometropic amblyopia (median, 8 years old) were enrolled along with 66 healthy controls of similar age and gender distribution. Best-corrected visual acuity (BCVA) was determined, and macular vessel density in the superficial and deep capillary plexuses (SCPs and DCPs, respectively) was measured by optical coherence tomography angiography before and after refractive correction and occlusion therapy. Changes in BCVA and macular SCP and DCP vessel density were measured after amblyopia treatment of 7.5 ± 4.4 months. Results. The amblyopic baseline BCVA, logMAR 0.42 ± 0.27, improved to logMAR 0.18 ± 0.18 in 14 patients (64%) after amblyopia treatment (P<0.001). In 8 patients (36%), there was no improvement in the BCVA. In amblyopic eyes with improved BCVA, the SCP density tended to increase in each parafoveal quadrant, while it tended to decrease in all quadrants of the fellow eyes. For patients in whom BCVA did not improve, the macular SCP vessel density tended to decrease in all quadrants of the amblyopic and fellow eyes. The posttreatment difference in SCP vessel density between amblyopic and fellow eyes was not significant. Multiple linear regression analysis showed that older age and greater foveal SCP vessel density were negatively correlated with BCVA improvement (P<0.018 and P<0.036, respectively). Conclusions. Macular vessel density tends to increase in anisometropic amblyopic eyes after successful treatment. Younger age and lower SCP macular density are predictive of a greater therapeutic effect of occlusion therapy

Short-Term Effects of Overnight Orthokeratology on Corneal Sensitivity in Chinese Children and Adolescents

Purpose. To assess the effects of the 3-month period of orthokeratology (OK) treatment on corneal sensitivity in Chinese children and adolescents. Methods. Thirty subjects wore overnight OK lenses in both eyes for 3 months and were assessed at baseline, 1 day, 1 week, 1 month, and 3 months after the treatment. Changes in corneal sensitivity were measured by the Cochet–Bonnet (COBO) esthesiometer at the corneal apex and approximately 2 mm from the temporal limbus. Changes in refraction and corneal topography were also measured. Results. Central corneal sensitivity suffered a significant reduction within the first month of the OK treatment period but returned to the baseline level at three months (F = 3.009, P=0.039), while no statistically significant difference occurred in temporal sensitivity (F = 2.462, P=0.074). The baseline of central corneal sensitivity correlated with age (r = −0.369, P=0.045). A marked change in refraction (uncorrected visual acuity, P<0.001; spherical equivalent, P<0.001) and corneal topographical condition (mean keratometry reading, P<0.001; eccentricity value, P<0.001; Surface Regularity Index, P<0.001) occurred, but none of these measurements were correlated with corneal sensitivity. Conclusions. A 3-month period OK treatment causes a reduction in central corneal sensitivity in Chinese children and adolescents but with a final recovery to the baseline level, which might be because neuronal adaptation occurred earlier in children and adolescents than in adults

A novel interleukin 33/ST2 signaling regulates inflammatory response in human corneal epithelium.

Interleukin (IL) 33, a member of IL-1 cytokine family, is well known to promote Th2 type immune responses by signaling through its receptor ST2. However, it is not clear whether ST2 is expressed by mucosal epithelium, and how it responds to IL-33 to induce inflammatory mediators. This study was to identify the presence and function of ST2 and explore the role of IL-33/ST2 signaling in regulating the inflammatory cytokine production in corneal epithelial cells. Human corneal tissues and cultured primary human corneal epithelial cells (HCECs) were treated with IL-33 in different concentrations without or with different inhibitors to evaluate the expression, location and signaling pathways of ST2 in regulating production of inflammatory cytokine and chemokine. The mRNA expression was determined by reverse transcription and real time PCR, and protein production was measured by enzyme-linked immunosorbent assay (ELISA), immunohistochemical and immunofluorescent staining. ST2 mRNA and protein were detected in donor corneal epithelium and cultured HCECs, and ST2 signal was enhanced by exposure to IL-33. IL-33 significantly stimulated the production of inflammatory cytokines (TNF-α, IL-1β and IL-6) and chemokine IL-8 by HCECs at both mRNA and protein levels. The stimulated production of inflammatory mediators by IL-33 was blocked by ST2 antibody or soluble ST2 protein. Interestingly, the IκB-α inhibitor BAY11-7082 or NF-κB activation inhibitor quinazoline blocked NF-κB p65 protein phosphorylation and nuclear translocation, and also suppressed the production of these inflammatory cytokines and chemokine induced by IL-33. These findings demonstrate that ST2 is present in human corneal epithelial cells, and IL-33/ST2 signaling plays an important role in regulating IL-33 induced inflammatory responses in ocular surface

Unique expression pattern and functional role of periostin in human limbal stem cells.

Periostin is a non-structural matricellular protein. Little is known about periostin in human limbal stem cells (LSCs). This study was to explore the unique expression pattern and functional role of periostin in maintaining the properties of human LSCs. Fresh donor corneal tissues were used to make cryosections for evaluation of periostin expression on ex vivo tissues. Primary human limbal epithelial cells (HLECs) were generated from limbal explant culture. In vitro culture models for proliferation and epithelial regeneration were performed to explore functional role of periostin in LSCs. The mRNA expression was determined by reverse transcription and quantitative real-time PCR (RT-qPCR), and the protein production and localization were detected by immunofluorescent staining and Western blot analysis. Periostin protein was found to be exclusively immunolocalized in the basal layer of human limbal epithelium. Periostin localization was well matched with nuclear factor p63, but not with corneal epithelial differentiation marker Keratin 3. Periostin transcripts was also highly expressed in limbal than corneal epithelium. In primary HLECs, periostin expression at mRNA and protein levels was significantly higher in 50% and 70% confluent cultures at exponential growth stage than in 100% confluent cultures at slow growth or quiescent condition. This expression pattern was similar to other stem/progenitor cell markers (p63, integrin β1 and TCF4). Periostin expression at transcripts, protein and immunoreactivity levels increased significantly during epithelial regeneration in wound healing process, especially in 16-24 hours at wound edge, which was accompanied by similar upregulation and activation of p63, integrin β1 and TCF4. Our findings demonstrated that periostin is exclusively produced by limbal basal epithelium and co-localized with p63, where limbal stem cells reside. Periostin promotes HLEC proliferation and regeneration with accompanied activation of stem/progenitor cell markers p63, integrin β1 and TCF4, suggesting its novel role in maintaining the phenotype and functional properties of LSC

Oxidative stress markers induced by hyperosmolarity in primary human corneal epithelial cells.

Oxidative stress has been known to be involved in pathogenesis of dry eye disease. However, few studies have comprehensively investigated the relationship between hyperosmolarity and oxidative damage in human ocular surface. This study was to explore whether and how hyperosmolarity induces oxidative stress markers in primary human corneal epithelial cells (HCECs). Primary HCECs were established from donor limbal explants. The hyperosmolarity model was made in HCECs cultured in isosmolar (312 mOsM) or hyperosmotic (350, 400, 450 mOsM) media. Production of reactive oxygen species (ROS), oxidative damage markers, oxygenases and anti-oxidative enzymes were analyzed by DCFDA kit, RT-qPCR, immunofluorescent and immunohistochemical staining and Western blotting. Compared to isosmolar medium, ROS production significantly increased at time- and osmolarity-dependent manner in HCECs exposed to media with increasing osmolarities (350-450 mOsM). Hyperosmolarity significantly induced oxidative damage markers in cell membrane with increased toxic products of lipid peroxidation, 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), and in nuclear and mitochondria DNA with increased aconitase-2 and 8-OHdG. Hyperosmotic stress also increased the mRNA expression and protein production of heme oxygenase-1 (HMOX1) and cyclooxygenase-2 (COX2), but reduced the levels of antioxidant enzymes, superoxide dismutase-1 (SOD1), and glutathione peroxidase-1 (GPX1). In conclusion, our comprehensive findings demonstrate that hyperosmolarity induces oxidative stress in HCECs by stimulating ROS production and disrupting the balance of oxygenases and antioxidant enzymes, which in turn cause cell damage with increased oxidative markers in membrane lipid peroxidation and mitochondrial DNA damage