Purpose: To evaluate dry eyes in children with vernal kerato-conjunctivitis (VKC) and correlate it with symptoms, clinical findings, and ocular surface analysis (OSA) parameters. Methods: Children with clinically diagnosed VKC underwent complete ophthalmological examination, Schirmer’s testing, modified ocular surface disease index (OSDI) scoring, Bonini grading, fluorescein tear-film break-up time (TBUT), VKC – Collaborative Longitudinal Evaluation of Keratoconus (CLEK) scoring, and OSA. Children with a TBUT of < 10 s were defined to have dry eyes. The above-mentioned parameters were compared between dry eye and non-dry eye VKC children. Results: The mean age of the 87 children included in the study was 9.1 ± 2.9 years. Dry eyes were seen in 60.9% [95% confidence interval (CI); 51% to 71%]. The mean TBUT was 13.4 ± 3.8 and 5.9 ± 1.9 s in non-dry and dry eye groups, respectively (P < 0.001). The mean value of Schirmer’s test was 25.9 ± 9.8 and 20.8 ± 8.6 mm in the non-dry and dry eye groups, respectively (P = 0.01). The two groups did not differ in their OSDI scores, Bonini grading, and CLEK scores. The OSA parameter of non-invasive break-up time (NIBUT) was 8.3 ± 3.2 s in non-dry eye group and 6.4 ± 2.9 s in dry eye group, P = 0.008. The lower lid Meibomian gland (MG) loss was 7.4% in non-dry eye group and 12.2% in dry eye group, P = 0.028. Other OSA parameters did not differ significantly among the two groups. Conclusion: Dry eyes are seen in two-thirds of pediatric VKC. Evaluation of dry eyes should be incorporated in their clinical evaluation. Among OSA parameters, NIBUT and lower lid MG loss are associated with dry eyes in pediatric VKC patients.

Judgments of facial attractiveness invariably accompany our perception of faces. Even neonates appear to be capable of making such judgments in a manner consistent with adults. This suggests that the processes supporting facial attractiveness require little, if any, visual experience to manifest. Here we investigate the resilience of these processes to several years of early‐onset visual deprivation. Specifically, we study whether congenitally blind children treated several years after birth possess the ability to rate facial attractiveness in a manner congruent to normally sighted individuals. The data reveal significant individual variability in the way each newly sighted child perceives attractiveness. This is in marked contrast to data from normally sighted controls who exhibit strong across‐subject agreement in facial attractiveness ratings. This variability may be attributable, in part, to atypical facial encoding strategies used by the newly sighted children. Overall, our results suggest that the development of facial attractiveness perception is likely to be vulnerable to early visual deprivation, pointing to the existence of a possible sensitive period early in the developmental trajectory.

AimsThe study aims to detect the underlying genetic defect in two autosomal dominant congenital cataract (ADCC) families.MethodsA detailed family history was collected, pedigrees were drawn, and slit-lamp examination and lens photography were performed. Mutation screening was carried out in the genes for crystallins and connexins by PCR and Sanger sequencing. Ethnically matched controls were tested for the identified variants. Different bioinformatics tools were used to assess the pathogenicity of the observed variants.ResultsIn an ADCC family with total cataract, a novel change (c.166A &gt; G) (p.Thr56Ala) in GJA8 was identified. In another ADCC family with nuclear cataract, c.134G &gt; C (p.Trp45Ser) in GJA3 has been detected. These variants co-segregated completely in patients in their respective families and were neither observed in unaffected family members nor in ethnically matched 100 controls, excluding them as polymorphisms.ConclusionsThe present study identifies a novel variant c.166A &gt; G (p.Thr56Ala) in GJA8 in an ADCC family having total cataract and a previously known mutation c.134G &gt; C (p.Trp45Ser) in GJA3 in another ADCC family. Thr56 in GJA8 seems to be a mutation hotspot, as previously an ADCC Mauritanian family harbored a different substitution (p.Thr56Pro) at the same codon, although for a different phenotype (nuclear cataract). Similarly, Trp45 in GJA3 appears as a mutation hotspot, as p.Trp45Ser has previously been reported for nuclear cataract in a Chinese ADCC family. p.Thr56 (GJA8) and p.Trp45 (GJA3) are in the extracellular loop 1 (EL1) in their respective connexin proteins, which, along with EL2, are essential for gap junction formation, hemichannel docking, and regulating the voltage gating of the channels. Hence, residues in these regions seem crucial for maintaining eye lens transparency.

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