Objectives: To assess the effectiveness of various atropine concentrations in managing myopia among children in East, South, and Southeast Asia, and to determine the most effective concentration.Methods: A systematic literature review was conducted using PubMed, Web of Science, Cochrane Library, and EMBASE. The search was limited to articles published up to 1 June 2024, and included studies in Chinese or English. Two researchers independently screened the literature, extracted relevant data, and assessed the data quality using the Revised Cochrane risk-of-bias 2 (RoB2) tool. A network meta-analysis was performed using Stata 14.2 software to compare the efficacy of different atropine concentrations in delaying myopia progression, measured by changes in refraction and axial length.Results: The analysis included 39 studies with 7,712 participants, examining 10 atropine concentrations ranging from 0.005% to 1%. Forest plots indicated that five concentrations (0.01%, 0.02%, 0.025%, 0.05%, and 1%) were more effective than a placebo in controlling myopia progression. The cumulative ordination plot indicated that 0.05% atropine most effectively delayed refraction change, which the mean change per year was 0.62D, while 1% was superior in slowing axial length progression, which the mean change per year was −0.43 mm. Considering both measures, 1% atropine showed the highest efficacy which the mean changes per year were 0.56D in spherical equivalent refraction and −0.43 mm in axial length, followed by 0.05% and 0.125% atropine.Conclusion: While 1% atropine demonstrated the highest efficacy in myopia control among East, South and Southeast Asian children, its use is not recommended due to increased adverse effects and a rapid rebound in myopia after cessation. Considering both efficacy and safety, 0.05% atropine is suggested as the optimal concentration for myopia management in this population.

Congenital aniridia is a rare autosomal dominant congenital ocular disorder. Genetic studies suggest that heterozygous mutations in the developmental regulator PAX6 gene or the related regulatory regions leading to haploinsufficiency are the main cause of congenital aniridia. In this study, the clinical characteristics and pathogenic mutation of a four-generation Chinese family with congenital aniridia were investigated. All members recruited in this study underwent comprehensive ophthalmic examinations. Targeted gene capture sequencing and Sanger sequencing were performed to screen and confirm the candidate pathogenicity gene and its mutation. A multiple alignment of homologous sequences covering the identified mutation from different species was investigated, and the mutant protein structure was predicted using Swiss-Model. Additionally, the prediction of pathogenicity was analyzed using the ACMG Guidelines. Thirteen patients in this pedigree were diagnosed with congenital aniridia. A novel heterozygous frameshift mutation (c.391_398dupATACCAAG, p.Ser133Argfs*8) in exon 7 of the PAX6 gene was identified in all affected individuals in the family. This study demonstrates that this frameshift mutation of the PAX6 gene might be the causative genetic defect of congenital aniridia in this family. This mutation is predicted to cause the premature truncation of the PAX6 protein, leading to the functional haploinsufficiency of PAX6, which may be the major molecular mechanism underlying the aniridia phenotype. To the best of our knowledge, this is the first report of a novel pathogenic PAX6 gene variant c.391_398dupATACCAAG(p.Ser133Argfs*8) identified in a Chinese family with congenital aniridia.

The subretinal injection technique is an important intraocular drug delivery modality that allows access to the subretinal space to directly act on target cells or the administration of medications, markedly improving the therapeutic efficacy of ocular diseases. Subretinal injection in experimental animals is a commonly used manipulation method for investigating vitreoretinal diseases, particularly when gene therapy and cell therapy studies are involved. In this study, we conducted a systematic review on the injection methods, operation sites, post-injection indicators, as well as the progress and significance of subretinal injection in experimental animals, discussed and compared the advantages and disadvantages of the subretinal injection technique, summarized its specific application of subretinal injection in experimental animals, and explored the development and application of this new technology of subretinal injection, hoping to offer insights that may facilitate the further development of this technology.

N-methyl-D-aspartate (NMDA)-induced retinal damage has been well studied in rodents, but the detailed mechanisms have not yet been characterized in nonhuman primates. Here, we characterized the retinal degenerative effects of NMDA on rhesus monkeys in vivo. NMDA saline or saline-only control was injected intravitreally to the randomly assigned eyes and contralateral eyes of four rhesus monkeys, respectively. The structural and functional changes of retina were characterized by optical coherence tomography and electroretinography on days 0, 4, 30 and 60 post injection. Both optic discs and macular areas of the NMDA-injected eyes initially presented with a transient retinal thickening, followed by continued retinal thinning. The initial, transient retinal thickening has also been observed in glaucoma patients, but this has not been reported in rodent NMDA models. This initial response was followed by loss of retina ganglion cells (RGCs), which is similar to glaucomatous optic neuropathy and other RGC-related retinal degenerations. The amplitudes of both the photopic negative response and pattern electroretinogram decreased significantly and remained low until the end of the study. Thus, the NMDA monkey model may serve as a more clinically relevant animal model of retinal damage.