We compared the therapeutic effects between botulinum toxin and surgery for acute acquired comitant esotropia (AACE) and analyze its clinical characteristics. The data of the 29 cases, who received treatment for AACE in the Ophthalmic Center of the First Affiliated Hospital of Zhengzhou University and Henan Provincial Ophthalmology Hospital between January 2016 and January 2017, were collected. The 29 cases with AACE were followed for 6 months or more, and received either botulinum toxin injection (group A with 13 cases) or squint correction (group B with 16 cases). The distant and near deviation angles were compared between the two groups before and after treatment. The success rate (total horizontal deviation of 10 prism diopters or less) and stereopsis were compared between the two groups at post-treatment 6 months. At the same time, the relations between distant and near deviation angles were analyzed among different myopia levels and different AACE types. Results indicated that he success rate was not significantly different at post-treatment 6 months (84.6% vs 81.3%, P = 1.00). The distant and near deviation angles were all significantly different one day and one month after treatment (all P < 0.05); but at post-treatment 6 months, they were not significantly different (all P > 0.05) between the two groups. There were no significant differences in the distant and near stereoacuity between the two groups at post-treatment 6 months (all P > 0.05). Among the 25 cases with myopia, the pre-treatment distant deviation angle was significantly higher than pre-treatment near deviation angle in the cases with myopia level >−2.5 D (P < 0.05), and the pre-treatment distant and near deviation angles were all significantly higher in the cases with type-IIAACE than in the cases with type-IIIAACE (all P < 0.05). This study suggests that Botulinum toxin is as effective as surgery in the treatment of AACE at post-treatment 6 months. For the cases with myopia level >−2.5 D, the pre-treatment distant deviation angle is significantly higher than pre-treatment near deviation angle; and both pre-treatment distant and near deviation angles are greater in the cases with type-IIAACE than in the cases with type-IIIAACE.

No abstract

Objective: To discover the possible underlying mechanism of Chlorogenic acid (CGA) in protecting against oxidative stress injury in glaucoma. Methods: LncRNA TUG1 and Nrf2 expressions were detected by qRT-PCR and Western blot. Retinal ganglion cell (RGC) viability and apoptosis were measured by MTT and flow cytometry, respectively. Reactive oxygen species (ROS) level was determined by reactive oxygen species assay kit. The interaction between lncRNA TUG1 and Nrf2 was confirmed by RNA pull-down and RIP assay. Results: IPL thickness and lncRNA TUG1 expression were significantly decreased in glaucoma mice model, and CGA treatment increased IPL thickness and lncRNA TUG1 expression. In vitro H2O2induced RGCs, RGC viability was significantly decreased, and ROS level and cell apoptosis were significantly increased. CGA up-regulated lncRNA TUG1 and Nrf2 expressions, decreased cell apoptosis and ROS production in RGCs, and increased RGCs viability. We further verified the interaction between lncRNA TUG1 and Nrf2, and proved Nrf2 was positively regulated by lncRNA TUG1. We found CGA promoted Nrf2 expression through lncRNA-TUG1, and further verified CGA protected RGCs from oxidative stress through regulating lncRNA TUG1/Nrf2. In vivo experiments showed TUG1 knockdown abrogated therapeutic effect of CGA on glaucoma. Conclusion: CGA increased RGC viability and decreased ROS level and RGC apoptosis after oxidative stress injury through lncRNA TUG1/Nrf2 pathway, which protected against glaucoma.

Congenital cataract (CC) is a clinical and genetically heterogeneous eye disease that primarily causes lens disorder and even amblyopic blindness in children. As the mechanism underlying CC is genetically inherited, identification of CC-associated gene mutations and their role in protein distribution are topics of both pharmacological and biological research. Through physical and ophthalmic examinations, two Chinese pedigrees with autosomal dominant congenital cataract (ADCC) were recruited for this study. Mutation analyses of CC candidate genes by next-generation sequencing (NGS) and Sanger sequencing revealed a novel missense mutation in CRYBB2 (p.V146L) and a deletion mutation in CRYAA (p.116_118del). Both mutations fully co-segregated were not observed in unaffected family members or in 100 unrelated healthy controls. The CRYBB2 missense mutation disrupts the distribution of CRYBB2 in human lens epithelial cells (HLEpiCs), and the CRYAA deletion mutation causes hyperdispersion of CRYAA. Furthermore, these two crystallin mutations result in aberrant expression of unfolded protein response (UPR) marker genes as well as apoptosis in HLEpiCs. Collectively, these findings broaden the genetic spectrum of ADCC.