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N6-methyladenosine (m6A) methylation/modification plays a critical role in various biological processes through post-transcriptional ribonucleic acid (RNA) modification, which involves RNA processing, nuclear export, translation and decay. Functionally, m6A modification may be involved in ocular cell growth and differentiation, stem cell identity, development, haemostasis and innate versus adaptive immunity. Aberrations in m6A methylation may mediate numerous pathological conditions in the eye, including microorganism infection, inflammation, autoimmune disease, senescence, degeneration, epithelial-mesenchymal transition, fibrosis, angiogenesis, tumorigenesis and complex eye diseases. In this review, we have discussed the relevance of m6A modification to precision medicine, stem cell directional differentiation, biomarkers of eye diseases and m6A methylation activators and inhibitors. In addition, we summarised the challenges and future research directions in the field related to visual function and eye diseases.

In this study, composite pear juice was processed by ultra-high pressure homogenization (UHPH) at four different pressures (50, 100, 150, and 200 MPa) with six different temperatures (4, 20, 30, 40, 60, and 80°C), then microorganism and physicochemical and nutritional properties of the samples were investigated. The counts of total aerobic bacteria (TAB) and yeasts and molds (YM) were reduced by 0.89-4.72 log10 CFU/ml and 0.40-3.03 log10 CFU/ml after processing, respectively. There was no significant change on total soluble solid and color, but significant decreases of pH and particle size value were observed, and the antioxidant activity, total phenolic content, viscosity, and suspension stability significantly increased in treated samples. Compared to the untreated samples, polyphenol oxidase (PPO) and peroxidase (POD) activity of UHPH-treated samples varied between 97%-126% and 81%-165%, respectively, indicating that the PPO and POD activities could be inactivated or activated by UHPH. This study introduced proper temperature combined with UHPH could improve the microbial inactivation and the quality of the compound juice.

Background: To compare the feature of ocular trauma between normalized period and the COVID-19 epidemic period in China, to provide a scientific basis for prevention and control eye injuries in special times in future.Methods: This study is a multi-center cross-sectional study with 30 participated hospitals involving the China Ocular Trauma Society members. All hospitalized cases who visited the ophthalmology department in participated hospitals with eye injuries during the normalized period (2019) and the COVID-19 epidemic period (2020) were included in this study. Demographic characteristic of cases, date of injury, sites and types of injury were collected.Results: This study involved 13525 (61cases with both eyes) injured cases. There were 7269 (53.74%) eye-injured cases and 6256 (46.26%) eye-injured cases in 2019 and 2020 separately. Compared with 2019, the incidence of ocular trauma in retirees, housewives and unemployed increased with year-on-year of 4.96%, 102.67% and 11.64% among all occupations. In 2020, the incidence of eye injuries decreased in all injury sites except for an increase in home (30.29% year-on-year). The incidence of mechanical eye injuries decreased, while that of non-mechanical eye injuries (Chemical/Thermal/Radiation) increased (47.45% year-on-year). There were 255 (3.50%, 255/7269) and 376 (6.01%, 376/6256) non-mechanical injured cases in 2019 and 2020 (Pearson chi2 = 47.33, P < 0.001) separately.Conclusions: During the COVID-19 epidemic period, the incidence of eye injuries decreased. The prevention and control measures should be focused on the non-mechanical injuries, and the retirees, unemployed and housewives during public events period in future.

An impaired blood-retinal barrier (BRB) leads to diabetic macular edema (DME), which is a major complication of Diabetic retinopathy (DR). Mediators such as inflammation cause BRB breakdown. However, the explicit mechanism of its disruption is largely unknown. In this study, we identified tumor necrosis factor ligand-related molecule 1A (TL1A) as a crucial factor which protect retinal endothelial cells integrity in DR. By providing both human and mouse data, we show that TL1A is significantly decreased in the retinas of DME patients and diabetic rodents. We further demonstrate that the loss of TL1A accelerated diabetes-induced retinal barrier breakdown. TL1A supplementation protects the diabetic retina against BRB breakdown. Mechanistically, TL1A stabilize intracellular junctions and protect vascular integrity by blocking SHP1-Src-regulated VE-cadherin phosphorylation. Collectively, our findings reveal that loss of TL1A in the retina leads to increased vascular permeability in DR, and that TL1A treatment is of potential therapeutic interest for the treatment of DME.

Purpose To characterize vitreous microparticles (MPs) in patients with traumatic proliferative vitreoretinopathy (PVR) and investigate their role in PVR pathogenesis. Methods Vitreous MPs were characterized in patients with traumatic PVR, patients with rhegmatogenous retinal detachment (RRD) complicated with PVR, and control subjects by flow cytometry. The presence of M2 macrophages in epiretinal membranes was measured by immunostaining. Vitreous cytokines were quantified by ELISA assay. For in vitro studies, MPs isolated from THP-1 cell differentiated M1 and M2 macrophages, termed M1-MPs and M2-MPs, were used. The effects and mechanisms of M1-MPs and M2-MPs on RPE cell proliferation, migration, and epithelial to mesenchymal transition were analyzed. Results Vitreous MPs derived from photoreceptors, microglia, and macrophages were significantly increased in patients with traumatic PVR in comparison with control and patients with RRD (PVR), whereas no significance was identified between the two control groups. M2 macrophages were present in epiretinal membranes, and their signature cytokines were markedly elevated in the vitreous of patients with traumatic PVR. Moreover, MPs from M2 macrophages were increased in the vitreous of patients with traumatic PVR. In vitro analyses showed that M2-MPs promoted the proliferation and migration of RPE cells via activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. However, M2-MPs did not induce the expression of fibrotic proteins, including fibronectin, α-smooth muscle actin, and N-cadherin in RPE cells. Conclusions This study demonstrated increased MP shedding in the vitreous of patients with traumatic PVR; specifically, MPs derived from M2 polarized macrophages may contribute to PVR progression by stimulating RPE cell proliferation and migration.

AimTo evaluate the long-term outcomes of intravitreal triamcinolone acetonide (TA) administration after posterior vitreous detachment (PVD) during pars plana vitrectomy (PPV) for patients with proliferative diabetic retinopathy (PDR).MethodsA total of 189 eyes (152 patients) who underwent PPV for severe PDR were reviewed. Intravitreal injection of TA (IVTA) was administered during PPV in 118 eyes (PPV+IVTA group), and 71 eyes did not receive IVTA (PPV group). Immediately after PVD, when most of the vitreous and proliferative membranes were removed, 0.1 mL TA (40 mg/mL) was injected into the vitreous cavity in the PPV+IVTA group. All patients were followed-up for least 12 months. Visual outcomes and postoperative complications were recorded and compared between the two groups.ResultsIVTA was helpful for proliferative membrane peeling and haemostasis during PPV. In the PPV+IVTA group, best-corrected visual acuity had significantly improved and the intraocular pressure was controlled well during the follow-up. The incidence of early recurrent vitreous haemorrhage after PPV was significantly lower in the PPV+IVTA group (1.7%) than in the PPV group (9.9%) (p=0.028).ConclusionThe administration of IVTA after PVD during PPV can effectively improve the final visual outcomes and prevent postoperative complications in patients with severe PDR.

Background To explore the association of cigarette smoking with retinal thickness and vascular structure in an elderly Chinese population. Methods This cross-sectional study enrolled employees and retirees aged over 50 years at Tianjin University of Sport from October 2020 to December 2020. Information on smoking status and lifestyle was obtained using a detailed questionnaire. All participants underwent full ophthalmic examination. OCTA image was acquired. Vascular and the thickness parameters in central fovea and peripapillary parameters were automatically calculated. Multiple linear regression analyses were utilized to assess the association of smoking with retinal thickness and vascular structure after controlling potential confounders. Results Compared with non-smoking adults, current smokers (β=-36.78; P = 0.01) and ever smokers (β=-35.45; P = 0.00) tended to have thinner macular fovea. Cigarettes daily, pack-years of smoking and CSI were negatively related to macular thickness (cigarettes daily: β=-1.43; pack-years: β=-14.73; CSI: β=-14.70), while they were positively associated with the circumference (cigarettes daily: β=0.03; pack-years: β=0.30; CSI: β=0.31) and the area of FAZ (cigarettes daily: β=0.01; pack-years: β=0.07). Conclusions Cigarette smoking seems associated with decreased macular fovea thickness and elevated circumference and area of the FAZ compared to non-smokers. Our data add to evidence of smoking on retinal thickness and the microvascular system in the macular area.

PURPOSE To estimate the prevalence, causes and risk factors of bilateral visual impairment in rural areas of Tianjin, China. METHODS A large population-based, cross-sectional study. A stratified random cluster sampling method was used to investigate 12 233 participants in all age groups living in rural Tianjin. Participants completed questionnaires and received professional ophthalmology examinations. RESULTS According to World Health Organization best-corrected visual acuity (BCVA) criteria, the crude prevalence of bilateral visual impairment (BCVA

Perfluorooctane sulfonate (PFOS) is the most typical compound as emerging persistent organic pollutants (POPs). It is very significant to monitor PFOS concentration in environmental samples. In this paper, a novel fluorescence probe based on a cationic perylene diimide derivative (PDI-Pyr) toward PFOS detection was designed and synthesized. The sensing properties were investigated systematically by spectroscopic techniques. The detection limit in the method was calculated to be 28 nmol/L. It was found that the formation of PDI-Pyr/PFOScomplex through electrostatic and hydrophobic interactions accounted for the mechanism of the fluorescent assay. This method could be further applied in real tap water samples and environmental samples such as soil extract. To the best of our knowledge, this work is the first report of PDI-based fluorescent sensor for PFOS determination.

Purpose Uncontrolled coagulation reactions contribute to pathological fibroproliferation in several organs, and yet their role in proliferative vitreoretinopathy (PVR) remains to be elucidated. In this study, we evaluated the profibrotic effects of FXa in RPE cells and in a mouse model of PVR. Methods FXa levels in the eyes of traumatic PVR patients and rabbit models of mechanical ocular trauma was measured by ELISA and immunohistochemistry. FXa-induced RPE EMT was assessed by examining cell proliferation, migration, tight junction changes, and expression of fibrotic markers. For in vivo study, FXa was injected into dispase-injured eyes, then intraocular fibrosis was evaluated by histological analysis and Western blotting. The therapeutic effect of FXa inhibitor was also examined in PVR mouse models. Results Vitreous FXa were higher in patients with traumatic PVR compared to patients with macular hole. Moreover, expressions of FXa and PAR1 were found in the epiretinal membranes from traumatic PVR patients. Vitreous FXa were markedly increased after mechanical ocular trauma in rabbits. In vitro, FXa stimulated RPE EMT characterized as ZO-1 disruption, compromised cell polarity, and increased fibronectin expressions. Co-injection of FXa and dispase in mice induced more severely damaged retinal structures, and increased α-SMA expressions than FXa or dispase treatment alone. Oral FXa or thrombin inhibitors significantly blocked intraocular fibrosis in PVR mouse models. FXa promoted phospho-activation of p38 in ARPE19 cells, which was dependent on PAR1. Moreover, TGF-βR inhibitor also significantly alleviated FXa-induced intraocular fibrosis in mice. Conclusions FXa promotes intraocular fibrosis in mice via mechanisms involving RPE activation.