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To explore the effect of phacoemulsification along with intraocular lens (IOL) implantation on the treatment of primary angle closure glaucoma (PACG), a total of 50 patients (54 eyes) with PCG who had undergone surgery were selected as the research objects, in which, there were 16 eyes with the acute PACG in pre-clinical stage, 20 eyes with acute PACG during acute attack, and 18 eyes with chronic PACG, and all patients received phacoemulsification along with IOL implantation therapy. The patient’s best corrected visual acuity, anterior chamber (AC), anterior depth, intraocular pressure (IOP), visual field, and fundus conditions were measured during the operation, after the operation, and during the follow-up period. The postoperative visual acuity of the patients with three types of PACG was greatly corrected, in which 30 eyes had corrected visual acuity above 0.5, and there were statistically significant differences (SSDs) (P < 0.05); angle closure of 54 eyes had different degrees of improvement, the opening degree of the acute angle closure is better than that of the chronic angle closure, and there were SSDs (P < 0.05); each of 54 eyes showed different degrees of deepening in the central AC, and there were SSDs (P < 0.05); postoperative IOP decreased greatly in all 54 eyes, and there were SSDs (P < 0.05). In conclusion, the IOL implantation based on phacoemulsification can effectively treat the PACG, at the same time reduce IOP, promote angle opening, enhance vision field of the patients, and ultimately achieve the purpose of improving surgical success.

To confirm the therapeutic efficacy of conbercept for the treatment of macular edema (ME) secondary to branch retinal vein occlusion (BRVO).In this prospective, randomized, and comparative study, patients were randomized and divided into conbercept (n = 18) and ranibizumab (n = 17) groups. After an initial intravitreal injection of either conbercept or ranibizumab, a pro re nata (PRN) strategy was adopted based on loss of visual acuity (VA) or increase in central macular thickness (CMT).All patients were followed for ≥6 months. Baseline best-corrected visual acuities (BCVAs) were 0.67 ± 0.37 and 0.511 ± 0.23 logMAR in the conbercept and ranibizumab groups, respectively (p = 0.087, t-test). Baseline CMTs were 512.5 ± 115.22 and 491.23 ± 114.72 µm in the conbercept and ranibizumab groups, respectively (p = 0.993, t-test). Significant improvements in BCVA and reduction of CMT were observed in both groups at each follow-up visit and compared to baseline values (p0.05, t-test). No significant differences in improvement of BCVA (p0.05, t-test) or reduction of CMT (p0.05, t-test) were noted in either group. Mean numbers of injections were 2.28 ± 0.96 and 2.65 ± 1.17 for the conbercept and ranibizumab groups, respectively (p = 0.478, t-test), with no statistically significant differences between the two groups.Intravitreal injection of conbercept is shown to be safe and effective for the treatment of ME secondary to BRVO, based on 6-month follow-up data.

Diabetic retinopathy (DR) occurs in almost all patients with diabetes and remains as one of the major causes of vision loss worldwide. Nevertheless, the molecular mechanisms underlying the pathogenesis of DR remain elusive. The present study aimed to investigate the role and association of Notch signaling and NADPH oxidase 4 (Nox4)‑mediated oxidative stress in high glucose (HG)‑treated retinal cells. Human retinal endothelial cells were cultured for various durations in RPMI‑1640 medium containing 30 mM glucose (HG) or 30 mM mannitol (MN) as an osmotic control; apoptotic cell death and reactive oxygen species (ROS) levels were assessed, respectively. Alterations in the expression profiles of Nox and Notch proteins were evaluated using reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Knockdown of Nox4 and recombination signal‑binding protein J (RBPj) was generated by transfection with specific small interfering (siRNA). Persistent activation of Notch signaling was induced via the overexpression of Notch intracellular domain (NICD). In the present study, time‑dependent increases in ROS production and cell death were detected in HG‑treated cells. Depletion of ROS by diphenyleneiodonium decreased HG‑induced cell death, and suppressed increases in caspase 3 activity and B‑cell lymphoma 2‑associated X protein levels. In HG‑treated cells, Nox4 expression was upregulated at the mRNA and protein levels, and inhibition of Nox4 by GKT137831 or knockdown of expression by siRNA Nox4 significantly reduced ROS levels and cell death. In the presence of HG, Notch1 expression levels were elevated, and increased NICD abundance was detected in whole cell lysates and nuclear fractions. Additionally, HG‑induced cell death was decreased by treatment with γ‑secretase inhibitor (GSI), but increased via the overexpression of NICD. The application of GSI or knockdown of RBPj by siRNA RBPj prevented increases in Nox4 expression within HG‑treated cells. The findings of the present study demonstrated that Nox4‑mediated ROS serves an important role in HG‑induced retinal cell damage, in which the activation of Notch signaling may be responsible for Nox4 upregulation. Therefore, inhibition of Notch signaling or Nox4 expression may be considered as potential therapeutic targets in patients with DR.