No abstract

To compare the efficiency, efficacy, and safety, as well as the educational value, of heads-up (three-dimensional visualization system-assisted) and traditional microscopic cataract surgery.Methods: This randomized noninferiority trial enrolled 242 eyes of 201 patients who received femtosecond laser-assisted cataract surgery. The questionnaire study enrolled 26 medical interns and 39 medical students. Patients received surgery under either a three-dimensional visualization system (3D group, 117 eyes) or traditional microscope (TM group, 125 eyes) after random allocation. The primary outcome was surgical time. The noninferiority margin of surgical time was 60 seconds. Secondary outcomes included ultrasound power, phacoemulsification time, visual acuity, intraocular pressure, endothelial cell density, central corneal thickness, complications, and observer satisfaction scores for surgical procedures.Results: Surgical time was 462.03 ± 80.36 seconds in the 3D group and 452.13 ± 76.63 seconds in the TM group (difference 9.90 seconds; 95% CI, -9.98 to 29.78; P = 0.365). Visual acuity and other perioperative parameters were comparable between the 3D group and the TM group (all P > 0.05). Incidences of both intraoperative and postoperative complications were low and not statistically different between groups (all P > 0.05). Across all observers, 3D surgery was superior to TM surgery for improving the degree of satisfaction (all P < 0.001). Conclusions:The surgical efficiency of heads-up cataract surgery is not inferior to traditional microscopic surgery. Both methods achieved similar efficacy and safety outcomes. Moreover, heads-up cataract surgery showed a significant advantage in medical education.Translational Relevance: Our findings show that heads-up cataract surgery has comparable efficiency, efficacy, and safety, as well as superior medical educational value, to TM surgery, which lays the foundation for promoting and popularizing this technology.

To improve the surface biocompatibility of the silicone intraocular lens (IOL), 2-methacryloyloxyethyl phosphorylcholine (MPC) was tethered onto the IOL through air plasma treatment. Chemical changes on the IOL surface were characterized by X-ray photoelectron spectroscopy (XPS) to confirm the covalent binding of MPC. Morphologies of the IOL surfaces were observed by scanning electron microscopy (SEM) to optimize the plasma treatment process. The hydrophilicity and biocompatibility of the control and modified IOLs were compared by the measurements of water contact angle, platelet adhesion, macrophage cell culture, and lens epithelial cell (LEC) attachment. It was found that, after the tethering of MPC, the hydrophilicity of the IOL can be improved significantly and permanently, and the platelet, macrophage, and LEC adhesion on the IOL surface are obviously suppressed, which indicated the enhancement of surface biocompatibility.

Excess accumulation of endogenous all-trans-retinal (atRAL) contributes to degeneration of the retinal pigment epithelium (RPE) and photoreceptor cells, and plays a role in the etiologies of age-related macular degeneration (AMD) and Stargardt's disease. In this study, we reveal that human RPE cells tolerate exposure of up to 5 µM atRAL without deleterious effects, but higher concentrations are detrimental and induce cell apoptosis. atRAL treatment significantly increased production of intracellular reactive oxygen species (ROS) and up-regulated mRNA expression of Nrf2, HO-1, and γ-GCSh within RPE cells, thereby causing oxidative stress. ROS localized to mitochondria and endoplasmic reticulum (ER). ER-resident molecular chaperone BiP, a marker of ER stress, was up-regulated at the translational level, and meanwhile, the PERK-eIF2α-ATF4 signaling pathway was activated. Expression levels of ATF4, CHOP, and GADD34 in RPE cells increased in a concentration-dependent manner after incubation with atRAL. Salubrinal, a selective inhibitor of ER stress, alleviated atRAL-induced cell death. The antioxidant N-acetylcysteine (NAC) effectively blocked RPE cell loss and ER stress activation, suggesting that atRAL-induced ROS generation is responsible for RPE degeneration and is an early trigger of ER stress. Furthermore, the mitochondrial transmembrane potential was lost after atRAL exposure, and was followed by caspase-3 activation and poly (ADP-ribose) polymerase cleavage. The results demonstrate that atRAL-driven ROS overproduction-induced ER stress is involved in cellular mitochondrial dysfunction and apoptosis of RPE cells.