BackgroundRetinal ganglion cell (RGC) death is the final consequence of many blinding diseases, where there is considerable variation in the time course and severity of RGC loss. Indeed, this process appears to be influenced by a wide variety of genetic and environmental factors. In this study we explored the genetic basis for differences in ganglion cell death in two inbred strains of mice.ResultsWe found that RGCs are more susceptible to death following optic nerve crush in C57BL/6J mice (54% survival) than in DBA/2J mice (62% survival). Using the Illumina Mouse-6 microarray, we identified 1,580 genes with significant change in expression following optic nerve crush in these two strains of mice. Our analysis of the changes occurring after optic nerve crush demonstrated that the greatest amount of change (44% of the variance) was due to the injury itself. This included changes associated with ganglion cell death, reactive gliosis, and abortive regeneration. The second pattern of gene changes (23% of the variance) was primarily related to differences in gene expressions observed between the C57BL/6J and DBA/2J mouse strains. The remaining changes in gene expression represent interactions between the effects of optic nerve crush and the genetic background of the mouse. We extracted one genetic network from this dataset that appears to be related to tissue remodeling. One of the most intriguing sets of changes included members of the crystallin family of genes, which may represent a signature of pathways modulating the susceptibility of cells to death.ConclusionDifferential responses to optic nerve crush between two widely used strains of mice were used to define molecular networks associated with ganglion cell death and reactive gliosis. These results form the basis for our continuing interest in the modifiers of retinal injury.

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PURPOSE. To investigate the effectiveness of a novel isoquinoline derivative, EDL-155, in killing retinoblastoma in vitro and in vivo. METHODS. Dose-response curves were generated in which Y79 retinoblastoma cells tagged with luciferase (Y79-Luc) were treated with serial concentrations of EDL-155. Electron microscopy was used to evaluate the ultrastructural morphology of EDL-155-treated Y79 cells. To determine whether autophagy was induced in EDL-155-treated Y79-Luc cells, staining with acridine orange and LC-3 immunoblot analysis was performed. To evaluate the efficacy of EDL-155 in vivo, Y79-Luc retinoblastoma cells were injected into the vitreous cavity of newborn rats, followed by periocular injections of EDL-155 (20 mg/kg/day) or an equivalent dosage of saline. RESULTS. EDL-155 appeared to destroy the retinoblastoma cells in vitro with an EC(50) of 9.1 micriM. EDL-155-treated retinoblastoma cells displayed a lack of viable mitochondria and the presence of autophagosomes wrapped in the characteristic double membranes. Acridine orange staining of EDL-155-treated retinoblastoma cells demonstrated the accumulation of vacuoles, and the immunoblots displayed a shift in molecular weight of LC-3, indicative of incorporation into autophagosome vesicles. In the retinoblastoma animal model, four doses of EDL-155 were delivered over 4 days, which was sufficient to see a significant decrease (P = 0.01) in viable intraocular tumors. Seven of the 25 rats treated with EDL-155 had no detectable living tumor. No significant decrease in viable tumor was observed in control animals. CONCLUSIONS. EDL-155 appears to eliminate retinoblastoma cells by disrupting mitochondria and inducing autophagy. Local delivery of EDL-155 may be an effective therapy for some types of ocular cancers.

Purpose To evaluate laser in situ keratomileusis (LASIK) flap thickness predictability and morphology by femtosecond (FS) laser and microkeratome (MK) using anterior segment optical coherence tomography. Methods Fifty-two candidates for the LASIK procedure were stratified into two groups: FS laser-assisted (Allegretto FS-200) and MK flap creation (Moria 2). Flap thickness was determined at five points. The side-cut angle was measured in three directions at the margin interface. LASIK flap assessment was performed one month postoperatively by Spectralis anterior segment optical coherence tomography. Results Fifty-two patients (93 eyes) were recruited; 49 eyes were stratified to the FS group and 44 eyes to the MK group. The FS group had relatively even flap configurations, and the MK group had meniscus-shaped flaps. Mean differences between planned and actual flap thickness were 12.93 ± 8.89 and 19.91 ± 5.77 µm in the FS and MK groups, respectively. In thin flaps (100 to 110 µm), there was a significant disparity between the two groups (7.80 ± 4.71 and 19.44 ± 4.46 µm in the FS and MK groups, respectively). However, in thicker flaps (130 µm), comparable flap thickness disparity was achieved (18.54 ± 9.52 and 20.83 ± 5.99 µm in the FS and MK groups, respectively). Mean side-cut angle was 74.29 ± 5.79 degrees and 32.34 ± 4.94 degrees in the FS and MK groups, respectively. Conclusions Comparable flap thickness predictability was achieved in thicker flaps (130 µm), while the FS laser technique yielded a more predictable result in thinner flaps (100 to 110 µm). Different flap morphology was observed in meniscus flaps in MK-LASIK and flap morphology in FS-LASIK.

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Purpose. To assess the efficacy and safety of a simple, noninvasive, “flap-sliding” technique for managing flap striae following laser in situ keratomileusis (LASIK). Methods. This prospective, interventional study included eyes with post-LASIK flap striae. All eyes underwent flap sliding 1-2 days after surgery. Following flap edge epithelialisation, a cellulose sponge was used to gently slide the flap perpendicular to the striae direction. This technique allows for flap striae treatment without flap lifting, avoiding any associated lifting complications. Uncorrected distance visual acuity (UDVA), corrected distance visual acuity (CDVA), and refractive error were monitored one day after the flap-sliding procedure. Results. Fifteen eyes (15 patients) with post-LASIK flap striae were managed using the flap-sliding technique. The procedure did not successfully relocate the flap striae in 1 eye, and flap elevation and floating (using a balanced salt solution) were required. Therefore, 14 eyes were included in post-flap-sliding analyses. The UDVA improved in all patients the first day after the flap-sliding procedure was performed, with 11 of 14 eyes (78.57%) reaching an UDVA of 20/25 or better. Complications following flap sliding occurred in 2 eyes (14.29%). One eye had intraoperative epithelial abrasion, and 1 eye had residual postoperative striae outside of the optical zone. Conclusion. The flap-sliding technique is a simple, noninvasive, efficient, and safe technique for managing post-LASIK flap striae that develop after epithelial healing in the early post-LASIK period. This trial is registered with NCT04055337.

Introduction:To present a case series of three female patients with punctate inner choroidopathy. We report the outcomes after an essentially long follow-up period of up to 14 years and provide evidence of the effectiveness of intravitreal injections of bevacizumab and dexamethasone 0.7 mg in punctate inner choroidopathy patients with choroidal neovascular membrane formation.Case series presentation:This is a retrospective case series of three female patients with punctate inner choroidopathy who were treated with intravitreal injections anti-vascular endothelial growth factor agent (bevacizumab, 1.25 mg/0.05 mL). Two patients also received intravitreal dexamethasone 0.7 mg. Once a choroidal neovascular membrane developed, the outcome was poor with a best-corrected visual acuity of 6/60 or counting fingers in the affected eyes. The patients were followed up for 5, 14 and 8 years.Conclusion:The use of dexamethasone 0.7 mg in punctate inner choroidopathy yielded encouraging results and long periods of stability. When choroidal neovascular membrane complicates the primary disease, the prognosis is unfavourable, especially if the macula integrity has already been considerably affected. On the contrary, aggressive early therapy and continued monthly monitoring can prevent severe fibrosis, as showed in previous reports. Further larger-scale studies are needed to evaluate the efficacy of intravitreal dexamethasone 0.7 mg and bevacizumab as an alternative treatment in non-infectious uveitis.

An interfacial adhesion improvement between low-density polyethylene (LDPE) and aluminum (Al) foil is an important challenge in designing multilayered packaging (TetraPak packaging type) due to insufficient inherent adhesion between both untreated materials. Therefore, extra adhesive layers are often used. The hydrophobic character of LDPE is responsible for poor adhesion to Al and can result in delamination. This study deals with the comparative study of the bulk modification of LDPE with various commercially available adhesive promoters with different chemical compositions to increase LDPE’s adhesive characteristics and ensure good adhesion in LDPE/Al laminates. A copolymer of ethylene and methacrylic acid; a terpolymer of ethylene, maleic anhydride, and acrylic ester; or maleated PE were used as adhesive promoters, and their effect on adhesion improvement of LDPE to Al was investigated. The best adhesion improvement was observed in LDPE-modified samples with maleated PE, while 0.1 wt.% additive content significantly increased peel resistance (from zero to 105 N/m). An additional increase in additive content (0.5 wt.%) in LDPE led to stronger adhesion forces than the cohesion forces in Al foil. Adding 0.5 wt.% of maleated PE into LDPE improved the LDPE/Al laminates’ adhesion and can be applied in multilayered lamination applications.