A retrospective analysis of visual function in patients with preoperatively diagnosed myopia, after implantation of Liberty® intraocular lens, including the influence of some factors like a kind of surgery, values of angle alpha and kappa, pupil size, values of higher order aberrations generated by the lens on visual acuity to far and near distances was done. Lens removal and Liberty® implantation was done 47 eyes, including in 13 patients in both eyes. In 7 eyes, it was a toric lens. A mean preoperative value of myopia was -6.72 Dsph. Cataract removal accounted for 55% of all procedures performed, the rest being Refractive Lens Exchange. Preoperative pupil size was between 3.6 and 6,4 mm. The average postoperative visual acuity to far distances was 0.13 (logMar), and to near distances was 0.51 (Snellen). Rare cases of insufficient quality of vision to intermediate distances, when the postoperative pupil size was greater than 4 mm, resolved after increasing light intensity in the room. A bigger values of higher order aberrations corresponded with lower values of preoperative visual acuity to far distances. A bigger values of angle alpha corresponded with lower values of postoperative visual acuity to far distances, which were significantly higher in cataract group. Visual acuity to far distances was also better in eye with bigger pupil size. A specific structure of the lens allows patients to see good to the near distances, even if the light intensity not perfect.
Macular Pigments (MPs), by absorbing potentially toxic short-wavelength (400–500 nm) visible light, provide protection against photo-chemical damage. A new method of MPs levels screening analyzes polarization-dependent absorption of blue light by MPs, which results in the entoptic phenomenon called Haidinger’s Brushes (HB). Subjects identify the direction of rotation of HB when presented with a circular stimulus illuminated with an even intensity of polarized white light in which the electric field vector was rotating either clockwise or anti-clockwise. The examination was performed at baseline and after 3 months of daily intake of 320 mg bilberry extract, from Vaccinium myrtillus L. and standardized to contain more than 36% of anthocyanins (anthocyanosides), in normal subjects and MPs improvement was recorded after 3 months of dietary supplements. The results suggest a challenging role of daily intake of 320 mg bilberry extract in macular pigment density improvement possibly due to a macular protection from oxidative damage by bilberry.
Severe damage of the ocular surface is still one of the leading causes of impaired vision. Next to widely used treatment methods, such as keratoplasty and usage of amniotic membrane, a new approach has been in the focus of the research for the past few years. This review presents possibilities for using nanofibrous materials in the treatment of corneal defects. There is a broad spectrum of natural and synthetic polymers suitable for this purpose. Thanks to their mechanical strength, nanofibrous scaffolds are durable, and due to their high porosity, they promote optimal cell growth and proliferation conditions. Those three-dimensional, thread-like structures can also be used as a drug delivery system for different substances, such as antibiotics or stem cells.
We report the case of a 56 year -old patient, with the notion of a neglected ocular trauma of the right eye 6 years ago, with a progressive decrease in visual acuity for 4 years. The ophthalmological examination of the right eye showed a visual acuity with finger movement, an ocular tone of 15 mmhg with a regressive cataract in the anterior segment with a retracted aspect and an embossed anterior surface. Ocular ultrasound was performed and returned normal. The ophthalmological examination of the left eye did not reveal any abnormality. A phacoemulsification cataract surgery was performed with a good postoperative evolution.
Background Epiretinal membranes in patients with proliferative vitreoretinopathy (PVR) consist of extracellular matrix and a number of cell types including retinal pigment epithelial (RPE) cells and fibroblasts, whose contraction causes retinal detachment. In RPE cells depletion of platelet-derived growth factor (PDGF) receptor (PDGFR)β suppresses vitreous-induced Akt activation, whereas in fibroblasts Akt activation through indirect activation of PDGFRα by growth factors outside the PDGF family (non-PDGFs) plays an essential role in experimental PVR. Whether non-PDGFs in the vitreous, however, were also able to activate PDGFRβ in RPE cells remained elusive. Methods The CRISPR/Cas9 technology was utilized to edit a genomic PDGFRB locus in RPE cells derived from an epiretinal membrane (RPEM) from a patient with PVR, and a retroviral vector was used to express a truncated PDGFRβ short of a PDGF-binding domain in the RPEM cells lacking PDGFRβ. Western blot was employed to analyze expression of PDGFRβ and α-smooth muscle actin, and signaling events (p-PDGFRβ and p-Akt). Cellular assays (proliferation, migration and contraction) were also applied in this study. Results Expression of a truncated PDGFRβ lacking a PDGF-binding domain in the RPEM cells whose PDGFRB gene has been silent using the CRISPR/Cas9 technology restores vitreous-induced Akt activation as well as cell proliferation, epithelial-mesenchymal transition, migration and contraction. In addition, we show that scavenging reactive oxygen species (ROS) with N-acetyl-cysteine and inhibiting Src family kinases (SFKs) with their specific inhibitor SU6656 blunt the vitreous-induced activation of the truncated PDGFRβ and Akt as well as the cellular events related to the PVR pathogenesis. These discoveries suggest that in RPE cells PDGFRβ can be activated indirectly by non-PDGFs in the vitreous via an intracellular pathway of ROS/SFKs to facilitate the development of PVR, thereby providing novel opportunities for PVR therapeutics. Conclusion The data shown here will improve our understanding of the mechanism by which PDGFRβ can be activated by non-PDGFs in the vitreous via an intracellular route of ROS/SFKs and provide a conceptual foundation for preventing PVR by inhibiting PDGFRβ transactivation (ligand-independent activation).
