Narayana Nethralaya

Foldable acrylic lenses are the most extensively used 'in the bag' monofocal or multifocal intraocular lenses (IOLs) in cataract surgery, toric lenses in astigmatism, and refractive lens exchange surgeries. When subluxation or dislocation of these lenses is encountered, they must be explanted as they cannot be fixed with conventional scleral fixation techniques. The 'pierce' technique is a novel way of fixing these lenses to the sclera, wherein a 9-0/10-0 polypropylene suture with a straight needle is passed through the IOL at the haptic-optic junction. The ends of the threads are sutured under the scleral flaps in a vertical fashion. This case series highlights the merits of refixing subluxated or dislocated IOLs in a closed or open globe technique and its utility in eyes with weakened capsular bags as it provides good centration, minimal tilt, and applicability to a wider range of foldable IOLs without eyelets, including premium IOLs.

Myogenic differentiation (MyoD), a class II basic helix-loop-helix transcription factor, regulates multiple cell functions, including fibrosis in many organs, but remains unknown in the cornea. This study characterized the expression of MyoD in non-fibrotic and fibrotic rabbit and human donor corneas and investigated the effects of MyoD gene silencing on corneal myofibroblast dedifferentiation in vitro and fibrosis in vivo. New Zealand White rabbits, human donor corneas, human corneal stromal fibroblasts (CSFs), and human corneal myofibroblasts (CMFs) were used. MyoD shRNA or scrambled shRNA was delivered into CMFs via Lipofectamine 3000 and rabbit cornea via 2-kDa polyethylenimine conjugated to gold nanoparticles (PEI2-GNPs). Quantitative real-time polymerase chain reaction (qRT-PCR), immunofluorescence, and western blotting quantified the expression of profibrotic genes, intermediate filaments, fibroblast-specific protein 1 (FSP1), and proliferation marker Ki67 in CMF-/+ MyoD gene silencing. MyoD expression was detected in human and rabbit corneal epithelium, stroma, and endothelium. MyoD levels were significantly greater in fibrotic human corneas (P < 0.001) and rabbit corneas (P < 0.0001) than corresponding non-fibrotic corneas. Also, CMFs had significantly greater MyoD levels than CSFs (P < 0.0001). MyoD shRNA-silenced CMFs acquired a characteristic fibroblast phenotype and showed reduced fibrotic genes, alpha smooth muscle actin (αSMA; P < 0.0001), fibronectin (FN; P = 0.0015), collagen type I (ColI; P = 0.0011), and collagen type IV (ColIV; P = 0.0053) mRNA levels compared to the scrambled shRNA-delivered CMFs. Further, immunofluorescence demonstrated increased vimentin (P < 0.001), FSP1 (P < 0.01), and Ki67 expression (P = 0.0349) and decreased desmin expression (P < 0.001) in MyoD shRNA-silenced CMFs than the scrambled shRNA-delivered CMFs. MyoD shRNA-delivered rabbit corneas had less scarring in vivo (P = 0.368). MyoD is expressed in cornea and could amend CMF dedifferentiation and fibrosis in an injured cornea. Additional studies are warranted to define the potential of MyoD in corneal fibrosis management.

Persistent optic disc bleeding during pars plana vitrectomy (PPV) is difficult to manage. This study aims to explore the use of fibrin glue as a novel agent to achieve hemostasis in such eyes. Interventional case series of patients with vitreous hemorrhage (VH) or tractional retinal detachment (TRD) due to proliferative diabetic retinopathy, retinal vein occlusion or retinal vasculitis, in whom fibrin glue was used intraoperatively for hemostasis. All the patients were followed up for 1 month. 14 eyes of 14 patients were included, of which 12 (85.7%) were male with mean age of 52 years. Surgery was performed in 10 eyes (71.4%) for VH and 4 eyes (28.6%) for TRD. The mean best corrected visual acuity (BCVA) improved from 1.33±0.53 Logarithm of the Minimum Angle of Resolution (logMAR) (20/428), to 0.42± 0.35 logMAR (20/53) 1 month after surgery (P = 0.002), 0.43± 0.32 logMAR (20/54) 3 months after surgery (p = 0.003) and 0.36±0.34 logMAR (20/46) at a mean of 7 months (p = 0.002) after the surgery. Post operative vitreous cavity hemorrhage occurred in 1 eye (7.1%), which did not require a repeat surgery. This report demonstrates the efficacy of fibrin glue used during vitrectomy in controlling persistent optic disc hemorrhage in a cohort of diverse etiologies. Persistent intraoperative optic disc bleeding is difficult to manage with adverse outcomes. Fibrin glue is a short acting bioadhesive, which has shown favorable outcomes when used in rhegmatogenous retinal detachment and macular hole surgeries. Our prospective interventional study shows that the use of fibrin glue is a valuable technique to manage optic disc bleeders, allowing for better and faster visual recovery, while reducing the incidences of rebleeding and reoperations. Of the 14 eyes included in our study, post-operative vitreous cavity hemorrhage occurred in just one case, which resolved spontaneously, and did not need any reoperation.

PurposeThe Standardization of Uveitis Nomenclature (SUN) criteria were introduced in 2021 to standardize the classification of uveitis subtypes. We evaluated the real-world applicability of these criteria for tubercular uveitis (TBU) using a computational definition mapped to the Ocular Autoimmune Systemic Inflammatory Infectious Study (OASIS) registry.MethodsThis observational retrospective cross-sectional study analyzed real-world baseline data from 372 clinician-diagnosed TBU cases within the multinational OASIS registry, all collected from 17 tertiary centers across 8 countries: India, Nepal, Indonesia, Switzerland, Ethiopia, Colombia, Argentina, and Chile. We mapped the SUN criteria to corresponding variables in the OASIS registry, and Boolean operators were used to generate a computational definition for TBU. The sensitivity of the SUN criteria in capturing clinician-diagnosed cases of TBU was evaluated.ResultsThe SUN criteria identified 15.9% (n = 59) of clinician-diagnosed TBU cases at baseline. Criterion f2 (evidence of TB infection) was met in 70.7% of cases (n = 263), and criterion f1 (TBU-compatible uveitic syndrome) was satisfied in 24.5% of cases (n = 91). Exclusion criterion successfully identified 99.5% of cases (n = 370). By country and anatomical location, cases in India and those with posterior uveitis had the highest concordance at 19.8% (n = 39) and 21.8% (n = 44), respectively. Bilateral TBU was more likely to satisfy the SUN criteria (P = 0.049).ConclusionsSUN classification criteria demonstrated low sensitivity for real-world TBU diagnosis at baseline, which may limit the number of cases available for enrollment in research studies. Further diagnostic refinement, clearer definition of application context, and longitudinal validation are needed to generate diagnostic criteria for clinical application.

To report a case of non-hereditary bilateral foveomacular and peripheral retinoschisis in a young female, with electrophysiological abnormalities in the absence of high myopia. A 25-year-old female with recent-onset diminution of vision in the left eye (LE) underwent comprehensive ophthalmic evaluation including best-corrected visual acuity (BCVA), slit lamp biomicroscopy, indirect ophthalmoscopy, optical coherence tomography (OCT), full field electroretinography (ERG) and genetic evaluation. BCVA at presentation was 6/6, N6 in the right eye(RE) and 6/9, N8 in the LE. The patient had a prior history of laser refractive surgery for moderate myopia. Anterior segment examination was unremarkable. Fundus evaluation revealed bilateral foveoschisis and peripheral retinal schisis. OCT showed retinoschisis predominantly involving outer plexiform and outer nuclear layer, along with mild vitreoschisis. Foveal detachment was noted in the LE. ERG demonstrated rod and cone system dysfunction, severe rod bipolar cell dysfunction in both eyes, and a borderline electronegative waveform in the LE. There was no family history, and clinical exome sequencing did not reveal any pathogenic variants associated with the phenotype. Electrophysiological abnormalities with bipolar cell dysfunction, similar to those seen in hereditary retinoschisis, can also occur in non-hereditary retinoschisis. Genetic evaluation is recommended to differentiate between the two, as ERG may show abnormalities in both.

Digital eye strain is a cross-system condition that arises from interactions between visual physiology and digital displays. As the use of screens has grown in work, education, and everyday life, researchers have sought to describe this condition through symptom questionnaires (CVS‑Q, CVSS17, DESQ), measurements of the ocular surface and blinking, tests of accommodation and vergence, and, in related visual fatigue studies, neurophysiological methods such as electromyography and electroencephalography (EEG). Nevertheless, these methods have usually examined individual mechanisms separately. Interventions-ranging from lubricating the ocular surface and filtering blue light to ergonomic changes, task‑specific refractive correction, and scheduled micro‑breaks-have seldom been guided by a unified mechanistic framework. This review compiles evidence from 128 studies to identify six mechanistic domains relevant for clinical assessment. These include ocular surface and blink dynamics, accommodation and vergence, musculoskeletal load, device-related optical stress, cognitive load, and neural markers. A systematic search of PubMed/MEDLINE, Embase, Scopus, and Web of Science was carried out through September 30th, 2025, in accordance with PRISMA guidelines. Eligible studies included randomized trials, controlled interventions, cohort studies, and laboratory experiments, with methodological quality evaluated using the Mixed Methods Appraisal Tool. Results across pediatric, adolescent, working‑age, and presbyopic groups indicate that cognitive load reduces blinking and destabilizes accommodation. Binocular incongruence links visual effort with trapezius activation, and EEG markers can precede subjective fatigue. Interventions aligned with these mechanisms-such as ocular surface care, accommodative/vergence correction, ergonomic optimization, and micro‑break scheduling-are supported across all domains. The review proposes a mechanism‑based triage model to assist clinicians in prioritizing interventions based on the patient's exposure profile, breaking neuro‑ocular feedback loops, and preserving functional performance in individuals exposed to screens. The framework provides an actionable, mechanism‑first triage checklist for optometric practice.

Carbon Quantum Dots (CQDs) were synthesized from Rheodiscolor leaf extract using Soxhlet extraction followed by a hydrothermal process in four variants: S1 (raw CQDs), S2 (5 % ethanol-CQDs), S3, and S4. UV–Visible absorption bands at 211–339 nm and excitation-dependent photoluminescence (315–475 nm) confirmed moderate quantum confinement. FTIR spectra identified O–H (∼3400 cm⁻¹) and C O (∼1645 cm⁻¹) groups, with additional C–H and C C bands in S2–S4 enhancing solubility. Electrochemical characterization using GCD and cyclic voltammetry (CV) revealed contrasting outcomes: GCD showed reduced capacitance of GCE for all CQD variants compared to KOH, with S1 retaining 45–54 % and S4 only 20–38 %, whereas CV indicated strong, stable performance of GCE for CQDs (S1–S3) (∼80–88 % of KOH) and moderate retention for CQD (S4) (43–60 %). These findings suggest that Rheodiscolor leaf-derived CQDs, especially S1–S3, are promising, sustainable, and tunable electrolyte materials for energy storage applications, with properties strongly influenced by synthesis conditions. Carbon Quantum Dots from Rheodiscolor leaves • Rheodiscolor leaf extract via green Soxhlet–hydrothermal method produced CQDs. • CQDs show UV-Vis absorption at 211–339 nm and PL emission at 315–475 nm. • Best electrochemical stability and reversibility were observed in S1 and S2. • S1-S3 showed 45–54 % (GCD) and 80–88 % (CV) vs KOH; S4 retained less. • Rheodiscolor CQDs show low-cost, sustainable electrolytes for flexible supercapacitors.

Purpose Familial exudative vitreoretinopathy (FEVR) is a rare genetic disorder characterized by incomplete retinal vascular development, leading to ischemia, aberrant neovascularization (NV), and retinal detachment (RD). This report describes a case of RD with concurrent NV and FEVR, successfully managed with encircling scleral buckling (SB) surgery without additional peripheral laser ablation. Case Description A 16-year-old female with high myopia presented with a four-day history of decreased vision in her right eye (RE). Fundus examination revealed subtotal RD involving the inferior and superonasal quadrants, multiple foci of NV in the inferior quadrant, peripheral avascular retina, and a thick subretinal gliotic band. The left eye (LE) displayed an attached retina with similar peripheral avascularity. Fluorescein angiography confirmed extensive peripheral avascularity and leaking neovascular fronds in the RE, consistent with FEVR. The patient underwent SB surgery in the RE using an encircling band without subretinal fluid drainage or transscleral cryotherapy. Over six weeks, serial examinations demonstrated progressive resolution of subretinal fluid, complete retinal reattachment, and regression of NV in the RE without additional laser treatment. Conclusion Early retinal reattachment with SB alone may be sufficient to achieve both anatomical reattachment and regression of NV in selected cases of FEVR-related tractional or rhegmatogenous RD, potentially reducing the need for adjunctive ablative therapy.

Protein kinases canonically suppress autophagy, yet how cells activate autophagy during stress remains unclear. Here we reveal that AKT1 kinase promotes autophagy through a non-canonical pathway. AKT2 loss triggers compensatory AKT1 activation, which phosphorylates telomerase reverse transcriptase (TERT) at Serine 824, driving nuclear translocation. Nuclear TERT assembles with FOXO3 and c-MYC into a transcriptional complex that activates PERK, initiating a feed-forward loop. PERK-ATF4 signaling amplifies autophagy gene transcription while inducing selective ERphagy through receptors TEX264 and CCPG1. Using C. elegans , mouse models, and human iPSCs, we demonstrate this AKT1-TERT-c-MYC-FOXO3 axis is evolutionarily conserved and essential for proteostasis in post-mitotic cells. We developed a first-in-class allosteric AKT2 inhibitor through structure-guided design that selectively triggers beneficial AKT1 compensation, restoring autophagy in diseased cells. These findings reveal a transcriptional mechanism linking AKT1 activation to autophagy and provide a therapeutic strategy for diseases with defective ER quality control.