Emer Chang

Introduction: Solar eclipses can cause solar retinopathy, but eclipse-related presentations may reflect public concern as well as true retinal injury. We evaluated the immediate ophthalmic service impact of the 12 August 2026 solar eclipse in the United Kingdom and characterised associated clinical, imaging, and online search findings. Methods: An observational case series was conducted at Birmingham and Midland Eye Centre, a tertiary eye casualty unit serving Birmingham and the wider West Midlands, England. Patients attending on 13 August 2026 with new visual symptoms or concern about ocular injury after viewing the Sun or eclipse were identified. Clinical characteristics, viewing behaviour, presenting and pinhole visual acuity, and multimodal retinal imaging findings were recorded, including optical coherence tomography, colour fundus photography, and fundus autofluorescence. Google Trends was used to assess contemporaneous UK online search interest in eclipse- and eye-related terms. Results: Of 128 eye casualty attendances on 13 August 2026, 10 (7.8%) were eclipse-related. Median age was 37.5 years, 7/10 (70%) patients were female, and 9/10 (90%) reported bilateral symptoms. Seven patients (70%) intentionally viewed the Sun or eclipse, and none reported confirmed use of certified eclipse glasses. Reduced or blurred vision was reported by 5/10 (50%) and photophobia by 4/10 (40%). Visual acuity was 6/9 or better in all 20 eyes and 6/6 or better in 17/20 (85%). Pinhole visual acuity was unchanged from presenting visual acuity in all 20 eyes. No clinically apparent macular abnormality or characteristic acute solar-retinopathy phenotype was identified. Google Trends showed a sharp, temporally concentrated increase in eclipse-related ocular searches around the eclipse, with several post-exposure queries showing marked increases or being classified as Breakout. Conclusions: The eclipse produced an immediate measurable burden on emergency ophthalmology services, with approximately 1 in 13 attendances on the following day being eclipse-related despite no definite acute solar retinopathy being identified. The accompanying increase in online search activity suggests substantial public concern with little demonstrable acute retinal pathology. As surveillance was restricted to the first full day after the eclipse, later presentations and longer-term symptom evolution cannot be excluded.

Aim: To evaluate the real-world effectiveness, durability, and safety of faricimab 6 mg in eyes with treatment-refractory retinal vein occlusion (RVO)-associated macular oedema (MO) in the United Kingdom (UK). Methods: This was a retrospective, single-centre observational study of eyes with RVO that were switched to faricimab after prior treatment with previous anti-vascular endothelial growth factor (anti-VEGF) agents. Baseline demographics, treatment history, pinhole visual acuity (VA), optical coherence tomography (OCT) biomarkers, and injection intervals were recorded. Eyes were treated using a treat-and-extend regimen without a loading phase. Functional, anatomical, durability, and safety outcomes were assessed over follow-up. Results: A total of 22 eyes from 22 patients were included, with a mean (SD) age of 67.9 (11.9) years and a mean (SD) RVO duration of 201.4 (153.1) weeks. Eyes had received a mean (SD) of 20.8 (16.9) prior anti-VEGF injections. The mean (SD) follow-up was 45.7 (15.8) weeks, with a mean (SD) of 5.9 (2.3) faricimab injections. There was no significant change in pinhole VA (53.5 (18.5) vs. 55.0 (18.8) letters, p = 0.08). The central subfield thickness (CST) reduced from 407.6 (102.1) to 377.0 (186.5) µm, and the maximum central retinal thickness from 483.6 (103.1) to 442.2 (187.2) µm, although these changes were not statistically significant (p > 0.05). The proportion of eyes with subretinal fluid (SRF) decreased from 18.2% to 4.5%, and intraretinal fluid (IRF) from 100% to 81.8%. Injection intervals between the first and second faricimab injections increased significantly from 4.9 (1.4) to 7.7 (3.4) weeks (final injection interval, p = 0.004). Six eyes (27.3%) discontinued faricimab, with three (13.6%) requiring an intravitreal dexamethasone implant following a suboptimal response. One eye (4.5%) developed transient intraocular pressure elevation; no cases of intraocular inflammation or endophthalmitis were observed. Conclusions: In this heavily pre-treated, chronic RVO cohort, switching to faricimab without a loading phase resulted in stable visual acuity, modest but non-significant anatomical improvements, and a significant extension in treatment intervals. These findings suggest that faricimab may provide durability benefits and disease stabilisation in treatment-refractory RVO, although functional gains may be limited in chronic disease. Further prospective studies are required to define optimal switching strategies.

Purpose: To assess the rate of retinal vascularisation derived from ultra-widefield (UWF) imaging-based retinopathy of prematurity (ROP) screening as predictor of type 1 ROP and characterise the effect of anti-VEGF therapy on vascularisation rate. Design: Retrospective, consecutive cohort study. Subjects: 132 eyes of 76 premature infants with mean gestational age (GA) of 26.0(±2.0SD) weeks and birth weight (BW) of 815(±264) g, who underwent longitudinal UWF imaging for ROP screening. Setting/Venue: Level 3 neonatal unit in Oxford, United Kingdom Methods: The extent of retinal vascularisation on each UWF image was measured as the ratio between ‘disc-to-temporal vascular front’ and ‘disc-to-fovea’ distance along a straight line bisecting the vascular arcades. Measurements from ≥3 timepoints plotted against post-menstrual age (PMA) enabled calculation of temporal vascularisation rate (TVR) for each eye. Using TVR, GA and BW as predictors, a machine learning model was created to classify eyes as either Group AB (no ROP and type 2 ROP) or Group C (type 1 ROP). The model was validated in a withheld cohort of 32 eyes (19 infants) of which 8 eyes (5 infants) required treatment. TVR in 37 eyes (20 infants) was compared before and after ultra-low-dose (0.16 mg) intravitreal bevacizumab treatment. Main Outcome Measures: Rate of retinal vascularisation. Results: Slower retinal vascularisation correlated with increasing ROP severity, with TVR being 29% slower in Group C eyes (n=50) than Group AB eyes (n=33 no ROP and n=49 type 2 ROP) (p=0.04). Our model correctly predicted ROP outcomes of 30/32 eyes, achieving a balanced accuracy of 95.8%. No significant change in TVR was found before and after bevacizumab treatment with mean post-treatment imaging follow-up of 7.7(±7.9) weeks (p=0.60 right eyes, p=0.71 left eyes). Conclusions: UWF imaging-based ROP screening enables quantification of retinal vascularisation rate, which can provide early prediction of type 1 ROP independent of BW and GA. Rate of physiological retinal vascularisation does not appear to be significantly affected by ultra-low-dose anti-VEGF treatment, which has significant implications for the development of peripheral avascular retina and timing of anti-VEGF intervention to prevent disease progression in high risk infants.

Objective: Mechanical and biologic cues drive cellular signaling in cartilage development, health, and disease. Primary cilia proteins, which are implicated in the transduction of biologic and physiochemical signals, control cartilage formation during skeletal development. This study was undertaken to assess the influence of the ciliary protein intraflagellar transport protein 88 (IFT88) on postnatal cartilage from mice with conditional knockout of the Ift88 gene (Ift88‐KO).Methods: Ift88^fl/fl and aggrecanCre^ERT2 mice were crossed to create a strain of cartilage‐specific Ift88‐KO mice (aggrecanCre^ERT2;Ift88^fl/fl). In these Ift88‐KO mice and Ift88^fl/fl control mice, tibial articular cartilage thickness was assessed by histomorphometry, and the integrity of the cartilage was assessed using Osteoarthritis Research Society International (OARSI) damage scores, from adolescence through adulthood. In situ mechanisms of cartilage damage were investigated in the microdissected cartilage sections using immunohistochemistry, RNAScope analysis, and quantitative polymerase chain reaction. Osteoarthritis (OA) was induced in aggrecanCre^ERT2;Ift88^fl/fl mice and Ift88^fl/fl control mice using surgical destabilization of the medial meniscus (DMM). Following tamoxifen injection and DMM surgery, the mice were given free access to exercise on a wheel.Results: Deletion of Ift88 resulted in progressive reduction in the thickness of the medial tibial cartilage in adolescent mice, as well as marked atrophy of the cartilage in mice during adulthood. In aggrecanCre^ERT2;Ift88^fl/fl mice at age 34 weeks, the median thickness of the medial tibial cartilage was 89.42 μm (95% confidence interval [95% CI] 84.00–93.49), whereas in Ift88^fl/fl controls at the same age, the median cartilage thickness was 104.00 μm (95% CI 100.30–110.50; P < 0.0001). At all time points, the median thickness of the calcified cartilage was reduced. In some mice, atrophy of the medial tibial cartilage was associated with complete, spontaneous degradation of the cartilage. Following DMM, aggrecanCre^ERT2;Ift88^fl/fl mice were found to have increased OARSI scores of cartilage damage. In articular cartilage from maturing mice, atrophy was not associated with obvious increases in aggrecanase‐mediated destruction or chondrocyte hypertrophy. Of the 44 candidate genes analyzed, only Tcf7l2 expression levels correlated with Ift88 expression levels in the microdissected cartilage. However, RNAScope analysis revealed that increased hedgehog (Hh) signaling (as indicated by increased expression of Gli1) was associated with the reductions in Ift88 expression in the tibial cartilage from Ift88‐deficient mice. Wheel exercise restored both the articular cartilage thickness and levels of Hh signaling in these mice.Conclusion: Our results in a mouse model of OA demonstrate that IFT88 performs a chondroprotective role in articular cartilage by controlling the calcification of cartilage via maintenance of a threshold of Hh signaling during physiologic loading.

Mechanical and biological cues drive cellular signalling in cartilage development, health, and disease. Proteins of the primary cilium, implicated in transduction of biophysiochemical signals, control cartilage formation during skeletal development, but their influence in post-natal cartilage remains unknown. Ift88 ^fl/fl and AggrecanCreER ^T2 mice were crossed to create a cartilage-specific, inducible knockout mouse AggrecanCreER ^T2 ;Ift88 ^fl/fl . Tibial articular cartilage (AC) thickness was assessed, through adolescence and adulthood, by histomorphometry and integrity by OARSI score. In situ mechanisms were investigated by immunohistochemistry (IHC), RNA scope and qPCR of micro-dissected cartilage. OA was induced by surgical destabilisation (DMM). Mice voluntarily exercised using wheels. Deletion of IFT88 resulted in progressive reductions in medial AC thickness during adolescence, and marked atrophy in adulthood. At 34 weeks of age, medial thickness was reduced from 104.00μm, [100.30-110.50, 95% CI] in Ift88 ^fl/fl to 89.42μm [84.00-93.49, 95% CI] in AggrecanCreER ^T2 ;Ift88 ^fl/fl (pAggrecanCreER ^T2 ;Ift88 ^fl/fl mice had increased OA scores. Atrophy in mature AC was not associated with obvious increases in aggrecanase-mediated destruction or chondrocyte hypertrophy. Ift88 expression positively correlated with Tcf7l2 , connective tissue growth factor ( Ctgf ) and Enpp1 . RNA scope revealed increased hedgehog (Hh) signalling ( Gli1) , associated with reductions in Ift88 , in AggrecanCreER ^T2 ;Ift88 ^fl/fl cartilage. Wheel exercise restored both AC thickness and levels of Hh signalling in AggrecanCreER ^T2 ;Ift88 ^fl/fl . Our results demonstrate that IFT88 is chondroprotective, regulating AC thickness, potentially by thresholding a Hh response to physiological loading that controls cartilage calcification.