Changes In Retinal Morphology Research Articles

Postoperative Proliferation Detection in Eyes Treated for Rhegmatogenous Retinal Detachment by WideField OCT Angiography.

Proliferative retinal changes may occur postsurgery for rhegmatogenous retinal detachment (RRD), possibly preceding recurrent detachment. This study aims to establish the groundwork for an imaging system capable of discerning changes in retinal vessel tortuosity after RRD repair, analyzing widefield optical coherence tomography angiography (WF-OCTA) images. Eighty-eight eyes of 86 patients with RRD who underwent surgical procedures and had repeated imaging with clear widefield optical coherence tomography (WF-OCT) and WF-OCTA on different postoperative days were enrolled in this retrospective study. We compared WF-OCTA images over time to identify alterations in retinal vessel tortuosity and observed regional changes in retinal morphology. After image processing, changes in retinal vessel tortuosity were detected in 66 quadrants. These changes, attributed to retinal traction from proliferative membranes, were observed in 56 quadrants, among which retinal thickness remained unchanged in seven sectors (12.5%) according to the WF-OCT map. In nine quadrants, changes in retinal vessel tortuosity were attributed to changes in subretinal fluid, aligning with observable variations in retinal thickness. Observation of vessel tortuosity changes using WF-OCTA can help detect early postoperative proliferative changes in eyes with RRD. Because WF-OCTA can detect minute vessel tortuosity changes, it can offer a noninvasive alternative for the detection of early postoperative proliferative changes.

Optical Imaging for Diabetic Retinopathy Diagnosis And Detection Using Ensemble Models

Diabetes, characterized by heightened blood sugar levels, can lead to a condition called Diabetic Retinopathy (DR), which adversely impacts the eyes due to elevated blood sugar affecting the retinal blood vessels. The most common cause of blindness in diabetics is thought to be Diabetic Retinopathy (DR), particularly in working-age individuals living in poor nations. People with type 1 or type 2 diabetes may develop this illness, and the risk rises with the length of diabetes and inadequate blood sugar management. There are limits to traditional approaches for the early identification of diabetic retinopathy (DR). In order to diagnose diabetic retinopathy, a model based on Convolutional neural network (CNN) is used in a unique way in this research. The suggested model uses a number of deep learning (DL) models, such as VGG19, Resnet50, and InceptionV3, to extract features. After concatenation, these characteristics are sent through the CNN algorithm for classification. By combining the advantages of several models, ensemble approaches can be effective tools for detecting diabetic retinopathy and increase overall performance and resilience. Classification and image recognition are just a few of the tasks that may be accomplished with ensemble approaches like combination of VGG19,Inception V3 and Resnet 50 to achieve high accuracy. The proposed model is evaluated using a publicly accessible collection of fundus images.VGG19, ResNet50, and InceptionV3 differ in their neural network architectures, feature extraction capabilities, object detection methods, and approaches to retinal delineation. VGG19 may excel in capturing fine details, ResNet50 in recognizing complex patterns, and InceptionV3 in efficiently capturing multi-scale features. Their combined use in an ensemble approach can provide a comprehensive analysis of retinal images, aiding in the delineation of retinal regions and identification of abnormalities associated with diabetic retinopathy. For instance, micro aneurysms, the earliest signs of DR, often require precise detection of subtle vascular abnormalities. VGG19′s proficiency in capturing fine details allows for the identification of these minute changes in retinal morphology. On the other hand, ResNet50′s strength lies in recognizing intricate patterns, making it effective in detecting neo neo-vascularization and complex hemorrhagic lesions. Meanwhile, InceptionV3′s multi-scale feature extraction enables comprehensive analysis, crucial for assessing macular edema and ischemic changes across different retinal layers.

Hyperglycemia-independent neonatal streptozotocin-induced retinopathy (NSIR) in rats.

Introduction: Chemicals, such as MNU (N-methyl-N-nitrosourea) and NaIO3 (sodium iodate), are widely used to induce retinal degeneration in rodents. Streptozotocin (STZ) is an analog of N-acetyl glucosamine in which an MNU moiety is linked to a hexose and has a special toxic effect on insulin-producing pancreatic β-cells. It is commonly used to induce hyperglycemia to model diabetes. While intracerebroventricular injection of STZ can produce Alzheimer's disease independent of hyperglycemia, most retinal studies using STZ focus on the effects of hyperglycemia on the retina, but whether STZ has any impact on retinal cells independent of hyperglycemia is unknown. We aimed to investigate the role of cytotoxicity of STZ in rat retina. Methods: Intravitreal or subcutaneous injection of STZ was performed on newborn rats. Electroretinogram (ERG) and H&E staining investigated retinal function and morphological changes. Retinal cell types, cell death, proliferation, inflammation, and angiogenesis were studied by immunostaining. RNA sequencing was performed to examine the transcriptome changes of retinal cells after intravitreal injection of STZ. Results: Intravitreal (5μg or 10μg) or subcutaneous (30mg/kg) injection of STZ at the early stage of newborn rats couldn't induce hyperglycemia but caused NSIR (Neonatal STZ-induced retinopathy), including reduced ERG amplitudes, retinal rosettes and apoptosis, cell cycle arrest, microglial activation, and delayed retinal angiogenesis. STZ did not affect the early-born retinal cell types but significantly reduced the late-born ones. Short-term and long-term hyperglycemia had no significant effects on the NSIR phenotypes. RNA sequencing revealed that STZ induces oxidative stress and activates the p53 pathway of retinal cells. Locally or systemically, STZ injection after P8 couldn't induce SINR when all retinal progenitors exit the cell cycle. Conclusion: NSIR in rats is independent of hyperglycemia but due to STZ's direct cytotoxic effects on retinal progenitor cells. NSIR is a typical reaction to STZ-induced retinal oxidative stress and DNA damage. This significant finding suggests that NSIR may be a valuable model for studying retinal progenitor DNA damage-related diseases, potentially leading to new insights and treatments.

Investigation of the pathophysiology of epiretinal membrane foveoschisis: An analysis of longitudinal changes in visual functions, retinal structures, and retinal traction force.

To analyze the pathophysiology of epiretinal membrane foveoschisis (ERM-FS) by evaluating the longitudinal changes in visual function and several optical coherence tomography (OCT) parameters. The medical records of 33 consecutive patients (35 eyes) with untreated ERM-FS were retrospectively reviewed. Best-corrected visual acuity (BCVA), M-CHARTS score, and OCT parameters including ERM area, maximum depth of retinal folds (MDRF), FS area, and FS circularity were evaluated. A wide range of FS area changes was observed at the final follow-up visit (59.68-240.45% of the baseline FS area). In the FS enlargement group, BCVA and mean M-CHARTS scores significantly worsened and MDRF significantly increased over time, whereas in the FS non-enlargement group, no significant change was observed in BCVA, mean M-CHARTS scores, or MDRF during the follow-up period. Multivariate logistic regression analyses revealed that MDRF (odds ratio: 1.05, 95% confidence interval: 1.00-1.10, P = 0.048) and FS circularity (odds ratio: 0.91, 95% confidence interval: 0.83-1.00, P = 0.043) were significantly associated with FS enlargement. ERM-FS encompasses diverse pathophysiologies. Since visual functions do not worsen in some cases, monitoring the changes in visual functions and retinal morphology over time is recommended to determine surgical indications.

Deep Learning‐Enabled Vasculometry Depicts Phased Lesion Patterns in High Myopia Progression

PurposeTo investigate the potential phases in myopic retinal vascular alterations for further elucidating the mechanisms underlying the progression of high myopia (HM). MethodsFor this retrospective study, participants diagnosed with high myopia at Beijing Tongren Hospital were recruited. Based on bionic mechanisms of human vision, an intelligent image processing model was developed and utilized to extract and quantify the morphological characteristics of retinal vasculatures in different regions measured by papilla-diameter (PD), including vascular caliber, arteriole-to-venule ratio (AVR), tortuosity, the angle of the vascular arch (AVA), the distance of the vascular arch (DVA), density, fractal dimension, and venular length. In addition, the optic disc and the area of peripapillary atrophy (PPA) were also quantified. The characteristics of the overall population, as well as patients aged less than 25 years old, were compared by different genders. Univariate and multiple linear regression analyses were conducted to investigate the correlation of retinal vasculature parameters with PPA width, and detailed trends of the vascular indicators were analyzed to explore the potential existence of staged morphological changes. FindingsThe study included 14,066 fundus photographs of 5775 patients (aged 41.2 ± 18.6 years), of whom 7379 (61.2 %) were female. The study included 12,067 fundus photographs of 5320 patients (aged 41.2 ± 18.6 years). Significant variations in the morphological parameters of retinal vessels were observed between males and females. After adjusting for age and sex, multiple linear regression analysis showed that an increased PPA width ratio was associated with lower AVA (1PD), DVA (1PD), vascular caliber (0.5–1.0 PD), tortuosity (0.5–1.0 PD), density and fractal dimension (all P < 0.001, Spearman’s ρ < 0). Overall, the changes in retinal vascular morphology showed two phases: tortuosity (0.5–1.0PD) and AVA (1PD) decreased rapidly in the first stage but significantly more slowly in the second stage, while vascular density and fractal dimension showed a completely opposite trend with an initial slow decline followed by a rapid decrease. ConclusionsThis study identified two distinct phases of retinal vascular morphological changes during the progression of HM. Traction lesions were predominant in the initial stage, while atrophic lesions were predominant in the later stage. These findings provide further insight into the development mechanism of HM from the perspective of retinal vasculature.

O-GlcNAc Modification Is a Promising Therapeutic Target for Diabetic Retinopathy.

Diabetic retinopathy (DR) is a very serious diabetes complication. Changes in the O-linked N-acetylglucosamine (O-GlcNAc) modification are associated with many diseases. However, its role in DR is not fully understood. In this research, we explored the effect of O-GlcNAc modification regulation by activating AMP-activated protein kinase (AMPK) in DR, providing some evidence for clinical DR treatment in the future. Bioinformatics was used to make predictions from the database, which were validated using the serum samples of diabetic patients. As an in vivo model, diabetic mice were induced using streptozotocin (STZ) injection with/without an AMPK agonist (metformin) or an AMPK inhibitor (compound C) treatment. Electroretinogram (ERG) and H&E staining were used to evaluate the retinal functional and morphological changes. In vitro, 661 w cells were exposed to high-glucose conditions, with or without metformin treatment. Apoptosis was evaluated using TUNEL staining. The protein expression was detected using Western blot and immunofluorescence staining. The angiogenesis ability was detected using a tube formation assay. The levels of O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) in the serum changed in the DR patients in the clinic. In the diabetic mice, the ERG wave amplitude and retinal thickness decreased. In vitro, the apoptotic cell percentage and Bax expression were increased, and Bcl2 expression was decreased in the 661 w cells under high-glucose conditions. The O-GlcNAc modification was increased in DR. In addition, the expression of GFAT/TXNIP O-GlcNAc was also increased in the 661 w cells after the high-glucose treatment. Additionally, the Co-immunoprecipitation(CO-IP) results show that TXNIP interacted with the O-GlcNAc modification. However, AMPK activation ameliorated this effect. We also found that silencing the AMPKα1 subunit reversed this process. In addition, the conditioned medium of the 661 w cells may have affected the tube formation in vitro. Taken together, O-GlcNAc modification was increased in DR with photoreceptor cell degeneration and neovascularization; however, it was reversed after activating AMPK. The underlying mechanism is linked to the GFAT/TXNIP-O-GlcNAc modification signaling axis. Therefore, the AMPKα1 subunit plays a vital role in the process.

Aspects of Histopathological and Ultrastructural Retinal Changes in Chronic Exposure to Hydroxychloroquine.

Background and Objective: Hydroxychloroquine sulfate (HCQ) is a lysosomotropic agent administered in systemic lupus erythematosus and rheumatoid arthritis that has fewer toxic effects than chloroquine. However, HCQ may still be responsible for retinal toxicity. In this study, we observed structural changes in the retinas of experimental rats after prolonged exposure to HCQ. Matherials and Methods: We investigated several aspects regarding retinal changes, at both the histopathological and ultrastructural levels. We used 96 male albino Wistar rats distributed into four equal groups (n = 24 per group): the first three groups were treated with different doses of HCQ (50, 100, and 200 mg/kg HCQ, injected intraperitoneally in a single dose daily), and the last group (the control group, n = 24) was treated with saline solution administered in the same way (0.4 mL of saline solution). The treated groups received HCQ daily for 4 months, and every month, six animals from each group were sacrificed to assess retinal changes. The eyes were examined via optical (OM) and electronic microscopy (EM). Statistical analysis was deployed, and results regarding retinal morpho-photometry were acquired. Results: We observed structural retinal changes in both high and low doses of HCQ; while high doses determined a significant thinning of the retina, lower doses caused retinal thickening. Morphological retinal changes upon exposure to HCQ are believed to be caused by accumulated HCQ in lysosomes found in retinal ganglion cells and in the inner nuclear and photoreceptor cell layers. Such changes were most evident in the group receiving HCQ intraperitoneally in doses of 100 mg/kg for a longer period (4 months). Conclusions: The present study highlights histopathological and ultrastructural retinal changes induced by chronic HCQ administration, which were strongly connected to the dosage and period of exposure.

CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models.

The purpose of this study was to investigate the protective effect of CD38 deletion on retinal ganglion cells (RGCs) in a mouse retinal ischemia/reperfusion (I/R) model and an optic nerve crush (ONC) model, and to elucidate the underlying molecular mechanisms. Retinal I/R and ONC models were constructed in mice. PCR was used to identify the deletion of CD38 gene in mice, hematoxylin and eosin (H&E) staining was used to evaluate the changes in retinal morphology, and electroretinogram (ERG) was used to evaluate the changes in retinal function. The survival of RGCs and activation of retinal macroglia were evaluated by immunofluorescence staining. The expression of Sirt1, CD38, Ac-p65, Ac-p53, TNF-α, IL-1β, and Caspase3 proteins in the retina was further evaluated by protein imprinting. In retinal I/R and ONC models, CD38 deficiency reduced the loss of RGCs and activation of macroglia and protected the retinal function. CD38 deficiency increased the concentration of NAD+, reduced the degree of acetylation of NF-κB p65 and p53, and reduced expression of the downstream inflammatory cytokines TNFα, IL-1β, and apoptotic protein Caspase3 in the retina in the ONC model. Intraperitoneal injection of the Sirt1 inhibitor EX-527 partially counteracted the effects of CD38 deficiency, suggesting that CD38 deficiency acts at least in part through the NAD+/Sirt1 pathway. CD38 plays an important role in the pathogenesis of retinal I/R and ONC injury. CD38 deletion protects RGCs by attenuating inflammatory responses and apoptosis through the NAD+/Sirt1 pathway.

Erratum in: Pentosan Polysulfate Sodium Causes Diminished Function and Subtle Morphological Changes in Retina and RPE of Mice.

Erratum in: Pentosan Polysulfate Sodium Causes Diminished Function and Subtle Morphological Changes in Retina and RPE of Mice.

Three-Year Follow-Up Study Investigating Changes in Retinal Vascular Morphology and the Relationship with Diabetic Retinopathy in Children with Type 1 Diabetes Mellitus.

This study aimed to investigate changes in retinal microvascular morphology and associated factors, and their relationship with diabetic retinopathy (DR) in children with type 1 diabetes mellitus (T1DM). Thirty-eight children enrolled in this 3-year follow-up study underwent complete ophthalmic examinations including fundus photography. Retinal vascular parameters were measured automatically and compared between baseline and follow-up. Multiple linear regression was used to investigate factors affecting changes in vascular parameters. Binary logistic regression was used to analyze the relationship between retinal microvascular morphology and DR. The caliber of all retinal vessels (within 1-1.5 papillary diameter [PD] from the center of the optic disc, p = 0.030; 1.5-2 PD, p = 0.003), arterioles, and venules (1.5-2 PD, p = 0.001) was narrower in nearly all regions in the follow-up group compared with the baseline group. Vascular tortuosity increased in the central part of the retina and decreased in the periphery. The density (1-1.5 PD, p = 0.030) and fractal dimension (p = 0.037) of retinal vessels were increased at the end of the follow-up compared with baseline. Retinal vascular caliber was independently correlated with DR (odds ratio 0.793 [95% confidence interval 0.633-0.993]; p = 0.044). Retinal microvascular morphology in children with T1DM varied with the disease course. Narrower retinal vessels may be an independent risk factor for DR. Results of this study emphasized the importance of regular follow-up of fundus vascular morphology for the detection of early DR in children with T1DM.

One year monitoring of retinal morphologic and functional changes in traumatic optic neuropathy patients

BackgroundTo analyze the morphologic and functional change in traumatic optic neuropathy (TON) divided by the mechanism of optic nerve injury.MethodsA retrospective analysis of 58 patients who were diagnosed as monocular TON from February 2015 to August 2021 was conducted at in CHA Bundang Medical Center in Seongnam, South Korea. The patients visited the clinic of the department of ophthalmology for more than 6 months and at least 4 times during this period.Results44 patients were classified as blunt TON patients, and 14 patients were surgical TON patients. The visual acuity showed significant decrease in traumatic eyes at the first visit after injury compared to fellow eyes and maintained the injured status during the 1-year follow-up period in blunt TON. In surgical TON, the visual acuity slightly improved during 1 month follow-up period. RNFL thickness tended to be decreased at 1 month after first visit blunt TON patients, which was earlier than surgical TON patients. GCIPL thickness showed earlier decreased than RNFL thickness in both blunt and surgical TON patients.ConclusionsIn both blunt and surgical TON eyes, there was a notable thinning in both RNFL and GCIPL, with particularly remarkable reduction in GCIPL in early phase. Therefore, analyzing each retinal layer thickness using OCT in conjunction with assessing visual function would be necessary. This combined approach is not only crucial for understanding clinical courses of each TON, but also predicting the morphological and functional deteriorations in TON.

A retinal vessel segmentation network with multiple-dimension attention and adaptive feature fusion

The incidence of blinding eye diseases is highly correlated with changes in retinal morphology, and is clinically detected by segmenting retinal structures in fundus images. However, some existing methods have limitations in accurately segmenting thin vessels. In recent years, deep learning has made a splash in the medical image segmentation, but the lack of edge information representation due to repetitive convolution and pooling, limits the final segmentation accuracy. To this end, this paper proposes a pixel-level retinal vessel segmentation network with multiple-dimension attention and adaptive feature fusion. Here, a multiple dimension attention enhancement (MDAE) block is proposed to acquire more local edge information. Meanwhile, a deep guidance fusion (DGF) block and a cross-pooling semantic enhancement (CPSE) block are proposed simultaneously to acquire more global contexts. Further, the predictions of different decoding stages are learned and aggregated by an adaptive weight learner (AWL) unit to obtain the best weights for effective feature fusion. The experimental results on three public fundus image datasets show that proposed network could effectively enhance the segmentation performance on retinal blood vessels. In particular, the proposed method achieves AUC of 98.30%, 98.75%, and 98.71% on the DRIVE, CHASE_DB1, and STARE datasets, respectively, while the F1 score on all three datasets exceeded 83%. The source code of the proposed model is available at https://github.com/gegao310/VesselSeg-Pytorch-master.

Effects of hemoglobin concentration on retinochoroidal vascular plexuses: an optical coherence tomography angiography study.

To evaluate retinal and choroidal microvascular structures using optical coherence tomography angiography (OCTA) in patients with anemia and polycythemia vera (PV). In this prospective study, 142 patients (142 eyes) were enrolled and divided into 3 groups: the anemia (n = 56), PV (n = 46), and healthy groups (n = 40, controls). For each patient, 6- × 6-mm macular angiography images were taken using an OCTA system (optovue, Inc., Fremont). For each eye analyzed, the software automatically measured vessel density (VD) in the superficial capillary plexus (SCP), deep capillary plexus (DCP; superior, nasal, temporal, and inferior quadrants), choriocapillaris (CC), and foveal avascular zone (FAZ). The OCTA analysis revealed that the VD of the DCP was significantly decreased in the superior and inferior hemispheres of the whole area, multiple quadrants of the perifovea, and CC with a 1-mm2 flow area in the anemia group compared with the PV group (p < 0.017), but the VD of the SCP did not show any significant difference in any quadrant between the two groups (p > 0.017). When compared with the healthy group, the anemia and PV groups showed a significant difference in multiple quadrants of the parafovea and temporal quadrant of the perifovea in the VD of the SCP and CC with a 2-mm2 flow area (p < 0.017). The FAZ and non-flow area did not manifest any significant difference between the groups (p > 0.017). The hemoglobin concentrations in the anemia, PV, and healthy groups were 8.11 ± 1.33, 17.5 ± 1.2, and 15.6 ± 0.73g/dL, respectively, indicating statistically significant differences between the groups (p < 0.001). In this study, quantitative OCTA analysis revealed a higher tendency for retinal and choroidal microvascular morphological changes in patients with anemia and PV. The outcomes of the current investigation can provide new insights into the retinal and choroidal pathophysiologies found in patients with hemoglobin abnormalities.

Study on the mechanism of 20-hydroxyeicosatetraenoic acid in retinal ischemia-reperfusion injury.

To explore the effect of 20-hydroxyeicosatetraenoic acid (20-HETE) on retinal ischemia-reperfusion injury (RIRI) and the protective effect of N-hydroxy-N'-(4-n-butyl-2-methylphenyl)formamidine (HET0016) on RIRI. Male Sprague-Dawley rats were randomly divided into the normal control group, experimental model group (RIRI group), experimental solvent group (RIRI + solvent group), and experimental treatment group (RIRI + HET0016 group). The levels of 20-HETE, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in the retina of rats at 24 h after reperfusion were measured by enzyme-linked immunosorbent assay. Hematoxylin-eosin staining was used to observe the retinal morphological and thickness changes at 24 h, 48 h, and 7 days after reperfusion. The number and localized expression of matrix metalloproteinase-9-positive cells in the retina of the rats at 24 h after reperfusion and the activation and localized expression of retinal microglia at 48 h after reperfusion were measured using an immunohistochemical method. The nuclear metastasis of nuclear factor kappa-B (NF-κB, p65) cells at 24 h after reperfusion was observed using an immunofluorescence method. Overall, 20-HETE might activate microglia to aggravate RIRI by the NF-κB pathway, but HET0016 has significant protective effects for the retina.

Pentosan Polysulfate Sodium Causes Diminished Function and Subtle Morphological Changes in Retina and RPE of Mice.

There are numerous reports of a distinctive maculopathy in adults exposed to pentosan polysulfate sodium (PPS), a drug prescribed to treat bladder discomfort associated with interstitial cystitis. We tested whether PPS treatment of mice injures RPE or retina to provide insight into the etiology of the human condition. Mice were fed PPS-supplemented chow over 14 months. RPE and retinal function was assessed by electroretinography (ERG) regularly. Following euthanasia, one eye was used for sagittal sectioning and histology, the contralateral for RPE flatmounting. ZO-1 positive RPE cell borders were imaged using confocal microscopy and cell morphology was analyzed using CellProfiler. After 10 months of PPS treatment, we observed diminution of mean scotopic c-wave amplitudes. By 11 months, we additionally observed diminutions of mean scotopic a- and b-wave amplitudes. Analysis of flatmounts revealed altered RPE cell morphology and morphometrics in PPS-treated mice, including increased mean en face cell area and geometric eccentricity, decreased RPE cell solidity and extent, and cytosolic translocation of alpha-catenin, all markers of RPE cell stress. Sex and regional differences were seen in RPE flatmount measures. Shortened photoreceptor outer segments were also observed. PPS treatment reduced RPE and later retina function as measured by ERG, consistent with a primary RPE injury. Post-mortem analysis revealed extensive RPE pleomorphism and polymegathism and modest photoreceptor changes. We conclude that PPS treatment of mice causes slowly progressing RPE and photoreceptor damage and thus may provide a useful model for some retinal pathologies.

Anterior Chamber and Retinal Morphological Changes During Accommodation in Different Age Ranges

Purpose Accommodation mainly affects the lens, a structure of the eyeball that degrades with age. The aim of this work was to study the morphological changes of different ocular structures during accommodation, both in the anterior pole and the posterior pole, which may also be involved in the accommodation process. Methods The study will be carried out by stimulating accommodation through lenses of -1.00, -3.00 and -5.00 D starting from the spherical equivalent (M) of each participant in different age groups, from 18 to 66 years. To obtain the M value, aberrometry was achieved, and retinal optical coherence tomography and anterior pole tomography were performed to evaluate the possible structural modifications (central and peripheral), while accommodation was progressively stimulated. Results It showed that as the accommodative demand increased, morphological changes were produced in retinal thickness, both in the central and peripheral retina, in all age groups. A thinning of the retina was observed in the central 3 mm, while significant progressive thickening was observed closer to the periphery (up to 6 mm from the fovea) as the required accommodative power increased. A decrease in the anterior chamber depth (ACD) and anterior chamber volume (ACV) was observed with increasing lens power. Conclusion Structural changes were observed in the central and peripheral retina, as well as in the ACD and ACV, while progressively greater accommodation was stimulated, showing that these structures were modified in the accommodation process even in advanced presbyopes.

Jednostronna jaskra wrodzona z wolooczem u dwóch sióstr – opis przypadków z długoterminową obserwacją

Primary congenital glaucoma is a rare condition but the most common form of glaucoma in infants. It occurs with variable frequency in different countries and ethnic groups. It is considered an autosomal recessively inherited disorder, but is known to occur as a result of de novo genetic mutations. It causes increased intraocular pressure on the background of congenital iridotrabeculodysgenesis and is a cause of severe optic neuropathy due to apoptotic degeneration of the retinal ganglion cell layer. We present the description of siblings with unilateral ipsilateral congenital glaucoma. Both sisters had corneal opacity and one had Haab’s striae at the time of diagnosis. Both patients underwent trabeculectomy by age one, less than 6 months after diagnosis. Results of regular follow-up examinations and long-term follow-up showed no changes in retinal morphology, no progression of the disease, and intraocular pressure stabilized over the long term.

Aniseikonia and retinal morphological changes in eyes undergoing macular hole surgery

Even after idiopathic macular hole (MH) surgery and with successful closure of MH, aniseikonia is a common postoperative symptom. We investigated the correlation of MH diameter, retinal displacement and retinal layer thicknesses with aniseikonia in 41 eyes of 41 patients undergoing MH surgery with internal limiting membrane peeling. Aniseikonia was measured with the New Aniseikonia Test. Retinal displacement (RD%) was defined as change of retinal distance between the temporal margin of the optic papilla and the intersection of the retinal vessels. Changes of thicknesses of the inner nuclear layer (INL%) and the outer retinal layer (OR%) were calculated. Aniseikonia improved postoperatively. Preoperative aniseikonia and their improvement at 6 months correlated with MH diameters (P = 0.004–0.046). Improvement of aniseikonia correlated with temporal RD% (P = 0.002–0.012). Improvement of vertical aniseikonia correlated with INL% at 2 weeks and with the nasal OR% at 1, 3, and 6 months (P = < 0.001–0.028). MH diameter and age were significant predictors for improvement of aniseikonia. The greater the temporal retina displacement, and the thinner the postoperative INL and OR, the greater the improvement of aniseikonia. MH diameter and age are strong predictors for improvement of aniseikonia after MH surgery.

Retrospective analysis of the progression of early dry age-related macular degeneration in patients receiving versus not receiving a multi-component nutraceutical for four years

Purpose: To retrospectively analyze the optical coherence tomography (OCT) changes in retinal morphology and progression in these changes in patients with early dry age-related macular degeneration (AMD) receiving versus not receiving a multi-component nutraceutical daily for four years. Material and Methods: We retrospectively analyzed disease progression in 52 patients (98 eyes) with early dry AMD who had been regularly followed up for four years. Group 1 was comprised of 24 patients (98 eyes) who had been receiving vitamin and mineral tablets containing the AREDS2 formulation plus resveratrol and vitamin D daily for four years. Group 2 was comprised of 28 patients (53 eyes) who had not been receiving any nutritional supplement. Retinal morphology was assessed by OCT and OCT angiography. Results: In group 1, best-corrected visual acuity (BCVA) did not change after completion of the 4-year observation period compared to baseline (0.6 ± 02, p = 0.72). In group 2, BCVA was 0.6 ± 0.2 at baseline and decreased to 0.2 ± 0.2 in four years (p ≤ 0.001). In patients with a low to moderate risk of progression in groups 1 and 2, the four-year progression rate was 15.4% and 45.4%, respectively, which corresponds to an annual progression rate of 3.8% and 11.3%, respectively. In patients with a high risk of progression in groups 1 and 2, the four-year progression rate was 26.3% and 80%, respectively, which corresponds to an annual progression rate of 6.5% and 20%, respectively. Patients who had early dry AMD eyes with a low to moderate risk of progression (and a high risk of progression) at baseline and were not taking the nutritional supplement, had 4.58 greater odds (95% CI, 1.291 – 16.267; р = 0.018) [and 11.2 greater odds (95% CI, 2.505 – 50.081; р = 0.0016)] of having AMD progression than those receiving the nutritional supplement daily for four years. Conclusion: A regular intake of tablets containing the AREDS2 formulation plus resveratrol and vitamin D slows the progression of early dry AMD, especially in eyes with a high risk of disease progression, and contributes to the preservation of visual function.

Long-term tralopyril exposure results in endocrinological and transgenerational toxicity: A two-generation study of marine medaka (Oryzias melastigma)

This study aims to investigate the impact of tralopyril, a newly developed marine antifouling agent, on the reproductive endocrine system and developmental toxicity of offspring in marine medaka. The results revealed that exposure to tralopyril (0, 1, 20 μg/L) for 42 days resulted in decreased reproductive capacity in marine medaka. Moreover, it disrupted the levels of sex hormones E2 and T, as well as the transcription levels of genes related to the HPG axis, such as cyp19b and star. Sex-dependent differences were observed, with females experiencing more pronounced effects. Furthermore, intergenerational toxicity was observed in F1 offspring, including increased heart rate, changes in retinal morphology and cartilage structure, decreased swimming activity, and downregulation of transcription levels of relevant genes (HPT axis, GH/IGF axis, cox, bmp4, bmp2, runx2, etc.). Notably, the disruption of the F1 endocrine system by tralopyril persisted into adulthood, indicating a transgenerational effect. Molecular docking analysis suggested that tralopyril's RA receptor activity might be one of the key factors contributing to the developmental toxicity observed in offspring. Overall, our study highlights the potential threat posed by tralopyril to the sustainability of fish populations, as it can disrupt the endocrine system and negatively impact aquatic organisms for multiple generations.