Anterior-segment optical coherence tomography (AS-OCT) supports cataract surgery planning by revealing corneal and crystalline lens geometry, but clinical workflows require fast, user-independent delineation of key interfaces in noisy scans. We address this need with an end-to-end pipeline tailored to low signal to noise ratio (SNR), preclinical AS-OCT: a systematic architecture search selects a U-Net with an ImageNet-pretrained EfficientNet-B2 encoder; a residual-driven, mask-guided non-local means stage suppresses background clutter while preserving boundaries; and a mask-to-surface conversion fits robust third-order polynomials to produce biometry-ready corneal and lenticular interfaces. Trained on 440 B-scans of rabbit eyes from a custom system, the model achieves mean Intersection-over-Union (IoU) of 0.957 ± 0.007 (cornea) and 0.978 ± 0.007 (lens) across five validation splits, with boundary root-mean-squared-error (RMSE) of 4.03-6.91 μ m between the predicted and manual reference surfaces. On an operator/time/subject-independent test set (n = 80), performance remains high-IoU 0.939 ± 0.008 (cornea) and 0.961 ± 0.009 (lens)-and the method outperforms a classical graph-search baseline. Despite limited training data and challenging image quality, the approach delivers accurate, robust surfaces suitable for downstream biometry.
{"title":"Automatic deep learning-based segmentation of cornea and lens in 2D OCT images of rabbit eyes.","authors":"Wannes De Martelaere, Haijun Lv, Hanrui Li, Xiuli Liu, Tingwei Quan, Shaoqun Zeng, Shangbin Chen, Xiaohua Lv","doi":"10.1016/j.exer.2026.110965","DOIUrl":"10.1016/j.exer.2026.110965","url":null,"abstract":"<p><p>Anterior-segment optical coherence tomography (AS-OCT) supports cataract surgery planning by revealing corneal and crystalline lens geometry, but clinical workflows require fast, user-independent delineation of key interfaces in noisy scans. We address this need with an end-to-end pipeline tailored to low signal to noise ratio (SNR), preclinical AS-OCT: a systematic architecture search selects a U-Net with an ImageNet-pretrained EfficientNet-B2 encoder; a residual-driven, mask-guided non-local means stage suppresses background clutter while preserving boundaries; and a mask-to-surface conversion fits robust third-order polynomials to produce biometry-ready corneal and lenticular interfaces. Trained on 440 B-scans of rabbit eyes from a custom system, the model achieves mean Intersection-over-Union (IoU) of 0.957 ± 0.007 (cornea) and 0.978 ± 0.007 (lens) across five validation splits, with boundary root-mean-squared-error (RMSE) of 4.03-6.91 μ m between the predicted and manual reference surfaces. On an operator/time/subject-independent test set (n = 80), performance remains high-IoU 0.939 ± 0.008 (cornea) and 0.961 ± 0.009 (lens)-and the method outperforms a classical graph-search baseline. Despite limited training data and challenging image quality, the approach delivers accurate, robust surfaces suitable for downstream biometry.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110965"},"PeriodicalIF":2.7,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Accurate quantification of axon density is pivotal in optic nerve-related studies, as axonal degeneration is a hallmark of numerous neurological disorders. This study introduces the Point Positioning and Counting Network (PPCNet), a novel point-annotation-based deep learning framework that overcomes the limitations of manual counting and existing automated tools. PPCNet integrates a VGG16 backbone with multiscale feature extraction and lateral fusion to generate high-resolution feature maps. A dual-branch architecture regresses spatial coordinates and classifies candidate points, enabling axonal-center localization and confidence scoring. An optimized Hungarian algorithm, incorporating Euclidean distance and confidence metrics, ensures one-to-one correspondence between predicted candidates and ground-truth points. The model is trained end-to-end using a hybrid loss combining mean squared error and cross-entropy. Evaluated on a goat optic nerve semi-thin section dataset, PPCNet significantly outperformed current state-of-the-art methods (Axonet 2.0 and AxonDeepSeg). In the test set, mean ± SD axon counts were 901.6 ± 225.6 for manual counting, 890.2 ± 227.3 for PPCNet, 918.8 ± 297.9 for Axonet2.0, and 1045 ± 275 for AxonDeepSeg. Linear regression analysis demonstrated superior agreement with manual counts (R2 = 0.939), surpassing Axonet 2.0 (R2 = 0.8612) and AxonDeepSeg (R2 = 0.9142). PPCNet also yielded a lower mean absolute error (MAE = 45.93) than those of the comparative models (97.50 and 146.33). Bland-Altman analysis confirmed narrower limits of agreement (-99.23 to 121.90) and reduced systematic bias. Confidence-interval analysis further supported PPCNet's reliability, showing substantial overlap with manual counts. In conclusion, PPCNet delivers sub-pixel-accurate automated axon quantification for optic nerve research, replacing tedious manual counting and traditional segmentation-based methods.
{"title":"Point positioning and counting network: A deep learning-based method for automatic axon counting.","authors":"Caiye Fan, Shurui Huang, Tinghui Huang, Rui Yao, Xudong Wang, Zuoping Tan, Yikui Zhang, Yuanyuan Wang","doi":"10.1016/j.exer.2026.110968","DOIUrl":"10.1016/j.exer.2026.110968","url":null,"abstract":"<p><p>Accurate quantification of axon density is pivotal in optic nerve-related studies, as axonal degeneration is a hallmark of numerous neurological disorders. This study introduces the Point Positioning and Counting Network (PPCNet), a novel point-annotation-based deep learning framework that overcomes the limitations of manual counting and existing automated tools. PPCNet integrates a VGG16 backbone with multiscale feature extraction and lateral fusion to generate high-resolution feature maps. A dual-branch architecture regresses spatial coordinates and classifies candidate points, enabling axonal-center localization and confidence scoring. An optimized Hungarian algorithm, incorporating Euclidean distance and confidence metrics, ensures one-to-one correspondence between predicted candidates and ground-truth points. The model is trained end-to-end using a hybrid loss combining mean squared error and cross-entropy. Evaluated on a goat optic nerve semi-thin section dataset, PPCNet significantly outperformed current state-of-the-art methods (Axonet 2.0 and AxonDeepSeg). In the test set, mean ± SD axon counts were 901.6 ± 225.6 for manual counting, 890.2 ± 227.3 for PPCNet, 918.8 ± 297.9 for Axonet2.0, and 1045 ± 275 for AxonDeepSeg. Linear regression analysis demonstrated superior agreement with manual counts (R<sup>2</sup> = 0.939), surpassing Axonet 2.0 (R<sup>2</sup> = 0.8612) and AxonDeepSeg (R<sup>2</sup> = 0.9142). PPCNet also yielded a lower mean absolute error (MAE = 45.93) than those of the comparative models (97.50 and 146.33). Bland-Altman analysis confirmed narrower limits of agreement (-99.23 to 121.90) and reduced systematic bias. Confidence-interval analysis further supported PPCNet's reliability, showing substantial overlap with manual counts. In conclusion, PPCNet delivers sub-pixel-accurate automated axon quantification for optic nerve research, replacing tedious manual counting and traditional segmentation-based methods.</p>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":" ","pages":"110968"},"PeriodicalIF":2.7,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-06DOI: 10.1016/j.exer.2026.110854
Yifei Zheng , Yequn Chen , Xuejun Gu , Mingzhe Wang , Chaozhong Zhang , Han Xu , Yang Zhou , Lihua Fang
This study was designed to measure rotational stability of four TIOLs with differences in haptic design in the capsular bag to provide insights for increasing postoperative rotational stability.Four different shapes of the TIOL models were reconstructed from real measurements and evaluated for their rotational stability in capsular bags of different diameters in vitro under simulated compression testing, as well as post-implantation analysis of rotation and stress. The TIOLs were compressed to a 10 mm diameter and assessed for bio-mechanical stability. There were significant differences in compressive force and axial displacement between models. Model D showed convex deformation of the optical surface when compressed to 10.5 mm, resulting in large variations in some internal parameters. When implanted into a 10.75 mm capsular bag, the rotational angles of different TIOLs ranged from 4.97° to 17.23°. Model C exhibited rotational angles between 3.06° and 9.93° in capsular bags of varying diameters. Model C showed higher stress at the optic-haptic junction, whereas Models A and D exhibited lower stress levels. Model A exhibited the lowest equatorial stress across capsular bags of different diameters.The rotational stability of TIOLs is significantly influenced by haptic design, with notable biomechanical differences among the models. This study provides valuable insights for optimizing TIOL designs to enhance postoperative rotational stability.
{"title":"Evaluating the rotational stability of toric intraocular lenses with different haptic designs using finite element analysis","authors":"Yifei Zheng , Yequn Chen , Xuejun Gu , Mingzhe Wang , Chaozhong Zhang , Han Xu , Yang Zhou , Lihua Fang","doi":"10.1016/j.exer.2026.110854","DOIUrl":"10.1016/j.exer.2026.110854","url":null,"abstract":"<div><div>This study was designed to measure rotational stability of four TIOLs with differences in haptic design in the capsular bag to provide insights for increasing postoperative rotational stability.Four different shapes of the TIOL models were reconstructed from real measurements and evaluated for their rotational stability in capsular bags of different diameters in vitro under simulated compression testing, as well as post-implantation analysis of rotation and stress. The TIOLs were compressed to a 10 mm diameter and assessed for bio-mechanical stability. There were significant differences in compressive force and axial displacement between models. Model D showed convex deformation of the optical surface when compressed to 10.5 mm, resulting in large variations in some internal parameters. When implanted into a 10.75 mm capsular bag, the rotational angles of different TIOLs ranged from 4.97° to 17.23°. Model C exhibited rotational angles between 3.06° and 9.93° in capsular bags of varying diameters. Model C showed higher stress at the optic-haptic junction, whereas Models A and D exhibited lower stress levels. Model A exhibited the lowest equatorial stress across capsular bags of different diameters.The rotational stability of TIOLs is significantly influenced by haptic design, with notable biomechanical differences among the models. This study provides valuable insights for optimizing TIOL designs to enhance postoperative rotational stability.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110854"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145922264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-24DOI: 10.1016/j.exer.2025.110827
Mengnan Wu, Mansha He, Yaolei Du
Keratoconus is a dilated corneal disorder caused by multiple factors, which is characterized by progressive thinning and protrusion of the paracentral cornea. It may be influenced both by genetic and environmental factors. Clinically, it manifests as significant irregular astigmatism in the affected eye, which can result in irreversible vision impairment that is challenging to correct with standard spectacles. Nevertheless, the specific hypoxia-related genes implicated in keratoconus, along with their diagnostic significance, remain inadequately explored. This research intend to explore the involvement of hypoxia-related differentially expressed genes in the pathogenesis of keratoconus, aiming to explore new diagnostic methods and therapeutic strategies. By employing bioinformatics methodologies, we analyzed RNA sequencing and microarray data from the GEO database to pinpoint differentially expressed genes associated with hypoxic conditions in keratoconus. Our analysis identified 490 differentially expressed genes, encompassing 62 genes that were upregulated and 428 that were downregulated, indicating their probable role in the advancement of keratoconus. Gene Ontology and pathway enrichment analyses showed that 43 HRDEGs were significantly enriched in various biological processes, underscoring the pivotal influence of hypoxia in the pathophysiology of keratoconus. Additionally, a support vector machine model highlighted nine hypoxia-related differentially expressed genes, while least absolute shrinkage and selection operator regression identified five genes suitable for modeling, culminating in two diagnostic models exhibiting high accuracy (AUC >0.9) for the early detection of keratoconus. Furthermore, the immune cell infiltration analysis revealed a positive association between DUSP1 and follicular helper T cells, as well as a negative association with resting mast cells, indicating an immune-related aspect in the progression of keratoconus. The results of our study lay the groundwork for subsequent investigations into the molecular pathways involved in keratoconus, as well as the creation of specialized diagnostic instruments.
{"title":"Role of hypoxia-related differentially expressed genes in pathogenesis of keratoconus and construction of diagnostic models","authors":"Mengnan Wu, Mansha He, Yaolei Du","doi":"10.1016/j.exer.2025.110827","DOIUrl":"10.1016/j.exer.2025.110827","url":null,"abstract":"<div><div>Keratoconus is a dilated corneal disorder caused by multiple factors, which is characterized by progressive thinning and protrusion of the paracentral cornea. It may be influenced both by genetic and environmental factors. Clinically, it manifests as significant irregular astigmatism in the affected eye, which can result in irreversible vision impairment that is challenging to correct with standard spectacles. Nevertheless, the specific hypoxia-related genes implicated in keratoconus, along with their diagnostic significance, remain inadequately explored. This research intend to explore the involvement of hypoxia-related differentially expressed genes in the pathogenesis of keratoconus, aiming to explore new diagnostic methods and therapeutic strategies. By employing bioinformatics methodologies, we analyzed RNA sequencing and microarray data from the GEO database to pinpoint differentially expressed genes associated with hypoxic conditions in keratoconus. Our analysis identified 490 differentially expressed genes, encompassing 62 genes that were upregulated and 428 that were downregulated, indicating their probable role in the advancement of keratoconus. Gene Ontology and pathway enrichment analyses showed that 43 HRDEGs were significantly enriched in various biological processes, underscoring the pivotal influence of hypoxia in the pathophysiology of keratoconus. Additionally, a support vector machine model highlighted nine hypoxia-related differentially expressed genes, while least absolute shrinkage and selection operator regression identified five genes suitable for modeling, culminating in two diagnostic models exhibiting high accuracy (AUC >0.9) for the early detection of keratoconus. Furthermore, the immune cell infiltration analysis revealed a positive association between <em>DUSP1</em> and follicular helper T cells, as well as a negative association with resting mast cells, indicating an immune-related aspect in the progression of keratoconus. The results of our study lay the groundwork for subsequent investigations into the molecular pathways involved in keratoconus, as well as the creation of specialized diagnostic instruments.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110827"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Excess consumption of added sugars, commonly delivered through sucrose and high-fructose corn syrup, has increased in parallel with obesity, metabolic syndrome, and type 2 diabetes. These systemic metabolic disturbances are consistently associated with a range of ocular conditions. However, whether high-fructose intake exerts independent and fructose-specific effects on ocular tissues remains uncertain, because most human evidence is indirect, often mediated through metabolic syndrome phenotypes, and frequently confounded by mixed dietary exposures and total energy intake. This review synthesizes mechanistic pathways that are plausibly enriched by fructose biology, including hepatic fructose metabolism with ATP depletion and uric acid generation, oxidative and inflammatory signaling, altered lipid handling, and gut barrier and microbiome perturbations. We evaluate how these systemic changes may intersect with ocular surface homeostasis, retinal neurovascular integrity, intraocular pressure regulation, and choroidal and macular vulnerability. Across dry eye disease, diabetic retinopathy, glaucoma-related outcomes, age-related macular degeneration and choroidal neovascular responses, and cataract, we distinguish fructose-specific exposure studies from metabolic syndrome only and mixed diet reports, and we emphasize limitations related to exposure definition, replication, and translation to humans. Overall, current evidence supports the view that excess fructose may amplify ocular susceptibility in metabolically stressed states, but direct causal links in humans remain preliminary. We conclude by outlining methodological priorities and testable study designs needed to clarify fructose-specific contributions to ocular disease risk. Some experimental findings, particularly those related to ocular-surface responses, originate from single research groups and require independent replication, underscoring that current evidence remains preliminary and hypothesis-generating.
{"title":"Sweet poison for the eyes: High-Fructose diets as drivers of metabolic disruption and ocular diseases - Insights and therapeutic horizons","authors":"Chen Chen , Chuyao Wang , Hongyu Li, Ting Wang, Xinwei Jiao","doi":"10.1016/j.exer.2026.110852","DOIUrl":"10.1016/j.exer.2026.110852","url":null,"abstract":"<div><div>Excess consumption of added sugars, commonly delivered through sucrose and high-fructose corn syrup, has increased in parallel with obesity, metabolic syndrome, and type 2 diabetes. These systemic metabolic disturbances are consistently associated with a range of ocular conditions. However, whether high-fructose intake exerts independent and fructose-specific effects on ocular tissues remains uncertain, because most human evidence is indirect, often mediated through metabolic syndrome phenotypes, and frequently confounded by mixed dietary exposures and total energy intake. This review synthesizes mechanistic pathways that are plausibly enriched by fructose biology, including hepatic fructose metabolism with ATP depletion and uric acid generation, oxidative and inflammatory signaling, altered lipid handling, and gut barrier and microbiome perturbations. We evaluate how these systemic changes may intersect with ocular surface homeostasis, retinal neurovascular integrity, intraocular pressure regulation, and choroidal and macular vulnerability. Across dry eye disease, diabetic retinopathy, glaucoma-related outcomes, age-related macular degeneration and choroidal neovascular responses, and cataract, we distinguish fructose-specific exposure studies from metabolic syndrome only and mixed diet reports, and we emphasize limitations related to exposure definition, replication, and translation to humans. Overall, current evidence supports the view that excess fructose may amplify ocular susceptibility in metabolically stressed states, but direct causal links in humans remain preliminary. We conclude by outlining methodological priorities and testable study designs needed to clarify fructose-specific contributions to ocular disease risk. Some experimental findings, particularly those related to ocular-surface responses, originate from single research groups and require independent replication, underscoring that current evidence remains preliminary and hypothesis-generating.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110852"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-08DOI: 10.1016/j.exer.2026.110856
Zhili Cui , Jun Kang
{"title":"Comment on “Precise biometric measurement of the mouse eye using optical coherence tomography based on optic-nerve-head imaging”","authors":"Zhili Cui , Jun Kang","doi":"10.1016/j.exer.2026.110856","DOIUrl":"10.1016/j.exer.2026.110856","url":null,"abstract":"","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110856"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-12DOI: 10.1016/j.exer.2026.110859
Suharsha Paidimarri, Nimesh B. Patel, Krista M. Beach, Jacinth J. Priscilla, Raman P. Sah, Manoj K. Manoharan, Rakesh Maldoddi, Lisa A. Ostrin
Purpose
To evaluate ocular rigidity in experimentally induced myopic eyes compared to contralateral control eyes in young rhesus monkeys.
Methods
Eight rhesus monkeys (Macaca mulatta) were reared with monocular form-deprivation from 24 days to 150 days of age. Refraction, axial length, and intraocular pressure (IOP) were measured biweekly. After 150 days, ocular rigidity was assessed in both eyes via anterior chamber cannulation, in which controlled changes in anterior chamber volume were used to calculate the coefficient of ocular rigidity using Friedenwald's equation. Paired t-tests were used to compare form-deprived and control eyes, and Pearson's correlations were used to examine relationships between ocular rigidity, refraction, and axial length.
Results
After 150 days, form-deprived eyes were significantly less hyperopic (+0.41 ± 3.89 D vs. +3.10 ± 3.01 D, P = 0.03) and had longer axial lengths (16.54 ± 0.81 mm vs. 15.90 ± 0.76 mm, P = 0.01) than control eyes. Mean ocular rigidity coefficients were not significantly different between form-deprived and control eyes (0.054 ± 0.008 vs. 0.050 ± 0.010 μL−1 P = 0.06).
Discussion
Form-deprivation myopia in young rhesus monkeys produced significant axial elongation and myopic shifts but did not significantly alter the coefficient of ocular rigidity. Although ocular rigidity showed a decreasing trend with increasing eye size, the limited range of axial lengths may have constrained statistical power to detect a small-to-moderate difference in the ocular rigidity coefficients between treated and control eyes. This work establishes direct in vivo assessment of ocular rigidity in a primate model, laying the groundwork for future approaches to examine ocular biomechanics in myopia.
目的评价实验性近视眼与对侧对照眼的眼强直。方法选取猕猴8只，在24 ~ 150日龄进行单眼形态剥夺饲养。每两周测量一次屈光、眼轴长度和眼内压。150天后，通过前房插管评估双眼眼僵硬度，其中前房容积的控制变化利用Friedenwald方程计算眼僵硬系数。配对t检验用于比较失形眼和对照眼，Pearson相关性用于检验眼强直、屈光度和眼轴长度之间的关系。结果150 D后，失形眼的远视程度显著低于对照组（+0.41±3.89 D vs +3.10±3.01 D, P = 0.03），眼轴长度显著高于对照组（16.54±0.81 mm vs 15.90±0.76 mm, P = 0.01）。失形眼和对照眼的平均眼刚度系数无显著差异（0.054±0.008 vs. 0.050±0.010 μL−1 P = 0.06）。年幼恒河猴形体剥夺性近视产生显著的眼轴伸长和近视眼移位，但对眼强直系数无显著影响。虽然眼硬度随眼睛尺寸的增大而下降，但轴向长度的有限范围可能限制了检测治疗眼和对照眼之间眼硬度系数的小到中等差异的统计能力。本研究在灵长类动物模型中建立了眼刚性的直接体内评估，为未来研究近视的眼生物力学奠定了基础。
{"title":"Ocular rigidity in eyes with experimental myopia","authors":"Suharsha Paidimarri, Nimesh B. Patel, Krista M. Beach, Jacinth J. Priscilla, Raman P. Sah, Manoj K. Manoharan, Rakesh Maldoddi, Lisa A. Ostrin","doi":"10.1016/j.exer.2026.110859","DOIUrl":"10.1016/j.exer.2026.110859","url":null,"abstract":"<div><h3>Purpose</h3><div>To evaluate ocular rigidity in experimentally induced myopic eyes compared to contralateral control eyes in young rhesus monkeys.</div></div><div><h3>Methods</h3><div>Eight rhesus monkeys (<em>Macaca mulatta</em>) were reared with monocular form-deprivation from 24 days to 150 days of age. Refraction, axial length, and intraocular pressure (IOP) were measured biweekly. After 150 days, ocular rigidity was assessed in both eyes via anterior chamber cannulation, in which controlled changes in anterior chamber volume were used to calculate the coefficient of ocular rigidity using Friedenwald's equation. Paired t-tests were used to compare form-deprived and control eyes, and Pearson's correlations were used to examine relationships between ocular rigidity, refraction, and axial length.</div></div><div><h3>Results</h3><div>After 150 days, form-deprived eyes were significantly less hyperopic (+0.41 ± 3.89 D vs. +3.10 ± 3.01 D, P = 0.03) and had longer axial lengths (16.54 ± 0.81 mm vs. 15.90 ± 0.76 mm, P = 0.01) than control eyes. Mean ocular rigidity coefficients were not significantly different between form-deprived and control eyes (0.054 ± 0.008 vs. 0.050 ± 0.010 μL<sup>−1</sup> P = 0.06).</div></div><div><h3>Discussion</h3><div>Form-deprivation myopia in young rhesus monkeys produced significant axial elongation and myopic shifts but did not significantly alter the coefficient of ocular rigidity. Although ocular rigidity showed a decreasing trend with increasing eye size, the limited range of axial lengths may have constrained statistical power to detect a small-to-moderate difference in the ocular rigidity coefficients between treated and control eyes. This work establishes direct <em>in vivo</em> assessment of ocular rigidity in a primate model, laying the groundwork for future approaches to examine ocular biomechanics in myopia.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110859"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-22DOI: 10.1016/j.exer.2025.110825
Yining Shen , Jinfang Huang , Leilei Zou , Yuanyang Huang , Rui Duan , Huiling Shen , Hong Liu
The increasing prevalence of myopia is a pressing public health concern. Robust experimental models are needed to investigate its mechanisms and evaluate potential interventions. Mouse models are particularly advantageous due to their concise and well-characterized genetic background, which facilitates genetic manipulation. However, the small head and eye size, combined with high activity levels of mice, present substantial challenges for the stable establishment of myopia models. The lens-induced myopia (LIM) model, closely resembling the natural progression of human myopia, offers significant research value. Here, we present an improved and reproducible mouse LIM model incorporating a 3D-printed head-mounted spectacle frame and custom-designed high-strength, wear-resistant resin lenses. The device was securely affixed to the skull using dental resin and tissue adhesive, ensuring long-term stability while minimizing interference with feeding and grooming behavior. Four-week induction with −25 diopter lenses in four-week-old C57BL/6J mice resulted in a mean myopic shift of 5.19 D and axial elongation of 110 μm. Electroretinography confirmed preserved retinal function, and the lens detachment rate remained below 15 %. No significant differences in general health status were observed between LIM and control groups. This optimized LIM model provides a reliable, well-tolerated platform for experimental myopia studies and is well-suited for mechanistic and interventional research in mice.
{"title":"An improved and more stable mouse model of lens-induced myopia","authors":"Yining Shen , Jinfang Huang , Leilei Zou , Yuanyang Huang , Rui Duan , Huiling Shen , Hong Liu","doi":"10.1016/j.exer.2025.110825","DOIUrl":"10.1016/j.exer.2025.110825","url":null,"abstract":"<div><div>The increasing prevalence of myopia is a pressing public health concern. Robust experimental models are needed to investigate its mechanisms and evaluate potential interventions. Mouse models are particularly advantageous due to their concise and well-characterized genetic background, which facilitates genetic manipulation. However, the small head and eye size, combined with high activity levels of mice, present substantial challenges for the stable establishment of myopia models. The lens-induced myopia (LIM) model, closely resembling the natural progression of human myopia, offers significant research value. Here, we present an improved and reproducible mouse LIM model incorporating a 3D-printed head-mounted spectacle frame and custom-designed high-strength, wear-resistant resin lenses. The device was securely affixed to the skull using dental resin and tissue adhesive, ensuring long-term stability while minimizing interference with feeding and grooming behavior. Four-week induction with −25 diopter lenses in four-week-old C57BL/6J mice resulted in a mean myopic shift of 5.19 D and axial elongation of 110 μm. Electroretinography confirmed preserved retinal function, and the lens detachment rate remained below 15 %. No significant differences in general health status were observed between LIM and control groups. This optimized LIM model provides a reliable, well-tolerated platform for experimental myopia studies and is well-suited for mechanistic and interventional research in mice.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110825"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-05DOI: 10.1016/j.exer.2026.110851
Yakun Wang , Xianyang Liu , Shuhao Zeng , Wenxian Yang , Fan Cao , Shengping Hou
Post-translational modifications (PTMs) encompass the spectrum of chemical covalent alterations that proteins undergo after being synthesized from mRNA. These modifications typically involve the covalent bonding of chemical groups or small protein molecules to the amino acid backbones or side chains. Currently, over 650 types of PTMs have been identified, including significant ones such as phosphorylation, ubiquitination, SUMOylation, methylation, acetylation, glycosylation, among other novel varieties like lactylation. However, a systematic review of PTMs associated with immune-mediated ocular diseases remains conspicuously absent in current literature. To fully understand the role of PTM in immune eye diseases, this review systematically introduces the regulatory mechanisms and functions of several important PTMs. Furthermore, this review also encapsulates the mechanisms of PTMs in several pivotal immune-related ocular conditions, specifically uveitis, age-related macular degeneration (AMD), dry eye disease (DED), and diabetic retinopathy (DR). By integrating current evidence, this work not only clarifies the pathogenic contributions of specific PTMs but also identifies their potential as therapeutic targets. Finally, we discuss future research directions and the challenges of translating PTM-based interventions into clinical practice for ocular immune disorders.
{"title":"The role and mechanism of post-translational modifications (PTMs) in immune-related eye diseases","authors":"Yakun Wang , Xianyang Liu , Shuhao Zeng , Wenxian Yang , Fan Cao , Shengping Hou","doi":"10.1016/j.exer.2026.110851","DOIUrl":"10.1016/j.exer.2026.110851","url":null,"abstract":"<div><div>Post-translational modifications (PTMs) encompass the spectrum of chemical covalent alterations that proteins undergo after being synthesized from mRNA. These modifications typically involve the covalent bonding of chemical groups or small protein molecules to the amino acid backbones or side chains. Currently, over 650 types of PTMs have been identified, including significant ones such as phosphorylation, ubiquitination, SUMOylation, methylation, acetylation, glycosylation, among other novel varieties like lactylation. However, a systematic review of PTMs associated with immune-mediated ocular diseases remains conspicuously absent in current literature. To fully understand the role of PTM in immune eye diseases, this review systematically introduces the regulatory mechanisms and functions of several important PTMs. Furthermore, this review also encapsulates the mechanisms of PTMs in several pivotal immune-related ocular conditions, specifically uveitis, age-related macular degeneration (AMD), dry eye disease (DED), and diabetic retinopathy (DR). By integrating current evidence, this work not only clarifies the pathogenic contributions of specific PTMs but also identifies their potential as therapeutic targets. Finally, we discuss future research directions and the challenges of translating PTM-based interventions into clinical practice for ocular immune disorders.</div></div>","PeriodicalId":12177,"journal":{"name":"Experimental eye research","volume":"264 ","pages":"Article 110851"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号