AIM: To investigate the relationship between choroidal thickness (CT) and primary open angle glaucoma (POAG) in highly myopic eyes across different categories of myopic atrophic maculopathy (MAM). METHODS: This observational analytical case–control study enrolled highly myopic patients. All participants underwent comprehensive ophthalmic examinations. CT was measured in peripapillary and macular regions using optical coherence tomography (OCT). Each eye was classified for POAG status and MAM category. Stepwise logistic regression was performed to identify factors independently associated with POAG. RESULTS: Among 248 highly myopic subjects, 37 (18 males, mean age 68.25±7.16y) had POAG (25 bilateral, 12 unilateral) and 211 (97 males, mean age 67.09±7.63y) were non-glaucomatous. Age and sex did not differ significantly between groups (both P>0.05). Seventy-eight patients had unilateral high myopia and 170 bilateral, yielding 418 highly myopic eyes, of which 58 (13.88%) had POAG. POAG prevalence across MAM categories (no lesion to complete macular atrophy) was 7.14%, 16.28%, 14.07%, 17.86%, and 17.14%, respectively (P=0.44). In the diffuse chorioretinal atrophy subgroup, POAG eyes showed significantly thicker CT in central, inner nasal, outer superior, inner superior, and inner inferior macular regions, and thinner central corneal thickness (all P<0.05). Stepwise logistic regression showed that only parafoveal inferior CT was independently associated with POAG in this subgroup (OR=1.017; 95%CI: 1.005–1.028; P<0.01). No significant CT–POAG association was found in other MAM categories. CONCLUSION: Increased macular CT is independently associated with POAG in highly myopic eyes with diffuse chorioretinal atrophy. This implies distinct pathogenic mechanisms underlying POAG development across different MAM categories in high myopia.

Advances in optical coherence tomography (OCT) technology allow a clear view of the vitreoretinal interface (VRI). The abnormality of the VRI is one of the common symptoms of high myopia, mainly including posterior vitreous detachment (PVD) and epiretinal membrane (ERM). They can cause severe damage to the structure and function of the retina, leading to permanent vision loss. Therefore, fully automated detection of abnormalities at the VRI is crucial for the management of high myopia. This paper presents a DS-YOLOv7 network aimed at accurately identifying abnormalities, including partial PVD, complete PVD, and ERM from retinal OCT images. Built upon the YOLOv7 network, the proposed model integrates the advanced dynamic snake convolution (DSConv) module to capture the curvilinear characteristics of lesions, and the mixture of attention and convolution (ACMix) module to improve the precision and robustness of feature extraction through effective fusion of self-attention mechanisms and convolution. Moreover, the introduction of the efficient complete intersection-over-union (ECIoU) loss function further enhances the coordinate regression capability of the model. Three-fold cross-validation on a dataset with 1973 OCT B-scans from 46 patients shows that the DS-YOLOv7 achieved superior performance in vitreoretinal interface abnormality detection, with mAP@0.5 of 0.714, mAP@0.75 of 0.438, and mAP@0.5:0.95 of 0.424. The proposed model can provide an accurate and efficient diagnostic tool for patients with high myopia.

Objective·To investigate the mechanism by which wingless-type MMTV integration site family member 5A (WNT5A) promotes the transition from ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) to chronic kidney disease (CKD).Methods·An IRI-induced AKI-to-CKD transition model was established in wild-type (WT) mice. Renal histopathological injury was assessed by hematoxylin-eosin (H-E) staining on the 3rd and the 14th day after IRI. Fibrosis was evaluated by Masson staining and immunohistochemistry for collagen type Ⅰ α1 chain (COL1A1). Wnt5a expression was quantified by RNA sequencing (RNA-seq), real-time quantitative PCR (qPCR), and Western blotting. Wnt5a heterozygous knockout (Wnt5a+/-) mice were used to establish the IRI-induced AKI-to-CKD transition model. Renal function was evaluated by serum creatinine (Scr) and blood urea nitrogen (BUN), and renal injury and fibrosis were assessed as described above. In vitro, a transforming growth factor-β (TGF-β)-induced fibrotic model was established in HK-2 cells (a human renal cortex proximal tubular epithelial cell line) with WNT5A overexpression. Differentially expressed genes identified by RNA-seq were subjected to Gene Ontology (GO) biological process enrichment analysis to identify key targets. Regulation of forkhead box protein P1 (FOXP1) by WNT5A was validated by qPCR and Western blotting. FOXP1 was overexpressed, or silenced in the context of WNT5A overexpression in HK-2 cells. Expression levels of notch receptor 2 (NOTCH2) pathway components, including NOTCH2, hairy/enhancer-of-split related with YRPW motif 1 (HEY1), and hairy and enhancer of split 1 (HES1), as well as fibrosis markers, including COL1A1 and vimentin (VIM), were analyzed by qPCR and Western blotting.Results·Wnt5a expression was increased in the renal tissue on the 3rd day after IRI, accompanied by marked tubular dilation and inflammatory cell infiltration. On the 14th day, Wnt5a expression was further increased, along with significant upregulation of fibrotic markers. Compared with WT mice, Wnt5a+/- mice exhibited reduced Scr and BUN levels on the 14th day after IRI, indicating improved renal function. FOXP1 expression was decreased, and tubular injury and renal fibrosis were attenuated in Wnt5a+/- mice. Mechanistically, WNT5A overexpression markedly upregulated FOXP1 in TGF-β-treated HK-2 cells. RNA-seq and GO analysis indicated significant enrichment of fibrosis-related processes and activation of the NOTCH signaling pathway. FOXP1 overexpression increased the mRNA and protein levels of NOTCH2 and its downstream targets HEY1 and HES1, along with elevated COL1A1 and VIM expression. In contrast, silencing FOXP1 in WNT5A-overexpressing cells reversed the upregulation of NOTCH2 pathway components and fibrosis markers.Conclusion·WNT5A upregulates the transcription factor FOXP1, which activates the NOTCH2 signaling pathway, thereby accelerating the IRI-induced AKI-to-CKD transition, and promoting renal fibrosis progression.

Introduction:This study evaluated the clinicopathological profiles and prognostic trajectories of nondiabetic renal disease (NDRD) subtypes coexisting with type 2 diabetes mellitus (T2D). Methods:The study cohort comprised of 123 patients with predominant NDRD subtypes: IgA nephropathy (T2D-IgAN, n = 52), membranous nephropathy (T2D-MN, n = 48), and podocytopathies (T2D-Podo, n = 23). Multivariate Cox regression was used to identify prognostic factors for renal outcomes over a median follow-up period of 80 months (interquartile range 62-102). Results:T2D-MN patients exhibited distinct characteristics compared to T2D-IgAN and T2D-Podo, including advanced age, higher incidence of nephrotic-range proteinuria and elevated total cholesterol. This group also demonstrated a greater susceptibility to atherosclerotic plaque formation. Pathological analysis revealed more severe glomerular sclerosis, interstitial inflammation, and C3 deposition in T2D-IgAN. Multivariate Cox regression identified three independent predictors of renal endpoints: glomerular C3 deposition (HR 3.021, 95% CI: 1.084-8.419), preserved estimated glomerular filtration rate (>60 mL/min/1.73 m2; HR 0.296, 95% CI: 0.110-0.796), and prolonged T2D duration (>10 years; HR 4.168, 95% CI: 1.389-12.503). Conclusion:These findings suggest that integrating clinical and pathological parameters enhances the prognostic accuracy of NDRD in patients with diabetes, enabling timely therapeutic interventions to mitigate complications in high-risk cases.

The automatic classification of retinal optical coherence tomography (OCT) images holds significant value for assisting in the diagnosis of related fundus diseases. However, it often faces challenges such as class imbalance and high inter-class similarity. In this paper, we propose a multi-perspective collaborative self-distillation network (MCSD-Net) for OCT image classification, which enables the model to learn through multi-perspective collaborative self-distillation mechanism and category aware contrastive learning strategy. Specifically, a multi perspective collaborative self-distillation mechanism is designed, which comprises structural distillation based on multi-stage feature fusion and historical distillation based on linear growth strategy, enhancing knowledge diversity from both structural and historical perspectives. A category-aware contrastive learning (CACL) strategy is designed, which constructs class-balanced batches to alleviate class imbalance and employs contrastive learning to strengthen the representation of intra-class and inter class features. Additionally, a direction-aware attention module (DAAM) is incorporated to extract features from horizontal and vertical directions, thereby improving feature discriminability. The proposed MCSD-Net is evaluated on a private myopic tractional maculopathy (MTM) retinal OCT dataset and two public OCT datasets (OCT2017 and OCTDL). Experimental results demonstrate that the proposed MCSD Net outperforms other state-of-the-art self-distillation based methods.

Myopic maculopathy (MM) is a major complication of high myopia and the leading cause of irreversible vision loss. Automated classification of MM is thus of great clinical importance for enabling precise treatment and preventing further deterioration. We propose a self-supervised learning framework, FreqMIM-Net, which leverages high-frequency information reconstruction based on masked image modeling for MM classification. The framework includes two stages: self-supervised feature representation learning and downstream classification. In the first stage, masked autoencoders are adopted as the baseline, and knowledge distillation is introduced to guide the student model in acquiring robust feature extraction ability from the teacher model. To better utilize fine-grained structural details, high-frequency components are used as the reconstruction target. In the downstream classification stage, center loss is employed to enhance the discriminative power of learned representations. Four public fundus image datasets, EyePACS, MMAC, PALM, and HPMI, were used for evaluation, with EyePACS for pretraining and the others for classification. Experimental results demonstrate that FreqMIM-Net consistently outperforms other mainstream self-supervised learning baselines trained under the same protocol and achieves competitive performance against recent retinal foundation models without the large-scale domain-specific retinal pretraining on the MM classification tasks.

Diabetic kidney disease (DKD) remains a major global health burden and the most common cause of ESKD. The therapeutic landscape has profoundly shifted from a glucocentric model to a multifaceted strategy focusing on the holistic management of cardiovascular-kidney-metabolic syndrome. This therapeutic paradigm is now anchored by four foundational pillars: renin-angiotensin-aldosterone system inhibitors, sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide-1 receptor agonists, and non-steroidal mineralocorticoid receptor antagonists, which collectively target complementary pathogenic pathways to slow DKD progression and reduce cardiovascular morbidity. Despite these advances, a high residual risk persists, driving kidney disease research into novel therapeutic targets. A large body of mechanistic studies demonstrates the critical roles of genetic and epigenetic modifications, persistent metabolic dysfunction, and inflammatory and fibrotic processes in DKD pathogenesis. Consequently, emerging investigational therapies are focused on histone-modifying enzymes, drugs to restore metabolic/lipid disorders, new anti-inflammatory and anti-fibrosis therapies, as well as stem cell-based interventions for their regenerative and immunomodulatory potential. The future of DKD management hinges on the successful clinical translation of these novel therapeutic approaches, which will require overcoming challenges in clinical trial design alongside current therapies, patient stratification for different therapeutic regimens using predictive biomarkers, and the exploration of synergistic combination therapies to ultimately personalize treatment strategies and enhance long-term kidney outcomes.

Preventing the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remains a considerable clinical challenge. In this study, we elucidate the role of WNT5A in accelerating the AKI-to-CKD transition and its underlying mechanisms. Renal biopsies from patients with AKI showed marked upregulation of WNT5A and its receptor, CD146, in proximal tubules, with higher expression in patients with CKD progression. In murine AKI models, Wnt5a knockdown attenuated CKD progression. Conversely, proximal tubular overexpression of Wnt5a exacerbated renal fibrosis in ischemia-reperfusion injury (IRI) mice, which was alleviated by Box5, a specific WNT5A antagonist. In vitro, WNT5A overexpression in transforming growth factor β (TGF-β)-stimulated HK-2 cells promoted CD146 upregulation, activated JNK phosphorylation, and enhanced SNAI1 expression. The genetic silencing of WNT5A/CD146 and JNK inhibition suppresses SNAI1 expression and attenuates fibrotic responses. Mechanistically, JNK-mediated c-JUN phosphorylation promoted its interaction with KLF5 at the SNAI1 promoter, driving renal fibrosis. Elevated serum levels of soluble CD146 correlated with renal function in patients with AKI and were higher in patients exhibiting CKD progression. Inhibition of WNT5A could serve as a therapeutic target for delaying renal fibrosis in AKI progression.

PURPOSE:To assess the longitudinal change of choroidal thickness (ChT) and tessellated fundus progression in Chinese adults over 4 years. METHODS:In this population-based longitudinal cohort study, 1646 right eyes of 1646 participants were examined. Fundus photographs were obtained and ChT was measured using swept-source optical coherence tomography. Participants were categorized into high-myopia, low-myopia, and non-myopia groups, and the tessellated fundus was graded 0-3 based on the fundus photographs. RESULTS:The mean baseline age, refractive error, axial length (AL), and macular ChT were 62.51 ± 9.89 years, -0.48 ± 3.18 D, 23.71 ± 1.58 mm, and 199.7 ± 77.3 μm, respectively. At the 4-year follow-up, a significant reduction in macular ChT of 4.05 ± 6.24, 4.44 ± 6.87, and 3.51 ± 5.17 μm per year was observed in the non-myopia, low-myopia, and high-myopia groups, respectively. Age, baseline ChT, and AL changes (with βnon-M = -78.439, βHM = -56.505) were independently related to the rate of macular ChT change (all p < 0.05). Furthermore, the decrease in the ChT distribution pattern varied with different refractive groups. Moreover, 4.31% of the participants had tessellated fundus progression; these participants had more ChT reduction over 4 years than those without tessellated fundus progression (p < 0.001). CONCLUSIONS:Choroidal thinning was found to be associated with age and AL elongation. For every 1 mm increase in AL, the decrease rate of ChT in the high-myopia group was slower than that in the non-myopia group. Progression of tessellated fundus was associated with a faster decrease in ChT, highlighting its potential as a biomarker for myopia progression.

IgA nephropathy (IgAN), the most common primary glomerular disease worldwide, progresses to end-stage renal disease (ESRD) in 30%–40% of patients. Despite its significant clinical burden, treatment options for IgAN remain limited. Recent advances in understanding disease mechanisms have led to the development of novel biologic agents, including Telitacicept, a recombinant fusion protein that targets the dysregulated B cell/plasma cell pathway by neutralizing B lymphocyte stimulator (BLyS) and A proliferation-inducing ligand (APRIL). This dual inhibition suppresses B cell-mediated autoimmune responses, offering a promising therapeutic approach. A phase II clinical trial has demonstrated Telitacicept's efficacy and safety in IgAN; however, real-world data are lacking. This study was designed to evaluate the real-world efficacy and safety of Telitacicept in Patients with IgAN. This study included 20 patients with biopsy-confirmed primary IgAN treated at Shanghai Sixth People's Hospital between 2023 and 2024. The average follow-up duration was 208.85 ± 96.82 days. Inclusion criteria included 24-hour urine protein levels >0.65 g and an estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m². All patients received subcutaneous Telitacicept at a dose of 160 mg per week for at least three months. Changes in clinical parameters, including 24-hour urine protein and eGFR, were assessed at 3 months and at the end of the study compared to baseline. Telitacicept-related adverse events were systematically recorded during the treatment period. After 3 months of Telitacicept treatment, the median 24-hour urine protein significantly decreased from 1.025 g/24 h at baseline to 0.59 g/24 h (z = −1.979, p < 0.05), while the median eGFR showed no significant change (69.78 mL/min/1.73 m² vs. 62.17 mL/min/1.73 m², p = 0.135). At the study endpoint, the median 24-hour urine protein further declined to 0.585 g/24 h (z = −1.96, p < 0.05), and the median eGFR remained stable (69.78 mL/min/1.73 m² to 58.03 mL/min/1.73 m², p = 0.904). The treatment was well-tolerated, with no reported adverse events such as respiratory infections, urinary tract infections, or injection site reactions. In this analysis of a small single-center cohort, Telitacicept demonstrated significant efficacy in reducing proteinuria and preserve renal function in patients with IgAN over both short-term (3-month) and long-term (≥6-month) treatment periods. Additionally, it exhibited an excellent safety profile, with no treatment-related adverse events observed. These findings support the further investigation and clinical application of Telitacicept in the management of IgAN.

Renal tubulointerstitial abnormalities predict diabetic kidney disease (DKD) progression, and targeting them may prevent DKD. Insulin-like growth factor binding-protein 7 (IGFBP7) is expressed in renal tubular cells and is elevated in both blood and urine during the early stages of human diabetes, serving as a predictor of the rate of disease progression. We showed that tubule- and glomerular-specific IGFBP7 promotes DKD, with tubular-derived IGFBP7 disrupting the renal microenvironment. IGFBP7 impairs mitochondrial bioenergetics in tubular cells, causing lipid accumulation, cell cycle arrest, interstitial inflammation, fibrosis, and glomerulosclerosis. These findings were substantiated by transgenic overexpression and the specific deletion of IGFBP7 in type 1/2 DKD mice. Mechanistically, IGFBP7 interacts with STAT3, promoting its acetylation/dimerization and downregulating mitochondrial bioenergetics. Our study identified levomefolic acid as a novel inhibitor of IGFBP7 and demonstrated its efficacy in mitigating the progression of DKD. Here we showed IGFBP7 is a promising therapeutic target for DKD.

Background:A key goal in managing patients with heterozygous disease-causing COL4A3 and COL4A4 (COL4A3/4) variants, affecting individuals spanning a broad age range, is to slow the development of chronic kidney disease (CKD). Whether age of onset is associated with the risk of CKD has not been investigated. Methods:In 294 patients (118 males) with heterozygous disease-causing COL4A3/4 variants in the Shanghai Registry of Alport Syndrome, we made the comparison of risk of CKD between those showing disease onset before 18 years old (early onset) or from 18 years and older (late onset). CKD were defined as onset of persistent albuminuria (albumin-to-creatinine ratio ≥30 mg/g) or CKD G2 (estimated glomerular filtration rate <90 ml/min/1.73 m2). Results:147 (50.0%) of patients had initial presentation of symptoms of kidney diseases when they were <18 years old [median age at onset, 5.0 years (IQR, 3.0-8.0 years)], and in the remainder when they were older [median age at onset, 30.0 years (IQR, 26.0-38.0 years)]. During a median follow-up of 3.0 years (IQR, 0-10.3 years), earlier disease onset showed significant associations with higher risk of albuminuria [hazard ratio (HR) 7.08, 95% confidence intervals (CI) 4.59-10.93] and CKD G2 (HR 3.49, 95%CI 1.57-7.75). Risk of albuminuria increased by 64%, and risk of CKD G2 increased by 34%, per 5-year step toward younger age at disease onset. Conclusions:Earlier onset of disease may predict higher risk of CKD in patients with heterozygous disease-causing COL4A3/4 variants. This association, if verified in large prospective studies, may help stratify patients by risk of worse prognosis, which can guide their management and preemptive nephroprotective treatment.

Paravascular retinal abnormalities (PRAs) are significant early signs of the progression from high myopia to pathological myopia, including paravascular microfold, inner and outer paravascular retinoschisis, paravascular cyst, and paravascular lamellar hole. It is challenging to segment these symptoms in OCT images due to their small and various sizes, blurred boundaries, and imbalanced distribution. To effectively address these challenges, we propose D(2)LFENet, a segmentation network based on a dual-decoder structure and a local feature enhancement (LFE) module. The network employs an improved HRNet as the baseline, integrating the LFE module to capture detailed local information and improve semantic feature representation. D(2)LFENet utilizes dual decoders, with the boundary segmentation decoder guiding the main segmentation branch, enhancing boundary definition and segmentation accuracy. Validated on a dataset from 78 high myopia patients at Shanghai General Hospital, D(2)LFENet achieves Dice similarity coefficients of 61.03%, 56.37%, 68.17%, 45.67%, and 34.31% for the above five types of PRAs, outperforming other state-of-the-art methods.

Background:Childhood obesity is a growing global concern and is associated with cardiometabolic comorbidities in adulthood. However, the association between childhood body size and age-related macular degeneration (AMD) in late life remains to be investigated. We aimed to explore the association between childhood obesity and incident AMD and the underlying anatomical and physiobiological mechanisms. Methods:We investigated the association between childhood body size and incident AMD using multivariable Cox regression models and its relation to retinal layer thickness using linear regression. We performed four-way decomposition mediation analyses to explore the underlying mechanism. Lastly, we used univariable Mendelian randomisation (UVMR) and multivariable Mendelian randomisation (MVMR) to evaluate and differentiate the causal effect of childhood and adulthood body mass index (BMI). Results:Over a median follow-up of 12.8 years, 5026 incident AMD cases occurred among 487 009 participants. Plumper childhood body size at age 10 conferred independent risk to incident AMD in later life (adjusted hazards ratio (aHR) = 1.13; 95% confidence interval (CI) = 1.03, 1.24, P = 0.007) and was associated with photoreceptor outer segment layer thinning. Adulthood BMI mediated the association between childhood plumper body size and incident AMD (pure indirect effect = 33%; 95% CI = 9.9, 56.9, P = 0.05). Mediation analysis of adulthood physiobiological and immuno-metabolic function showed that 17 peripheral biomarkers of 7 categories significantly mediated the aforementioned pathway, with HbA1c and cystatin C showing the two largest effects. Mendelian randomisation suggested a potential causal association between childhood BMI and AMD (UVMR inverse variance weighted (IVW) odd ratio (OR) = 1.50; 95% CI = 1.09, 2.08, P = 0.013), independent of adulthood BMI (MVMR adulthood BMI-adjusted IVW OR = 1.29; 95% CI = 1.03, 1.61, P = 0.024). Conclusions:Childhood obesity may be a causal risk factor for incident AMD in later life, partially mediated by persistent obesity and physiobiological memory. Prevention of retinal degenerative diseases should therefore begin in childhood, whereby children should be encouraged and supported to maintain a normal body size.

Aims To investigate myopic maculopathy in Chinese children with high myopia and its association with choroidal and retinal changes. Methods This cross-sectional study included Chinese children aged 4–18 years with high myopia. Myopic maculopathy was classified by fundus photography and retinal thickness (RT) and choroidal thickness (ChT) in the posterior pole were measured by swept-source optical coherence tomography. A receiver operation curve was used to determine the efficacy of fundus factors in classifying myopic maculopathy. Results In total, 579 children aged 12.8±3.2 years with a mean spherical equivalent of −8.44±2.20 D were included. The proportions of tessellated fundus and diffuse chorioretinal atrophy were 43.52% (N=252) and 8.64% (N=50), respectively. Tessellated fundus was associated with a thinner macular ChT (OR=0.968, 95% CI: 0.961 to 0.975, p<0.001) and RT (OR=0.977, 95% CI: 0.959 to 0.996, p=0.016), longer axial length (OR=1.545, 95% CI: 1.198 to 1.991, p=0.001) and older age (OR=1.134, 95% CI: 1.047 to 1.228, p=0.002) and less associated with male children (OR=0.564, 95% CI: 0.348 to 0.914, p=0.020). Only a thinner macular ChT (OR=0.942, 95% CI: 0.926 to 0.959, p<0.001) was independently associated with diffuse chorioretinal atrophy. When using nasal macular ChT for classifying myopic maculopathy, the optimal cut-off value was 129.00 µm (area under the curve (AUC)=0.801) and 83.85 µm (AUC=0.910) for tessellated fundus and diffuse chorioretinal atrophy, respectively. Conclusion A large proportion of highly myopic Chinese children suffer from myopic maculopathy. Nasal macular ChT may serve as a useful index for classifying and assessing paediatric myopic maculopathy. Trial registration number NCT03666052 .

To identify the relationship of macular outward scleral height (MOSH) with axial length (AL), macular choroidal thickness (ChT), peripapillary atrophy (PPA), and optic disc tilt in Chinese adults. In this cross-sectional study, 1088 right eyes of 1088 participants were enrolled and assigned into high myopia (HM) and non-HM groups. MOSH was measured in the nasal, temporal, superior, and inferior directions using swept-source optical coherence tomography images. The clinical characteristics of MOSH and the association of MOSH with AL, macular ChT, PPA, and tilt ratio were analysed. The mean age of participants was 37.31 ± 18.93 years (range, 18–86 years), and the mean AL was 25.78 ± 1.79 mm (range, 21.25–33.09 mm). MOSH was the highest in the temporal direction, followed by the superior, nasal, and inferior directions (all p < 0.001). The MOSH of HM eyes was significantly higher than that of non-HM eyes, and it was positively correlated with AL in the nasal, temporal, and superior directions (all p < 0.001). Macular ChT was independently associated with the average MOSH (B = −0.190, p < 0.001). Nasal MOSH was positively associated with the PPA area and the presence of a tilted optic disc (both p < 0.01). Eyes with a higher MOSH in the superior (odds ratio [OR] = 1.008; p < 0.001) and inferior directions (OR = 1.006; p = 0.009) were more likely to have posterior staphyloma. MOSH is an early indicator of scleral deformation, and it is correlated positively with AL and negatively with ChT. A higher nasal MOSH is associated with a larger PPA area and the presence of a tilted optic disc. Higher MOSH values in the superior and inferior directions were risk factors for posterior staphyloma. The study was registered at www.clinicaltrials.gov (Reg. No. NCT03446300).

Optical coherence tomography (OCT) has become the leading imaging technique in diagnosing and treatment planning for retinal diseases. Retinal OCT image segmentation involves extracting lesions and/or tissue structures to aid in the decisions of ophthalmologists, and multi-class segmentation is commonly needed. As the target regions often spread widely inside the retina, and the intensities and locations of different categories can be close, good segmentation networks must possess both global modeling capabilities and the ability to capture fine details. To address the challenge in capturing both global and local features simultaneously, we propose HyFormer, an efficient, lightweight, and robust hybrid network architecture. The proposed architecture features parallel Transformer and convolutional encoders for independent feature capture. A multi-scale gated attention block and a group positional embedding block are introduced within the Transformer encoder to enhance feature extraction. Feature integration is achieved in the decoder composed of the proposed three-path fusion modules. A class activation map-based cross-entropy loss function is also proposed to improve segmentation results. Evaluations are performed on a private dataset with myopic traction maculopathy lesions and the public AROI dataset for retinal layer and lesion segmentation with age-related degeneration. The results demonstrate HyFormer's superior segmentation performance and robustness compared to existing methods, showing promise for accurate and efficient OCT image segmentation. .

Background The relationship between integrated lifestyles, mental status and their impact on overall well-being has attracted considerable attention. This study aimed to evaluate the association between lifestyle factors, depression and diabetic retinopathy (DR) in adults aged 18–64 years. Methods A cohort of 3482 participants diagnosed with diabetes was drawn from the National Health and Nutrition Examination Survey (NHANES) spanning the years 1999–2018. DR was defined based on self-reported diabetic retinopathy diagnoses by professional physicians, relying on Diabetes Interview Questionnaires. Subgroup analysis was employed to assess lifestyle and psychological factors between participants with DR and those without, both overall and stratified by diabetic duration. Continuous variables were analyzed using the student’s t test, while weighted Rao-Scott χ 2 test were employed for categorical variables to compare characteristics among the groups. Results Of the 3482 participants, 767 were diagnosed with diabetic retinopathy, yielding a weighted DR prevalence of 20.8%. Patients with DR exhibited a higher prevalence of heavy drinking, depression, sleep deprivation, and insufficient physical activity compared to those without DR. Furthermore, multivariable logistic regression analysis revealed that sleeping less than 5 h (OR = 3.18, 95%CI: 2.04–4.95, p < 0.001) and depression (OR = 1.35, 95%CI:1.06–1.64, p = 0.025) were associated with a higher risk of DR, while moderate drinking (OR = 0.49, 95%CI: 0.32–0.75, p = 0.001) and greater physical activity (OR = 0.64, 95%CI: 0.35–0.92, p = 0.044) were identified as protective factors. Conclusions Adults aged 18–64 years with DR exhibited a higher prevalence of lifestyle-related risk factors and poorer mental health. These findings underscore the need for concerted efforts to promote healthy lifestyles and positive emotional well-being in this population.