Vascular endothelial growth factor A (VEGFA) plays a critical role in the pathogenesis of diabetic macular edema (DME) in patients with type 2 diabetes mellitus (T2DM). Herein, we sought to determine whether palmitoylation modulates the stability and function of VEGFA in the context of DME. VEGFA protein levels were measured by western blotting in retinal pigment epithelial (RPE) tissues from mice and in cultured RPE cell lines. Palmitoylation of VEGFA was assessed using acyl‑biotin exchange (ABE) and Click‑iT pulldown assays. Cell proliferation was evaluated with the Cell Counting Kit‑8 (CCK‑8) assay. The interaction between VEGFA and zinc finger DHHC-type containing 19 (ZDHHC19) was examined by co‑immunoprecipitation. Retinal histopathology in DME mice was evaluated by hematoxylin‑eosin (H E) staining. VEGFA levels were elevated in the RPE of DME mice compared with those of T2DM mice. Pharmacological inhibition of palmitoylation with 2‑bromopalmitate (2‑BP) reduced VEGFA protein expression in cultured cells. ZDHHC19 was identified as the palmitoyltransferase responsible for VEGFA. Wild‑type ZDHHC19 failed to palmitoylate the VEGFA‑C387A mutant, and the catalytically inactive ZDHHC19‑C142S mutant also lacked activity toward VEGFA. Overexpression of wild‑type VEGFA or ZDHHC19 significantly promoted RPE cell proliferation, whereas the VEGFA‑C387A and ZDHHC19‑C142S mutants had no effect. Consistent with these in vitro findings, wild‑type VEGFA or ZDHHC19 overexpression exacerbated DME development in mice, while the corresponding mutants did not significantly affect disease progression. ZDHHC19‑mediated palmitoylation of VEGFA contributes to DME pathogenesis and may serve as a potential therapeutic target and biomarker for this disease.

Glaucoma is a leading cause of irreversible blindness worldwide. One hallmark of glaucoma is the degeneration of retinal ganglion cells (RGCs). In this study, a dual role for growth hormone-releasing hormone receptor (GHRHR) modulation under glaucoma-relevant conditions and complementary injury paradigms involving the RGCs is identified. Using acute IOP elevation (retinal ischemia-reperfusion), chronic ocular hypertension (microbead-induced), and traumatic axonal injury (optic nerve crush) models, we show that GHRHR deficiency preserves RGC survival and uniquely restores visual functions-contrasting with GHRHR activation, which solely promotes cellular survival. Single-cell transcriptomic analysis uncovers RGC-specific alterations in genes associated with ferroptosis, lipid metabolism, oxidative stress, and mitochondrial dynamics. At the mechanistic level, GHRHR deficiency prevents the pathological downregulation of key anti-ferroptotic mediators GPX4 and FTH1 while suppressing pro-ferroptotic factors ACSL4 caused by glaucomatous neurodegeneration. This multifaceted regulation attenuated iron accumulation, lipid peroxidation, and reactive oxygen species (ROS) accumulation, effects that are diminished by the ferroptosis inducer RSL3. Notably, in mitochondria damaged primary RGCs, pharmacological GHRHR inhibition replicates these benefits, reducing lipid peroxidation and mitochondrial ROS to bolster RGC survival. Collectively, these findings establish GHRHR inhibition as a potent therapeutic strategy for glaucomatous neurodegeneration, synergistically rescuing both structural and functional integrity of the retina.

Neovascular age-related macular degeneration (nAMD) and proliferative diabetic retinopathy (PDR) continue to be significant contributors to permanent visual impairment. Although anti-vascular endothelial growth factor (anti-VEGF) therapy has substantially improved disease management, recurrent neovascularization, persistent leakage, incomplete treatment response, subretinal fibrosis in nAMD, and fibrovascular membrane formation or tractional complications in PDR indicate that disease progression involves mechanisms beyond VEGF signaling alone. Cellular senescence-a stress-induced condition marked by persistent cell-cycle arrest, altered stress responses, and context-dependent senescence-associated secretory phenotype (SASP) activity-has been identified as a potential pathogenic amplifier in posterior-segment neovascular diseases. Chronic oxidative stress, hyperglycemia, hypoxia, metabolic dysfunction, and inflammation in the retina and choroid may induce senescence-associated or senescence-like remodeling in retinal pigment epithelial cells, Müller glia, endothelial cells, and pericytes. Nonetheless, conclusive evidence of bona fide cellular senescence in human ocular tissues remains scarce and varies markedly across cell types and disease contexts. This review integrates direct experimental evidence, marker-based observations, and inferred mechanistic insights to delineate a proposed, evidence-based senescence-associated feed-forward amplification model. In this model, chronic pathological stress may initiate or reinforce senescence-related programs, whereas SASP factors, extracellular vesicles, and immune microenvironment remodeling may further amplify angiogenic, inflammatory, vascular, and fibrotic dysfunction. Importantly, this model should be interpreted as a hypothesis-generating, non-exclusive framework rather than a fully established causal pathway. We also compare disease-specific features of nAMD and PDR, discuss methodological challenges in defining retinal senescence, and evaluate the translational potential and safety concerns of senolytics and SASP-modulating strategies as adjuncts to anti-VEGF therapy. Rather than presenting cellular senescence as a fully established causal driver, this review frames senescence-associated remodeling as a context-dependent, evidence-stratified amplifying component within this proposed feed-forward framework.

BackgroundHyperreflective materials (HRMs), enigmatic biomarkers observed in diabetic retinopathy (DR), exhibit poorly characterized pathophysiological origins and clinical implications.MethodsThis retrospective cross-sectional study investigates the spatial distribution patterns of HRMs subtypes and their integrative relationships with retinal microvascular architecture, structural remodeling, and systemic metabolic parameters in 205 DR eyes. HRMs were systematically classified via multimodal optical coherence tomography angiography (OCTA) analysis, incorporating topographic localization (inner vs. outer retinal), reflectivity profiles, morphometric dimensions, posterior shadowing artifacts, and decorrelation signal. Quantitative correlations were established between HRMs subtypes and OCTA-derived vascular parameters (intraretinal microvascular abnormalities [IRMA], non-perfusion [NP] areas, microaneurysms), diabetic macular edema (DME) status, and systemic metabolic indices (glycemic control, lipid profiles, renal function, inflammatory markers).ResultsSix distinct HRMs phenotypes were identified: inner retinal hyperreflective spots (IRHFs), outer retinal hyperreflective spots (ORHFs), intraretinal hard exudates (IRHE), outer retinal hard exudates (ORHE), decorrelation-positive HRMs, and cotton-wool spots. Spatial mapping revealed predominant HRMs colocalization with IRMA territories (75.4% IRHFs, 89.5% ORHFs, 90.8% IRHE, 94% ORHE), while 19% of IRHFs and 8.7% of ORHFs overlapped NP zones. Decorrelation-positive HRMs demonstrated dual associations with IRMA (77.6%) and microaneurysms (21.0%). DME eyes exhibited significantly elevated HRMs density within IRMA and NP regions (P < 0.001). Multivariate analysis identified dyslipidemia as a strong predictor of HRMs burden.ConclusionsThese findings establish HRMs as spatially resolved biomarkers of diabetic retinal pathophysiology, reflecting compartment specific interactions between microvascular incompetence (IRMA-associated barrier failure), ischemic remodeling (NP zones), and systemic metabolic dysregulation. The colocalization of HRMs subtypes with IRMA walls and leakage-prone microaneurysms supports their putative role as optical signatures of lipoprotein extravasation and inflammatory lipidotoxicity in DR progression.

To better understand the complexity of the tumor microenvironment and to identify novel treatment strategies for uveal melanoma (UVM), we analyzed single-cell RNA sequencing (scRNA-seq) data from eight primary UVM eye tissues and three metastatic UVMs in the liver (GSE139829). We integrated this with bulk RNA-seq data from UVM patients derived from TCGA-UVM and GSE84976 cohorts. Our study focused on cytokine signaling in immune-related genes (CSIRGs), revealing distinct cellular compositions, intercellular interactions, and prognostic implications in UVM. We identified 137 cytokine signaling-related genes in UVM, with ISG20 significantly upregulated and linked to advanced stages and poor prognosis. Recognized for immune regulation, ISG20 emerged as a key survival predictor and therapeutic target from a risk model using Cox regression and LASSO, effectively categorizing patients by survival risk. Furthermore, differential drug response analysis revealed distinct sensitivities to drugs between the risk groups. Immune infiltration analysis showed a diverse immune landscape, potentially influencing response to immunotherapy. Structural prediction using AlphaFold 2 technology and molecular docking analyses revealed interactions between ISG20 and the therapeutic candidate decitabine. This study combines scRNA-seq analysis with structural biology approaches to unravel the molecular complexity of UVM, emphasizing the prognostic and therapeutic relevance of CSIRGs, particularly ISG20.

Precise multi-class retinal disease recognition faces challenges from inter/intra-class variations and imbalanced distributions. While Convolution Neural Network (CNNs) effectively capture salient lesions, they struggle with subtle lesions and exhibit bias toward frequent diseases. We propose a Retinal Lesion Fusion Network (RLF-Net) with two novel modules: a Retinal Lesion Feature Fusion (RLFF) module combining a SAlient Lesion Enhancement (SALE) block, SUbtle Lesion Enhancement (SULE) block, and Fast Fourier Transform Fusion (FFTF) block to adaptively integrate multi-scale lesion features and a Retinal Screening of Diseases (RSD) module mitigating class imbalance by equally weighting disease-specific feature differences. Additionally, we design a hybrid loss merging supervised contrastive learning and cross-entropy to enhance discriminative power. Evaluations on a clinical Fundus Fluorescein Angiography (FFA) dataset and two public fundus benchmarks demonstrate RLF-Net's superiority over state-of-the-art methods. Our approach advances multi-class retinal diagnosis by addressing critical limitations in feature representation and class imbalance, particularly improving recognition of subtle lesions and rare diseases through synergistic feature fusion and balanced optimization strategies.

Purpose:Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in the elderly, characterized by chronic retinal inflammation and immune dysregulation. While myeloid cells have been increasingly implicated in AMD pathogenesis, the specific immune subsets responsible remain poorly defined. This study aimed to identify causal immune cell populations and elucidate their functional roles in AMD progression. Methods:We employed an integrative multiomics strategy encompassing Mendelian randomization (MR) analysis using genome-wide association study summary statistics, single-cell RNA sequencing (scRNA-seq) analysis of retinal pigment epithelium (RPE)/choroid tissues from patients with AMD and healthy controls (GSE230348), and flow cytometric (FCM) validation in a sodium iodate-induced dry AMD mouse model. Results:MR analysis identified a significant causal association between CD64 expression on CD14⁻CD16⁻ monocytes and increased AMD risk (odds ratio, 1.179; P < 0.001). scRNA-seq profiling revealed a pronounced enrichment of CD14⁻CD16⁻ monocytes in AMD tissues, with FCGR1A (CD64) expression specifically localized within this subset. Pseudotime trajectory analysis demonstrated dynamic activation and differentiation states among monocyte populations in AMD. Ligand-receptor interaction modeling identified three major signaling pathways, MIF-CD74-CXCR4, IGF1-IGF1R, and SEMA3C-PLXND1, mediating interactions between CD14⁻CD16⁻ monocytes and RPE cells. FCM analysis of retinal single-cell suspensions in AMD mice confirmed a significantly higher proportion of CD64⁺ myeloid cells compared to controls. Conclusions:This study identifies CD64⁺CD14⁻CD16⁻ monocytes as potential contributors to AMD and reveals their putative immunomodulatory crosstalk with RPE cells. These findings highlight CD64 as a promising biomarker and therapeutic target for mitigating myeloid-driven inflammation in AMD.

Objective The aim of this study is to compare the efficacy of plate fixation via the tarsal sinus approach with screw fixation alone in treating Sander type II, III, and IV fractures. Method Between 2016 and 2023, a comprehensive study encompassing 73 patients and 78 feet with calcaneus fractures was conducted. The investigation compared the efficacy of open reduction plate fixation (ORPF) (18 cases) against open reduction screw fixation (ORSF) (60 cases). Parameters such as operation duration, intraoperative blood loss, hospital stay duration, postoperative imaging metrics (including calcaneal length, width, height, Bohler Angle, Gissane Angle, and Angle of calcaneus varus), postoperative complications, and the AOFAS score one year post-surgery were meticulously analyzed and compared across both treatment groups. Results No significant discrepancies were observed between the two groups concerning calcaneal dimensions, including length, width, height, Bohler Angle, Gissane Angle, and Angle of calcaneus varus post-operation (p > 0.05). Moreover, throughout the long-term postoperative monitoring period, no notable distinctions were evident in these parameters between the two groups. Notably, the ORSF group exhibited reduced intraoperative hemorrhage (p = 0.026), shorter procedural duration (p = 0.028), and fewer occurrences of postoperative complications such as pain or superficial infections. However, the incidence of long-term postoperative complications did not demonstrate statistical significance. Furthermore, there were no discernible variations in AOFAS scores between the groups at the latest follow-up assessment. Conclusion Both open reduction screw internal fixation and open reduction plate internal fixation have been shown to be effective methods for clinically treating calcaneal fractures, with both techniques yielding positive postoperative imaging results. However, internal fixation with open reduction screws has been found to have several advantages over open reduction plate internal fixation, including less bleeding, shorter operation time, and fewer short-term complications.

BackgroundProliferative diabetic retinopathy (PDR), a major cause of blindness, is characterized by complex pathogenesis. This study integrates single-cell RNA sequencing (scRNA-seq), Non-negative Matrix Factorization (NMF), machine learning, and AlphaFold 2 methods to explore the molecular level of PDR.MethodsWe analyzed scRNA-seq data from PDR patients and healthy controls to identify distinct cellular subtypes and gene expression patterns. NMF was used to define specific transcriptional programs in PDR. The oxidative stress-related genes (ORGs) identified within Meta-Program 1 were utilized to construct a predictive model using twelve machine learning algorithms. Furthermore, we employed AlphaFold 2 for the prediction of protein structures, complementing this with molecular docking to validate the structural foundation of potential therapeutic targets. We also analyzed protein−protein interaction (PPI) networks and the interplay among key ORGs.ResultsOur scRNA-seq analysis revealed five major cell types and 14 subcell types in PDR patients, with significant differences in gene expression compared to those in controls. We identified three key meta-programs underscoring the role of microglia in the pathogenesis of PDR. Three critical ORGs (ALKBH1, PSIP1, and ATP13A2) were identified, with the best-performing predictive model demonstrating high accuracy (AUC of 0.989 in the training cohort and 0.833 in the validation cohort). Moreover, AlphaFold 2 predictions combined with molecular docking revealed that resveratrol has a strong affinity for ALKBH1, indicating its potential as a targeted therapeutic agent. PPI network analysis, revealed a complex network of interactions among the hub ORGs and other genes, suggesting a collective role in PDR pathogenesis.ConclusionThis study provides insights into the cellular and molecular aspects of PDR, identifying potential biomarkers and therapeutic targets using advanced technological approaches.

Purpose This study aims to explore glucose-6-phosphate dehydrogenase (G6PD) activity in diabetic retinopathy (DR) and its correlation with inflammatory factors, elucidating the regulatory role of G6PD in DR pathology. Methods A total of 151 T2DM patients were divided into three groups: diabetes without retinopathy (DNR, n = 59), non-proliferative retinopathy (NPDR, n = 46) and proliferative retinopathy (PDR, n = 49). Plasma G6PD activity was measured by a Randox G6PD kit and compared between these groups. Then the G6PD activity was correlated with inflammatory cytokines and metabolic parameters in these patients. A STZ-induced diabetic rat model was established, G6PD activity was validated by western blot and immunofluorescence staining in the retina of this model. Results Plasma G6PD activity decreased in the order of DNR, NPDR and PDR groups (P<0.01). G6PD activity was negatively correlated with IL-6, IL-8, TNF-α, cholesterol, and LDL (r = -0.1625, -0.1808, -0.1865, -0.1747, r = -0.1807, P<0.05). Multiple regression analysis showed TNF-α, IL-6, and LDL were independent related factors for G6PD. Logistic regression analysis showed G6PD, triglyceride, cholesterol, IL-8, TNF-α, and macular edema were influencing factors for T2DM with DR. Western Blot analysis indicated a significant reduction of G6PD expression in the retina, and immunofluorescence staining showed distribution of G6PD especially in the retinal endothelium cell decreased. Conclusion G6PD may play an important role in DR occurrence and progression, with decreased expression correlating closely with lipid metabolism and inflammatory factors.

The complement system is a protein response system with a precise regulatory mechanism, which has the functions of mediating inflammation, regulating immune response, dissolving cells and clearing immune complexes. Diabetic retinopathy(DR)is a common and severe ocular complication of diabetes and one of the common irreversible blinding eye diseases in ophthalmology, and its pathogenesis is complex, including hypoxia, oxidative stress, inflammation and abnormal polyol metabolism pathway. In recent years, there has been more and more evidence that dysregulation and inflammation of immune system are important factors in the pathogenesis of DR, and a variety of complement proteins play an important role in key processes such as inflammation regulation and angiogenesis. Therefore, the central purpose of this review is to discuss the role of the complement system and related regulatory proteins in DR, with the aim of elucidating the close relationship between the complement proteins and the occurrence and development of DR, and providing important references and new ideas for the prevention and treatment of DR. At the same time, the clinical research of complement system-targeted drugs is further elaborated.

It is known that the actin cytoskeleton and its associated cellular interactions in the trabecular meshwork (TM) and juxtacanalicular tissues mainly contribute to the formation of resistance to aqueous outflow of the eye. Fibulin-3, encoded by EFEMP1 gene, has a role in extracellular matrix (ECM) modulation, and interacts with enzymatic ECM regulators, but the effects of fibulin-3 on TM cells has not been explored. Here, we report a stop codon variant (c.T1480C, p.X494Q) of EFEMP1 that co-segregates with primary open angle glaucoma (POAG) in a Chinese pedigree. In the human TM cells, overexpression of wild-type fibulin-3 reduced intracellular actin stress fibers formation and the extracellular fibronectin levels by inhibiting Rho/ROCK signaling. TGFβ1 up-regulated fibulin-3 protein levels in human TM cells by activating Rho/ROCK signaling. In rat eyes, overexpression of wild-type fibulin-3 decreased the intraocular pressure and the fibronectin expression of TM, however, overexpression of mutant fibulin-3 (c.T1480C, p.X494Q) showed opposite effects in cells and rat eyes. Taken together, the EFEMP1 variant may impair the regulatory capacity of fibulin-3 which has a role for modulating the cell contractile activity and ECM synthesis in TM cells, and in turn may maintain normal resistance of aqueous humor outflow. This study contributes to the understanding of the important role of fibulin-3 in TM pathophysiology and provides a new possible POAG therapeutic approach.

Instrument-tissue interaction detection task, which helps understand surgical activities, is vital for constructing computer-assisted surgery systems but with many challenges. Firstly, most models represent instrument-tissue interaction in a coarse-grained way which only focuses on classification and lacks the ability to automatically detect instruments and tissues. Secondly, existing works do not fully consider relations between intra- and inter-frame of instruments and tissues. In the paper, we propose to represent instrument-tissue interaction as quintuple and present an Instrument-Tissue Interaction Detection Network (ITIDNet) to detect the quintuple for surgery videos understanding. Specifically, we propose a Snippet Consecutive Feature (SCF) Layer to enhance features by modeling relationships of proposals in the current frame using global context information in the video snippet. We also propose a Spatial Corresponding Attention (SCA) Layer to incorporate features of proposals between adjacent frames through spatial encoding. To reason relationships between instruments and tissues, a Temporal Graph (TG) Layer is proposed with intra-frame connections to exploit relationships between instruments and tissues in the same frame and inter-frame connections to model the temporal information for the same instance. For evaluation, we build a cataract surgery video (PhacoQ) dataset and a cholecystectomy surgery video (CholecQ) dataset. Experimental results demonstrate the promising performance of our model, which outperforms other state-of-the-art models on both datasets.

Objective: This study aimed to investigate the surgical approaches, clinical efficacy, and indications of a novel acetabular anatomical locking plate for acetabular fractures involving the quadrilateral plate. Methods: Patients with acetabular fracture treated with the novel acetabular quadrilateral anatomical locking plates in our department from December 2017 to June 2020 were collected. According to the fracture types, a 1:1 matched-pair analysis was carried out and patients treated with reconstruction plates were selected. These 2 groups of patients were included in the observation group and control group, respectively, and ultimately each group included 11 patients. The time between injury and definitive surgery, surgical approaches, operation time, intraoperative blood loss volume, intraoperative blood transfusion volume, postoperative blood transfusion volume, fracture union time, reduction loss, and postoperative complications were recorded. The fracture reduction quality and hip function were respectively evaluated by Matta's grading system and the modified Merle D'Aubigne-Postel grading system. A comparison was made to observe whether the 2 groups had differences in the preceding clinical parameters. Results: As for the observation group, the mean operation time was 327.82 +/- 137.46 min (range: 120 similar to 580 min; median: 323 min), the mean intraoperative blood loss volume was 1745.46 +/- 2103.98 mL (range: 300 similar to 7000 mL; median: 1000 mL), and the mean intraoperative blood transfusion volume was 1526.18 +/- 1617.46 mL (range: 0 similar to 5130 mL; median: 900 mL), and the mean postoperative blood transfusion volume was 254.55 +/- 439.01 mL (range:0 similar to 1400 mL; median:0 mL). During the follow-up period ranging from 9 to 28 months, 1 incision lipoliquefaction, 1 heterotopic ossification, and 1 traumatic arthritis were recorded. According to Matta's grading system, 4 anatomic reductions, 6 imperfect reductions, and 1 poor reduction were recorded, and the rate of satisfactory reduction quality was 90.91%. According to the modified Merle D'Aubigne-Postel grading system, 5 excellent, 4 good, 1 fair, and 1 poor were recorded, and the rate of satisfactory hip function was 81.82%. As for the control group, the mean operation time was 273.18 +/- 99.15 min (range: 120 similar to 450 min; median: 270 min), the mean intraoperative blood loss volume was 1122.73 +/- 469.77 mL (range: 300 similar to 1500 mL; median: 1500 mL), and the mean intraoperative blood transfusion volume was 608.55 +/- 363.71 mL (range: 0 similar to 1086 mL; median: 758 mL), the mean postoperative blood transfusion volume was 281.82 +/- 430.86 mL (range:0 similar to 1000 mL; median:0 mL). During the follow-up period ranging from 9 to 42 months, 2 instances of traumatic arthritis and 1 femoral head necrosis were recorded. According to Matta's grading system, 2 anatomic reductions, 6 imperfect reductions, and 3 poor reductions were recorded, and the rate of satisfactory reduction quality was 72.73%. According to the modified Merle D'Aubigne-Postel grading system, 1 excellent, 7 good, 0 fair, and 3 poor were recorded, and the rate of satisfactory hip function was 72.73%. All the patients obtained fracture union, and no reduction loss was recorded. According to statistical analysis, there were no significant differences between the 2 groups in the time between the injury and definitive surgery, surgical approaches, intraoperative blood loss volume, intraoperative blood transfusion volume, postoperative blood transfusion volume, rate of satisfactory reduction quality, hip function score, and rate of satisfactory hip function. Conclusions: Through 3 kinds of anterior approaches, the novel anatomical locking plate can be used to fix acetabular fractures involving the quadrilateral plate including anterior wall fractures, anterior column fractures, transverse fractures, and double-column fractures, which can obtain satisfactory fracture reduction quality, limit the medial displacement of the quadrilateral plate effectively, restore the postoperative hip function well, and obtain a comparable clinical efficacy as the reconstruction plate.

AIM: To analyze the changes of serum homocysteine(Hcy), vitamin B12(VitB12)and folic acid in the serum of patients with diabetic retinopathy(DR), and to explore their significance in the occurrence and development of DR.METHODS: A case-control study was designed. A total of 95 patients with DR(DR group), 94 patients with diabetes mellitus(DM group)treated in endgcrinology department and 87 patients with age-related cataract(normal control group)from the ophthalmology department of Shenzhen People's Hospital between July 2021 and January 2022 were selected. Fasting venous blood was collected and serum was separated. The concentration of Hcy in serum was detected by enzyme linked immunosorbent assay(ELISA), and chemiluminescence immunoassay was used to detect the concentration of VitB12 and folic acid. Pearson linear correlation analysis was used to evaluate the correlation between Hcy and clinical parameters. Multivariate linear regression analysis was used to evaluate the main factors which affect Hcy level. Receiver operating characteristic(ROC)curve was designed to analyze the diagnostic value of serum Hcy, VitB12 and folic acid in DR.RESULTS: The concentration of serum Hcy in DR group was 16.52±3.54 μmol/L, which was significantly higher than that in DM group(10.86±3.47 μmol/L)and control group(6.84±1.39 μmol/L; all P<0.05); The concentration of VitB12 in the serum of the control group was 501.79±108.95 pmol/L, which was higher than that in DM group(478.57±57.85 pmol/L)and DR group(455.88±181.49 pmol/L), but the difference was not statistically significant(P=0.054); The concentration of folic acid in serum of control group was 10.31±2.43 nmol/L, which was higher than that of DM group(9.94±1.90 nmol/L)and DR group(7.27±2.79 nmol/L), and the difference between DR group and DM group was statistically significant(P<0.05); In DR group, Hcy expression was weakly positively correlated with triglyceride and low density lipoprotein(r=0.208, P=0.043; r=0.240, P=0.019). Multivariate linear regression showed that low density lipoprotein was an important factor which affect the expression of Hcy in DR patients. ROC curve shows that Hcy has important value in the diagnosis of DR.CONCLUSIONS: Hcy, VitB12 and folic acid are differentially expressed in DR group, DM group and normal control group. Hcy may be involved in the pathogenesis of DR, and it has important value in the diagnosis of DR. In addition, low density lipoprotein is also an important factor which affects the expression of Hcy.

In computer-assisted surgeries, monocular depth estimation plays an important role, which provides navigation for surgeons by computing precise depth information. In recent years, depth estimation has achieved significant breakthroughs with the application of deep learning. However, the lack of depth ground truth in the ophthalmology surgery scene has become an obstacle to the development of depth estimation in this scene. To resolve this problem, we built one synthetic dataset for cataract surgeries. The dataset contains information on RGB images, depth maps, and segmentation masks. We also adopt the state-of-the-art methods of depth estimation on this dataset as the baseline model to build the benchmark. We also analyze the generalization of the baseline models trained on the synthetic dataset to the real surgical scene.

AIM: To evaluate the efficacy and safety of different Conbercept treatment on diabetic macular edema(DME)with 3+PRN and 5+PRN.METHODS: Retrospective case-control study. A total of 51 patients(92 eyes)with DME who were treated in our hospital during December 2019 and June 2020 were included, and they were divided into 3+PRN group with 26 cases(48 eyes)and 5+PRN group with 25 cases(44 eyes). All patients received monthly follow-up for 12mo and the changes of best-corrected visual acuity(BCVA)and central macular thickness(CMT), the number of intravitreal injections and the occurrence of complications were compared and observed in the two groups.RESULTS:After follow-up for 12mo, there was no difference in the average injection times between the 3+PRN group and the 5+PRN group(7.24±0.91 times vs. 7.56±1.04 times, P=0.117). The BCVA and CMT of the two groups improved at 3, 6, 9, and 12mo after treatment compared with those before treatment(all P<0.05), and the BCVA and CMT of the 5+PRN group were better than those of the 3+PRN group at 6, 9, and 12mo after treatment(all P<0.05). During the follow-up period, no serious adverse events occurred in the two groups of patients, and the total incidence of ocular adverse events in the two groups was 27%. All adverse events were improved after symptomatic treatment.CONCLUSION: Both the 3+PRN and 5+PRN treatment strategy of Conbercept can treat DME safely and effectively, the total times of injection were comparable. However, the BCVA and CMT improved more in the 5+PRN group than that in 3+PRN group.