Diabetic retinopathy (DR) is increasingly recognized as a neurovascular disease driven by early retinal neurovascular dysfunction. Current therapies primarily alleviate vascular leakage but offer limited neuroprotection. Here, we have identified microRNA-15a-5p (miR-15a-5p) as an endogenous regulator of retina structure and function and evaluated its therapeutic potential against early stage DR. Using db/db mice, we investigated the effects of intravitreal delivery of a miR-15a-5p agomir initiated at 12 weeks of age. miR-15a-5p treatment preserved retinal structure and visual function, attenuated Müller cell gliosis and microglial activation, reduced neuronal apoptosis, and mitigated progressive synaptic and neuronal loss. Furthermore, miR-15a-5p alleviates blood-retinal barrier breakdown, reduces vascular leakage and leukostasis, and suppresses acellular capillary formation. Mechanistically, we identified Acyl-coenzyme A binding domain containing 3 protein (ACBD3), a Golgi-resident scaffold protein, serves as a direct functional target of miR-15a-5p. In vitro, suppression of ACBD3 by miR-15a-5p preserved Golgi integrity and limited pro-inflammatory microglial polarization, and in vivo, ACBD3 knockdown reduced retinal glial activation, inflammation, and apoptosis. Importantly, miR-15a-5p knockout mice exhibited Golgi fragmentation in the retina, supporting a critical role for miR-15a-5p in maintaining Golgi integrity. Our data suggest that miR-15a-5p is a promising clinical candidate for treatment of DR.

In this study, we aimed to identify subclinical retinal and choroidal changes in patients with type 2 diabetes mellitus without diabetic retinopathy (NDR) over two years and evaluate the risk factors associated with diabetic retinal neurodegeneration (DRN). In this prospective cohort study, retinal and choroidal thicknesses were measured using optical coherence tomography (OCT), and OCT angiography was used to analyze vessel density. Among 8020 eyes, 6644 were control eyes, and 1376 were NDR eyes, with 808 eyes completing the 2-year follow-up assessment. The NDR group exhibited significantly thinner overall retinal thickness (RT), ganglion cell-inner plexiform layer, and choroidal thickness compared to the control group (P = 0.043, P = 0.013, and P = 0.031, respectively). Additionally, the NDR group showed significant annual thinning in 3-mm overall RT, retinal nerve fiber layer, and ganglion cell complex thickness, with losses of − 1.14 μm/y, − 0.27 μm/y, and − 0.62 μm/y, respectively. Factors such as age, female sex, cardiovascular events, and axial length were negatively associated with DRN. Our patient cohort demonstrated that DRN precedes the microvascular changes characteristic of DR and progresses over time. Choroidal morphological features were altered and may correspond to DRN.

Excessive artificial light at night (ALAN) disrupts circadian rhythms and may accelerate ocular aging; however, personal objective dosimetry data linking evening light exposure to specific age-related eye diseases (AREDs) remain sparse. The objective of the study is to determine whether personal high-intensity light exposure during the evening transition window (20:00–23:30) is associated with the risk of incident age-related macular degeneration (AMD), cataracts, and glaucoma. This prospective cohort study utilized data from the UK Biobank. Participants (n = 82,826) were monitored for 7 days via wrist-worn accelerometers equipped with high-resolution light sensors between 2013 and 2015. Individuals with baseline eye diseases were excluded. Average light intensity (lux) during the evening transition period (20:00–23:30) was categorized by percentiles (top 10

Aims To evaluate the potential causal role of sleep traits (STs) on diabetic retinopathy (DR). Methods The cross-sectional study included 23,851 patients with type 2 diabetes from the UK Biobank and used multivariate logistic models to investigate the observational association between STs and DR. Genetic correlation analysis and two-sample Mendelian randomization (MR) were conducted using ST data from the UK Biobank and DR data from the FinnGen consortium to investigate the genetic and causal associations between STs and DR. Results Patients who experienced daytime sleepiness often/all of the time had a higher risk for DR (OR: 1.40; 95% CI, 1.09–1.79; p = .008) compared with those who sometimes/never/rarely experienced daytime sleepiness. Genetic correlations between several STs and DR were detected by cross-trait linkage disequilibrium score regression. MR suggested a causal effect of self-reported daytime sleepiness (OR: 4.08; 95% CI, 1.44–11.61; p = .008), and accelerator-derived sleep duration (OR: 0.73; 95% CI, 0.54–0.98; p = .036) and sleep efficiency (OR: 0.54; 95% CI, 0.36–0.80; p = .002) on DR. Conclusions STs may have a potential causal role for DR. Attention should be paid to the STs of patients for better prevention and treatment of DR.

To evaluate the surgical results of scleral buckling (SB) combined with a noncontact wide-angle viewing system with a cannula-based 25G endo-illumination for the management of rhegmatogenous retinal detachments (RRDs) with subretinal proliferation, as well as undetected retinal breaks, in young adults, to explore characteristics of the undetected breaks. The medical records of 26 young RRD patients with undetected retinal breaks and subretinal proliferations who underwent encircling using an SB combined noncontact wide-angle viewing system with a cannula-based 25G endo-illumination were assessed, as were their follow-ups at 1 and 6 months after surgery. Retinal breaks were found and treated in 24 (92.3

The pyroptosis of retinal Müller cells is intricately linked to the pathogenesis of diabetic retinopathy (DR). Ubiquitin-fold modifier 1 (UFM1)-mediated UFMylation plays an important role in insulin and diabetes mellitus metabolism and regulates cell death such as apoptosis and pyroptosis. UFM1-specific protease 2 (UFSP2) mediates the maturation of the UFM1 precursor and thus affects UFMylation reaction. However, its role in DR remains unknown. The aim of our study was to determine the mechanism and upstream regulation of UFSP2 on the pyroptosis of rat retinal Müller cells. Pathological changes, UFSP2 expression and succinate accumulation were determined in retinal tissues of db/db diabetic mice via Hematoxylin and eosin and immunofluorescence staining and biochemical analysis. High glucose (HG) was used to construct a DR cell model using rat retinal Müller cells (rMC-1). Ufsp2 RNA interference and overexpression plasmids were constructed to determine the effects of UFSP2. Pyroptosis and reactive oxygen species (ROS) levels were assessed via flow cytometry. Inflammatory cytokine (IL-1β and IL-18) levels and key molecular markers related to pyroptosis (NLRP3, ASC, Caspase-1p20, GSDMD-N) were measured by enzyme linked immunosorbent assay and Western blot, respectively. Succinate-mediated H3K3me3 enrichment in Ufsp2 promoter region was measured by chromatin immunoprecipitation. In vivo experiments revealed that the UFSP2 expression and succinate levels were increased in retinal tissues of db/db diabetic mice with thinning of retinal thickness. Moreover, in vitro experiments showed that The mRNA and protein levels of Ufsp2 exhibited a time-dependent increase under HG conditions. Upon Ufsp2 knockdown, the elevated oxidative stress, inflammatory responses, and pyroptosis stimulated by HG were significantly suppressed. The effect of Ufsp2 overexpression on pyroptosis and inflammatory responses was consistent with the HG stimulation, whereas the UFSP2-induced heightened levels of pyroptosis as well as the inflammatory state were significantly reversed when co-administered with NLRP3 inhibitor or ROS inhibitor. Further activating NLRP3 inflammasome using LPS + ATP stimulation revealed that the knockdown of Ufsp2 resulted in inhibited pyroptosis levels and inflammatory responses, while the Ufsp2 overexpression markedly increased pyroptosis and inflammatory responses. Lastly, succinate was demonstrated to influence Ufsp2 transcription, as well as the expression of H3K3me3 and its enrichment in the Ufsp2 promoter region, ultimately affecting pyroptosis and inflammatory responses. Succinate-mediated Ufsp2 transcription promotes pyroptosis in rMC-1 cells by activating NLRP3 inflammasome and oxidative stress.

Functional hyper-connectivity in hippocampus has been recently observed in patients with an early stage of type 2 diabetes, however, the structural connectivity between hippocampus and other regions of the brain and its effects on neuropsychological performance are still unknown. Participants (82 patients with type 2 diabetes and without peripheral microvascular complications; 75 healthy controls) underwent detailed cognitive assessment and diffusion MRI. Probabilistic tractography based on a multifiber model was performed to investigate the fiber connections between hippocampus and other regions of the brain. The differences in hippocampal connectivity between groups were compared with age, sex, body mass index and education as covariates. The association between hippocampal connectivity and cognitive performances in patients with diabetes were further investigated. Patients had lower Stroop Accuracy and longer Stroop Reaction Time compared with age-, sex-, education-matched controls. Although lower hippocampal connectivities to widespread brain regions were observed in diabetic group, there were no statistical differences after FDR adjustment. Moreover, the strength of fiber connections was not associated with any cognitive performance in patients with diabetes. Taken together, worse executive function was observed in patients with an early stage of type 2 diabetes. However, it might not be related to hippocampal fiber connectivity. These findings suggested that structural connectivity in hippocampus was not an early predictor for diabetes-associated cognitive decrements.

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.

Abstract Background Limited studies have investigated the correlation between fat distribution and the risk of diabetic retinopathy (DR) in the general population with diabetes. The relationship between obesity and DR remains inconclusive, possibly due to using simple anthropometric measures to define obesity. This study investigates the relationships between the android-to-gynoid fat ratio (A/G ratio, measured using dual-energy X-ray absorptiometry) and DR within the US population with diabetes. Methods The study used a population-based, cross-sectional approach based on the 2003–2006 and 2011–2018 data of the National Health and Nutrition Examination Survey (NHANES). Multivariable logistic regression analyses were performed on participants with diabetes to evaluate the contribution of body mass index (BMI), waist-to-height ratio (WHtR), and A/G ratio to the prevalence of DR. Results The prevalence of DR was 22.2, 21.2, and 17.6% among participants with A/G ratios <1.0, 1.0–1.2, and ≥1.2, respectively. After adjusting sex, age, ethnicity, diabetes duration, hemoglobin A1c level, blood pressure level, and non-high-density lipoprotein cholesterol level, a higher A/G ratio (≥1.2) was independently associated with decreased odds of DR (odds ratio [OR], 0.565; 95% CI: 0.372–0.858) compared with the A/G ratio of 1.0–1.2. Associations between a higher A/G ratio and DR remained statistically significant after adjusting for BMI (OR, 0.567; 95% CI: 0.373–0.861) and WHtR (OR, 0.586; 95% CI: 0.379–0.907). Moreover, these associations remained statistically significant in analyses using the ethnic-specific tertiles for the A/G ratio. In sex-stratified models, these correlations remained in males. There was a significant inverse association between the A/G ratio and diabetes duration in males, which persisted after multivariable adjustments (p < 0.05). Conclusions A novel finding indicates that a higher A/G ratio is associated with a reduced likelihood of DR in males with diabetes. The results from NHANES underscore the importance of considering imaging-based fat distribution as a critical indicator in clinical practice.

Background Diabetic vascular complications share common pathophysiological mechanisms, but the relationship between diabetes‐related macrovascular complications (MacroVCs) and incident diabetic microvascular complications remains unclear. We aimed to investigate the impact of MacroVCs on the risk of microvascular complications. Methods and Results There were 1518 participants with type 1 diabetes (T1D) and 20 802 participants with type 2 diabetes from the UK Biobank included in this longitudinal cohort study. MacroVCs were defined by the presence of macrovascular diseases diagnosed after diabetes at recruitment, including coronary heart disease, peripheral artery disease, stroke, and ≥2 MacroVCs. The primary outcome was incident microvascular complications, a composite of diabetic retinopathy, diabetic kidney disease, and diabetic neuropathy. During a median (interquartile range) follow‐up of 11.61 (5.84–13.12) years and 12.2 (9.50–13.18) years, 596 (39.3%) and 4113 (19.8%) participants developed a primary outcome in T1D and type 2 diabetes, respectively. After full adjustment for conventional risk factors, Cox regression models showed significant associations between individual as well as cumulative MacroVCs and the primary outcome, except for coronary heart disease in T1D (T1D: diabetes coronary heart disease: 1.25 [0.98–1.60]; diabetes peripheral artery disease: 3.00 [1.86–4.84]; diabetes stroke: 1.71 [1.08–2.72]; ≥2: 2.57 [1.66–3.99]; type 2 diabetes: diabetes coronary heart disease: 1.59 [1.38–1.82]; diabetes peripheral artery disease: 1.60 [1.01–2.54]; diabetes stroke: 1.50 [1.13–1.99]; ≥2: 2.66 [1.92–3.68]). Subgroup analysis showed that strict glycemic (glycated hemoglobin <6.5%) and blood pressure (<140/90 mm Hg) control attenuated the association. Conclusions Individual and cumulative MacroVCs confer significant risk of incident microvascular complications in patients with T1D and type 2 diabetes. Our results may facilitate cost‐effective high‐risk population identification and development of precise prevention strategies.

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.

Controlled metabolic factors and socioeconomic status (SES) was crucial for prevention of diabetic retinopathy (DR). The study aims to assess the metabolic factors control and SES among working-age adults (18–64 years) with diabetes compared to older adults (65 years and older). Totals of 6738 participants with self-reported diagnosed diabetes from National Health and Nutrition Examination Survey were included, of whom 3482 were working-age and 3256 were elderly. The prevalence of DR, metabolic factors control, and the impact of SES and diabetic duration on DR was estimated. Subgroup analysis among working-age adults was employed across different diabetic duration and SES level. The prevalence of DR was 20.8

This case report documents progression of myelinated retinal nerve fibers in a young boy from age 6 months to 2 years.

AIMS:To investigate the precise association between BMI and waist circumference (WC) and diabetic complications, including retinopathy (DR), nephropathy (DN) and peripheral neuropathy (DPN).METHODS:A multivariable-adjusted Cox proportional hazard model was used to evaluate the observed association from 30,541 UK Biobank participants with diabetes. A two-sample Mendelian randomization (MR) framework was applied to summary-level GWASs of BMI and WC comprising a total of 461,460 and 462,166 participants from UK Biobank to explore the potential causal association.RESULTS:Higher BMI and WC were associated with increased risks of DR, DN, and DPN (HR (95% CI), per-SD increase: BMI: DR 1.09 (1.04-1.13), DN 1.37 (1.33-1.41), DPN 1.27 (1.20-1.34); WC: DR 1.11 (1.07-1.16), DN 1.41 (1.36-1.46), DPN 1.38 (1.30-1.45)) in the UK Biobank cohort. Univariate MR indicated that increased BMI and WC were causal risk factors for these complications (OR (95% CI), per-SD increase: BMI: DR 1.33 (1.22-1.45), DN 1.74 (1.47-2.07), DPN 2.20 (1.67-2.90); WC: DR 1.43 (1.27-1.61), DN 2.03 (1.62-2.55), DPN 2.80 (1.99-3.92)), and the effect sizes remained significant after adjustment for glycated hemoglobin.CONCLUSIONS:Prospective observational and MR analyses provided evidence that high BMI and WC may represent potential causal risk factors for diabetic microvascular complications. Weight control might modify the risks of these complications independently of glycemic control and should be considered as a therapeutic recommendation.

Endothelial dysfunction is a critical and initiating factor of the vascular complications of diabetes. Inflammation plays an important role in endothelial dysfunction regulated by epigenetic modifications. N6-methyladenosine (m6A) is one of the most prevalent epigenetic modifications in eukaryotic cells. In this research, we identified an m6A demethylase, fat mass and obesity-associated protein (FTO), as an essential epitranscriptomic regulator in diabetes-induced vascular endothelial dysfunction. We showed that enhanced FTO reduced the global level of m6A in hyperglycemia. FTO knockdown in endothelial cells (ECs) resulted in less inflammation and compromised ability of migration and tube formation. Compared with EC Ftofl/fl diabetic mice, EC-specific Fto-deficient (EC FtoΔ/Δ) diabetic mice displayed less retinal vascular leakage and acellular capillary formation. Furthermore, methylated RNA immunoprecipitation sequencing (MeRIP-Seq) combined with RNA-Seq indicated that Tnip1 served as a downstream target of FTO. Luciferase activity assays and RNA pull-down demonstrated that FTO repressed TNIP1 mRNA expression by erasing its m6A methylation. In addition, TNIP1 depletion activated NF-κB and other inflammatory factors, which aggravated retinal vascular leakage and acellular capillary formation, while sustained expression of Tnip1 by intravitreal injection of adeno-associated virus alleviated endothelial impairments. These findings suggest that the FTO-TNIP1-NF-κB network provides potential targets to treat diabetic vascular complications.

Background: Transient receptor potential channel 6 (TRPC6) is reported to be involved in the pathogenesis of diabetic complications, but its role in diabetic retinopathy (DR) remains unknown. The aim of our study was to determine the role and mechanism of TRPC6 in DR.Methods: High glucose was used to construct a DR cell model using rat retinal Muller cells (rMC-1). Intracellular Ca2+, reactive oxygen species (ROS) and cell pyroptosis were evaluated by flow cytometry. Protein levels of NLRP3, pro-caspase-1, active caspase-1, gasdermin D (GSDMD), GSDMD-N, TRPC6 and H3K27ac were detected by Western blot. mRNA levels of EP300 and TRPC6 were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Levels of IL-113 and IL-18 were estimated by enzyme linked immunosorbent assay (ELISA). The interaction between EP300 and TRPC6 was validated by a chromatin immunoprecipitation assay.Results: The knockdown of TRPC6 reduced inflammation and cell pyroptosis in HG induced rMC-1 cells, whereas overexpression of TRPC6 had the opposite effects. The inhibition of ROS and NLRP3 reversed TRPC6-mediated cell pyroptosis in the DR cell model. In addition, EP300 increased the expression of H3K27ac and TRPC6 to promote cell pyroptosis, which was suppressed by the knockdown of TRPC6.Conclusions: Our study revealed a novel EP300/H3K27ac/TRPC6 signaling pathway that may contribute to HG induced Muller cell pyroptosis. TRPC6 played a novel role in Muller cell pyroptosis triggered by HG, and may be a potential target for DR treatment in the future.

INTRODUCTION Walking pace is associated with various health-related outcomes. The aim of this study was to investigate the association between self-reported walking pace and the incidences of diabetic microvascular complications among participants with type 2 diabetes (T2D). METHODS Self-reported walking pace was classified as brisk, average, or slow. The outcomes were the incidences of diabetic retinopathy, diabetic neuropathy, and diabetic nephropathy. COX proportional hazards models adjusted for sociodemographic, lifestyle, and health-related factors were used to estimate hazard ratios (HRs) and 95% CIs. RESULTS A total of 14 518 participants with T2D in the UK Biobank (mean age 59.7 ± 7.0 years, 5028 [34.6%] women) were included. During a median follow-up of 12.5 (interquartile range: 11.6-13.4) years, 2980 participants developed diabetic microvascular complications. After adjusting for confounding factors, and compared with brisk walkers, slow walkers had a multivariable-adjusted HR of 1.98 (95% CI 1.58, 2.47) for composite diabetic microvascular complications, 1.54 (95% CI 1.11, 2.14) for diabetic retinopathy, 3.26 (95% CI 2.08, 5.11) for diabetic neuropathy, and 2.32 (95% CI 1.91, 2.82) for diabetic nephropathy. Average walking pace was associated with a higher risk for diabetic nephropathy (HR 1.51, 95 CI% 1.27-1.79) compared with brisk walking. Additionally, ≥1 diabetic microvascular complication occurred in 447 (14.7%) of participants with brisk walking pace, 1702 (19.5%) with average walking pace, and 831 (30.4%) with slow walking pace. Time from study recruitment to first diagnosis was shorter in participants who reported a slow walking pace, compared with brisk or average walkers. Among participants who had diabetic nephropathy as their first diagnosis, slow walking pace was associated with subsequent risk of a second diabetic microvascular complication (HR 3.88, 95 CI% 2.27-6.60). CONCLUSIONS Self-reported slow walking pace is associated with a higher risk of diabetic microvascular complications among participants with T2D in this population-based cohort study.

This study investigated the characteristics of refractive status, visual acuity, and retinal morphology in children with a history of receiving intravitreal ranibizumab for retinopathy of prematurity (ROP). Children 4–6 years of age were enrolled and divided into the following four groups: group 1, children with a history of ROP who had been treated with intravitreal ranibizumab; group 2, children with a history of ROP who had not received any treatment; group 3, premature children without ROP; and group 4, full-term children. Refractive status, peripapillary retinal nerve fiber layer (RNFL), and macular thickness were measured. A total of 204 children were enrolled. In group 1, myopic shift was not noted, but poorer best corrected visual acuity (BCVA) and shorter axial length were observed. Significantly lower peripapillary RNFL thickness in the average total and superior quadrant, higher central subfield thickness, lower parafoveal retinal thickness in average total, superior, and nasal and temporal quadrants were observed in group 1 than in the other groups. The poor BCVA in patients with ROP was correlated with the lower RNFL thickness in the superior quadrant. Conclusion: Children with a history of type 1 ROP treated with ranibizumab did not show a myopic shift but did show abnormal retinal morphology and the poorest BCVA among all groups. We suggest that pediatric ophthalmologists should always pay attention to visual development in patients with ROP with a history of intravitreal ranibizumab.

Abstract Background To investigate the prevalence and predictors of retinal breaks reopening after vitrectomy with air tamponade in rhegmatogenous retinal detachment (RRD). Methods A retrospective cohort study was conducted in Shanghai General Hospital. Chart review was performed among 1715 patients with primary RRD who received pars plana vitrectomy (PPV) with air tamponade as initial management. Patients were followed up for recurrence. The clinical features of the eyes with retinal breaks reopening were recorded. Logistic regression was constructed to investigate the predictors for breaks reopening. Results A total of 137 (7.99%) patients had recurrent retinal detachment after PPV with air tamponade. The causes of surgery failure included new or missed retinal breaks (48.9%), reopening of original tears (43.8%) and proliferative vitreoretinopathy (7.3%). The median time to recurrence for the patients with breaks reopening was 18.0 days. Multivariate logistic regression indicated that the presence of retinal break(s) ≥ 1.5 disc diameters (DD) (odds ratio [OR]: 2.68, 95% confidence interval [CI]: 11.04–6.92, P = 0.041), and shorter period for restricted activities (OR: 0.94, 95% CI: 0.89–0.99, P = 0.020) were the independent predictors for breaks reopening. Conclusions Breaks reopening is an important cause for retinal redetachment after PPV with air tamponade in primary RRD. The first 2–4 weeks after surgery is the “risk period” for breaks reopening. Special attention should be paid for patients with retinal break(s) ≥ 1.5 DD. A prolonged period for restricted activities is recommended.

Abstract Background The aim of our research was to prospectively explore the clinical value of a deep learning algorithm (DLA) to detect referable diabetic retinopathy (DR) in different subgroups stratified by types of diabetes, blood pressure, sex, BMI, age, glycosylated hemoglobin (HbA1c), diabetes duration, urine albumin‐to‐creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR) at a real‐world diabetes center in China. Methods A total of 1147 diabetic patients from Shanghai General Hospital were recruited from October 2018 to August 2019. Retinal fundus images were graded by the DLA, and the detection of referable DR (moderate nonproliferative DR or worse) was compared with a reference standard generated by one certified retinal specialist with more than 12 years of experience. The performance of DLA across different subgroups stratified by types of diabetes, blood pressure, sex, BMI, age, HbA1c, diabetes duration, UACR, and eGFR was evaluated. Results For all 1674 gradable images, the area under the receiver operating curve, sensitivity, and specificity of the DLA for referable DR were 0.942 (95% CI, 0.920‐0.964), 85.1% (95% CI, 83.4%‐86.8%), and 95.6% (95% CI, 94.6%‐96.6%), respectively. The DLA showed consistent performance across most subgroups, while it showed superior performance in the subgroups of patients with type 1 diabetes, UACR ≥ 30 mg/g, and eGFR < 90 mL/min/1.73m2. Conclusions This study showed that the DLA was a reliable alternative method for the detection of referable DR and performed superior in patients with type 1 diabetes and diabetic nephropathy who were prone to DR.