Allergy Test Dosage of Fluorescein Detects Diabetic Retinopathy Changes in Fundus Fluorescein Angiography.

BACKGROUND: The aims of this study were to evaluate the feasibility of allergy test dosage of fluorescein sodium (1%) for Diabetic Retinopathy (DR) detection in Fundus Fluorescein Angiography (FFA) examination as compared to the regular dosage (20%). METHODS: Totally 77 eyes from 42 DR patients were included in this prospective study. Capillary non-perfusion area, neovascularization, diabetic macular edema and microaneurysms were measured by FFA and compared at 1, 5 and 15 min after intravenous injection of 1% or 20% fluorescein sodium. RESULTS: There was no statistically significant difference in the proportions of capillary non-perfusion area and diabetic macular edema as well as the amount of neovascularization between the 1% and 20% fluorescein sodium groups. Yet, the 1% group had a significantly a smaller number of microaneurysms than the 20% group at 1 min (p < 0.001) and a smaller number of eyes with diabetic macular edema than the 20% group at 5 (p = 0.032) and 15 min (p = 0.015). The images from patients with clear vitreous had better quality than the images from patients with vitreous opacity (all p < 0.05, except comparison on neovascularization at 5 min: p > 0.999). All examined indexes showed high correlations between the 1% and 20% groups (r > 0.8, p < 0.001). CONCLUSIONS: This study demonstrated that 1% fluorescein sodium could detect the changes of DR comparably to the regular dosage.

Automatic Detection of Peripheral Retinal Lesions From Ultrawide-Field Fundus Images Using Deep Learning.

PURPOSE: To establish a multilabel-based deep learning (DL) algorithm for automatic detection and categorization of clinically significant peripheral retinal lesions using ultrawide-field fundus images. METHODS: A total of 5958 ultrawide-field fundus images from 3740 patients were randomly split into a training set, validation set, and test set. A multilabel classifier was developed to detect rhegmatogenous retinal detachment, cystic retinal tuft, lattice degeneration, and retinal breaks. Referral decision was automatically generated based on the results of each disease class. t -distributed stochastic neighbor embedding heatmaps were used to visualize the features extracted by the neural networks. Gradient-weighted class activation mapping and guided backpropagation heatmaps were generated to investigate the image locations for decision-making by the DL models. The performance of the classifier(s) was evaluated by sensitivity, specificity, accuracy, F 1 score, area under receiver operating characteristic curve (AUROC) with 95% CI, and area under the precision-recall curve. RESULTS: In the test set, all categories achieved a sensitivity of 0.836-0.918, a specificity of 0.858-0.989, an accuracy of 0.854-0.977, an F 1 score of 0.400-0.931, an AUROC of 0.9205-0.9882, and an area under the precision-recall curve of 0.6723-0.9745. The referral decisions achieved an AUROC of 0.9758 (95% CI= 0.9648-0.9869). The multilabel classifier had significantly better performance in cystic retinal tuft detection than the binary classifier (AUROC= 0.9781 vs 0.6112, P < 0.001). The model showed comparable performance with human experts. CONCLUSIONS: This new DL model of a multilabel classifier is capable of automatic, accurate, and early detection of clinically significant peripheral retinal lesions with various sample sizes. It can be applied in peripheral retinal screening in clinics.

CXCL5/CXCR2 modulates inflammation-mediated neural repair after optic nerve injury.

BACKGROUND: Previous studies reported that mild inflammation promotes retinal ganglion cell (RGC) survival and axonal regeneration after optic nerve (ON) injury with involvement of infiltrating macrophages and neutrophils. Here we aimed to evaluate the involvement and regulation of the main inflammatory chemokine pathway CXCL5/CXCR2 in the inflammation-mediated RGC survival and axonal regeneration in mice after ON injury. METHODS: The expressions and cellular locations of CXCL5 and CXCR2 were confirmed in mouse retina. Treatment effects of recombinant CXCL5 and CXCR2 antagonist SB225002 were studied in the explant culture and the ON injury model with or without lens injury. The number of RGCs, regenerating axons, and inflammatory cells were determined, and the activation of Akt andSTAT3 signaling pathways were evaluated. RESULTS: Cxcr2 and Cxcl5 expressions were increased after ON and lens injury. Addition of recombinant CXCL5 promoted RGC survival and neurite outgrowth in retinal explant culture with increase in the number of activated microglia, which was inhibited by SB225002 or clodronate liposomes. Recombinant CXCL5 also alleviated RGC death and promoted axonal regeneration in mice after ON injury, and promoted the lens injury-induced RGC protection with increase in the number of activated CD68+ cells. SB225002 inhibited lens injury-induced cell infiltration and activation, and attenuated the promotion effect on RGC survival and axonal regeneration through reduction of lens injury-induced Akt activation. CONCLUSIONS: CXCL5 promotes RGC survival and axonal regeneration after ON injury and further enhances RGC protection induced by lens injury with CD68+ cell activation, which is attenuated by CXCR2 antagonist. CXCL5/CXCR2 could be a potential therapeutic target for RGC survival promotion after ON injury.