Purpose Central serous chorioretinopathy (CSC) is a retinal disease that frequently shows resolution and recurrence with serous detachment of the neurosensory retina. Here, we present a deep learning analysis of subretinal fluid (SRF) lesion segmentation in fundus photographs to evaluate CSC. Methods We collected 194 fundus photographs of SRF lesions from the patients with CSC. Three graders manually annotated of the entire SRF area in the retinal images. The dataset was randomly separated into training (90%) and validation (10%) datasets. We used the U-Net segmentation model based on conditional generative adversarial networks (pix2pix) to detect the SRF lesions. The algorithms were trained and validated using Google Colaboratory. Researchers did not need prior knowledge of coding skills or computing resources to implement this code. Results The validation results showed that the Jaccard index and Dice coefficient scores were 0.619 and 0.763, respectively. In most cases, the segmentation results overlapped with most of the reference areas in the annotated images. However, cases with exceptional SRFs were not accurate in terms of prediction. Using Colaboratory, the proposed segmentation task ran easily in a web-based environment without setup or personal computing resources. Conclusions The results suggest that the deep learning model based on U-Net from the pix2pix algorithm is suitable for the automatic segmentation of SRF lesions to evaluate CSC. Translational Relevance Our code implementation has the potential to facilitate ophthalmology research; in particular, deep learning–based segmentation can assist in the development of pathological lesion detection solutions.
Dry eye disease (DED) is one of the most prevalent ocular diseases but has limited treatment options. Cystic fibrosis transmembrane conductance regulator (CFTR), a major chloride channel that stimulates fluid secretion in the ocular surface, may pave the way for new therapeutic strategies for DED. Herein, we report the optimization of Cact-3, a potent CFTR activator with poor solubility, to 16d, a potent CFTR activator with suitable solubility for eye drop formulation. Notably, 16d was well distributed in target tissues including cornea and conjunctiva with minimal systemic exposure in rabbit. Topical ocular instillation of 16d significantly enhanced tear secretion and improved corneal erosion in a mouse model of DED. In addition, 16d significantly reduced mRNA expression of pro-inflammatory cytokines including IL-1β, IL-17, and TNF-α and MMP2 in cornea and conjunctiva of DED mice.
Purpose We investigated a role of bone morphogenic protein 7 (BMP7), a member of the TGF-β superfamily on pathogenic mechanism of Graves’ orbitopathy (GO). The therapeutic effects of BMP7 on inflammation and fibrosis were evaluated in cultured Graves’ orbital fibroblasts. Methods Expression of BMP7 was compared in cultured orbital tissue explants from GO (n = 12) and normal control (n = 12) subjects using real-time PCR. Orbital fibroblasts were cultured from orbital connective tissues obtained from GO (n = 3) and normal control patients (n = 3). Cells were pretreated with recombinant human BMP7 (rhBMP7) before stimulation with TGF-β, IL-1β, and TNF-α. Fibrosis-related proteins and inflammatory cytokines were analyzed by Western blotting. The activation of signaling molecules in inflammation and fibrosis was also analyzed. Results The expressions of BMP7 mRNA were lower in GO orbital tissues than control. Fibrosis-related proteins, fibronectin, collagen 1α, and α-SMA induced by TGF-β were suppressed by treating rhBMP7, and rhBMP7 upregulated TGF-β induced SMAD1/5/8 protein expression, whereas downregulated SMAD2/3. Increased pro-inflammatory molecules, IL-6, IL-8, and intercellular adhesion molecule-1 (ICAM-1) by IL-1β or TNF-α were blocked by rhBMP7 treatment, and the expression of phosphorylated NFκB and Akt was suppressed by rhBMP7 treatment. Conclusions BMP7 transcript levels were downregulated in Graves’ orbital tissues. Exogenous BMP7 treatment showed inhibitory effects on the production of profibrotic proteins and proinflammatory cytokines in orbital fibroblasts. Our results provide a molecular basis of BMP7 as a new potential therapeutic agent through the opposing mechanism of profibrotic TGF-β/SMAD signaling and proinflammatory cytokine production.
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