End-to-End Automatic Classification of Retinal Vessel Based on Generative Adversarial Networks with Improved U-Net.

The retinal vessels in the human body are the only ones that can be observed directly by non-invasive imaging techniques. Retinal vessel morphology and structure are the important objects of concern for physicians in the early diagnosis and treatment of related diseases. The classification of retinal vessels has important guiding significance in the basic stage of diagnostic treatment. This paper proposes a novel method based on generative adversarial networks with improved U-Net, which can achieve synchronous automatic segmentation and classification of blood vessels by an end-to-end network. The proposed method avoids the dependency of the segmentation results in the multiple classification tasks. Moreover, the proposed method builds on an accurate classification of arteries and veins while also classifying arteriovenous crossings. The validity of the proposed method is evaluated on the RITE dataset: the accuracy of image comprehensive classification reaches 96.87%. The sensitivity and specificity of arteriovenous classification reach 91.78% and 97.25%. The results verify the effectiveness of the proposed method and show the competitive classification performance.

Mouse mesenchymal stem cell-derived exosomal miR-466f-3p reverses EMT process through inhibiting AKT/GSK3ß pathway via c-MET in radiation-induced lung injury.

BACKGROUND: Radiation-induced lung fibrosis (RILF) is a common complication of thoracic radiotherapy. Alveolar epithelial cells play a crucial role in lung fibrosis via epithelial-mesenchymal transition (EMT). Exosomes derived from mesenchymal stem cells own the beneficial properties to repair and regeneration of damaged tissues, however the underlying mechanisms remain poorly understood. METHODS: Mouse mesenchymal stem cells-derived exosomes (mMSCs-Exo) were isolated by differential centrifugation, and their protective effects were assessed in vivo and in vitro, respectively. EMT-associated proteins were measured via western blot assay and/or immunofluorescence staining. The miRNA expression was measured by microarray assay and qPCR. Furthermore, bioinformatics prediction with KEGG analysis, luciferase assay, and rescue experiments were performed to explore the molecular mechanism underlying miR-466f-3p. RESULTS: mMSCs-Exos were efficiently isolated ranging from 90-150 nm with high expression of exosomal markers (CD63, TSG101, and CD9). mMSCs-Exos administration efficiently relieved radiation-induced lung injury with less collagen deposition and lower levels of IL-1ß and IL-6. Meanwhile, in vitro results showed mMSCs-Exos treatment obviously reversed EMT process induced by radiation. Among enriched miRNA cargo in exosomes, miR-466f-3p was primarily responsible for the protective effects via inhibition of AKT/GSK3ß pathway. Our mechanistic study further demonstrated that c-MET was the direct target of miR-466f-3p, whose restoration partially abrogated mMSCs-Exo-mediated inhibition in both EMT process and AKT/GSK3ß signaling activity induced by radiation. CONCLUSIONS: Our findings indicated that exosomal miR-466f-3p derived from mMSCs may possess anti-fibrotic properties and prevent radiation-induced EMT through inhibition of AKT/GSK3ß via c-MET, providing a promising therapeutic modality for radiation-induced lung fibrosis.

[Association between murine double minute 2 expression and AngII and ceramide induced endothelial cells apoptosis].

OBJECTIVE: To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis. METHOD: Human umbilical endothelial cells (ECs) were cultured in vitro and treated with angiotensin II alone or in combination with losartan (an inhibitor of AT1), PD123319 (an inhibitor of AT2) and FB1 (an inhibitor of ceramidase) respectively. ECs were also treated with different doses of C2-ceramide. The apoptosis of ECs was detected with Tunel, the mdm2 mRNA and protein expressions were measured with reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: PD123319 and FB1 but not losartan inhibited AngII induced ECs apoptosis and down-regulated the AngII induced increased mdm2 expressions. C2-ceramide also induces ECs apoptosis and down-regulated mdm2 expressions at protein and mRNA levels in a dose-dependent manner. CONCLUSIONS: AngII binding with AT2 induces ECs apoptosis via ceramide. AngII and ceramide induce EC apoptosis by inhibiting mdm2.