ABSTRACT
To tackle the problems of over-reliance on traditional experience, poor troubleshooting robustness, and slow response by maintenance personnel to changes in faults in the current aircraft health management field, this paper proposes the use of a knowledge graph. The knowledge graph represents troubleshooting in a new way. The aim of the knowledge graph is to improve the correlation between fault data by representing experience. The data source for this study consists of the flight control system manual and typical fault cases of a specific aircraft type. A knowledge graph construction approach is proposed to construct a fault knowledge graph for aircraft health management. Firstly, the data are classified using the ERNIE model-based method. Then, a joint entity relationship extraction model based on ERNIE-BiLSTM-CRF-TreeBiLSTM is introduced to improve entity relationship extraction accuracy and reduce the semantic complexity of the text from a linguistic perspective. Additionally, a knowledge graph platform for aircraft health management is developed. The platform includes modules for text classification, knowledge extraction, knowledge auditing, a Q&A system, and graph visualization. These modules improve the management of aircraft health data and provide a foundation for rapid knowledge graph construction and knowledge graph-based fault diagnosis.
ABSTRACT
The protective activity of scopoletin (SPT) against glucose-induced cataract has been attributed to attenuation of aldose reductase activity and oxidative stress in a rat model. The present investigation was aimed to study the protective effect and mechanism of SPT in retinal ganglia cells (RGC) under oxidative stress and apoptosis induced by hyperglycemia. The RGC-5 cells were pre-conditioned with variable SPT concentrations for 6 hours and then subjected to hyperglycemia for 48 hours. The cell viability, mito- chondrial membrane potential (MMP) and oxidative stress markers were quantified. Western blotting was employed to screen the expression of mitogen-activated protein kinase (MAPK) and various apoptosis related proteins. SPT blocked the high-glucose induced cell injury and normalized the mitochondrial functioning via lowering the loss of MMP and release of cytochrome c. Pretreatment with SPT suppressed the enhanced ROS, malondialdehyde, and protein carbonyl content triggered by high-glucose exposure in RGC-5 cells. SPT normalized the apoptotic proteins in RGC-5 cells. The phosphorylation of c-Jun N-terminal kinases (JNK) and p38 MAPK in RGC-5 due to hyperglycemia was attenuated by SPT. Overall, SPT exhibited a protective effect in RGC-5 cells exposed to a high-glucose environment via its antioxidant efficacy, inhibition of apoptosis and modulation of the ROS-dependent p38/JNK signaling cascade.
ABSTRACT
BACKGROUND/AIMS: In this study, the molecular mechanisms of miR-27b and lipoprotein lipase (LPL) that regulate human adipose-derived mesenchymal stem cells (hASCs) adipogenic differentiation were detected. METHODS: Microarray analysis was applied to screen for differentially expressed miRNAs and mRNA during hASCs adipocyte differentiation induction. MiR-27b and LPL were found to have abnormal expression. Then, a dual luciferase reporter assay was employed to validate the targeting relationship between miR-27b and LPL. We also utilized qRT-PCR, western blot, cellular immunofluorescence and an oil red O staining assay to analyze the regulation of miR-27b and LPL during adipogenic differentiation. RESULTS: The microarray analysis demonstrated that, during adipogenic differentiation, miR-27b was down-regulated, while LPL was up-regulated but tended to become stable 14 days after induction. A dual luciferase reporter assay confirmed the negative targeting regulatory relationship between miR-27b and LPL. After overexpressing and silencing miR-27b, LPL was found to be reversely regulated by miR-27b according to qRT-PCR and western blot. The fat-formation-related biomarkers CCAAT-enhancer binding protein α (c/EBPα) and peroxisome proliferator-activated receptors γ (PPARγ) had decreasing levels after over-expressing miR-27b or knockdown of LPL followed by adipogenic differentiation. Meanwhile, the oil red O staining assay revealed that the accumulation of lipid droplets decreased. There was no change in the expression of c/EBPα, PPARγ, or lipid droplet accumulation when overexpressing miR-27b and LPL. CONCLUSION: During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.
