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Substation network security is the key to maintaining the stable operation of power systems. In the face of growing threats of network attacks, traditional security protection measures have been brutal to meet the needs of modern power systems. Research on substation network security, situational awareness strategies, and remote operation and maintenance of equipment is essential to improve network defense capability and ensure the continuity and reliability of power supply. This study explores effective security situational awareness methods and remote operation and maintenance techniques to provide new solutions for substation network security. This paper builds an efficient network attack detection model by introducing linear discriminant analysis (LDA) and radial basis function (RBF) neural networks. The experiment uses the KDD Cup99 dataset, which is preprocessed to provide the model training and testing data. The LDA-RBF model in this paper outperforms the traditional RNF neural and BP neural networks regarding recognition rate. Specifically, the recognition rate reaches 90.2% for the Smurf attack and 100% for the Ipsweep attack. The proposed model of the study also performs well in terms of leakage and false alarm rates, with an overall recognition rate of 97.00%. This study proposes a network security situational awareness strategy and equipment remote operation and maintenance method that can effectively enhance substation networks’ security and operation and maintenance efficiency.

Type 2 diabetic osteoporosis (T2DOP) is a skeletal metabolic syndrome characterized by impaired bone remodeling due to type 2 diabetes mellitus, and there are drawbacks in the present treatment. Osteoking (OK) is widely used for treating fractures and femoral head necrosis. However, OK is seldom reported in the field of T2DOP, and its role and mechanism of action need to be elucidated. Consequently, this study investigated whether OK improves bone remodeling and the mechanisms of diabetes‐induced injury. We used db/db mice as a T2DOP model and stimulated MC3T3‐E1 cells (osteoblast cell line) with high glucose (HG, 50 mM) and advanced glycation end products (AGEs, 100 µg/mL), respectively. The effect of OK on T2DOP was assessed using a combined 3‐point mechanical bending test, hematoxylin and eosin staining, and enzyme‐linked immunosorbent assay. The effect of OK on enhancing MC3T3‐E1 cell differentiation and mineralization under HG and AGEs conditions was assessed by an alkaline phosphatase activity assay and alizarin red S staining. The AGEs/insulin‐like growth factor‐1(IGF‐1)/β‐catenin/osteoprotegerin (OPG) pathway‐associated protein levels were assayed by western blot analysis and immunohistochemical staining. We found that OK reduced hyperglycemia, attenuated bone damage, repaired bone remodeling, increased tibial and femoral IGF‐1, β‐catenin, and OPG expression, and decreased receptor activator of nuclear kappa B ligand and receptor activator of nuclear kappa B expression in db/db mice. Moreover, OK promoted the differentiation and mineralization of MC3T3‐E1 cells under HG and AGEs conditions, respectively, and regulated the levels of AGEs/IGF‐1/β‐catenin/OPG pathway‐associated proteins. In conclusion, our results suggest that OK may lower blood glucose, alleviate bone damage, and attenuate T2DOP, in part through activation of the AGEs/IGF‐1/β‐catenin/OPG pathway. [ABSTRACT FROM AUTHOR]

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder which can contribute to memory loss and cognitive damage in the elderly; moreover, evidence from clinical and animal studies demonstrated that AD always exhibit severe cognitive deficits. However, the effects of donepezil medications on cognition are controversial. Additionally, it is unclear whether donepezil can protect neurons to improve cognitive function through the brain-derived neurotropic factor (BDNF)/tyrosine receptor kinase B (TrkB) signalling pathway in the tree shrew (TS), which has a closer evolutionary relationship to primates than rodents. Here, we designed a study on an amyloid-β1-40 (Aβ1-40)-induced TS model of AD and investigated the molecular mechanism by which donepezil protects neurons and improves cognitive function through activating the BDNF/TrkB signalling pathway. The results showed that donepezil could rescue Aβ1-40-induced spatial cognition deficits, and reverse Aβ1-40-induced temporal horn along with ADC enlargement in the TS brain. Meanwhile, it suppressed Aβ1-40-induced neuronal damage and loss of body weight. Intriguingly, donepezil could increase the choline acetyl transferase (ChAT) expression level and reduce the fibrillary acid protein (GFAP) expression level in the hippocampus and cortex of TS. Additionally, donepezil significantly upregulated the expression level of BDNF, as well as the phosphorylated level of TrkB. These results suggested that donepezil could protect neurocytes from senility and ameliorate learning and memory impairment in the TS model of AD, which appeared to be through regulating the cholinergic system and inhibiting the BDNF/TrkB-dependent signalling pathway. Moreover, the study underlines the potency of TS to be a novel animal model for research on AD, and it deserves intensive attention. [ABSTRACT FROM AUTHOR]