Stroke is a common disease in clinical practice, which seriously endangers people’s physical and mental health. The neurovascular unit (NVU) plays a key role in the occurrence and development of ischemic stroke. Different from other classical types of cell death such as apoptosis, necrosis, autophagy, and pyroptosis, ferroptosis is an iron-dependent lipid peroxidation-driven new form of cell death. Interestingly, the function of NVU and stroke development can be regulated by activating or inhibiting ferroptosis. This review systematically describes the NVU in ischemic stroke, provides a comprehensive overview of the regulatory mechanisms and key regulators of ferroptosis, and uncovers the role of ferroptosis in the NVU and the progression of ischemic stroke. We further discuss the latest progress in the intervention of ferroptosis as a therapeutic target for ischemic stroke and summarize the research progress and regulatory mechanism of ferroptosis inhibitors on stroke. In conclusion, ferroptosis, as a new form of cell death, plays a key role in ischemic stroke and is expected to become a new therapeutic target for this disease.

The nervous system is important, because it regulates the physiological function of the body. Neurons are the most basic structural and functional unit of the nervous system. The synapse is an asymmetric structure that is important for neuronal function. The chemical transmission mode of the synapse is realized through neurotransmitters and electrical processes. Based on vesicle transport, the abnormal information transmission process in the synapse can lead to a series of neurorelated diseases. Numerous proteins and complexes that regulate the process of vesicle transport, such as SNARE proteins, Munc18-1, and Synaptotagmin-1, have been identified. Their regulation of synaptic vesicle secretion is complicated and delicate, and their defects can lead to a series of neurodegenerative diseases. This review will discuss the structure and functions of vesicle-based synapses and their roles in neurons. Furthermore, we will analyze neurotransmitter and synaptic functions in neurodegenerative diseases and discuss the potential of using related drugs in their treatment.

Background AXL, a TAM tyrosine kinase receptor, plays an essential role in the pathogenesis of various solid tumours. This study explores the role of AXL and its ligand PROS1 in the generation and biological behaviour of papillary thyroid cancer (PTC). Methods The expression levels of AXL in PTC cancer tissue were analysed using immunohistochemistry (IHC) staining. The expression levels of AXL in PTC and normal thyroid cell lines were analysed using real-time quantitative polymerase chain reaction (RT-qPCR). CCK-8 was used to assess the proliferation of the PTC cell line with and without the effect of the AXL inhibitor (R428). Scratching assays played a role in evaluating the cell migration rate. Results PROS1 and AXL were expressed in TPC-1, B-CPAP, and Nthy-Ori 3–1 cells at different levels. Expression was significantly higher in PTC cell lines (TPC-1 and B-CPAP) than in the normal thyroid cell line (Nthy-Ori 3–1) (p < 0.05). In addition, AXL expression in PTC tissues was significantly higher than in adjacent normal tissues (p < 0.05). CCK-8 experiments confirmed that R428 suppresses the proliferation of PTC cell lines in a dose-dependent manner, with an increase in concentration from 0.5 to 4 μM, decreasing the inhibitory effect (p < 0.01). In addition, R428 inhibited PTC cell line migration to different degrees in a range of concentrations from 0.5 to 2 μM compared to control cells (p < 0.01). Conclusion PROS1 and its downstream receptor AXL expression were significantly higher in PTC than in normal thyroid cells. AXL expression was also higher in human PTC tissues than in normal thyroid tissues. Inhibiting the PROS1-AXL-mediated TAM signaling pathway via the AXL blocker R428 suppressed the proliferation and migration of human PTC cells, highlighting the role of this cascade in human PTC development and progression.

Upon the teenagers’ failure to obtain the plenty of physical exercises at the growth and development stage, the related central nervous system is prone to degeneration and the physical fitness starts to decline gradually. In fact, through monitoring the exercise process real-timely and quantifying the exercise data, the adolescent physical training can be effectively conducted. For such process, it involves two issues, i.e., the real-time data monitoring and data quantification evaluation. Therefore, this paper proposes a novel method based on Reinforcement Learning (RL) and Markov model to monitor and evaluate the physical training effect. Meanwhile, the RL is used to optimize the adaptive bit rate of surveillance video and help the real-time data monitoring; the Markov model is employed to evaluate the health condition on the physical training. Finally, we develop a real-time monitoring system on exercise data and compare with the state-of-the-art mechanisms based on this system platform. The experimental results indicate that the proposed performance optimization mechanism can be more efficient to conduct the physical training. Particularly the average evaluation deviation rate based on Markov model is controlled within 0.16%.

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