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With the development of the times, UAVs are gradually promoted and popularized in military and civil fields, and the future airspace will also face more security risks. This paper combines the graph theory network algorithm to plan the initial path of UAV inspection and completes the dynamic collision avoidance path planning in the process of UAV inspection through the established joint model of UAV inspection sensing and avoidance. At the same time, the ant colony algorithm is introduced to improve the graph theory network algorithm to solve the dynamic collision avoidance optimal path in the process of UAV inspection. On this basis, simulation experiments of path planning design for UAV collision avoidance and kinematic simulation with two-fold priority judgment are carried out, and the kinematic parameters corresponding to the collision avoidance path are selected as the analysis anchor points. The extreme values of horizontal speed, climb speed, trajectory inclination angular rate, and heading angular rate are 31.6 m/s, 3 m/s, 5.7°/s, and 18.4°/s, respectively, which are within the given constraints, and verify the reasonableness and effectiveness of the proposed optimization scheme. The average time of the proposed algorithm is 0.0458s, which is much lower than the corresponding 0.7105s of the original scheme algorithm, through data comparison of simulation experiments and experimental validation. Using a graph theory network algorithm, the proposed optimization scheme is more efficient and stable and has a higher success rate for collision avoidance.

Bone defects are characterized by a hypoxic environment, which affects bone tissue repair. However, the role of hypoxia in the repair of alveolar bone defects remains unclear. Human periodontal ligament stem cells (hPDLSCs) are high‐quality seed cells for repairing alveolar bone defects, whose behavior changes under hypoxia. However, their mechanism of action is not known and needs to be elucidated. We hypothesized that hypoxia might be beneficial to alveolar bone defect repair and the osteogenic differentiation of hPDLSCs. To test this hypothesis, cobalt chloride (CoCl2) was used to create a hypoxic environment, both in vitro and in vivo. In vitro study, the best osteogenic effect was observed after 48 h of hypoxia in hPDLSCs, and the AKT/mammalian target of rapamycin/eukaryotic translation initiation factor 4e‐binding protein 1 (AKT/mTOR/4EBP‐1) signaling pathway was significantly upregulated. Inhibition of the AKT/mTOR/4EBP‐1 signaling pathway decreased the osteogenic ability of hPDLSCs under hypoxia and hypoxia‐inducible factor 1 alpha (HIF‐1α) expression. The inhibition of HIF‐1α also decreased the osteogenic capacity of hPDLSCs under hypoxia without significantly affecting the level of phosphorylation of AKT/mTOR/4EBP‐1. In vitro study, Micro‐CT and tissue staining results show better bone regeneration in hypoxic group than control group. These results suggested that hypoxia promoted alveolar bone defect repair and osteogenic differentiation of hPDLSCs, probably through AKT/mTOR/4EBP‐1/HIF‐1α signaling. These findings provided important insights into the regulatory mechanism of hypoxia in hPDLSCs and elucidated the effect of hypoxia on the healing of alveolar bone defects. This study highlighted the importance of physiological oxygen conditions for tissue engineering. [ABSTRACT FROM AUTHOR]

Bone defects are characterized by a hypoxic environment, which affects bone tissue repair. However, the role of hypoxia in the repair of alveolar bone defects remains unclear. Human periodontal ligament stem cells (hPDLSCs) are high-quality seed cells for repairing alveolar bone defects, whose behavior changes under hypoxia. However, their mechanism of action is not known and needs to be elucidated. We hypothesized that hypoxia might be beneficial to alveolar bone defect repair and the osteogenic differentiation of hPDLSCs. To test this hypothesis, cobalt chloride (CoCl 2 ) was used to create a hypoxic environment, both in vitro and in vivo. In vitro study, the best osteogenic effect was observed after 48 h of hypoxia in hPDLSCs, and the AKT/mammalian target of rapamycin/eukaryotic translation initiation factor 4e-binding protein 1 (AKT/mTOR/4EBP-1) signaling pathway was significantly upregulated. Inhibition of the AKT/mTOR/4EBP-1 signaling pathway decreased the osteogenic ability of hPDLSCs under hypoxia and hypoxia-inducible factor 1 alpha (HIF-1α) expression. The inhibition of HIF-1α also decreased the osteogenic capacity of hPDLSCs under hypoxia without significantly affecting the level of phosphorylation of AKT/mTOR/4EBP-1. In vitro study, Micro-CT and tissue staining results show better bone regeneration in hypoxic group than control group. These results suggested that hypoxia promoted alveolar bone defect repair and osteogenic differentiation of hPDLSCs, probably through AKT/mTOR/4EBP-1/HIF-1α signaling. These findings provided important insights into the regulatory mechanism of hypoxia in hPDLSCs and elucidated the effect of hypoxia on the healing of alveolar bone defects. This study highlighted the importance of physiological oxygen conditions for tissue engineering., (© 2024 The Authors. Cell Biology International published by John Wiley & Sons Ltd on behalf of International Federation of Cell Biology.)

A series of highly reduced Mo red clusters {Mo 28 } (1), {Mo 30 } (2), and {Mo 40 } (3) are synthesized from the rational assembly of planar {MoV4} building blocks and employed for proton conduction. 3 exhibits the best conductivity of 7.56 × 10 -3 S cm -1 under optimal conditions due to the most efficient hydrogen-bonding network.