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Although the suspension gap between a maglev train and its track is narrow, it has a significant impact on the aerodynamic performance of the train. This study investigated the effect of the suspension gap on the wake flow of a superconducting maglev train traveling at a speed of 600 km/h by comparing the aerodynamics and flow field structure of a tail car (TC) with suspension gaps of 8, 10, 12, and 14 cm. The results showed that with increasing suspension gap, the vortex structures in the wake region move closer to the TC, the airflow from the suspension gap inhibits the high-pressure region of the wake, and the pressure and velocity fluctuations significantly increase near the nose tip of the TC. Moreover, the suspension gap was found to have a significant impact on lift and almost no effect on drag. Increasing the suspension gap leads to a balance in the lift between the head car (HC) and the TC; as the gap continues to increase, the lift ratio of the HC and TC rapidly decreases. [ABSTRACT FROM AUTHOR]

Doxorubicin-induced cardiotoxicity (DIC) is one of the most severe side effects of doxorubicin, yet the underlying mechanisms remain incompletely understood. Our results showed that Neutrophil extracellular traps (NETs) accumulated in plasma and cardiac tissue after doxorubicin treatment. The inhibition of NETs formation by Pad4 gene ablation significantly attenuated doxorubicin-induced arrhythmia, prolonged survival time and reduced the levels of Troponin T (cTnT) and creatine kinase MB (CK-MB) in mice. In addition, reductions in left ventricular fractional shortening and ejection fraction induced by doxorubicin were more severe in WT mice than in Pad4 -/- mice. Immunostaining and qPCR analyses revealed that NETs activated macrophages to release pro-inflammatory cytokines such as IL-18, IL-1β, and TNF-α. IL-18, in turn, activated T cells to produce IFN-γ, which, along with TNF-α, downregulated the expression of Cx43, thereby inducing cardiac conduction abnormalities. We identify that IL-18-IFN-γ-Cx43-induced cardiac conduction abnormalities triggered by neutrophil extracellular traps is the key molecular and cellular determinants of DIC. Furthermore, targeting NETs formation using ozone therapy significantly alleviated DIC. This study highlights the critical role of NETs in the development of DIC and proposes ozone therapy as a potential therapeutic strategy for treating DIC., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025. Published by Elsevier B.V.)

Opioids, such as morphine, are the most potent drugs used to treat pain. Long-term use results in high tolerance to morphine. High mobility group box-1 (HMGB1) has been shown to participate in neuropathic or inflammatory pain, but its role in morphine tolerance is unclear. In this study, we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive days. We found that morphine induced rat spinal cord neurons to release a large amount of HMGB1. HMGB1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4 receptor expression in microglia, thereby inducing morphine tolerance. Glycyrrhizin, an HMGB1 inhibitor, markedly attenuated chronic morphine tolerance in the mouse model. Finally, compound C (adenosine 5'-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin (heme oxygenase-1 inhibitor) alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-SY5Y cell model of morphine tolerance, and alleviated morphine tolerance in the mouse model. These findings suggest that morphine induces HMGB1 release via the adenosine 5'-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway, and that inhibiting this signaling pathway can effectively reduce morphine tolerance., Competing Interests: None