ABSTRACT
In this paper, a multifunctional device and a design method are proposed based on the vanadium dioxide (VO2)-assisted metamaterial structure. The structure comprises several layers arranged from top to bottom, including a VO2 patch layer, a polyimide (PI) dielectric layer, an elliptical metal layer, a VO2 thin film layer, another PI dielectric layer, and a bottom metal layer. The research results show that the metamaterial structure enables linear-to-linear (LTL) polarization conversion and linear-to-circular (LTC) polarization conversion across multiple frequency bands when the VO2 is in the insulating state. Moreover, as the VO2 material undergoes a transition from the insulating state to the metallic state, the multifunctional structure can function as a broadband absorber, exhibiting an absorption rate of over 90% within the frequency range of 1.751-3.853 THz, with a relative bandwidth of 75%. This versatile conversion device holds great potential for applications in terahertz system and smart system fields.
ABSTRACT
OBJECTIVES: To investigate the molecular mechanism of edaravone (EDA) in improving the post-traumatic brain injury (TBI) dysfunction in learning and memory. METHODS: In vitro and in vivo TBI models were established using hydrogen peroxide (H2O2) treatment for hippocampal nerve stem cells (NSCs) and surgery for rats, followed by EDA treatment. WST 1 measurement, methylthiazol tetrazolium assay, and flow cytometry were performed to determine the activity, proliferation, and apoptosis of NSCs, and malondialdehyde (MDA), lactic dehydrogenase (LDH), and reactive oxygen species (ROS) detection kits were used to analyze the oxides in NSCs. RESULTS: Following EDA pretreatment, NSCs presented with promising resistance to H2O2-induced oxidative stress, whereas NSCs manifested significant increases in activity and proliferation and a decrease in apoptosis. Meanwhile, for NSCs, EDA pretreatment reduced the levels of MDA, LDH, and ROS, with a significant upregulation of Nrf2/antioxidant response element (ARE) signaling pathway, whereas for EDA-treated TBI rats, a significant reduction was observed in the trauma area and injury to the hippocampus, with improvement in memory and learning performance and upregulation of Nrf2/ARE signaling pathway. CONCLUSIONS: EDA, by regulating the activity of Nrf2/ARE signal pathway, can improve the TBI-induced injury to NSCs and learning and memory dysfunction in rats.
Subject(s)
Antioxidant Response Elements , Brain Injuries, Traumatic , Edaravone , Learning , Memory , NF-E2-Related Factor 2 , Animals , Apoptosis/drug effects , Brain Injuries, Traumatic/drug therapy , Brain Injuries, Traumatic/metabolism , Brain Injuries, Traumatic/physiopathology , Edaravone/pharmacology , Learning/drug effects , Memory/drug effects , NF-E2-Related Factor 2/metabolism , Oxidative Stress/drug effects , Rats , Reactive Oxygen Species/metabolism , Signal Transduction/drug effectsABSTRACT
OBJECTIVES: To investigate the molecular mechanism of edaravone (EDA) in improving the post-traumatic brain injury (TBI) dysfunction in learning and memory. METHODS: In vitro and in vivo TBI models were established using hydrogen peroxide (H2O2) treatment for hippocampal nerve stem cells (NSCs) and surgery for rats, followed by EDA treatment. WST 1 measurement, methylthiazol tetrazolium assay, and flow cytometry were performed to determine the activity, proliferation, and apoptosis of NSCs, and malondialdehyde (MDA), lactic dehydrogenase (LDH), and reactive oxygen species (ROS) detection kits were used to analyze the oxides in NSCs. RESULTS: Following EDA pretreatment, NSCs presented with promising resistance to H2O2-induced oxidative stress, whereas NSCs manifested significant increases in activity and proliferation and a decrease in apoptosis. Meanwhile, for NSCs, EDA pretreatment reduced the levels of MDA, LDH, and ROS, with a significant upregulation of Nrf2/antioxidant response element (ARE) signaling pathway, whereas for EDA-treated TBI rats, a significant reduction was observed in the trauma area and injury to the hippocampus, with improvement in memory and learning performance and upregulation of Nrf2/ARE signaling pathway. CONCLUSIONS: EDA, by regulating the activity of Nrf2/ARE signal pathway, can improve the TBI-induced injury to NSCs and learning and memory dysfunction in rats.
