城市快速路作为重要交通走廊,其合流区交通调度更为复杂。为保障智能网联车辆(Connected and Automated Vehicle, CAV)在城市快速路合流区高效、安全、舒适行驶,基于城市快速路合流区的换道特征,开展了考虑换道风险动态评估结果的CAV换...城市快速路作为重要交通走廊,其合流区交通调度更为复杂。为保障智能网联车辆(Connected and Automated Vehicle, CAV)在城市快速路合流区高效、安全、舒适行驶,基于城市快速路合流区的换道特征,开展了考虑换道风险动态评估结果的CAV换道决策模型的相关研究。首先,对换道车辆与邻车进行时空重叠分析,将分析结果作为潜在风险判别依据,对存在时空重叠的CAV及其邻车计算换道碰撞时间(Lane Change Time to Collision, LCTTC),实现换道风险动态评估;然后,将换道风险动态评估结果融入多目标奖励函数优化的DQN(Deep Q-Network)网络结构,并综合考虑车辆行驶高效性、安全性与舒适性等因素,提出具有风险感知的SIDQN(Security Improvement Deep Q-Network)换道决策;最后,通过仿真试验进行验证。研究结果表明:相较于对比策略,提出的SIDQN策略换道成功率保持在95%以上,且运行平均速度不低于21.008 m·s^(-1);此外,在复杂的交通合流场景中,融入安全性奖励的SIDQN策略表现出最佳安全性,其LCTTC平均占比仅为9.56%,远低于其他对比策略,同时事故率统计结果持续保持较低水平;在舒适性方面,SIDQN策略下换道次数仅为4次,连续换道和无效换道次数均为1次,并显著降低了频繁换道和极端加速减速操作次数,提升了乘客的舒适体验。提出的换道决策模型综合性能优势明显,可为智能网联环境下城市快速路合流区CAV安全换道决策研究提供参考。展开更多
Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type ...Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type calcium channels.T-type calcium channel blockers,such as pimozide and mibefradil,have been shown to prevent cerebral ischemia/reperfusion injury-induced brain injury.However,the role of Cav3.2 channels in cerebral ischemia/reperfusion injury remains unclear.Here,in vitro and in vivo models of cerebral ischemia/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia/reoxygenation exposure in primary hippocampal neurons.The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons.We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia/reperfusion injury.Cav3.2 knockout markedly reduced infarct volume and brain water content,and alleviated neurological dysfunction after cerebral ischemia/reperfusion injury.Additionally,Cav3.2 knockout attenuated cerebral ischemia/reperfusion injury-induced oxidative stress,inflammatory response,and neuronal apoptosis.In the hippocampus of Cav3.2-knockout mice,calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia/reperfusion injury.These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin/nuclear factor of activated T cells 3 signaling.Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia/reperfusion injury.展开更多
Allergic inflammation is closely related to the activation of mast cells(MCs),which is regulated by its intracellular Ca^(2+) plevel,but the intake and effects of the intracellular Ca^(2+) premain unclear.The Ca^(2+) ...Allergic inflammation is closely related to the activation of mast cells(MCs),which is regulated by its intracellular Ca^(2+) plevel,but the intake and effects of the intracellular Ca^(2+) premain unclear.The Ca^(2+) pinflux is controlled by members of Ca^(2+) pchannels,among which calcium voltage-gated channel subunit alpha1 C(CaV1.2)is the most robust.This study aimed to reveal the role and underlying mechanism of MC CaV1.2 in allergic inflammation.We found that CaV1.2 participated in MC activation and allergic inflammation.Nimodipine(Nim),as a strong CaV1.2-specific antagonist,ameliorated allergic inflammation in mice.Further,CaV1.2 activation in MC was triggered by phosphatizing at its Ser1928 through protein kinase C(PKC),which calcium/calmodulin-dependent protein kinase II(CaMKII)catalyzed.Overexpression or knockdown of MC CaV1.2 influenced MC activation.Importantly,CaV1.2 expression in MC had detrimental effects,while its deficiency ameliorated allergic pulmonary inflammation.Results provide novel insights into CaV1.2 function and a potential drug target for controlling allergic inflammation.展开更多
文摘城市快速路作为重要交通走廊,其合流区交通调度更为复杂。为保障智能网联车辆(Connected and Automated Vehicle, CAV)在城市快速路合流区高效、安全、舒适行驶,基于城市快速路合流区的换道特征,开展了考虑换道风险动态评估结果的CAV换道决策模型的相关研究。首先,对换道车辆与邻车进行时空重叠分析,将分析结果作为潜在风险判别依据,对存在时空重叠的CAV及其邻车计算换道碰撞时间(Lane Change Time to Collision, LCTTC),实现换道风险动态评估;然后,将换道风险动态评估结果融入多目标奖励函数优化的DQN(Deep Q-Network)网络结构,并综合考虑车辆行驶高效性、安全性与舒适性等因素,提出具有风险感知的SIDQN(Security Improvement Deep Q-Network)换道决策;最后,通过仿真试验进行验证。研究结果表明:相较于对比策略,提出的SIDQN策略换道成功率保持在95%以上,且运行平均速度不低于21.008 m·s^(-1);此外,在复杂的交通合流场景中,融入安全性奖励的SIDQN策略表现出最佳安全性,其LCTTC平均占比仅为9.56%,远低于其他对比策略,同时事故率统计结果持续保持较低水平;在舒适性方面,SIDQN策略下换道次数仅为4次,连续换道和无效换道次数均为1次,并显著降低了频繁换道和极端加速减速操作次数,提升了乘客的舒适体验。提出的换道决策模型综合性能优势明显,可为智能网联环境下城市快速路合流区CAV安全换道决策研究提供参考。
基金supported by the Natural Science Foundation of Anhui Province of China,No.2208085Y32Scientific Research Plan Project of Anhui Province of China,No.2022AH020076the Chen Xiao-Ping Foundation for the Development of Science and Technology of Hubei Province,No.CXPJJH12000005-07-115(all to CT).
文摘Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury.Various calcium channels are involved in cerebral ischemia/reperfusion injury.Cav3.2 channel is a main subtype of T-type calcium channels.T-type calcium channel blockers,such as pimozide and mibefradil,have been shown to prevent cerebral ischemia/reperfusion injury-induced brain injury.However,the role of Cav3.2 channels in cerebral ischemia/reperfusion injury remains unclear.Here,in vitro and in vivo models of cerebral ischemia/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia/reoxygenation exposure in primary hippocampal neurons.The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons.We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia/reperfusion injury.Cav3.2 knockout markedly reduced infarct volume and brain water content,and alleviated neurological dysfunction after cerebral ischemia/reperfusion injury.Additionally,Cav3.2 knockout attenuated cerebral ischemia/reperfusion injury-induced oxidative stress,inflammatory response,and neuronal apoptosis.In the hippocampus of Cav3.2-knockout mice,calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia/reperfusion injury.These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin/nuclear factor of activated T cells 3 signaling.Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia/reperfusion injury.
基金funded by National Natural Science Foundation of China(Grant Nos.:81930096 and 82274063).
文摘Allergic inflammation is closely related to the activation of mast cells(MCs),which is regulated by its intracellular Ca^(2+) plevel,but the intake and effects of the intracellular Ca^(2+) premain unclear.The Ca^(2+) pinflux is controlled by members of Ca^(2+) pchannels,among which calcium voltage-gated channel subunit alpha1 C(CaV1.2)is the most robust.This study aimed to reveal the role and underlying mechanism of MC CaV1.2 in allergic inflammation.We found that CaV1.2 participated in MC activation and allergic inflammation.Nimodipine(Nim),as a strong CaV1.2-specific antagonist,ameliorated allergic inflammation in mice.Further,CaV1.2 activation in MC was triggered by phosphatizing at its Ser1928 through protein kinase C(PKC),which calcium/calmodulin-dependent protein kinase II(CaMKII)catalyzed.Overexpression or knockdown of MC CaV1.2 influenced MC activation.Importantly,CaV1.2 expression in MC had detrimental effects,while its deficiency ameliorated allergic pulmonary inflammation.Results provide novel insights into CaV1.2 function and a potential drug target for controlling allergic inflammation.
