文中将匝道控制中的协同调控思想引入停车场出口管理中,将停车场出口闸机抬杆频率作为控制和优化变量,设计定时控制、感应控制策略调节离场车辆速率以保证区域通行效率.以上海金鼎超大型地下停车平台作为验证实例,基于SUMO(simulation o...文中将匝道控制中的协同调控思想引入停车场出口管理中,将停车场出口闸机抬杆频率作为控制和优化变量,设计定时控制、感应控制策略调节离场车辆速率以保证区域通行效率.以上海金鼎超大型地下停车平台作为验证实例,基于SUMO(simulation of urban mobility)仿真平台模拟不同时段下实施不同策略时外部路网状态变化.结果表明:所提出的控制策略能够显著缓解区域路网的拥堵状况,提升动态交通的平均速度,同时降低外部道路交叉口的排队.展开更多
Small ubiquitin-related modifier(SUMOylation)is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload.However,the functi...Small ubiquitin-related modifier(SUMOylation)is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload.However,the function of SUMOylation after myocardial infarction(MI)and the molecular details of heart cell responses to SUMO1 deficiency have not been determined.In this study,we demonstrated that SUMO1 protein was inconsistently abundant in different cell types and heart regions after MI.However,SUMO1 knockout significantly exacerbated systolic dysfunction and infarct size after myocardial injury.Single-nucleus RNA sequencing revealed the differential role of SUMO1 in regulating heart cells.Among cardiomyocytes,SUMO1 deletion increased the Nppa^(+)Nppb^(+)Ankrd1^(+)cardiomyocyte subcluster pro-portion after MI.In addition,the conversion of fibroblasts to myofibroblasts subclusters was inhibited in SUMO1 knockout mice.Importantly,SUMO1 loss promoted proliferation of endothelial cell subsets with the ability to reconstitute neovascularization and expressed angiogenesis-related genes.Computational analysis of ligand/receptor interactions suggested putative pathways that mediate cardiomyocytes to endothelial cell communication in the myocardium.Mice preinjected with cardiomyocyte-specific AAV-SUMO1,but not the endothelial cell-specific form,and exhibited ameliorated cardiac remodeling following MI.Collectively,our results identified the role of SUMO1 in cardiomyocytes,fibroblasts,and endothelial cells after MI.These findings provide new insights into SUMO1 involvement in the patho-genesis of MI and reveal novel therapeutic targets.展开更多
文摘文中将匝道控制中的协同调控思想引入停车场出口管理中,将停车场出口闸机抬杆频率作为控制和优化变量,设计定时控制、感应控制策略调节离场车辆速率以保证区域通行效率.以上海金鼎超大型地下停车平台作为验证实例,基于SUMO(simulation of urban mobility)仿真平台模拟不同时段下实施不同策略时外部路网状态变化.结果表明:所提出的控制策略能够显著缓解区域路网的拥堵状况,提升动态交通的平均速度,同时降低外部道路交叉口的排队.
基金the Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medi-cine(Grant No.:ZYYCXTD-D-202207)the National Natural Science Foundation of China(Grant Nos.:82270304,81774050,and 81901526)+1 种基金the Tianjin Special Project of New Generation Artificial Intelligence Technology(Project No.:18ZXZNSY00260)the Ministry of Education of People's Republic of China“Program for Innovative Research Team in University”(Project No.:IRT_16R54).
文摘Small ubiquitin-related modifier(SUMOylation)is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload.However,the function of SUMOylation after myocardial infarction(MI)and the molecular details of heart cell responses to SUMO1 deficiency have not been determined.In this study,we demonstrated that SUMO1 protein was inconsistently abundant in different cell types and heart regions after MI.However,SUMO1 knockout significantly exacerbated systolic dysfunction and infarct size after myocardial injury.Single-nucleus RNA sequencing revealed the differential role of SUMO1 in regulating heart cells.Among cardiomyocytes,SUMO1 deletion increased the Nppa^(+)Nppb^(+)Ankrd1^(+)cardiomyocyte subcluster pro-portion after MI.In addition,the conversion of fibroblasts to myofibroblasts subclusters was inhibited in SUMO1 knockout mice.Importantly,SUMO1 loss promoted proliferation of endothelial cell subsets with the ability to reconstitute neovascularization and expressed angiogenesis-related genes.Computational analysis of ligand/receptor interactions suggested putative pathways that mediate cardiomyocytes to endothelial cell communication in the myocardium.Mice preinjected with cardiomyocyte-specific AAV-SUMO1,but not the endothelial cell-specific form,and exhibited ameliorated cardiac remodeling following MI.Collectively,our results identified the role of SUMO1 in cardiomyocytes,fibroblasts,and endothelial cells after MI.These findings provide new insights into SUMO1 involvement in the patho-genesis of MI and reveal novel therapeutic targets.
