针对智能小车转向时跟踪精度差、响应时间较慢的问题,提出了一种基于机器视觉的智能小车转向系统的滑模控制方法。首先,以感知路面信息的智能小车为研究对象,对其转向系统进行了原理分析及数学建模。通过对永磁直流电机工作过程的分析,...针对智能小车转向时跟踪精度差、响应时间较慢的问题,提出了一种基于机器视觉的智能小车转向系统的滑模控制方法。首先,以感知路面信息的智能小车为研究对象,对其转向系统进行了原理分析及数学建模。通过对永磁直流电机工作过程的分析,建立了电枢电压平衡方程和转矩平衡方程,得出了相应的传递函数,并采用实验方法对传递函数参数进行了辨识。其次,针对上述被控对象,设计了滑模控制器,并进行了稳定性证明。利用Matlab/Simulink仿真结果验证了滑模控制算法的有效性。理论结果和实验验证相结合表明,相较于PID(proportional integral differential)控制,滑模控制具有较好的跟踪精度和响应速度。在频率为20 Hz时,跟踪精度提高了89.3%。此外,滑模控制能够克服系统的不确定性,尤其是对于非线性系统,显示出良好的控制效果。展开更多
The effects of ATP-sensitive mitochondrial K + channel(mitoK ATP) on mitochondrial membrane potential(Δψm),cell proliferation and protein kinase C alpha(PKCα) expression in airway smooth muscle cells(ASMCs) were in...The effects of ATP-sensitive mitochondrial K + channel(mitoK ATP) on mitochondrial membrane potential(Δψm),cell proliferation and protein kinase C alpha(PKCα) expression in airway smooth muscle cells(ASMCs) were investigated.Thirty-six Sprague-Dawley(SD) rats were immunized with saline(controls) or ovalbumin(OVA) with alum(asthma models).ASMCs were cultured from the lung of control and asthma rats.ASMCs were treated with diazoxide(the potent activator of mitoK ATP) or 5-hydroxydencanote(5-HD,the inhibitor of mitoK ATP).Rhodamine-123(R-123) was used to detect Δψm.The expression of PKCα protein was examined by using Western blotting,while PKCα mRNA expression was detected by using real-time PCR.The proliferation of ASMCs was measured by MTT assay and cell cycle analysis.In diazoxide-treated normal ASMCs,the R-123 fluorescence intensity,protein and mRNA levels of PKCα,MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls.The ratio of G 0 /G 1 cells was decreased(P<0.05) in diazoxide-treated ASMCs from normal rats.However,there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group.In untreated and diazoxide-treated ASMCs of asthmatic rats,the R-123 fluorescence intensity,protein and mRNA levels of PKCα,MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group.Furthermore,in comparison to ASMCs from asthmatic rats,these values were considerably increased in asthmatic group treated with diazoxide(P<0.05).After exposure to 5-HD for 24 h,these values were decreased as compared with asthma control group(P<0.05).In ASMCs of asthma,the signal transduction pathway of PKCα may be involved in cell proliferation,which is induced by the opening of mitoK ATP and the depolarization of Δψm.展开更多
文摘针对智能小车转向时跟踪精度差、响应时间较慢的问题,提出了一种基于机器视觉的智能小车转向系统的滑模控制方法。首先,以感知路面信息的智能小车为研究对象,对其转向系统进行了原理分析及数学建模。通过对永磁直流电机工作过程的分析,建立了电枢电压平衡方程和转矩平衡方程,得出了相应的传递函数,并采用实验方法对传递函数参数进行了辨识。其次,针对上述被控对象,设计了滑模控制器,并进行了稳定性证明。利用Matlab/Simulink仿真结果验证了滑模控制算法的有效性。理论结果和实验验证相结合表明,相较于PID(proportional integral differential)控制,滑模控制具有较好的跟踪精度和响应速度。在频率为20 Hz时,跟踪精度提高了89.3%。此外,滑模控制能够克服系统的不确定性,尤其是对于非线性系统,显示出良好的控制效果。
基金supported by grants from Natural Science Foundation of Hubei Province,China (No. 2010CDB096)the National Key Technology R&D Program of the 12th National Five-year Development Plan of China (No. 2012BAI05B01)
文摘The effects of ATP-sensitive mitochondrial K + channel(mitoK ATP) on mitochondrial membrane potential(Δψm),cell proliferation and protein kinase C alpha(PKCα) expression in airway smooth muscle cells(ASMCs) were investigated.Thirty-six Sprague-Dawley(SD) rats were immunized with saline(controls) or ovalbumin(OVA) with alum(asthma models).ASMCs were cultured from the lung of control and asthma rats.ASMCs were treated with diazoxide(the potent activator of mitoK ATP) or 5-hydroxydencanote(5-HD,the inhibitor of mitoK ATP).Rhodamine-123(R-123) was used to detect Δψm.The expression of PKCα protein was examined by using Western blotting,while PKCα mRNA expression was detected by using real-time PCR.The proliferation of ASMCs was measured by MTT assay and cell cycle analysis.In diazoxide-treated normal ASMCs,the R-123 fluorescence intensity,protein and mRNA levels of PKCα,MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls.The ratio of G 0 /G 1 cells was decreased(P<0.05) in diazoxide-treated ASMCs from normal rats.However,there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group.In untreated and diazoxide-treated ASMCs of asthmatic rats,the R-123 fluorescence intensity,protein and mRNA levels of PKCα,MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group.Furthermore,in comparison to ASMCs from asthmatic rats,these values were considerably increased in asthmatic group treated with diazoxide(P<0.05).After exposure to 5-HD for 24 h,these values were decreased as compared with asthma control group(P<0.05).In ASMCs of asthma,the signal transduction pathway of PKCα may be involved in cell proliferation,which is induced by the opening of mitoK ATP and the depolarization of Δψm.
