为了充分利用非圆信号共轭相关不为零的特性,提高空间到达角(direction of arrival,DOA)和极化参数估计精度,提出了一种信号DOA和极化参数估计的稳健算法.即构造2个非圆信号的4阶累积量矩阵,引入旋转不变子空间(estimation of signal pa...为了充分利用非圆信号共轭相关不为零的特性,提高空间到达角(direction of arrival,DOA)和极化参数估计精度,提出了一种信号DOA和极化参数估计的稳健算法.即构造2个非圆信号的4阶累积量矩阵,引入旋转不变子空间(estimation of signal parameters via rotational invariance techniques,ESPRIT)算法思想,利用这2个矩阵之间的旋转不变特性求出旋转因子,实现信号DOA和极化参数更精确估计.与2阶相域ESPRIT相比,改进的算法适用于任意极化状态的信号,提高估计信号的利用率,同时利用4阶累积量对高斯噪声的抑制性处理相关噪声,使估计信号的精度有了明显提升,并通过仿真结果验证了改进算法的有效性.展开更多
Objective: To investigate the underlying neurobiological mechanism of the protective effect of electroacupuncture (EA) during cerebral ischemia-reperfusion (CI-R). Methods: In the first part of the study, 15 SD rats w...Objective: To investigate the underlying neurobiological mechanism of the protective effect of electroacupuncture (EA) during cerebral ischemia-reperfusion (CI-R). Methods: In the first part of the study, 15 SD rats were evenly randomized into control group, CI-R-48h model group and CI-R-48h+EA group. The cortical apoptosis and expression of Bcl-2 and Bax proteins in each group were detected by flow cytometer (FCM). In the second part of the study, 75 SD rats were evenly randomized into control, CI-R-3min, CI-R-3min+EA, CI-R-48h and CI-R-48h+EA groups. Cortical norepinephrine (NE) concentration was detected by fluorescence spectrometer. CI-R model was established by occlusion of the bilateral common carotid arteries and reperfusion. EA (4～16 Hz, 1～3 V) was applied to “Shuigou”(水沟 GV 26) and “Chengjiang”(承浆 CV 24) for 30 min before CI and after reperfusion respectively. Results: In the first part of this study, results indicated that the number of the apoptotic neurons and the apoptosis rate of CI-R-48h group were significantly higher than those of control group; while comparison between CI-R-48h+EA and CI-R-48h groups showed that the number of the apoptotic neurons and the apoptosis rate of the former group were significantly lower than those of the later group (P<0.05). In comparison with control group, after CI-48h, Bax expression was up-regulated significantly and Bcl-2 down-regulated markedly (P<0.05). Comparison between CI-R-48h and CI-R-48h+EA group indicated that Bax expression of the later group was significantly lower than that of the former group, while Bcl-2 expression of CI-R-48h+EA group was significantly higher than that of CI-R-48h group (P<0.05), suggesting that EA could reverse CI induced reactions of these two indexes. In the second part of the study, in comparison with control group, NE concentration in cerebral cortex of CI-R-3min group increased significantly (P<0.05); while NE content of CI-R-3min+EA group was significantly lower than that of CI-R-3min group (P<0.05). No significant difference was found between CI-R-3min group and control group in cortical NE levels; and no significant changes were found about NE levels in CI-R-48h and CI-R-48h+EA groups, suggesting that EA could inhibit the increase of cortical NE level in the early stage of CI. Conclusion: Changes of NE concentration in the cerebral cortex during the earlier period of CI-R is possibly related to the incidence of cortical apoptosis. EA can reduce the increase of NE due to CI and thus may inhibit CI-induced cortical apoptosis.展开更多
文摘为了充分利用非圆信号共轭相关不为零的特性,提高空间到达角(direction of arrival,DOA)和极化参数估计精度,提出了一种信号DOA和极化参数估计的稳健算法.即构造2个非圆信号的4阶累积量矩阵,引入旋转不变子空间(estimation of signal parameters via rotational invariance techniques,ESPRIT)算法思想,利用这2个矩阵之间的旋转不变特性求出旋转因子,实现信号DOA和极化参数更精确估计.与2阶相域ESPRIT相比,改进的算法适用于任意极化状态的信号,提高估计信号的利用率,同时利用4阶累积量对高斯噪声的抑制性处理相关噪声,使估计信号的精度有了明显提升,并通过仿真结果验证了改进算法的有效性.
文摘Objective: To investigate the underlying neurobiological mechanism of the protective effect of electroacupuncture (EA) during cerebral ischemia-reperfusion (CI-R). Methods: In the first part of the study, 15 SD rats were evenly randomized into control group, CI-R-48h model group and CI-R-48h+EA group. The cortical apoptosis and expression of Bcl-2 and Bax proteins in each group were detected by flow cytometer (FCM). In the second part of the study, 75 SD rats were evenly randomized into control, CI-R-3min, CI-R-3min+EA, CI-R-48h and CI-R-48h+EA groups. Cortical norepinephrine (NE) concentration was detected by fluorescence spectrometer. CI-R model was established by occlusion of the bilateral common carotid arteries and reperfusion. EA (4～16 Hz, 1～3 V) was applied to “Shuigou”(水沟 GV 26) and “Chengjiang”(承浆 CV 24) for 30 min before CI and after reperfusion respectively. Results: In the first part of this study, results indicated that the number of the apoptotic neurons and the apoptosis rate of CI-R-48h group were significantly higher than those of control group; while comparison between CI-R-48h+EA and CI-R-48h groups showed that the number of the apoptotic neurons and the apoptosis rate of the former group were significantly lower than those of the later group (P<0.05). In comparison with control group, after CI-48h, Bax expression was up-regulated significantly and Bcl-2 down-regulated markedly (P<0.05). Comparison between CI-R-48h and CI-R-48h+EA group indicated that Bax expression of the later group was significantly lower than that of the former group, while Bcl-2 expression of CI-R-48h+EA group was significantly higher than that of CI-R-48h group (P<0.05), suggesting that EA could reverse CI induced reactions of these two indexes. In the second part of the study, in comparison with control group, NE concentration in cerebral cortex of CI-R-3min group increased significantly (P<0.05); while NE content of CI-R-3min+EA group was significantly lower than that of CI-R-3min group (P<0.05). No significant difference was found between CI-R-3min group and control group in cortical NE levels; and no significant changes were found about NE levels in CI-R-48h and CI-R-48h+EA groups, suggesting that EA could inhibit the increase of cortical NE level in the early stage of CI. Conclusion: Changes of NE concentration in the cerebral cortex during the earlier period of CI-R is possibly related to the incidence of cortical apoptosis. EA can reduce the increase of NE due to CI and thus may inhibit CI-induced cortical apoptosis.
