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The Stabilization and 3D Visual Simulation of the Triple Inverted Pendulum based on CGA-PIDNN
Xiu-Ling Zhang,Hong-Min Fan,Jia-Yin Zang,Liang Zhao,Shuang Hao 제어·로봇·시스템학회 2015 International Journal of Control, Automation, and Vol.13 No.4
Aiming at the triple inverted pendulum which is a strong coupling, multivariable, high-order and unsteady system, a design method of the controller based on PID neural network (PIDNN) optimized by cloud genetic algorithm (CGA) is proposed, this method is called CGA-PIDNN. CGA can be applied to learn and train the PIDNN connection weights. CGA can overcome the defect of the slow convergence rate and premature convergence for genetic algorithm (GA). PIDNN is a simple and normative network which is easy to be realized and has a good dynamic performance. The CGA-PIDNN control system of triple inverted pendulum is verified with MATLAB simulation test. The comparison results with the control effect of PIDNN control system optimized by standard GA (GA-PIDNN) are presented first. Then in LabVIEW environment, by using the combination of virtual reality technology and MATLAB, the three-dimensional (3D) animation simulation model of the triple inverted pendulum CGA-PIDNN control system is built. The simulation results indicate that CGA-PIDNN control method is effective, whose control effects are superior to those by GA-PIDNN control, it is believed that CGAPIDNN is effective and will become a promising candidate of control methods.
Fang, Yi,Liu, Xiaofang,Zhao, Libo,Wei, Zhongna,Jiang, Daoli,Shao, Hua,Zang, Yannan,Xu, Jia,Wang, Qian,Liu, Yang,Peng, Ye,Yin, Xiaoxing The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5
The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, $40{\mu}g/kg$ i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7-36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.
Yi Fang,Xiaofang Liu,Libo Zhao,Zhongna Wei,Daoli Jiang,Hua Shao,Yannan Zang,Jia Xu,Qian Wang,Yang Liu,Ye Peng,Xiaoxing Yin 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.5
The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7-36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7-36) (10, 20, 40 μg/kg i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7- 36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7-36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7-36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.