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        Role of Dehydrocorybulbine in Neuropathic Pain After Spinal Cord Injury Mediated by P2X4 Receptor

        Wang, Zhongwei,Mei, Wei,Wang, Qingde,Guo, Rundong,Liu, Peilin,Wang, Yuqiang,Zhang, Zijuan,Wang, Limin Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.2

        Chronic neuropathic pain is one of the primary causes of disability subsequent to spinal cord injury. Patients experiencing neuropathic pain after spinal cord injury suffer from poor quality of life, so complementary therapy is seriously needed. Dehydrocorybulbine is an alkaloid extracted from Corydalis yanhusuo. It effectively alleviates neuropathic pain. In the present study, we explored the effect of dehydrocorybulbine on neuropathic pain after spinal cord injury and delineated its possible mechanism. Experiments were performed in rats to evaluate the contribution of dehydrocorybulbine to P2X4 signaling in the modulation of pain-related behaviors and the levels of pronociceptive interleukins and proteins after spinal cord injury. In a rat contusion injury model, we confirmed that chronic neuropathic pain is present on day 7 after spinal cord injury and P2X4R expression is exacerbated after spinal cord injury. We also found that administration of dehydrocorybulbine by tail vein injection relieved pain behaviors in rat contusion injury models without affecting motor functions. The elevation in the levels of pronociceptive interleukins ($IL-1{\beta}$, IL-18, MMP-9) after spinal cord injury was mitigated by dehydrocorybulbine. Dehydrocorybulbine significantly mitigated the upregulation of P2X4 receptor and reduced ATP-evoked intracellular $Ca^{2+}$ concentration. Both P2XR and dopamine receptor2 agonists antagonized dehydrocorybulbine's antinociceptive effects. In conclusion, we propose that dehydrocorybulbine produces antinociceptive effects in spinal cord injury models by inhibiting P2X4R.

      • KCI등재

        Role of Dehydrocorybulbine in Neuropathic Pain After Spinal Cord Injury Mediated by P2X4 Receptor

        Zhongwei Wang,Wei Mei,Qingde Wang,Rundong Guo,Peilin Liu,Yuqiang Wang,Zijuan Zhang,Limin Wang 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.2

        Chronic neuropathic pain is one of the primary causes of disability subsequent to spinal cord injury. Patients experiencing neuropathic pain after spinal cord injury suffer from poor quality of life, so complementary therapy is seriously needed. Dehydrocorybulbine is an alkaloid extracted from Corydalis yanhusuo. It effectively alleviates neuropathic pain. In the present study, we explored the effect of dehydrocorybulbine on neuropathic pain after spinal cord injury and delineated its possible mechanism. Experiments were performed in rats to evaluate the contribution of dehydrocorybulbine to P2X4 signaling in the modulation of pain-related behaviors and the levels of pronociceptive interleukins and proteins after spinal cord injury. In a rat contusion injury model, we confirmed that chronic neuropathic pain is present on day 7 after spinal cord injury and P2X4R expression is exacerbated after spinal cord injury. We also found that administration of dehydrocorybulbine by tail vein injection relieved pain behaviors in rat contusion injury models without affecting motor functions. The elevation in the levels of pronociceptive interleukins (IL-1β, IL-18, MMP-9) after spinal cord injury was mitigated by dehydrocorybulbine. Dehydrocorybulbine significantly mitigated the upregulation of P2X4 receptor and reduced ATP-evoked intracellular Ca2+ concentration. Both P2XR and dopamine receptor2 agonists antagonized dehydrocorybulbine’s antinociceptive effects. In conclusion, we propose that dehydrocorybulbine produces antinociceptive effects in spinal cord injury models by inhibiting P2X4R.

      • DIGITAL REALIZATION OF ROTOR POSITION DETECTION FOR PERMANENT MAGNET SYNCHRONOUS MOTOR SERVO SYSTEM

        Guo Qingding,Wang Limei,Luo Ruifu 전력전자학회 1995 ICPE(ISPE)논문집 Vol.1995 No.10

        This paper presents an effective digital realization method for detecting the rotor position of high performance sinusoid drive permanent magnet synchronous motor ( PMSM) servo system. The system adopts two chips of INTEL8098 The rotor position of PMSM is detected by resolver and calculated by microcomputer. The hardware and software are designed and analyzed Experimental result demonstrates that this method is capable to acquire precise position signal of rotor and improve performance of the servo system.

      • POSITION CONTROL OF BRUSHLESS DC MOTOR SERVO SYSTEM BASED ON NEURAL NETWORK

        Guo Qingding,Luo Ruifu,Wang Limei 전력전자학회 1995 ICPE(ISPE)논문집 Vol.1995 No.10

        This paper describes a DSP based neural network controller of high performance brushless DC motor servo system It has a multi-layer feedforward structure and adopts DSP(TMS320C30) as its operation element. Learning scheme and designing method is discussed Simulation and experiment result are presented and the performance of neural network controllers is studied.

      • A NEW ALGORITHM OF VARIABLE STRUCTURE SLIDING MODE CONTROL FOR AC POSITION SERVO SYSTEM

        Guo Qingding,Wang Limei,Fu Qiang 전력전자학회 1995 ICPE(ISPE)논문집 Vol.1995 No.10

        This paper describes a new algorithm of variable structure sliding mode (VSSM) control for a high performance sinusoid drive permanent magnet synchronous motor (PMSM) position servo system. Simulation result demonstrates that the new algorithm promises strong robustness and good performance of the systern.The chattering has been alleviated effectively.

      • FULLY DIGITAL PERMANENT MAGNET SYNCHRONOUS MOTOR SERVO SYSTEM BASED ON DSP

        Guo Qingding,Luo Ruifu,Wang Limei 전력전자학회 1995 ICPE(ISPE)논문집 Vol.1995 No.10

        This paper describes a high performance fully digital implementation of a PMSM servo system. On the basis of vector control principle, the system is controlled by an INTEL8031 and a DSP(TMS320C25) A new self-tuning PID algorithm based on IATE optimal rule is used in speed loop Experimental result demonstrates that the system is capable to improve performance in terms of precision of control action, dynamic response and flexibility, even when system parameters are varied.

      • COMPLETERY DIGITAL AC SERVO SYSTEM USING NEURAL NETWORK CONTROLLER

        Guo Qingding,Wang Limei,Luo Ruifu 전력전자학회 1995 ICPE(ISPE)논문집 Vol.1995 No.10

        This paper describes a neural network controller for a completely digital permanent magnet synchronous motor servo system. Learning scheme and design method are presented The control circuit is realized by software. DSP ( TMS320C30) and singie-chip microcomputer INTEL (8098) are adopted in the system Simulation results show that the controller using neural network makes the servo system achieve fast response, non -over- shot and good robustness against disturbance.

      • Oxidative Stress–Mediated Thrombospondin-2 Upregulation Impairs Bone Marrow–Derived Angiogenic Cell Function in Diabetes Mellitus

        Bae, Ok-Nam,Wang, Jie-Mei,Baek, Seung-Hoon,Wang, Qingde,Yuan, Hong,Chen, Alex F. American Heart Association, Inc. 2013 Arteriosclerosis, thrombosis, and vascular biology Vol.33 No.8

        <P><B>Objective—</B></P><P>Circulating angiogenic cells play an essential role in angiogenesis but are dysfunctional in diabetes mellitus characterized by excessive oxidative stress. We hypothesize that oxidative stress–mediated upregulation of thrombospondin-2 (TSP-2), a potent antiangiogenic protein, contributes to diabetic bone marrow–derived angiogenic cell (BMAC) dysfunction.</P><P><B>Approach and Results—</B></P><P>BMACs were isolated from adult male type 2 diabetic db/db mice and control db/+ (C57BLKS/J) mice. In Matrigel tube formation assay, angiogenic function was impaired in diabetic BMACs, accompanied by increased oxidative stress and nicotinamide adenine dinucleotide phosphate oxidase activity. BMAC angiogenic function was restored by overexpression of dominant negative Rac1 or by overexpression of manganese superoxide dismutase. TSP-2 mRNA and protein were both significantly upregulated in diabetic BMACs, mediated by increased oxidative stress as shown by a decrease in TSP-2 level after overexpression of dominant negative Rac1 or manganese superoxide dismutase. Silencing TSP-2 by its small interfering RNA in diabetic BMACs improved BMAC function in tube formation, adhesion, and migration assays. Notably, the upregulation of TSP-2 was also found in BMACs from streptozotocin-induced type 1 diabetic mice, and normal BMACs with high glucose treatment. let-7f, a microRNA which has been related to endothelial angiogenic function, is found to play key role in TSP-2 increase, but let-7f did not directly interact with TSP-2 mRNA.</P><P><B>Conclusions—</B></P><P>The upregulation of TSP-2 mediated by increased oxidative stress contributes to angiogenesis dysfunction in diabetic BMACs.</P>

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