The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Xiao-yun Feng - One of the best experts on this subject based on the ideXlab platform.
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Power Calculation for Direct Power Control of Single-Phase Three-Level Rectifiers Without Phase-Locked Loop
Ieee Transactions on Industrial Electronics, 2016Co-Authors: Jun Peng Ma, Jun Hui Zhao, Wen Sheng Song, Shi Lei Jiao, Xiao-yun FengAbstract:Synchronization unit such as single-phase grid Voltage phase-locked loop (PLL) is essential to control scheme in single-phase converters. However, the design of PLL is not simple and increases the complexity of control system, and the performance of PLL could be impacted by the waveform quality of the Main Voltage. Therefore, in this paper, a novel single-phase power calculation method without PLL is proposed to improve the performance of single-phase three-level rectifier which is widely used in railway traction drive system. Moreover, a strategy to compensate phase angle and power calculation error is presented to improve the power calculation precision and enlarge operation range. Then the compensation strategy and the single-phase power calculation method are combined with a common direct power control (DPC) to form a no-PLL control system for single-phase three-level rectifiers. Finally, performance of the proposed scheme is verified through experimental tests and compared with two traditional PLL-based control schemes.
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deadbeat predictive power control of single phase three level neutral point clamped converters using space vector modulation for electric railway traction
IEEE Transactions on Power Electronics, 2016Co-Authors: Wen Sheng Song, Liang Zhou, Xiao-yun FengAbstract:This paper presents an alternative approach to address the control and modulation problem of single-phase three-level converters applied in the high-speed railway electrical traction drive system. Following the principle of deadbeat predictive direct torque control of ac motors, this paper discusses an improved direct power control (DPC) method based on a deadbeat active and reactive power prediction technique. Comparing with the conventional PI-based DPC scheme, the proposed deadbeat predictive DPC scheme can provide these advantageous features: lower current harmonics and THD index, lower active and reactive power ripples, and fewer adjusted parameters. Moreover, compared with PI-based DPC with the PI parameters optimization, this approach can also easily obtain fast dynamic response but without the Main Voltage orientation. A single-phase three-level space vector pulse width modulation (SVPWM) with inherent neutral-point Voltage balancing capability is adopted, which can be combined with DPC scheme as an overall control and modulation system. A series of simulation and experimental tests have been conducted to demonstrate an excellent performance of the deadbeat predictive DPC. In addition, the neutral-point-Voltage balancing ability of the adopted SVPWM method has been verified.
H. Peter Larsson - One of the best experts on this subject based on the ideXlab platform.
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KCNE1 Separates the Main Voltage Sensor Movement and Channel Opening in KCNQ1/KCNE1 Channels
Biophysical Journal, 2014Co-Authors: Rene Barro-soria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, H. Peter LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
Peter H Larsson - One of the best experts on this subject based on the ideXlab platform.
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kcne1 separates the Main Voltage sensor movement and channel opening in kcnq1 kcne1 channels
Biophysical Journal, 2014Co-Authors: Rene Barrosoria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, Peter H LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
Kevin J Sampson - One of the best experts on this subject based on the ideXlab platform.
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kcne1 separates the Main Voltage sensor movement and channel opening in kcnq1 kcne1 channels
Biophysical Journal, 2014Co-Authors: Rene Barrosoria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, Peter H LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
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KCNE1 Separates the Main Voltage Sensor Movement and Channel Opening in KCNQ1/KCNE1 Channels
Biophysical Journal, 2014Co-Authors: Rene Barro-soria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, H. Peter LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
Sara I Liin - One of the best experts on this subject based on the ideXlab platform.
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kcne1 separates the Main Voltage sensor movement and channel opening in kcnq1 kcne1 channels
Biophysical Journal, 2014Co-Authors: Rene Barrosoria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, Peter H LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
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KCNE1 Separates the Main Voltage Sensor Movement and Channel Opening in KCNQ1/KCNE1 Channels
Biophysical Journal, 2014Co-Authors: Rene Barro-soria, Sara I Liin, Marta E Perez, Santiago Rebolledo, Robert S Kass, Kevin J Sampson, H. Peter LarssonAbstract:The IKs channel is a slowly activating potassium channel that generates one of the potassium currents that limits the duration of the cardiac action potential. The IKs channel consists of 4 pore forming alpha subunits (KCNQ1) and 2-4 beta subunits (KCNE1). The four KCNQ1 subunits form functional potassium channels, but the KCNE1 beta subunit is necessary to recapitulate the slow activation kinetics of the IKs channel. The mechanism by which KCNE1 slows the kinetics of KCNQ1 channels is a matter of current controversy. Here, we use a combination of Voltage clamp fluorometry (VCF) and gating current measurements to show that IKs channel activation occurs in two steps: (1) mutually independent Voltage sensor movements in the four KCNQ1 subunits generate the Main gating charge movement and underlie the delay in the activation time course of the KCNQ1/KCNE1 currents, (2) a slower and concerted conformational change of all four Voltage sensors and the gate, which opens the KCNQ1/KCNE1 channel. Gating currents develop with a similar time and Voltage dependence as the first fluorescence component, as if the first component reports on the Main S4 charge movement. In contrast to other Kv channels, the Voltage dependences of the Main Voltage sensor movement and channel opening are separated by over 100 mV. The two activation steps in KCNQ1/KCNE1 channels can be farther separated by a disease-causing mutation in KCNE1. We determine rates and Voltage dependence of the gating transitions to construct a model for KCNQ1/KCNE1 channels. Our model is consistent with that KCNQ1/KCNE1 channel has a fast S4 movement at negative Voltages that moves the majority of gating charge and a slower second conformational change at positive Voltages that moves a smaller amount of gating charge and opens the gate.
