Voltage Tail Research Articles

An Improved Fourier-Series-Based IGBT Model by Mitigating the Effect of Gibbs Phenomenon at Turn on

The Fourier-series-based insulated-gate bipolar transistor (IGBT) model has been very effective in simulating its switching behaviors and meanwhile, reflecting carrier dynamics. However, in turn-on process, such a model has difficulty in distinguishing the boundary between undepleted area and depletion layer of the drift region due to Gibbs phenomenon and therefore, cannot accurately describe the carrier behavior of carrier storage region (CSR). In this study, the Fourier-series-based model is modified to determine the more precise depletion layer edge for turn on. This is achieved by utilizing the actual characteristics of the carrier concentration gradient at the edge of CSR in turn-on process. Such a modified model is implemented in MATLAB/Simulink and it can better reflect the depletion layer and simulate the distribution of both the carrier concentration and electric field during turn-on process. It corrects the unreasonable voltage tail caused by the error of drift region voltage calculation in previous models. The results of the proposed model under both the resistive load and inductive load are in good agreement with TCAD. Such a modified model can more accurately simulate both carrier dynamics and switching behaviors in the turn-on process.

Accumulative effect of partial discharges at impulse voltage wave tail

This study describes a technique for evaluating partial discharges at fast impulse voltages. Fast transient voltages are increasingly present in power equipment and industrial environments due to the ubiquitous application of power electronics switching devices. Special attention should be paid to the dangers caused by the accumulative effect of repetitive impulse voltages on electrical insulation. This study describes a method of analysing partial discharges occurring during impulse voltage stimuli. A repetitive train of pulses is applied to a dielectric specimen and the accumulated PD pattern is obtained. This study focuses on the reverse discharges which occur during the tail part of the impulse voltage waveform acquired in time-resolved mode. Investigations of the partial discharges in the wave tail can potentially lead to greater degradation of the insulation due to the formation of longer, repetitive sequence occurring along the decaying impulse voltage tail. Experiments were performed which investigated the influence of rise time, fall time and peak voltage on discharge pattern reshaping, intensity and time to inception on the tail. In the future, such an approach might be further developed for diagnostic applications and for extended factory tests.

A Buck-Boost Transformerless DC–DC Converter Based on IGBT Modules for Fast Charge of Electric Vehicles

A transformer-less Buck-Boost direct current–direct current (DC–DC) converter in use for the fast charge of electric vehicles, based on powerful high-voltage isolated gate bipolar transistor (IGBT) modules is analyzed, designed and experimentally verified. The main advantages of this topology are: simple structure on the converter’s power stage; a wide range of the output voltage, capable of supporting contemporary vehicles’ on-board battery packs; efficiency; and power density accepted to be high enough for such a class of hard-switched converters. A precise estimation of the loss, dissipated in the converter’s basic modes of operation Buck, Boost, and Buck-Boost is presented. The analysis shows an approach of loss minimization, based on switching frequency reduction during the Buck-Boost operation mode. Such a technique guarantees stable thermal characteristics during the entire operation, i.e., battery charge cycle. As the Buck-Boost mode takes place when Buck and Boost modes cannot support the output voltage, operating as a combination of them, it can be considered as critically dependent on the characteristics of the semiconductors. With this, the necessary duty cycle and voltage range, determined with respect to the input-output voltages and power losses, require an additional study to be conducted. Additionally, the tolerance of the applied switching frequencies for the most versatile silicon-based powerful IGBT modules is analyzed and experimentally verified. Finally, several important characteristics, such as transients during switch-on and switch-off, IGBTs’ voltage tails, critical duty cycles, etc., are depicted experimentally with oscillograms, obtained by an experimental model.

Counterflow diffusion flame oscillations induced by ns pulse electric discharge waveforms

Repetitive ns pulse, dielectric barrier discharge voltage waveforms, combined with a tail several ms long, are used to induce oscillations of a counterflow atmospheric pressure diffusion flame. A baseline ns pulse discharge operated at 10 Hz results in a relatively modest oscillatory response of the flame, which becomes more pronounced in burst mode operation, at the same burst repetition rate of 10 Hz. This effect is most likely caused by the residual electric field after the discharge pulse, producing the electrohydrodynamic (EHD) force (“ion wind”) on the charges generated during the discharge, although plasma chemistry and Joule heating by the discharge may also contribute. Manipulating the external circuit to add a variable duration tail to the discharge pulse, without changing the pulse shape during breakdown or the pulse repetition rate, considerably enhances the impulse of the EHD force and increases the amplitude of the flame oscillations. To quantify this effect, the electric field distribution between the electrodes during and after the discharge pulse is measured by ps Electric Field Induced Second Harmonic (E-FISH) diagnostic. The results show that the electric field is maintained during the voltage tail, although it is lower compared to the Laplacian field due to the charge accumulation on the dielectric sleeves covering the electrodes. The time scale of the flame oscillations at the present conditions, of the order of ∼10 ms, is limited by the relatively slow momentum transfer from the ions to the neutral species. The present results demonstrate feasibility of enhancing the flame control authority, by combining a high peak ionization fraction generated by a ns pulse discharge with the EHD force applied on a long time scale, using a single plasma generator.

Cause of Pulse Artefacts Inherent to the Electrodes of Neuromodulation Implants.

The current pulses delivered through platinum electrodes by medical implants to recruit neurons give rise to slowly decaying voltage tails, called "artefacts." These tails make measurement of evoked potentials following the pulses very difficult. We present an evidence to show that in a typical clinical scenario, these tails are mostly caused by the concentration gradients of species induced in the electrical double layer adsorbed onto the surface of both stimulating and passive electrodes. A compact model is presented that allows the simulation of these artefacts. The model is verified against measurements made in saline. This shows that electrode artefacts are an intrinsic property of the conductive electrodes of a lead.

Design and Implementation of Flash ADC for Low Power Applications

Flash ADC is one of the most preferred architectures for high speed analog-to-digital data conversion applications. The comparator is a building block of virtually all analog-to-digital converter architecture. The kickback noise in the comparator is one of the important factor which leads to power dissipation. Hence the objective of this project is to design and implement a 4 bit Flash ADC by using effective comparator which reduces the kick back noise. Reduction of the kickback noise makes it possible to drive the ADC with higher impedance, which in turn reduces the power dissipation. Here the design of different types of comparators such as Preamplifier based, Double Tail Latch Type Voltage, Dynamic comparator and Double Tail Dual Rail Dynamic Latched comparators are analyzed. The Dynamic comparator without kickback noise is proposed for the flash ADC due its less power consumption. The proposed ADC offers a low-power solution with reduced Kickback noise. This design is simulated and analyzed in 90nm technology in Cadence virtuoso. Simulation results are tabulated and analysis has been done with graphical representation. The proposed flash ADC consumes 7.846mW power at sampling rate of 0.8 GS/s. When compared with previous work, this architecture showed 21.54% reduction in power consumption.

Design and Investigative Aspects of RF-Low Power 0.18-µm based CMOS Differential Ring Oscillator

This manuscript presents the designing and investigative aspects of a low power, wide frequency range, and delay cell based 3 and 5-stage ring oscillator for RF-Ultra-WideBand application. The wide range of frequency is achieved by using two variable voltage sources i.e. control voltage source (Vcntrl) and tail current source (Vtail). A tail current improvement is responsible to control the charging and discharging time of oscillator. Moreover, the push-pull configuration is also used to attain high frequency. In addition, the proposed work presents the effect of control voltage and tail current source on the oscillator frequency. This work establishes a relation between oscillator frequency and its power consumption. This work also gives a comparison between 3stage and 5-stage ring oscillator. The circuit is implemented in 180 nm CMOS process provided by TSMC. The designed oscillator is measured to cover a frequency range of 1.3 – 5.7 GHz for 3-stage and 1.99 – 3.12 GHz for 5-stage ring oscillator. The simulated circuit draws 0.510 mW of average power for 3-stage ring oscillator and 0.719 mW average power for 5-stage ring oscillator.

Effect of Azelastine on Cardiac Repolarization of Guinea-Pig Cardiomyocytes, hERG K+ Channel, and Human L-type and T-type Ca2+ Channel

Azelastine is a second generation histamine H1–receptor antagonist used as an anti-asthmatic and anti-allergic drug that can induce QT prolongation and torsades de pointes. We investigated the acute effects of azelastine on human ether-a-go-go-related gene (hERG) channels, action potential duration (APD), and L-type (ICa,L) and T-type Ca2+ current (ICa,T) to determine the electrophysiological basis for its proarrhythmic potential. Azelastine increased the APD at 90% of repolarization concentration dependently, with an IC50 of 1.08 nM in guinea-pig ventricular myocytes. We examined the effects of azelastine on the hERG channels expressed in Xenopus oocytes and HEK293 cells using two-microelectrode voltage-clamp and patch-clamp techniques. Azelastine induced a concentration-dependent decrease of the hERG current amplitude at the end of the voltage steps and tail currents. The IC50 for the azelastine-induced block of the hERG currents expressed in HEK293 cells was 11.43 nM, while the drug inhibited ICa,L and ICa,T with IC50 values of 7.60 and 26.21 μM, respectively. The S6 domain mutations, Y652A partially attenuated and F656A abolished hERG current block. These results suggest that azelastine is a potent blocker of hERG channels rather than ICa,L or ICa,T, providing molecular mechanisms for the arrhythmogenic side effects during the clinical administration of azelastine.

Heavy-Ion Induced Threshold Voltage Tails in Floating Gate Arrays

We studied heavy-ion effects on floating gate memories, focusing on the generation of tails in the threshold voltage distributions after irradiation. Using both experiments and simulations based on the Geant4 toolkit, we provide new insight, distinguishing two types of events, large events and small events, which are responsible for the secondary peak and the intermediate region in the post-rad threshold distribution, respectively. Both are well correlated with the energy deposited in the FG. Implications for error rate predictions are discussed.

Physics-Based Model of Planar-Gate IGBT Including MOS Side Two-Dimensional Effects

An existing physics-based insulated gate bipolar transistor (IGBT) model, which has been proven accurate for both inductive turn-off and inductive turn-on simulations, is modified to account for planar-gate IGBT 2-D effects at the MOS end of the drift region. The modification is based on a steady-state solution of carrier distribution in the JFET region of the IGBT. The accuracy of this solution is verified through a set of finite element simulations. The improved accuracy of the modified model in terms of on-state forward drop and voltage tail at turn-on is verified through comparison with experimental results.

Turn-on Performance of Reverse Blocking IGBT (RB IGBT) and Optimization Using Advanced Gate Driver

Turn-on performance of a reverse blocking insulated gate bipolar transistor (RB IGBT) is discussed in this paper. The RB IGBT is a specially designed IGBT having ability to sustain blocking voltage of both the polarities. Such a switch shows superior conduction but much worst switching (turn- on) performances compared to a combination of an ordinary IGBT and blocking diode. Because of that, optimization of the switching performance is a key issue that makes the RB IGB not well accepted in the real applications. In this paper, the RB IGBT turn-on losses and reverse recovery current are analyzed for different gate driver techniques, and a new gate driver is proposed. Commonly used conventional gate drivers do not have capability for the switching dynamics optimization. In contrast to this, the new proposed gate driver provides robust and simple way to control and optimize the reverse recovery current and turn-on losses. The collector current slope and reverse recovery current are controlled by the means of the gate emitter voltage control in feedforward manner. In addition, the collector emitter voltage slope is controlled during the voltage falling phase by the means of inherent increase of the gate current. Therefore, the collector emitter voltage tail and the total turn- on losses are reduced, independently on the reverse recovery current. The proposed gate driver was experimentally verified and the results presented and discussed.

Evaluation of thrust force generated for a robotic fish propelled with polypyrrole actuators

AbstractSwimming‐type robotic fish are being developed as mobile sensor platforms that have the potential to outperform existing underwater vehicles in terms of manoeuvrability, miniaturisation and silent operation. Conducting polymer actuators are potential candidates for propelling a flapping tail fin for a robotic fish. This study introduces a method for directly measuring the thrust force generated by a polypyrrole (PPy) powered tail fin. The effects of voltage stimulus (waveform shape and frequency) and tail fin shape on the thrust force were determined. A square wave voltage input was shown to generate the highest thrust forces as fast bending actuation was induced. The thrust force tended to decrease at higher operating frequencies as a result of the reduced actuation occurring in the PPy layers. Increases in the tail fin area tended to lower the frequency where the peak in thrust force was achieved. Tail fin shape was also shown to be important to the force‐frequency behaviour. When attached to an untethered robotic fish, the swimming speed tended to increase with increasing voltage input frequency. There was also an optimum frequency that enabled the fastest acceleration from rest that happened to be higher than the frequency that gave the peak thrust force. This was presumed to be due to the complicated swimming behaviour involving the side‐to‐side movement of the fish nose at low flap frequencies. The study provides valuable insight into the means for tailoring polymer actuator performance to achieve maximum fish swimming speeds. Copyright © 2010 Society of Chemical Industry

Blockade of HERG K+ channel by isoquinoline alkaloid neferine in the stable transfected HEK293 cells

We studied the effects of isoquinoline alkaloid neferine (Nef) extracted from the seed embryo of Nelumbo nucifera Gaertn on Human ether-à-go-go-related gene (HERG) channels stably expressed in human embryonic kidney (HEK293) cells using whole-cell patch clamp technique, western blot analysis and immunofluorescence experiment. Nef induced a concentration-dependent decrease in current amplitude according to the voltage steps and tail currents of HERG with an IC(50) of 7.419 microM (n(H) -0.5563). Nef shifted the activation curve in a significantly negative direction and accelerated recovery from inactivation and onset of inactivation, however, slowed deactivation. In addition, it had no significant influence on steady-state inactivation curve. Western blot and immunofluorescence results suggested Nef had no significant effect on the expression of HERG protein. In summary, Nef can block HERG K(+) channels that functions by changing the channel activation and inactivation kinetics. Nef has no effect on the generation and trafficking of HERG protein. A blocked-off HERG channel was one mechanism of the anti-arrhythmic effects by Nef.

Role of connexin 32 hemichannels in ATP release from Schwann cells

The X-linked Charcot Marie Tooth (CMTX) is an inherited disease due to mutations in connexin 32 (Cx32) gene expressed in Schwann cells (SC) of peripheral nerves. In SC, Cx32 localizes in the paranodes, in the Schmidt Lanterman incisures and in the cell surface. Cx32 can form “reflexive” gap junction channels as well as functional hemichannels open upon membrane depolarization. We have explored the permeability of Cx32 hemichannels to ATP, in SC and in a heterologous expression system. Murine sciatic nerve trunks release ATP under electrical or mechanical stimulation, as determined by the luciferase reaction. Luminescence imaging revealed that ATP release is especially intense at the SC paranodes, which contain the highest immunofluorescent label for Cx32. Cultured adult SC have a high expression of Cx32 and under mechanical stimulus release ATP being insensitive to exocytosis blockers like brefeldin A. In Xenopus oocytes expressing human Cx32, we measured simultaneously the hemichannel currents and the release of ATP elicited by a square depolarizing pulse up to +100 mV. Depolarizing pulses induced characteristic slowly activating outward currents and when the membrane potential returned to the holding voltage tail currents coinciding with the peak of ATP release. The deconvolution of the light signal revealed that the time courses of the tail current and the ATP release were coincident. We established a direct relationship between the amount of ATP released and the amplitude of tail current. Applying positive voltages closer to the ATP reversal potential during the tail current reduced the amount of ATP released. Five different single amino acid mutants of Cx32, described in CMTX, affecting intracellular, extracellular or transmembrane domains, were tested. Those mutations deeply inhibited or abolished the hemichannel currents and the ATP release.

An IGBT Gate Driver for Feed-Forward Control of Turn-on Losses and Reverse Recovery Current

This paper addresses the problem of turn on performances of an insulated gate bipolar transistor (IGBT) that works in hard switching conditions. The IGBT turn on dynamics with an inductive load is described, and corresponding IGBT turn on losses and reverse recovery current of the associated freewheeling diode are analysed. A new IGBT gate driver based on feed-forward control of the gate emitter voltage is presented in the paper. In contrast to the widely used conventional gate drivers, which have no capability for switching dynamics optimisation, the proposed gate driver provides robust and simple control and optimization of the reverse recovery current and turn on losses. The collector current slope and reverse recovery current are controlled by means of the gate emitter voltage control in feed-forward manner. In addition the collector emitter voltage slope is controlled during the voltage falling phase by means of inherent increase of the gate current. Therefore, the collector emitter voltage tail and the total turn on losses are significantly reduced. The proposed gate driver was experimentally verified and compared to a conventional gate driver, and the results are presented and discussed in the paper.

Maprotiline block of the human ether-a-go-go-related gene (HERG) K+ channel

Maprotiline, an atypical antidepressant, can induce prolonged QT and torsades de pointes. We studied the effects of maprotiline on human ether-a-go-go-related gene (HERG) channels expressed in Xenopus oocytes and HEK293 cells. Maprotiline induced a concentration-dependent decrease in current amplitudes at the end of the voltage steps and tail currents of HERG. The V1/2 values in the absence and presence of 1-20 microM maprotiline were not significantly different, while the values decreased according to the concentrations of the drug at 50-300 microM. The IC50 for a maprotiline block of HERG current in Xenopus oocytes did not change according to depolarization; 39.5 +/- 3.2 microM at -40 mV and 43.6 +/- 2.8 microM at +40 mV. The block of HERG by maprotiline was examined after treatment of trinitrobenzene sulfonic acid (TNBS), an amino-group reagent that neutralizes the positively charged amino-groups of peptide N-terminal and lysine residues. TNBS inhibited the change of V1/2 values induced by 50-300 mM maprotiline, and aggravated the drug-induced gmax decrease. The IC50 for the maprotiline-induced blockade of HERG currents in HEK293 cells at 36 degrees C was 0.13 microM at +20 mV. Our findings suggest that the arrhythmogenic side effects of maprotiline are caused by a blockade of HERG and possibly by a blockade of delayed rectifier K+ channel.

Blockade of HERG human K + channel and IKr of guinea pig cardiomyocytes by prochlorperazine

Prochlorperazine, a drug for the symptomatic control of nausea, vomiting and psychiatric disorders, can induce prolonged QT, torsades de pointes and sudden death. We studied the effects of prochlorperazine on human ether- a- go- go-related gene ( HERG) channels expressed in Xenopus oocytes and also in the delayed rectifier K + current of guinea pig cardiomyocytes. Prochlorperazine induced a concentration-dependent decrease in current amplitudes at the end of the voltage steps and tail currents of HERG. The IC 50 for a prochlorperazine block of HERG current in Xenopus oocytes progressively decreased relative to the degree of depolarization, from 42.1 μM at − 40 mV to 37.4 μM at 0 mV to 22.6 μM at + 40 mV. The block of HERG by prochlorperazine was use-dependent, exhibiting a more rapid onset and a greater steady-state block at higher frequencies of activation, while there was partial relief of the block with reduced frequencies. In guinea pig ventricular myocytes, bath applications of 0.5 and 1 μM prochlorperazine at 36 °C blocked rapidly activating delayed rectifier K + current by 38.9% and 76.5%, respectively, but did not significantly block slowly activating delayed rectifier K + current. Our findings suggest that the arrhythmogenic side effects of prochlorperazine are caused by a blockade of HERG and the rapid component of the delayed rectifier K + current rather than by a blockade of the slow component.

Inhibition of Human ether-a-go-go-Related Gene K+ Channel and IKr of Guinea Pig Cardiomyocytes by Antipsychotic Drug Trifluoperazine

Trifluoperazine, a commonly used antipsychotic drug, has been known to induce QT prolongation and torsades de pointes, which can cause sudden death. We studied the effects of trifluoperazine on the human ether-a-go-go-related gene (HERG) channel expressed in Xenopus oocytes and on the delayed rectifier K(+) current of guinea pig cardiomyocytes. The application of trifluoperazine showed a dose-dependent decrease in current amplitudes at the end of voltage steps and tail currents of HERG. The IC(50) for a trifluoperazine block of HERG current progressively decreased according to depolarization: IC(50) values at -40, 0, and +40 mV were 21.6, 16.6, and 9.29 microM, respectively. The voltage dependence of the block could be fitted with a monoexponential function, and the fractional electrical distance was estimated to be delta = 0.65. The block of HERG by trifluoperazine was use-dependent, exhibiting more rapid onset and greater steady-state block at higher frequencies of activation; there was partial relief of the block with decreasing frequency. In guinea pig ventricular myocytes, bath applications of 0.5 and 2 microM trifluoperazine at 36 degrees C blocked the rapidly activating delayed rectifier K(+) current by 32.4 and 72.9%, respectively; however, the same concentrations of trifluoperazine failed to significantly block the slowly activating delayed rectifier K(+) current. Our findings suggest the arrhythmogenic side effect of trifluoperazine is caused by a blockade of HERG and the rapid component of the delayed rectifier K(+) current rather than by the blockade of the slow component.

Mechanisms of adrenergic control of sino-atrial node discharge.

Among the mechanisms proposed for the increase in discharge of sino-atrial node (SAN) by norepinephrine (NE) are an increase in the hyperpolarization-activated current I(f) and in the slow inward current I(Ca,L). If I(f) is the primary mechanism, cesium (a blocker of I(f)) should eliminate the positive chronotropic effect of NE. If I(Ca,L), is involved, [Ca(2+)](o) should condition NE effects. We studied the electrophysiological changes induced by NE in isolated guinea pig SAN superfused in vitro with Tyrode solution (both SAN dominant and subsidiary pacemaker mechanisms are present) as well as with high [K(+)](o), higher Cs(+) or Ba(2+) (only the dominant pacemaker mechanism is present). In Tyrode solution, NE (0.5-1microM) increased the SAN rate and adding Cs(+) (approximately 12 mM) caused a decaying voltage tail during diastole in subsidiary pacemakers. NE enhanced the Cs(+)-induced tail, and increased the rate but less than in Tyrode solution. In higher [Cs(+)](o) (15- 18 mM), Ba(2+) (1 mM) or Ba(2+) plus Cs(+) (10 mM) dominant action potentials (not followed by a tail) were present and NE accelerated them as in Tyrode solution. In high [K(+)](o), NE increased the rate in the absence and presence of Cs(+), Ba(2+) or Ba(2+) plus Cs(+). In these solutions, NE increased the overshoot and maximum diastolic potential of dominant action potentials (APs) and increased the rate by steepening diastolic depolarization and shifting the threshold for upstroke to more negative values. High [Ca(2+)](o) alone increased the rate and NE enhanced this action, whereas low [Ca(2+)](o) reduced or abolished the increase in rate by NE. In SAN quiescent in high [K(+)](o) plus indapamide, NE induced spontaneous discharge by decreasing the resting potential and initiating progressively larger voltage oscillations. Thus, NE increases the SAN rate by acting primarily on dominant APs in a manner consistent with an increase of I(Ca,L) and I(K) and under conditions where I(f) is either blocked or not activated. NE INITIATES spontaneous discharge by inducing voltage oscillations unrelated to I(f).

FMRFamide modulates potassium currents in circadian pacemaker neurons of Bulla gouldiana

The peptide FMRFamide (Phe-Met-Arg-Phe-NH 2) is known to modulate the circadian pacemaker found in the eye of the marine snail Bulla gouldiana. In the present study, we investigated the cellular mechanisms underlying this modulation by examining the effects of FMRFamide on the membrane properties of the circadian pacemaker cells, known as basal retinal neurons in this preparation. Bath application of FMRFamide (0.1–1 μM) increased the membrane conductance, and hyperpolarized the membrane potential of these neurons. Next, perforated-patch recordings were used to demonstrate that FMRFamide reversibly increased the outward current amplitude due to an augmentation of a non-inactivating calcium-independent current. Reversal potential of the tail currents and its dependence on extracellular potassium concentration suggested potassium ions as the charge carrier for this current. The peptide-modulated outward current was blocked by 54% after bath application of the potassium channel blocker tetraethylammonium chloride and completely blocked by substituting cesium for intracellular potassium. Voltage dependence, activation kinetics and tail current kinetics of the FMRFamide-modulated current were consistent with values found for the delayed rectifier current. Overall, our data suggest that FMRFamide modulates a delayed rectifier potassium current and at least one other, less voltage-dependent conductance. This provides a mechanistic explanation for FMRFamide’s ability to both shift the phase and attenuate light-induced phase shifts of the circadian pacemaker in B. gouldiana.