Forward Mode Operation Research Articles

A Study on Control Algorithm of Thyristor Dual Converter System for DC Electricity Supply of Urban Railway

Most of systems that supplying electric power to operate an electric train of an urban railway to supply power by converting AC into DC through trolly wire, there are two rectification methods to converting AC into DC, with diodes or thyristor. Rectification method using thyristor is composed by 12 pulse thyristor converter with forward and reverse connection. Forward connection thyristor converter supplies electric power to trolly wire as forward mode operation, Reverse connection thyristor converter returns surplus trolly wire voltage to AC top main when regenerative electric power occurs according to regenerative braking, which reduces 20% operating power of an electric train. Rectification method using thyristor is appropriate for an electric train of an urban railway for improving operation efficiency and reducing greenhouse gases. In this paper, propose a dual converter using thyristor system for an urban railway substations and a control algorithm, and the validity of the proposed control technique is verified by the fabrication and experiment of 10 kW scale reduction model.

A Scheme of a Resonant Forward-Flyback Converter With Suppressed Frequency Variation

This letter proposes a simple and low-cost scheme to soft switch an isolated converter. The new circuit merges resonant forward converters and flyback converters by using shared power transformers and primary switches. Specifically, the resonant forward mode operation fulfills soft-switching for the primary switches, and the flyback mode operation resets the transformers by directly delivering the energy to the output. This also allows us a lower ratio between the leakage inductance and the magnetizing inductance. Thus, the main attraction is that simpler structure is utilized to regulate the output voltage for a resonant converter with a constant switching frequency, and higher power efficiency is achievable by taking the full use of transformer magnetizing energy. Also, an input-series-output-parallel connection is utilized to further reduce the voltage stress on the primary side. In addition to detailed theoretical analysis, experimental results verify the feasibility and effectiveness of the proposed concept.

Monolithic optical link in silicon-on-insulator CMOS technology.

This work presents a monolithic laterally-coupled wide-spectrum (350 nm < λ < 1270 nm) optical link in a silicon-on-insulator CMOS technology. The link consists of a silicon (Si) light-emitting diode (LED) as the optical source and a Si photodiode (PD) as the detector; both realized by vertical abrupt n+p junctions, separated by a shallow trench isolation composed of silicon dioxide. Medium trench isolation around the devices along with the buried oxide layer provides galvanic isolation. Optical coupling in both avalanche-mode and forward-mode operation of the LED are analyzed for various designs and bias conditions. From both DC and pulsed transient measurements, it is further shown that heating in the avalanche-mode LED leads to a slow thermal coupling to the PD with time constants in the ms range. An integrated heat sink in the same technology leads to a ∼ 6 times reduction in the change in PD junction temperature per unit electrical power dissipated in the avalanche-mode LED. The analysis paves way for wide-spectrum optical links integrated in smart power technologies.

Total Ionizing Dose Effects on a High-Voltage (&gt;30V) Complementary SiGe on SOI Technology

Total ionizing dose (TID) effects are evaluated for a high-voltage (>30 V) complementary SiGe on SOI technology. Devices are irradiated with 10-keV X-rays at doses up to 5 Mrad(SiO2). The results depend strongly on collector-to-emitter bias, in both forward- and inverse-mode. An anomalous reduction in current gain at high injection in forward-mode operation is observed at doses >500 krad(SiO2). Calibrated 2-D TCAD simulations suggest that this high injection phenomenon is primarily due to interface traps near the STI/Si interface, which is exhibited as a collector resistance increase in the forward Gummel characteristics. Additionally, a strong collector doping dependence is observed, which indicates that this is primarily driven by the thick and lightly doped collector used in this technology. These results illustrate, that high concentrations of interface traps at the STI can have a strong impact on the forward-mode TID response of SiGe HBTs.

Na+ Dysregulation Coupled with Ca2+ Entry through NCX1 Promotes Muscular Dystrophy in Mice

Unregulated Ca(2+) entry is thought to underlie muscular dystrophy. Here, we generated skeletal-muscle-specific transgenic (TG) mice expressing the Na(+)-Ca(2+) exchanger 1 (NCX1) to model its identified augmentation during muscular dystrophy. The NCX1 transgene induced dystrophy-like disease in all hind-limb musculature, as well as exacerbated the muscle disease phenotypes in δ-sarcoglycan (Sgcd(-/-)), Dysf(-/-), and mdx mouse models of muscular dystrophy. Antithetically, muscle-specific deletion of the Slc8a1 (NCX1) gene diminished hind-limb pathology in Sgcd(-/-) mice. Measured increases in baseline Na(+) and Ca(2+) in dystrophic muscle fibers of the hind-limb musculature predicts a net Ca(2+) influx state due to reverse-mode operation of NCX1, which mediates disease. However, the opposite effect is observed in the diaphragm, where NCX1 overexpression mildly protects from dystrophic disease through a predicted enhancement in forward-mode NCX1 operation that reduces Ca(2+) levels. Indeed, Atp1a2(+/-) (encoding Na(+)-K(+) ATPase α2) mice, which have reduced Na(+) clearance rates that would favor NCX1 reverse-mode operation, showed exacerbated disease in the hind limbs of NCX1 TG mice, similar to treatment with the Na(+)-K(+) ATPase inhibitor digoxin. Treatment of Sgcd(-/-) mice with ranolazine, a broadly acting Na(+) channel inhibitor that should increase NCX1 forward-mode operation, reduced muscular pathology.

Abstract 279: Inositol Triphosphate Receptor Activation Alters the Electrical Properties of Human Ventricular Myocytes

The recognition that ryanodine receptor (RyR) dysfunction is associated to arrhythmogenic diseases raises the possibility that alternative Ca2+ release channels alter the electrical properties of ventricular myocytes. The aim of this study was to determine whether inositol triphosphate receptor (IP3R)-mediated Ca2+ mobilization modulates Ca2+ cycling and electrical behavior in LV myocytes. Cells were obtained from human and mouse hearts and the expression and function of IP3Rs were evaluated. IP3Rs were identified in isolated myocytes by immunocytochemistry and Western blotting. In field-stimulated cells, IP3R activation via Gq-protein receptor agonists (ET-1, ATP) or enhancer of ligand affinity (thimerosal) increased diastolic Ca2+ and transient amplitude by 11% and 44%, respectively. Additionally, extra-systolic Ca2+ release and sustained Ca2+ elevations were detected. These effects were prevented by inhibition of IP3 production or by IP3R blockade. Importantly, myocytes obtained from mice infected in vivo with small hairpin RNA (shRNA) targeting IP3R type 2, failed to respond to Gq-protein receptor agonists. In patch-clamped human and mouse cells, changes in Ca2+ transient properties following IP3R activation were accompanied by a decrease in resting potential, action potential (AP) prolongation, and emergence of arrhythmic events. In mouse cardiomyocytes, assessment of excitation-contraction coupling gain and blockade of RyR channels under IP3R stimulation, excluded the contribution of RyRs to the effects induced by IP3R activation. In voltage-clamped cells, IP3R agonists promoted transient inward currents at the membrane potential of -70 mV and increased a nickel-sensitive current in the range of potentials corresponding to forward mode operation of the Na-Ca exchanger. To establish whether enhanced Ca2+ load was responsible for the altered electrical properties under IP3R activation, conditions buffering cytosolic Ca2+ levels were employed. Under these circumstances, IPR stimulation failed to prolong the AP and to induce arrhythmias. In conclusions, our observations demonstrate that Ca2+ mobilization via IP3Rs directly alters the electrical properties of human and rodent myocytes.

Optimal Design and Analysis of a DC—DC Synchronous Converter Using Genetic Algorithm and Simulated Annealing

This paper presents the application of Genetic Algorithm (GA) and Simulated Annealing (SA) techniques for optimal design and analysis of a DC—DC converter with synchronous rectification normally used in battery charge/discharge circuits in DC uninterruptible power supply systems. Converter models for simulation are designed for the forward and backup modes of operation. The results are analysed and compared to those of the expected ideal operation to confirm the validity of the models. An objective function of the converter efficiency in the forward mode operation is derived based on the steady-state values of simulation model. A constrained optimization on the objective function is performed using GA and SA, and optimal parameters are derived. The design and analysis of the converter are performed using software tools within the MATLAB/SIMULINK environment for GA. The derived optimal parameters of the converter from GA are compared with those obtained with SA technique.

The Na+/Ca2+ exchange blocker SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in canine ventricular cardiomyocytes

This study was designed to evaluate the effects of the Na(+)/Ca(2+) exchange (NCX) inhibitor SEA0400 on Ca(2+) handling in isolated canine ventricular myocytes. Intracellular Ca(2+) ([Ca(2+)](i)) transients, induced by either field stimulation or caffeine flush, were monitored using Ca(2+) indicator dyes. [Ca(2+)](i)-dependent modulation of the inhibitory effect of SEA0400 on NCX was characterized by the changes in Ni(2+)-sensitive current in voltage-clamped myocytes. Sarcoplasmic reticulum (SR) Ca(2+) release and uptake were studied in SR membrane vesicles. Gating properties of single-ryanodine receptors were analysed in lipid bilayers. Ca(2+) sensitivity of the contractile machinery was evaluated in chemically skinned myocytes. In myocytes paced at 1 Hz, neither diastolic [Ca(2+)](i) nor the amplitude of [Ca(2+)](i) transients was significantly altered by SEA0400 up to the concentration of 1 microM, which was shown to inhibit the exchange current. The blocking effect of SEA0400 on NCX decreased with increasing [Ca(2+)](i), and it was more pronounced in reverse than in forward mode operation at every [Ca(2+)](i) examined. The rate of decay of the caffeine-induced [Ca(2+)](i) transients was decreased significantly by 1 microM SEA0400; however, this effect was only a fraction of that observed with 10 mM NiCl(2). Neither SR Ca(2+) release and uptake nor cell shortening and Ca(2+) sensitivity of the contractile proteins were influenced by SEA0400. The lack of any major SEA0400-induced shift in Ca(2+) transients or contractility of myocytes can well be explained by its limited inhibitory effect on NCX (further attenuated by elevated [Ca(2+)](i) levels) and a concomitant reduction in Ca(2+) influx due to the predominantly reverse mode blockade of NCX and suppression of L-type Ca(2+) current.

Changes in intracellular calcium concentration in response to hypertonicity in bovine articular chondrocytes

Intracellular calcium concentration ([Ca 2+] i) in articular chondrocytes changes during mechanical challenges associated with joint movements, because of the fluctuation of the extracellular osmotic environment during joint loading. Matrix synthesis by chondrocytes is modulated by loading patterns, possibly mediated by variations in intracellular composition, including [Ca 2+] i. The present study has employed the Ca 2+-sensitive fluoroprobe Fura-2 to determine the effects of hypertonic shock on intracellular Ca 2+ concentration ([Ca 2+] i) and to characterise the mechanisms involved in the response for isolated bovine articular chondrocytes. In cells subjected to a hypertonic shock, [Ca 2+] i rapidly increased by approximately 300%, reaching a maximal value within 50 s following the hypertonic shock with a recovery of more than 90% towards the initial [Ca 2+] i within 5 min. The effect was inhibited by removal of extracellular Ca 2+ ions, but not by thapsigargin, indicating that the rise in [Ca 2+] i is only a result of influx from the extracellular medium. The rise was insensitive to inhibitors of L-type voltage-activated Ca 2+ channels, TRPV channels or stretch-activated cation channels. Non-specific inhibitors of Ca 2+ channels like CdCl 2, NiCl 2, LaCl 3 and ZnCl 2 significantly attenuated the response, although the extent in which CdCl 2 and NiCl 2 (both of them inhibitors of annexin-mediated Ca 2+ fluxes) inhibited the response was significantly greater. The rise was also sensitive to KBR7943, inhibitor of NCE reverse mode and trifluoperazine, inhibitor of the activity of annexins. Hypertonic shock also produced also hyperpolarisation of chondrocytes ( E m measured by means of Di-BA-C 4(3), a membrane potential sensitive dye), which was inhibited by TEA-Cl and BaCl, but was not affected by changing the extracellular solution to Ca 2+-free HBS. Inhibition of hyperpolarisation completely abolished the [Ca 2+] i rise following hypertonic shock. Treatment with retinoic acid, which can increase the activity of annexins as Ca 2+ transport pathways caused a significant increase in [Ca 2+] i. The recovery of [Ca 2+] was inhibited by benzamil and was dependent on extracellular Na +, but was unaffected by Na-orthovanadate, an inhibitor of plasma Ca 2+-ATPase. We conclude that in response to hypertonic shock, NCE reverse mode and annexins are the pathways responsible for the [Ca 2+] i increase, while forward mode operation of NCE is responsible for the subsequent extrusion of Ca 2+ and recovery of [Ca 2+] i towards initial values.

Extrusion of intracellular calcium ion after in vitro ischemia in the rat hippocampal CA1 region.

Simultaneous recordings of intracellular Ca(2+) ([Ca(2+)](i)) signal and extracellular DC potential were obtained from the CA1 region in 1-[6-amino-2-(5-carboxy-2-oxazolyl)-5-benzofuranyloxy]-2-(2-amino-5-methylphenoxy)-ethane-N,N,N',N'-tetraacetic acid penta-acetoxymethyl ester (Fura-2/AM)-loaded rat hippocampal slices. Superfusion with oxygen- and glucose-deprived medium (in vitro ischemia) for 5-6 min produced a rapid rise of the [Ca(2+)](i) level in the stratum radiatum (rising phase of the [Ca(2+)](i) signal), which occurred simultaneously with a rapid negative DC potential (rapid negative potential). When oxygen and glucose were reintroduced, the increased [Ca(2+)](i) signal diminished rapidly (falling phase of the [Ca(2+)](i) signal) during the generation of a slow negative DC potential (slow negative potential), which occurred within 1 min from the onset of the reintroduction. Thereafter, the [Ca(2+)](i) signal partially and the slow negative potential completely returned to the preexposure level approximately 6 min after the reintroduction. The changes in [Ca(2+)](i) signal during and after in vitro ischemia were very similar to the changes in the membrane potential of glial cells. The rising and falling phases of [Ca(2+)](i) signal corresponded to the rapid depolarization and a depolarizing hump, respectively, in the repolarizing phase of glial cells. A prolonged application of in vitro ischemia or a reintroduction of either glucose or oxygen suppressed the falling phase after ischemic exposure. The application of ouabain (30 microM) generated both a rapid negative potential and a rapid elevation of [Ca(2+)](i), but no slow negative potential or rapid reduction in [Ca(2+)](i) were observed. When oxygen and glucose were reintroduced to slices in the Na(+)-free or ouabain- or Ni(2+)-containing medium, the falling phase was suppressed. The falling phase was significantly accelerated in Ca(2+)- and Mg(2+)-free with EGTA-containing medium. In contrast, the falling phase was significantly slower in the Ca(2+)-free with high Mg(2+)- and EGTA-containing medium. The falling phase of the [Ca(2+)](i) signal after ischemic exposure is thus considered to be primarily dependent on the reactivation of Na(+), K(+)-ATPases, while the extrusion of cytosolic Ca(2+) via the forward-mode operation of Na(+)/Ca(2+) exchangers in glial cells is thought to be directly involved in the rapid reduction of [Ca(2+)](i) after ischemic exposure.

Na+/Ca2+ exchanger activity induces a slow DC potential after in vitro ischemia in rat hippocampal CA1 region.

In rat hippocampal CA1 neurons recorded intracellularly from tissue slices, a rapid depolarization occurred approximately 5 min after application of ischemia-simulating medium. In extracellular recordings obtained from CA1 region, a rapid negative-going DC potential (rapid DC potential) was recorded, corresponding to a rapid depolarization. When oxygen and glucose were reintroduced after generating the rapid depolarization, the membrane further depolarized and the potential became 0 mV after 5 min. Contrary, the DC potential began to repolarize slowly and subsequently a slow negative-going DC potential (slow DC potential) occurred within 1 min. A prolonged application of ischemia-simulating medium suppressed the slow DC potential. Addition of a high concentration of ouabain in normoxic medium reproduced a rapid but not a slow DC potential. The slow DC potential was reduced in low Na+- or Co2+-containing medium, but was not affected in low Cl-, high K+ or K+-free medium, suggesting that the slow DC potential is Na+-and Ca2+-dependent. Ni2+ (Ca2+ channel blocker as well as the Na+/Ca2+ exchanger blocker) and benzamil hydrochloride (Na+/Ca2+ exchanger blocker) reduced the slow DC potential dose-dependently. These results suggest that the slow DC potential is mediated by forward mode operation of Na+/Ca2+ exchangers in non-neuronal cells, and that reactivation of Na+, K+-ATPase is necessary to the Na+/Ca2 +exchanger activity.

Cloning, sequencing and expression of the 67-kDa collagen-binding annexin from chicken growth plate matrix vesicles

Intracellular calcium concentration ([Ca2+]i) in articular chondrocytes changes during mechanical challenges associated with joint movements, because of the fluctuation of the extracellular osmotic environment during joint loading. Matrix synthesis by chondrocytes is modulated by loading patterns, possibly mediated by variations in intracellular composition, including [Ca2+]i. The present study has employed the Ca2+-sensitive fluoroprobe Fura-2 to determine the effects of hypertonic shock on intracellular Ca2+ concentration ([Ca2+]i) and to characterise the mechanisms involved in the response for isolated bovine articular chondrocytes. In cells subjected to a hypertonic shock, [Ca2+]i rapidly increased by approximately 300%, reaching a maximal value within 50 s following the hypertonic shock with a recovery of more than 90% towards the initial [Ca2+]i within 5 min. The effect was inhibited by removal of extracellular Ca2+ ions, but not by thapsigargin, indicating that the rise in [Ca2+]i is only a result of influx from the extracellular medium. The rise was insensitive to inhibitors of L-type voltage-activated Ca2+ channels, TRPV channels or stretch-activated cation channels. Non-specific inhibitors of Ca2+ channels like CdCl2, NiCl2, LaCl3 and ZnCl2 significantly attenuated the response, although the extent in which CdCl2 and NiCl2 (both of them inhibitors of annexin-mediated Ca2+ fluxes) inhibited the response was significantly greater. The rise was also sensitive to KBR7943, inhibitor of NCE reverse mode and trifluoperazine, inhibitor of the activity of annexins. Hypertonic shock also produced also hyperpolarisation of chondrocytes (Em measured by means of Di-BA-C4(3), a membrane potential sensitive dye), which was inhibited by TEA-Cl and BaCl, but was not affected by changing the extracellular solution to Ca2+-free HBS. Inhibition of hyperpolarisation completely abolished the [Ca2+]i rise following hypertonic shock. Treatment with retinoic acid, which can increase the activity of annexins as Ca2+ transport pathways caused a significant increase in [Ca2+]i. The recovery of [Ca2+] was inhibited by benzamil and was dependent on extracellular Na+, but was unaffected by Na-orthovanadate, an inhibitor of plasma Ca2+-ATPase. We conclude that in response to hypertonic shock, NCE reverse mode and annexins are the pathways responsible for the [Ca2+]i increase, while forward mode operation of NCE is responsible for the subsequent extrusion of Ca2+ and recovery of [Ca2+]i towards initial values.

Hot-carrier effects in Hydrogen-passivated p-channel polycrystalline-Si MOSFET's

The dependence of hot-carrier effects on channel length and stress-bias voltage in hydrogen-passivated accumulation-mode p-channel polycrystalline-Si MOSFET's operating in the saturation region has been studied, Before stress, these devices exhibit a minimum value of current at V GS ≈ 0 V but as V GS increases above 0 V, they show an increase in (leakage) current due to field-enhanced generation of carriers near the drain. After stress, the current at V GS ≈ 0 V increases slightly with respect to its pre-stress value. However, the current then monotonically decreases as V GS increases above 0 V unlike the situation before stress. No change in reverse mode (source and drain reversed) characteristics and no change in the ON-state (V GS < 0 V) forward-mode characteristic was observed after stress. These observations are shown to be due to hot-carrier-induced acceptor-type interface states near the drain in forward-mode operation.

A ladder structure for millimeter waves

A planar structure, closely related to the stub-supported ring and bar structure, is analyzed using Fletcher's method. The computed dispersion characteristics and interaction impedances show that it should prove useful in millimeter generators. Experiments at X band have shown that oscillation bands of over 1.7 : 1 are possible working on a backward mode. Forward-mode operation with higher output powers, but with a more restricted bandwidth can also be realized.