BURNING MODES OF A BIPOLAR PULSED DISCHARGE IN CO2

We have studied the burning modes of the bipolar pulsed discharge in CO2 within the frequency range between 20 and 300 kHz and the duty cycle of 11...97 %. The current and voltage waveforms within the pressure range between 0.1 to 1 Torr were registered. We have established that the duty cycle values may affect the axial structure of the discharge considerably causing the voltage drop redistribution across the electrodes. The bipolar pulsed discharge may burn in a high-current mode (with cathode sheaths near every electrode) as well as in a low-current one (with a low discharge current and weak glow). The transition between these modes may be observed at high duty cycle values. We have found that one may make a shift of the complete oscilloscope voltage pattern higher or lower along the voltage axis and produce a self-bias constant voltage the value and sign of which depend on the duty cycle, amplitude and frequency of the applied voltage.

The Electrical Behavior of Pd/AIN/Semiconductor Thin Film Hydrogen Sensing Structures

The device on Si substrates behaves as an MIS capacitor and the response to hydrogen is given by a shift of the capacitance vs. bias profile along the bias voltage axis, whereas the device on SiC behaves as a rectifying diode and the presence of hydrogen causes a shift of the forward current vs. voltage plot. The relatively large forward current, in both cases, indicates that there is measurable electrical transport across the AlN layer, but at the same temperature the turn on bias is different. Either structure contains two rectifying contacts in series, namely a Schottky contact between Pd and AlN and a heterojunction between AlN and the substrate.

Critical Considerations in Polymer Thin-Film Transistor (TFT) Dielectrics

We present a study of aqueous and plasma anodised aluminium oxide (Al2O3) and its performance in thin film transistors (TFTs). The current through the oxide was measured with aluminium electrodes and with one of the electrode replaced by poly(3-hexylthiophene)(P3HT). The current increased by up to 2 orders of magnitude with P3HT. The current increased further when the polymer was doped with different percentages of 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ). It was also found to be dependent on the thickness of the polymer film. Surprisingly, the oxide current fell to its initial value when the polymer film was removed. Two mechanisms may explain the behaviour in these devices: charge injection and/or displacement. C-V plots were obtained from the MOS capacitors and were frequency dependent. They also showed substantial hysteresis, with a lateral shift along the voltage axis. This indicates the presence of a mobile species that increases with the concentration of dopant. We deduce that much of the increased gate current is associated with displacement currents induced by ion motion.

Plasma Etching Damage to Ferroelectric SrBi2Ta2O9 (SBT) Thin Films and Capacitors

The effects of reactive ion etching damage on the electrical properties of Pt/SBT/Pt capacitors have been investigated. The plasma treated SBT/Pt layers showed a significant decrease in remanent polarization compared with that of the reference sample. The remanent polarization of the plasma treated layers varied with the gas ratios of the Cl2/Ar plasma. XPS analysis of the plasma treated SBT/Pt samples showed that the surface composition was significantly changed as the gas ratios were varied, which resulted in a polarization decrease in the plasma treated samples. Plasma treatment also caused a voltage shift of the hysteresis loops along the voltage axis. The magnitude of the voltage shift was increased for the chlorine-rich plasma. The results of surface analysis revealed that the voltage shift is caused by oxygen deficiency at the SBT surface. Based on our experimental results, reactive ion etching damage was explained in terms of physical and electrical effects of the plasma on the electrical properties of the ferroelectric Pt/SBT/Pt capacitors.

Effects of oxidant stress on steady-state background currents in isolated ventricular myocytes

Free radicals and oxidant stress have previously been shown to induce depolarization, transient action potential prolongation, and automaticity. We have investigated the ionic basis of these electrophysiological changes in isolated rabbit ventricular cells. Oxidant stress was generated by the photoactivation of rose bengal, and, in current-clamp experiments, the effects of oxidant stress on the action potential were confirmed. In voltage-clamp studies, oxidant stress decreased both inward and outward current through the inward-rectifier potassium channel, and the slope conductance (measured at the voltage-axis intercept near the resting membrane potential) was decreased from 40 +/- 8 to 25 +/- 6 nS (n = 6). Transient inward currents were induced on repolarization after a depolarizing clamp step, suggesting that the cells were calcium overloaded. In addition, oxidant stress activated a steady-state membrane conductance that showed a slight outward-going rectification and a reversal potential of approximately 0 mV. Evidence is presented to indicate that this reflects an increase in the conductance of the calcium-activated nonselective cation channel. The slope conductance of this calcium-activated channel (measured at the voltage-axis intercept) increased with prolonged exposure to oxidant stress (from 0.5 to 12 nS after 7 min), indicating that the intracellular free calcium increased gradually during the maintained application of rose bengal. These results suggest that oxidant stress depolarizes the cell membrane by reducing the inward-rectifier potassium current and by activating a calcium-activated membrane conductance. Both factors may contribute to the oxidant stress-induced changes in action potential duration and automaticity.

Modification of sodium channel gating by lanthanum. Some effects that cannot be explained by surface charge theory.

In clonal pituitary (GH3) cells we studied the changes in sodium channel gating caused by substitution of La3+ for Ca2+ ion. Gating of sodium channels was simplified by using intracellular papain to remove inactivation. To quantify La effects, we empirically fitted closing and the late phase of opening of the channels with single exponentials, determined the opening (a) and closing (b) rate, and plotted these rates as a function of Vm (membrane voltage). The midpoint of the fraction open-Vm curve was also determined. Changing from Ca to La shifted the curves for these three measures of Na channel gating along the voltage axis and changed their shape somewhat. Surface charge theory, in the form usually presented, predicts equal shifts of all three curves, with no change in shape. We found, however, that the shift for each of the measurements was different. 2 mM La, for example, shifted opening kinetics by +52 mV (i.e., 52 mV must be added to the depolarization to make activation in 2 mM La as fast as in 2 mM Ca), the fraction open voltage curve by +42.5 mV, and the closing rate curve by +28 mV. The shift was an almost linear function of log [La] for each of the measures. The main finding is that changing from 2 mM Ca to 10 microM La causes a positive shift of the opening rate and fraction open curves, but a negative shift of the closing rate curve. The opposite signs of the two effects cannot be explained in terms of surface charge theory. We briefly discuss some alternatives to this theory.

Anticonvulsants modify inactivation but not activation processes of sodium channels in Myxicola axons

The effects of pronase and the anticonvulsant drugs diphenylhydantoin, bepridil, and sodium valproate on fast and slow Na+ inactivation were examined in cut-open Myxicola giant axons with loose patch-clamp electrodes applied to the internal surface. Pronase completely eliminated fast Na+ inactivation without affecting the kinetics of Na+ activation or the maximum Na+ conductance. The time and voltage dependences of slow inactivation following pronase treatment were identical to those measured before enzyme application in the same axons. All three anticonvulsants slowed the time course of recovery from fast Na+ inactivation in untreated axons, and shifted the steady-state fast inactivation curve in the hyperpolarizing direction along the voltage axis. Anticonvulsants enhanced steady-state slow inactivation and retarded recovery from slow inactivation in both untreated and pronase-treated axons. Although some quantitative differences were seen, the order of potency of the anticonvulsants on slow Na+ inactivation was the same as that for recovery from fast inactivation.