Correlation between Battery Voltage under Loaded Condition and Estimated State of Charge at Valve-Regulated Lead Acid Battery on Discharge Condition using Open Circuit Voltage Method

One of the common methods that developed to predict state of charge is open circuit voltage (OCV) method. The problem which commonly occurs is to find the correction parameter between open circuit voltage and loaded voltage of the battery. In this research, correlation between state of charge measurement at loaded condition of a Panasonic LC-VA1212NA1, which is a valve-regulated lead acid (VRLA) battery, and open circuit voltage had been analyzed. Based on the results of research, correlation between battery’s measured voltage under loaded condition and open circuit voltage could be approached by two linearization area. It caused by K v ’s values tend to increase when measured voltage under loaded condition V M < 11.64 volt. However, K v values would be relatively stable for every V M ≥ 11.64 volts. Therefore, estimated state of charge value, in respect to loaded battery voltage, would increase slower on V M < 11.64 volts and faster on other range.

Minimum dropout voltage on a serial pnp transistor of a moderately loaded voltage regulator in a gamma radiation field

The main examined value in an experiment performed on moderately loaded voltage regulators was the serial pnp transistor?s minimum dropout voltage, followed by the data on the base current and forward emitter current gain. Minimum dropout voltage decreased by up to 12%, while the measured values of the forward emitter current gain decreased by 20-40% after the absorption of a total ionizing dose of 500 Gy. The oxide trapped charge increased the radiation tolerance of the serial lateral pnp transistor owing to the suppression of interface trap formation above the base area. Current flow through the serial transistor of the voltage regulator had an influence on the decrease in the power pnp transistor?s forward emitter current gain. Due to the operation with a moderate load of 100 mA, loss of emitter injection efficiency was not as important as during the operation with high current density, thus eliminating the negative influence of emitter crowding on the radiation hardness of the voltage regulator. For a moderate load, gain in the negative feedback reaction was enough to keep output voltage in the anticipated range. Only information procured from tests of the minimum dropout voltage on the moderately loaded voltage regulators were not sufficient for unequivocal determination of the examined integrated circuit?s radiation hardness.

On-line monitoring of base current and forward emitter current gain of the voltage regulator's serial pnp transistor in a radiation environment

A method of on-line monitoring of the low-dropout voltage regulator's operation in a radiation environment is developed in this paper. The method had to enable detection of the circuit's degradation during exploitation, without terminating its operation in an ionizing radiation field. Moreover, it had to enable automatic measurement and data collection, as well as the detection of any considerable degradation, well before the monitored voltage regulator's malfunction. The principal parameters of the voltage regulator's operation that were monitored were the serial pnp transistor's base current and the forward emitter current gain. These parameters were procured indirectly, from the data on the voltage regulator's load and quiescent currents. Since the internal consumption current in moderately and heavily loaded devices was used, the quiescent current of a negligibly loaded voltage regulator of the same type served as a reference. Results acquired by on-line monitoring demonstrated marked agreement with the results acquired from examinations of the voltage regulator's maximum output current and minimum dropout voltage in a radiation environment. The results were particularly consistent in tests with heavily loaded devices. Results obtained for moderately loaded voltage regulators and the risks accompanying the application of the presented method, were also analyzed.

Mitochondrial Ca2+ uptake is important over low [Ca2+]i range in arterial smooth muscle

Mitochondrial Ca2+ uptake is usually thought to occur only when intracellular Ca2+concentration ([Ca2+]i) is high. We investigated whether mitochondrial Ca2+ removal participates in shaping [Ca2+]i signals in arterial smooth muscle over a low [Ca2+]irange. [Ca2+]i was measured using fura 2-loaded, voltage-clamped cells from rat femoral arteries. Both diazoxide and carbonyl cyanide m-chlorophenylhydrazone (CCCP) depolarized the mitochondria. Diazoxide application increased resting [Ca2+]i, suggesting that Ca2+ is sequestered in mitochondria. Over a low [Ca2+]i range, diazoxide and CCCP slowed Ca2+ removal rate, determined after a brief depolarization. When [Ca2+]i was measured during sustained depolarization to −30 mV, CCCP application increased [Ca2+]i. When Ca2+ transients were repeatedly evoked by caffeine applications, CCCP application elevated resting [Ca2+]i. Caffeine-induced Ca2+ transients were compared before and after CCCP application using the half decay time, or time required to reduce increase in [Ca2+]i by 50% ( t ½). CCCP treatment significantly increased t ½. These results suggest that Ca2+ removal to mitochondria in arterial smooth muscle cells may be important at a low [Ca2+]i.

Control of Maximum Sarcoplasmic Reticulum Ca Load in Intact Ferret Ventricular Myocytes

In steady state, the Ca content of the sarcoplasmic reticulum (SR) of cardiac myocytes is determined by a balance among influx and efflux pathways. The SR Ca content may be limited mainly by the ATP-supplied chemical potential that is inherent in the gradient between SR and cytosol. That is, forward Ca pumping from cytosol to SR may be opposed by energetically conservative reverse pumping dependent on intra-SR free [Ca]. On the other hand, SR Ca loading may be limited by dissipative pathways (pump slippage and/or pump-independent leak). To assess how SR Ca content is limited, we loaded voltage-clamped ferret ventricular myocytes cumulatively with known amounts of Ca via L-type Ca channels (ICa), using Na-free solutions to prevent Na/Ca exchange. We then measured the maximal resulting caffeine-released SR Ca content under control conditions, as well as when SR Ca pumping was accelerated by isoproterenol (1 μM) or slowed by thapsigargin (0.2–0.4 μM). Under control conditions, SR Ca content reached a limit of 137 μmol·liter cytosol−1 (nonmitochondrial volume) when measured by integrating caffeine-induced Na/Ca exchange currents (∫INaCaXdt) and of 119 μmol·liter cytosol−1 when measured using fluorescence signals dependent on changes in cytosolic free Ca ([Ca]i). When Ca-ATPase pumping rate was slowed 39% by thapsigargin, the maximal SR Ca content decreased by 5 (∫INaCaXdt method) or 23% (fluorescence method); when pumping rate was increased 74% by isoproterenol, SR Ca content increased by 10% (fluorescence method) or 20% (∫INaCaXdt method). The relative stability of the SR Ca load suggests that dissipative losses have only a minor influence in setting the SR Ca content. Indeed, it appears that the SR Ca pump in intact cells can generate a [Ca] gradient approaching the thermodynamic limit.

Intracellular pH-regulating ion transport mechanisms in parietal cell basolateral membrane vesicles

Na(+)-H+ and Cl(-)-base exchangers on the parietal cell have been demonstrated by several authors. Controversy exists concerning a basolateral Na(+)-HCO3- cotransporter in the parietal cell. To clarify this issue, we prepared highly enriched basolateral membrane (BLM) and apical-tubulovesicular membrane (to serve as negative controls) vesicles from rabbit fundic mucosa. Na(+)-H+ exchange was demonstrated by measuring pH gradient-driven amiloride-sensitive 22Na+ uptake and Na+ gradient-driven proton uptake into voltage-clamped BLM but not into apical-tubulovesicular vesicles. Anion exchange was demonstrated by measuring 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-inhibitable influx of 36Cl- into Cl(-)- or HCO3(-)-loaded voltage-clamped BLM vesicles. Na(+)-HCO3- cotransport was assessed by comparing HCO3(-)-driven 22Na uptake with uptake driven by an identical pH gradient. No significant difference was found between 22Na uptake in the presence and absence of HCO3-; 1 mM amiloride inhibited 22Na uptake > 90% in both conditions, whereas 2 mM DIDS had no effect. In BLM vesicles prepared from rabbit renal cortex, however, a HCO3- gradient stimulated 22Na uptake much more than an equivalent pH gradient, and DIDS inhibited this HCO3- gradient-driven 22Na uptake. This indicates that our experimental setup was suitable to detect a Na(+)-HCO3- cotransporter if present. Our data suggest that the parietal cell BLM contains Na(+)-H+ exchangers and Cl(-)-HCO3- exchangers but no Na(+)-HCO3- cotransporter.