Initial Rapid Rise Research Articles

Tribocharging of the magnetic hard disk drive head–disk interface

As head–disk separation diminishes and the sensitivity of magnetic recording transducers increases, the effects of spurious charge buildup caused by friction become an increasing concern. We have investigated some of the characteristics of tribocharging during frictional contact between head and media typically found in magnetic hard disk drives. From constant velocity tests with an electrically isolated head contacting the laser texture zone, we find that current and voltage are closely related, both undergoing a rapid initial rise followed by a long-term rise. We have found that the long-term rise is controlled by the rate of discharge and that the overall magnitude of both current and voltage is dependent upon the rate of rotation. Additionally, we find that the magnitude of current and voltage increases sequentially from test to test, suggesting that wear is occurring at the interface. We develop models for wear-induced tribocharging and surface potential difference-induced tribocharging and contrast their predictions for charge generations as functions of velocity. These models suggest that wear is the dominant tribocharging mechanism.

Modeling Excess Retrieval in Rat Melanotroph Membrane Capacitance Records

We have used the patch-clamp technique to monitor changes in membrane capacitance ( C m) elicited by fast and spatially homogeneous rises in cytosolic calcium concentration ([Ca 2+] i) using flash photolysis of NP-EGTA. Average peak [Ca 2+] i amplitudes of 20–25 μM triggered three different types of responses in C m: (i) In 42% of cells, a rise in [Ca 2+] i activated a monotonic increase in C m followed by a slow decline to resting values; (ii) In 30% of cells, the rise in C m was clearly characterized by two dynamic components, consisting of a rapid and a slow exo–endocytosis cycle; (iii) In 28% of cells, after the initial rapid rise in C m, endocytosis exhibited excess retrieval that was characterized by a decline in C m below resting C m. The aim of this work is to develop a unified mathematical model with a minimum number of parameters that would describe all the observed types of responses. Three models were considered: Model A, a model with a single component of exo-endocytosis cycle; model B, a model consisting of a sum of two independent dynamic components; and model C, a model in which, in addition to the two dynamic components as in model B, excess retrieval due to a lipid flow through the reversal closing of the fusion pore during the rapid component of exo-endocytosis cycle was considered. The results show that the latter model describes all the types of responses in C m recorded in rat melanotrophs. The association of excess retrieval exclusively with the rapid, but not the slow, exocytosis indicates that some fusing vesicles mediate a lipidic flux during the reversal closing of the fusion pore, whereas those entering the slow phase of exocytosis may fuse with the plasma membrane completely and are retrieved by other endocytic machinery, independent of the lipid flow that might have occurred as the fusion pore opened permanently.

Ion transport by sheep distal airways in a miniature chamber.

Ion transport and the electric profile of distal airways of sheep lungs were studied in a miniature polypropylene chamber with a 1-mm aperture. Small airways with an inner diameter < 1 mm were isolated, opened longitudinally, and then mounted as a flat sheet onto the 1-mm aperture where it was glued and secured with an O-ring. Both sides of the tissue were bathed with identical physiological solutions at 37 degrees C and oxygenated. Pooled data from 27 distal airways showed an inner airway diameter of 854 +/- 22 (SE) microm and a transepithelial potential difference (PD) of 1.86 +/- 0.29 mV, lumen negative. Short-circuit current (I(sc)) was 25 +/- 3.5 microA/cm(2), tissue resistance was 96 +/- 14 Omega, and conductance was 15.2 +/- 1.7 mS/cm(2). At baseline, amiloride-sensitive Na transport accounted for 51% of I(sc) (change in I(sc) = 9.7 +/- 2.6 microA/cm(2); n = 8 airways), corresponding to 0.36 microeq. cm(-2). h(-1). Treatment with 0.1 mM bumetanide did not reduce the I(sc) (n = 5 airways). Exposure to 1 microM Ca ionophore A-23187 raised the I(sc) by 9 microA/cm(2) (47%; P < 0.03; n = 6 airways). The latter effect was blunted by bumetanide. Carbachol at 1 microM provoked a biphasic response, an initial rapid rise in I(sc) followed by a decline (n = 3 airways). There was no significant increase in PD or I(sc) in response to isoproterenol or dibutyryl cAMP. The data suggest that Na absorption constitutes at least 50% of baseline transport activity. Cl or other anion secretion such as HCO(3) appears to be present and could be stimulated by raising intracellular Ca.

TheV−EUV Delay for Dwarf Nova Outbursts: A Case Study for VW Hydri, U Geminorum, and SS Cygni

We present a parameter study using time dependent calculations of the thermal limit cycle model for dwarf nova outbursts. Our goal is to delineate the dependence of the delay between the initial rapid rise of the visual and EUV fluxes during the start of an outburst on model parameters, concentrating on three bright, nearby systems for which complete optical and EUV observations exist - VW Hyi, U Gem, and SS Cyg. For these systems we infer that the outburst must be triggered at ~0.7-0.8 of the outer disk radius to produce delays which are in accord with observations. We also see a stagnation or period of slow warming (first noted by Mineshige) during the early stages of thermal instability, but find it does not influence the V-EUV delay since it precedes the rapid rise in V at the start of the outburst. We find that if one decreases the surface density in the inner disk, interior to the instigation radius, the V-EUV delay can be lengthened by as much as a factor of two. In addition, we find there to be a weak relation between the V-EUV delay and the value of the alpha viscosity parameter in quiescence.

Effects on the optokinetic system of midline lesions in the pretectum of monkeys

The nucleus of the optic tract (NOT), an important visuo-motor relay between the retina and preoculomotor structures, is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits and rats. In addition to its projection to the vestibular nuclei, the NOT has a prominent projection to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs in OKN, we cut the posterior commissure in three Macaca fuscata. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and both eyes viewing. OKN was recorded in response to counter-clockwise and clockwise stimulation at stimulus velocities of 30 degrees/s, 60 degrees/s and 90 degrees/s. After control data were gathered, the posterior commissure was transected with an operating knife. Before the animal was sacrificed, biocytin, an anterograde tracer, was injected into the left NOT in order to confirm that all of the commissural fibers had been cut. Although the midline lesions decreased the initial rapid rise and steady state OKN slow-phase velocity in all three animals, there were no directional differences observed during monocular clockwise or counter-clockwise visual stimulation to either eye. In two of the three animals, there were no significant differences in the time-constants of optokinetic after nystagmus (OKAN) after the lesion. In the remaining animal, the time-constants decreased at stimulus velocities of 30 degrees/s and 60 degrees/s. In conclusion, gain reduction in the rapid rise and steady state slow-phase velocity of OKN can be explained by removal of an excitatory signal mediated by commissural fibers to inhibitory interneurons in the contralateral NOT. However, interrupting the commissural fibers had no effect on the velocity storage mechanism, because the time-constants of OKAN mostly remained largely unchanged by the lesion.

ATP consumption by uncoupled mitochondria activates sarcolemmal K(ATP) channels in cardiac myocytes.

We tested whether close coupling exists between mitochondria and sarcolemma by monitoring whole cell ATP-sensitive K(+) (K(ATP)) current (I(K,ATP)) as an index of subsarcolemmal energy state during mitochondrial perturbation. In rabbit ventricular myocytes, either pinacidil or the mitochondrial uncoupler dinitrophenol (DNP), which rapidly switches mitochondria from net ATP synthesis to net ATP hydrolysis, had little immediate effect on I(K,ATP). In contrast, in the presence of pinacidil, exposure to 100 microM DNP rapidly activated I(K,ATP) with complex kinetics consisting of a quick rise [time constant of I(K,ATP) increase (tau) = 0.13 +/- 0.01 min], an early partial recovery (tau = 0.43 +/- 0.04 min), and then a more gradual increase. This DNP-induced activation of I(K,ATP) was reversible and accompanied by mitochondrial flavoprotein oxidation. The F(1)F(0)-ATPase inhibitor oligomycin abolished the DNP-induced activation of I(K,ATP). The initial rapid rise in I(K,ATP) was blunted by atractyloside (an adenine nucleotide translocator inhibitor), leaving only a slow increase (tau = 0.66 +/- 0.17 min, P < 0.01). 2,4-Dinitrofluorobenzene (a creatine kinase inhibitor) slowed both the rapid rise (tau = 0.20 +/- 0.01 min, P < 0.05) and the subsequent declining phase (tau = 0.88 +/- 0.19 min, P < 0.05). From single K(ATP) channel recordings, we excluded a direct effect of DNP on K(ATP) channels. Taken together, these results indicate that rapid changes in F(1)F(0)-ATPase function dramatically alter subsarcolemmal energy charge, as reported by pinacidil-primed K(ATP) channel activity, revealing cross-talk between mitochondria and sarcolemma. The effects of mitochondrial ATP hydrolysis on sarcolemmal K(ATP) channels can be rationalized by reversal of F(1)F(0)-ATPase and the facilitation of coupling by the creatine kinase system.

Acetylcholine increases intracellular Ca2+ in the rat pituitary folliculostellate cells in primary culture.

Pituitary folliculostellate cells (FSCs) are thought to partially inhibit pituitary hormone secretion through a paracrine mechanism. In this process, one of the important questions is what factors regulate the function of FSCs. Because ACh is synthesized in and possibly released from the corticotrophs and lactotrophs, we examined whether FSCs respond to ACh by the method of Ca2+ imaging in primary cultured FSCs from male Wistar rats. ACh (30 nM-3 microM) increased intracellular calcium concentration ([Ca2+](i)) of FSCs in a concentration-dependent manner, with an initial rapid rise followed by a relatively sustained increase. The complete block of the response by atropine and pirenzepine suggests involvement of muscarinic receptors. Depletion of the stored Ca2+ by thapsigargin blocked the response completely. Blockers of phospholipase C, U-73122 and neomycin, suppressed significantly the rise of [Ca2+](i). These results suggest that ACh increases [Ca2+](i) in FSCs by activating phospholipase C, presumably through activation of M(1) receptors. The rise in [Ca2+](i) could trigger a variety of Ca2+-dependent cellular processes, including the synthesis and release of bioactive substances, which in turn act on endocrine cells.

The effects of ramp stretches on active contractions in intact mammalian fast and slow muscle fibres.

The effects of a ramp stretch (amplitude <6% muscle fibre length (L0), speed < 13L0 s(-1)) on twitch tension and twitch tension re-development were examined in intact mammalian (rat) fast and slow muscle fibre bundles. The experiments were done in vitro at 20 degrees C and at an initial sarcomere length of 2.68 microm. In both fibre types, a stretch applied during the rising phase of the twitch response (including the time of stimulation) increased the re-developed twitch tension (15-35%). A stretch applied before the stimulus had little or no effect on the twitch myogram in fast muscle fibres, but it increased the twitch tension (approximately 5%) in slow muscle fibres. A similar stretch had little or no effect on tetanic tension in either muscle fibre type. In general, the results indicate that the contractile-activation mechanism may be stretch sensitive and this is particularly pronounced in slow muscle fibres. Recorded at a high sampling rate and examined at an appropriate time scale, the transitory tension response to a stretch rose in at least two phases; an initial rapid tension rise to a break (break point tension, P1a) followed by a slower tension rise (apparent P2a) to a peak reached at the end of the stretch. Plotted against stretch velocity, P1a tension increased in direct proportion to stretch velocity (viscous-like) whereas, P2a tension (calculated as peak tension minus P1a tension) increased with stretch velocity to a plateau (visco-elastic). Examined at the peak of a twitch, P1a tension had a slope (viscosity coefficient) of 1.8 kN m(-2) per L0 s(-1) in fast fibres and 4.7 kN m(-2) per L0 s(-1) in slow muscle fibres. In the same preparations, P2a tension had a relaxation time of 8 ms in the fast muscle fibres and 25 ms in the slow muscle fibres. The amplitudes of both tension components scaled with the instantaneous twitch tension in qualitatively the same way as the instantaneous fibre stiffness. These fast/slow fibre type differences probably reflect differences in their cross-bridge kinetics.

Characterization of platelet-activating factor-induced cytosolic calcium mobilization in human eosinophils.

Activated eosinophils play an important role in the pathogenesis of bronchial asthma and other allergic diseases, and platelet-activating factor (PAF) is a potent activator of eosinophils. To characterize the cytosolic Ca2+ ([Ca2+]i) mobilization in human eosinophils in response to PAF. [Ca2+]i responses to PAF were examined in human eosinophils using a microscopic fura-2 fluorescence-ratio imaging system. PAF caused a significant and dose-dependent increase in (Ca2+)i, which consisted of an initial rapid rise followed by a sustained elevation. This PAF-induced (Ca2+)i rise was inhibited by WEB 2086, a specific PAF receptor antagonist. The addition of 5 mM EGTA or 1 mM Ni2+ to a nominally Ca2+-free solution did not appreciably reduce the initial rise but significantly inhibited the sustained rise. The application of a protein kinase C inhibitor, Ro31-8220, augmented the sustained increase by PAF. Thapsigargin, a microsomal Ca2+ ATPase inhibitor, induced no appreciable change in a nominally Ca2+-free solution but induced a marked increase in (Ca2+)i when changed to a Ca2+-containing solution. The initial rapid rise and the following sustained rise in (Ca2+)i by PAF depends on Ca2+ release from the intracellular Ca2+ stores and Ca2+ influx, respectively, which are regulated by protein kinase C in human eosinophils. Furthermore, the so called Ca2+-capacitative entry is possibly involved in the Ca2+ influx from the extracellular solution in human eosinophils.

Modeling stop-consonant releases for synthesis

This study is part of a project leading to rule-based speech synthesis using the HLsyn synthesizer. In HLsyn, stop-consonant releases are generated by controlling the time variation of a constriction that is formed by the lips, the tongue blade, or the tongue body. In order to generate a consonant release that is perceptually acceptable and that has acoustic characteristics that match those of normal speech, it was found that the trajectory of the consonant release (cross-sectional area versus time) had to exhibit an initial rapid rise, followed by a delay in which the rise was interrupted, followed finally by a final rise. The burst at the consonant release is generated by the airflow through the constriction during the time that the rise is delayed. A model of the time course of this three-stage release of the articulator has been developed, taking into account the role of the intraoral pressure, the tapering formed by the articulator, and the glottal area. The model shows that the delay between the initial and final area increases is progressively longer for labials, alveolars, and velars, in agreement with acoustic data on the burst duration. [Work supported in part by NIH Grant Nos. MH52358 and DC00075.]

The Holocene depositional history of the IJzer palaeovalley (Western Belgian coastal plain) with reference to the factors controlling the formation of intercalated peat beds

Detailed stratigraphic and sedimentological work, together with radiocarbon datings of the Holocene coastal deposits in the IJzer palaeovalley was performed in order to document the formation of the sedimentary sequence in relation to the controlling factors, to reveal the stratigraphical significance of intercalated peat beds, and to reconstruct the depositional history. Because of the many controversies relating to these topics, the Belgian literature has been reviewed. An initial rapid sea-level rise prior to ca. 7800 cal BP resulted in a rapid shift of the facies belts across the palaeovalley and was associated with rapid filling with no formation of intercalated peat beds. A deceleration in the rate of the sea-level rise with sufficient sediment supply produced rapid facies changes registered as frequent alternations of mud, peat and gyttja in the sedimentary sequence deposited between ca. 7800 and 6000 cal BP. The facies changes are determined by a sedimentological control related to the tidal channel and creek network, and not by sea-level fluctuations. Periods of peat growth lasted longer and the lateral extension became more widespread as deceleration of the sea-level rise and filling of the plain continued. This was associated with progradation of the shoreface from ca. 6000 cal BP onwards. Tidal conditions returned to the area from ca. 4000 cal BP onwards. This return was accompanied by erosion and landward migration of the shoreface and channel network. This study demonstrates that the tripartite stratigraphy using Dunkerque and Calais as units should be abandoned in favour of lithological and sedimentological descriptions and age determinations together with environmental interpretation.

Optokinetic eye movements elicited by an apparently moving visual pattern in guinea pigs

Based on known anatomical and physiological properties, guinea pigs could be expected to show a lack of cortical impact on the basic properties of optokinetic nystagmus (OKN) such as eye movements elicited by a rotating striped drum. The present study aimed to clarify the question of whether the guinea pig's brainstem-mediated circuit is capable of generating horizontal OKN with the animal binocularly viewing a stationary stroboscopically illuminated striped pattern (apparent-motion OKN). A striped drum with a pattern periodicity of 2.37 degrees was rotated around the animal. The OKN buildup under real stimulation conditions was found to be largely devoid of a rapid initial rise in slow-phase eye velocity (direct OKN component). Only in a few recordings was a slight initially faster acceleration seen eliciting slow-phase eye velocities of 2 degrees/s at the most. The lack of a rapid initial rise proves that the optokinetic reflex loop does not possess a functionally significant cortically mediated component. To achieve apparent-motion OKN, initially in each recording real-motion OKN was elicited by the constantly illuminated rotating pattern. Then, 60 or 90 s later the drum was stopped and the illumination switched over from constant to flashing light. Following Grüsser and Behrens (1979), we calculated an apparent stimulus velocity (= flash frequency x 2.37 degrees) and an apparent OKN gain. We found that all animals continued in nystagmus under the flashing light condition. The slow-phase eye velocity was the same as under real pattern motion, with gain values of between 0.36 and 0.7. In two animals we produced an apparent gain close to unity by suddenly doubling the flash interval, i.e., halving the apparent drum velocity. This gain, however, did not remain at a high level: The slow-phase eye velocity decreased until the previous lower gain was reached again. The data indicate that cortical mechanisms are not necessary to produce nystagmus under apparent-motion stimulation and neither phi nor sigma phenomena of motion perception satisfactorily explain the apparent-motion OKN in the guinea pig. Our data provide evidence that the brainstem-located velocity storage mechanism plays a decisive role in keeping the eye in motion under apparent-motion stimulation.

Prostaglandin F2α-induced Ca++ oscillations in human myometrial cells and the role of RU 486

Objective:We sought to examine the change of cytosolic calcium concentration caused by prostaglandin F2α and RU 486 in cultured human myometrial cells. Study Design:Human myometrial cells obtained from 16 nonpregnant women were loaded with fura 2, and the intracellular cytosolic calcium concentrations were measured by the use of wavelength spectrophotofluorometry. Results:Application of prostaglandin F2α (2.8 μmol/L) caused an initial rapid rise in cytosolic calcium concentration followed by sustained cytosolic calcium oscillations at an average frequency of 0.43 ± 0.04 min−1 and an amplitude in the range of 296.82 ± 27.16 nmol/L. The oscillatory activity was not affected by increasing the concentration of prostaglandin F2α but varied by changing the concentration of extracellular cytosolic calcium concentration. The cytosolic calcium oscillations were suppressed by caffeine, 2,5-di-tert-butylhydroquinone, and lanthanum but not affected by ryanodine. Verapamil decreased the amplitude but not the frequency of oscillations. The progesterone antagonist RU 486 at a concentration of 10−8 to 10−5 mol/L had no significant effect on the basal intracellular cytosolic calcium. However, RU 486 (10−5 mol/L) significantly increased the frequency but not the amplitude of intracellular cytosolic calcium oscillations induced by prostaglandin F2α. Conclusions:The results indicate that prostaglandin F2α-stimulated cytosolic calcium oscillations are mediated by an increase in both cytosolic calcium release from inositol 1,4,5-trisphosphate-sensitive cytosolic calcium stores and a cytosolic calcium influx from the extracellular space. Moreover, RU 486 seems to directly regulate prostaglandin F2α-induced intracellular cytosolic calcium in human myometrial cells.

Long term variability in solar wind velocity and IMF intensity and the relationship between solar wind parameters &amp; geomagnetic activity

A study is carried out on the mean monthly values of in situ observations of solar wind velocity (V) and the intensity of interplanetary magnetic field, B to elucidate their long term variations using the technique of singular spectrum analysis. It is shown that B exhibits a clear solar cycle signal with progressively deepening minimum and a well-defined longer period variation but V is marked by a ~9-yr cycle. Time variations in the amplitude of 16-month periodicity, observed sporadically in the velocity earlier by others are clearly brought out, as also the characteristic amplitude changes in a 42-month signal in velocity. It appears that time intervals which show certain significant fluctuations in B are marked by the absence of similar signal in V. aa index is next used as a proxy for solar wind velocity, after establishing a good correlation between Ap and observed V so that we could examine the evolution of different periodicities over 14 solar cycles. A significant trend with least value in 1900 and a near-linear rise up to 1960 is shown to be the main feature of the velocity change. The solar cycle component in V lags the solar activity peak by ~22 months. Streams emanating from coronal holes in the declining phase seem to be the most dominant contributor to the 11-year variation in velocity. The anomalous pattern of changes in V observed in cycle 20 is not present in any of the other 13 cycles. Statistical relationships between V, B and plasma density (N) with Ap are studied and it is shown that over three solar cycles (20, 21 and 22) the patterns are almost the same with a slight change observed in cycle 21. IMF B and Ap are linearly related over a wide range of Ap values from close to 0 up to about 60, whereas density/Ap relation appears insignificant. In case of V, an initial rapid rise in V causes moderate changes in Ap but for velocity in excess of 700 km/sec, the enhancement in geomagnetic activity is more rapid. From the statistical relation of several other solar wind/IMF parameters, their variability and combinations with Ap, one sees linear relation for solar wind electric field, n/s component of IMF and variability in the components of B. An estimate is made of the base level of the magnetosphere, corresponding to quiet levels of geomagnetic activity.

Sintering Anomaly in Silica-Titania Sol-Gel Films

Sol-gel processing has been successfully applied to the preparation of silica-titania planar waveguides for integrated optics. In order to achieve low loss guides, proper densification is essential. A series of single layer silica-titania films were deposited by spin-coating on Si substrates from precursor sols prepared by mixing tetraethylorthosilicate (TEOS) with titanium tetra-iso-propoxide (TPOT). The thermal densification behavior of these thin gel films was followed by measuring their refractive index, by ellipsometry, as a function of the temperature, between 300–900°C and the heating time; an anomalous sintering behavior was found, consisting of a rapid initial rise in film density (calculated from the refractive index) at any heat-treatment temperature, followed by a pronounced minimum at times of the order of 3 minutes, after which the density slowly increased until the maximum plateau value, reached at each temperature.

Late Quaternary sea-level changes along the Tyrrhenian coast near Orbetello (Tuscany, central Italy): palaeoenvironmental reconstruction using ostracods

A multidisciplinary study has been carried out on a 51 m long core, drilled on coastal lowlands near the Albegna River (Tuscany, Central Italy). Both sedimentological and faunal analyses (ostracods and molluscs) indicate a coastal lagoon environment repeatedly influenced both by the rising Holocene sea and the Albegna River alluvial inflow. δ 13C, δ 18O, Mg/Ca, Sr/Ca and 87Sr/ 86Sr analyses were performed on Cyprideis torosa shells in order to detail the influence of Albegna River freshwater on the coastal lagoon water. The analytical data illustrate the difficulties of using geochemical proxies in marginal marine settings. Four radiocarbon dates provide a chronostratigraphy for the early Holocene part of the core. The data are used to reconstruct Late Pleistocene to early Holocene palaeoenvironments along this part of the coast and show the development of freshwater environments followed by a coastal brackish lagoon formed in response to the initial Holocene rapid rise in relative sea level. An attempt is made to relate sediments and age data from the core to the relative sea-level curve for the Tyrrhenian Sea.

Mechanisms of calcium transport in human endothelial cells subjected to hyperthermia

We have probed the mechanisms by which severe heat alters cytosolic calcium ion concentrations (Cai) in individual cultured human endothelial cells (ATCC ♯1998). Cells adhering to glass coverslips were heated to as high as 50°C and Cai determined by means of a fluorescence laser imaging system using the calcium-sensitive dye, indo-1, in the presence of thapsigargin, and in Na-free and Ca-free media. Baseline Cai varied between 175–225 nM. When cells were heated to 50°C in a complete Ca-containing medium, there was first a transient fall in Cai, then a rapid rise of 50–100 nM in Cai, followed by a slower, secondary rise of 50–75 nM. Depleting the intracellular calcium stores with thapsigargin blocked both the transient fall and the secondary rise in Cai. Placement of the cells into a Ca-free medium blocked both the transient fall and the initial rapid rise, while use of a Na-free buffer prevented the initial rapid rise only. These data suggest that in human endothelial cells, extreme heat accelerates the CaATPase pumps of the intracellular Ca stores causing the transient fall in Cai which is soon followed by activation of the reverse mode of the Na/Ca exchanger to cause the initial rapid rise in Cai. The Ca-release channels of the intracellular stores become activated by heat to cause the secondary, slow rise in Cai. This preliminary work indicates that the application of heat to cultured cells can be a useful probe to examine the kinetics and unmask mechanisms of intracellular Ca fluctuations.

Silica increases cytosolic calcium and causes cell injury in renal cell lines.

The purpose of this study was to clarify the effect of silica-induced cytosolic free calcium mobilization and cell injury in immortalized cell lines from transgenic mice kidney harboring SV40 T-antigen gene. The proximal convoluted tubule (S1)- and the inner medullary collecting tubule (IMCT)-originated cell lines were used. Cytosolic free calcium concentration ([Ca2+]i) was measured employing Fura-2 fluorescence and cell injury was evaluated by a vital dye exclusion procedure. Silica increased [Ca2+]i in a concentration-dependent manner in S1 (60 micrograms/ml-600 micrograms/ml) and IMCT (6 micrograms/ml-600 micrograms/ml). Silica caused a biphasic increase in [Ca2+]i which was composed of an initial rapid rise and following sustained phase. Ca2+ removal from the medium resulted in abolishment of initial and sustained phase of silica (600 micrograms/ml)-induced [Ca2+]i in both cell lines. Silica-induced cell injury was increased in a dose-dependent manner. This silica-induced cell injury was attenuated by the pretreatment with EGTA (100 microM) and nifedipine (1 microM). Cellular ATP content ([ATP]i) by silica also decreased in a concentration-dependent manner. The relationship between [Ca2+]i and [ATP]i showed that [ATP]i depletion caused [Ca2+]i to rise. This study suggests that 1) the elevation of [Ca2+]i caused by silica is due mainly to influx through plasma membrane Ca2+ channel and non specific membrane damage (at high concentration) and 2) nephrotoxicity of silica shows site-specificity within the kidney.

EFFECTS OF HYPOXIA, CALCIUM, CARBACHOL, ATROPINE AND TETRODOTOXIN ON THE FILLING OF THE IN-VITRO RABBIT WHOLE BLADDER

The urinary bladder stores urine at low intravesical pressure and empties the urine efficiently and completely. Bladder compliance is the property that allows the bladder to fill to near capacity without a large increase in intravesical pressure. The current study utilized an in vitro whole bladder model to determine the effects of hypoxia, alterations in extracellular calcium concentration, carbachol and atropine on bladder capacity and compliance. Mature male New Zealand White rabbits were used in this study. The urinary bladder was excised from the rabbit together with a short segment of proximal urethra and mounted in a 400 ml. isolated bath containing Tyrode's buffer. Bladder filling was started by opening the bladder to a saline reservoir placed 80 cm. above the bladder. Intravesical pressure, rate of pressure increase, rate of volume increase, and maximal volume were digitally recorded. The bladder filling was repeated while the whole bladder was subjected to hypoxia, high calcium concentration, the presence of EGTA, carbachol, atropine and tetrodotoxin respectively. Results are summarized as follows: 1) Bladder filling was biphasic. There was an initial rapid rise in intravesical pressure followed by a slower rise. The final bladder volume averaged 46 ml. 2) Hypoxia significantly decreased the initial rate of the rise in intravesical pressure, increased the rate of bladder filling, and increased bladder volume by 43%. 3) Incubation of the bladder in the presence of EGTA also significantly decreased the initial rate of intravesical pressure rise, increased the rate of filling and increased bladder volume by 39%. 4) High concentrations of calcium increased the initial rate of rise in intravesical pressure. 5) Carbachol significantly increased the rate of intravesical pressure rise, decreased the rate of bladder filling, and decreased bladder volume. 6) Atropine and tetrodotoxin (TTX) had no effects on bladder filling. In summary, alterations in muscle tone had significant effects on bladder capacity and compliance.

EFFECTS OF HYPOXIA, CALCIUM, CARBACHOL, ATROPINE AND TETRODOTOXIN ON THE FILLING OF THE IN-VITRO RABBIT WHOLE BLADDER

Purpose The urinary bladder stores urine at low intravesical pressure and empties the urine efficiently and completely. Bladder compliance is the property that allows the bladder to fill to near capacity without a large increase in intravesical pressure. The current study utilized an in vitro whole bladder model to determine the effects of hypoxia, alterations in extracellular calcium concentration, carbachol and atropine on bladder capacity and compliance. Methods Mature male New Zealand White rabbits were used in this study. The urinary bladder was excised from the rabbit together with a short segment of proximal urethra and mounted in a 400 ml. isolated bath containing Tyrode's buffer. Bladder filling was started by opening the bladder to a saline reservoir placed 80 cm. above the bladder. Intravesical pressure, rate of pressure increase, rate of volume increase, and maximal volume were digitally recorded. The bladder filling was repeated while the whole bladder was subjected to hypoxia, high calcium concentration, the presence of EGTA, carbachol, atropine and tetrodotoxin respectively. Results Results are summarized as follows: 1) Bladder filling was biphasic. There was an initial rapid rise in intravesical pressure followed by a slower rise. The final bladder volume averaged 46 ml. 2) Hypoxia significantly decreased the initial rate of the rise in intravesical pressure, increased the rate of bladder filling, and increased bladder volume by 43%. 3) Incubation of the bladder in the presence of EGTA also significantly decreased the initial rate of intravesical pressure rise, increased the rate of filling and increased bladder volume by 39%. 4) High concentrations of calcium increased the initial rate of rise in intravesical pressure. 5) Carbachol significantly increased the rate of intravesical pressure rise, decreased the rate of bladder filling, and decreased bladder volume. 6) Atropine and tetrodotoxin (TTX) had no effects on bladder filling. Conclusion In summary, alterations in muscle tone had significant effects on bladder capacity and compliance.