[Is orthodontic correction in late cases of Angle class II(2) possible with functional orthodontic appliances?].
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Biomedical subjects
E Stefani
Publications and source records attributed to E Stefani.
Simultaneous measurements of Ca2+ currents and intracellular Ca2+ concentrations in single skeletal muscle fibers of the frog.
The relationship between Ca2+ current amplitudes and myoplasmic Ca2+ transients was studied in single muscle fibers. Segments of muscle fibers were voltage-clamped in a double Vaseline gap chamber. Ca2+ transients were measured as an optical signal derived from the interaction between Ca2+ and the dye antipyrylazo III. The cells were maintained at -90 mV. Ca2+ currents were detected at pulse potentials to -50 mV, reached a maximum value at 0 mV, were reduced in size for larger depolarizations, and reversed at about 40 mV. Ca2+ transients were also detected at -50 Mv and progressively increased in size with larger pulse potentials up to 10 mV. Depolarizations to voltages greater than 10 mV did not further increase the size of the transient. The magnitude and time course of transients from 10 to 70 mV were almost identical Ca2+ fluxes into the myoplasm (Ca2+ input fluxes) were calculated from the Ca2+ transients applying a removal model. The size of the input fluxes increased with depolarization up to 0 mV. Between 0 and 70 mV the peak input flux slightly increased, while the flux measured at 200 ms remained unchanged. In conclusion, Ca2+ transients and input fluxes were not reduced during pulses to large positive potentials, even though a drastic reduction of Ca2+ current occurred at these potentials. These observations make it very unlikely that a voltage-dependent Ca2+ entry is the triggering signal for contraction.
Animals↗
Rescue of a wild-type MDCK cell by a ouabain-resistant mutant.
When wild-type MDCK cells (W-MDCK) were cocultured in mixed monolayers with a ouabain-resistant mutant (R-MDCK), the wild-type cells were protected from the effect of ouabain up to concentrations as high as 100 microM. Rescue depended on the dose of ouabain and on the proportion of each cell type in the coculture. The survival of R-MDCK cells at 1 microM ouabain was not endangered by varying from 1:9 to 9:1 the proportion of W-MDCK cells to be rescued. Ouabain binding revealed two kinds of binding sites in R-MDCK cells, one with high and the other with low affinity. Only the high affinity site was present in W-MDCK cells. Electron probe analysis of individual cells revealed that rescued cells kept a high K and a low Na intracellular contents, similar to control cells. Histograms of intracellular K/Na in cocultured cells treated with ouabain were unimodal. Using microinjection of Lucifer yellow or electrophysiological techniques we estimated that at most 13% of the R-MDCK and W-MDCK cells may be connected at a given time through cell-to-cell junctions. Therefore permanent cell-to-cell communication did not seem to play a central role in the rescue. W-MDCK cells cocultured with R-MDCK cells and subsequently separated, were not rescued. Thus rescue did not seem to depend on the transfer from R-MDCK to W-MDCK cells of either ouabain-resistant Na-K pumps or of information to synthesize them. It is speculated that intercellular communications were sporadic events, so that all cells may become intermittently connected and rescued.
Animals↗
Skeletal muscle Ca2+ channels.
Ca2+ channels are widely distributed among different cell types. We shall describe in this paper kinetic properties of voltage-dependent slow Ca2+ channels in mammalian and frog skeletal muscle fibres. In addition, recent data on a fast-activated Ca2+ channel will be presented. Finally, the possible physiological role of the channel will be considered.
Action Potentials↗
A fast-activated inward calcium current in twitch muscle fibres of the frog (Rana montezume).
Voltage-clamp experiments were performed at 18 degrees C in intact twitch muscle fibres of the frog using the three micro-electrode technique. Membrane currents were recorded in the presence of 120 mM-tetraethylammonium-methanesulphonate and 10 mM-Ca2+. The recording solution was made hypertonic by adding 350 mM-sucrose to avoid contraction. Two components of inward current in the absence of external Na+ were observed. Depolarization induced a fast-activated inward current of small amplitude in addition to the well-known slow, transient Ca2+ current (ICa,s). Both components of inward current persisted in the presence of tetrodotoxin. They practically disappeared on replacing external Ca2+ with Mg2+ and were blocked by millimolar additions of Cd2+ to the bath. Thus, the fast-activated component of inward current was also carried by Ca2+ (ICa,f). Neither ICa,f nor ICa,s were reduced by 5 microM-diltiazem. During 400 ms depolarizations ICa,f was detected at approximately -60 mV, 30 mV more negative than the membrane potentials at which ICa,s appeared. At about 0 mV the time constant for activation was 5 ms for ICa and 150 ms for ICa,s. ICa,f did not significantly decline during depolarizations up to 2s in duration at membrane potentials between -60 and -30 mV. ICa,f tended to disappear as a function of time on exposure to the hypertonic recording solution. Its maximum amplitude decreased from about -25 microA/cm2 during the first 5 min to about -5 microA/cm2 after 25 min while ICa.s remained practically unchanged (maximum peak amplitude of about -60 microA/cm2). These results indicate the existence of two types of voltage-dependent CA2+ channels in intact muscle fibres. The kinetic properties of fast-activated Ca2+ channels suggest that they significantly activate during a single twitch.
Action Potentials↗
Calcium action potentials and calcium currents in tonic muscle fibres of the frog (Rana pipiens).
Slow action potentials were evoked in cruralis tonic and twitch fibres of the frog after drastically reducing the Cl- and K+ conductances. Tonic fibres were identified by their electrical characteristics. They had an effective resistance (Reff) of 50 +/- 6 M omega (n = 27) and a membrane time constant (tau m) of 440 +/- 70 ms (n = 8). In twitch fibres Reff = 2.9 +/- 0.3 M omega (n = 16) and tau m = 50 +/- 4 ms (n = 6). In tonic fibres the slow action potential had a threshold of -50 to -60 mV and a peak amplitude of -10 mV. In twitch fibres the slow action potential had a threshold of -40 mV and reached a peak amplitude of +40 mV. The responses were blocked by the addition of Cd2+ (2 mM) or Co2+ (5 mM). These results strongly suggest that Ca2+ is the main carrier of current during the response. Using the three-micro-electrode voltage-clamp technique a slow inward membrane current underlying the Ca2+ potential could be described in tonic muscle fibres. The slow inward current was mainly carried by Ca2+, since it was reduced when external Ca2+ concentration was lowered or when Cd2+ (2 mM) was added. Moreover, Ca2+ was the only cation in the solution that could carry inward current. It had a mean threshold of -60 mV, reached a maximum value at ca. 0 mV, ranged from 24 to 28 microA/cm2 and had a mean reversal potential of +35 mV. In about half of the examined tonic fibres inward current declined with time, only slowly. This can either be explained by there being less contamination by K+ outward current, or by the presence of two types of Ca2+ channels in the tonic fibre membrane.
Action Potentials↗
Effects of external calcium on potassium contractures in tonic muscle fibers of the frog (Rana pipiens).
K+ contractures of tonic bundles from cruralis muscle of the frog were studied with different K+ concentrations (10-120 mM). K+ contractures had an initial transient phase followed by a sustained tension. The amplitude of the sustained tension diminished with high K+ concentration (80-120 mM). However, in all cases, tension was maintained for several minutes. External Ca2+ reduction practically abolished the sustained phase of the K+ contractures. The initial phase was also reduced and tension spontaneously relaxed. The curve relating the peak tension with log [K+]o, showed that the threshold was not affected but the peak tension was reduced to about 70% in low-Ca2+ saline (0 Ca2+ + 3 mM-Mg2+) and 50% in Ca2+-free saline (1 mM-EGTA + 3 mM-Mg2+). The dependence of the sustained tension on external Ca2+ was further confirmed by Ca2+ withdrawal and re-establishment and/or by Ni2+ substitution for Ca2+ before or during K+ contractures. These results indicate that external Ca2+ had to be continuously present to maintain the tension during K+ contractures and that Ni2+ was not able to restore the normal temporal course of K+ contracture. The sustained phase was diminished by blocking agents of Ca2+ channels, such as nifedipine (1 microM) and diltiazem (1-10 microM). The present results can be explained by a direct control of the Ca2+ currents on K+ contracture or by specific interactions between external Ca2+ and Ca2+-binding sites in the membrane.
Animals↗
Electrical properties and morphology of single vascular smooth muscle cells in culture.
Single vascular smooth muscle cells (VSMC) were isolated from the caudal artery and vein and studied after 2 or 3 days in culture. Current clamp with intracellular microelectrodes and "whole-cell" voltage-clamp techniques were used. Also, scanning and transmission electron microscopy studies were performed, revealing morphological characteristics of smooth muscle in culture. Cells could contract in response to electrical and chemical stimuli. The passive membrane properties recorded with intracellular microelectrodes in a mammalian saline were as follows: 1) for artery, resting potential Vm = -56 +/- 5 mV (mean +/- SD), input resistance Rin = 590 +/- 35 M omega, membrane time constant tau m = 19 +/- 2 ms, membrane capacity C/cm2 = 1.3 +/- 0.2 microF/cm2, and length constant lambda = 900 +/- 40 micron; and 2) for vein, Vm = -66 +/- 3 mV, Rin = 450 +/- 25 M omega, tau m = 19 +/- 2 ms, C/cm2 = 1.0 +/- 0.1 microF/cm2, and lambda = 1,300 +/- 200 micron. The values calculated for a short cable and the observed change of the membrane potential as a single exponential, in response to hyperpolarizing pulses of current, both indicate that the cell membrane behaves as an isopotential surface. With hyperpolarizing pulses, both cell types gave linear voltage-current (V-I) relationships with a constant slope, Rin. On the other hand, depolarizing pulses elicited outward rectification. Voltage-clamp experiments show an outward voltage-dependent K+ current (IK) when the cell membrane is depolarized beyond approximately equal to -40 mV from holding levels approximately equal to -60 mV. Maximum slope conductances were of approximately 120 microS/cm2. Blocking of K+ channels with tetraethylammonium ions did not unmask an inward current. These results indicate that VSMC from rat caudal artery and vein in culture have K+ channels responsible for the graded depolarization of the cell membrane in response to an electrical stimulus. Furthermore, this experimental approach seems to be adequate to further study the electrical responses of VSMC from vessels at distinct stages of development, and to follow these responses as the cells change in a defined environment.
Animals↗
[Minor orthodontic measures in a periodontally involved dentition].
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Adult↗
Changes in paracellular and cellular ionic permeabilities of monolayers of MDCK cells infected with influenza or vesicular stomatitis viruses.
MDCK cells (epithelioid line derived from the kidney of a normal dog) form monolayers which retain the properties of transporting epithelia. In these cells viruses bud asymmetrically: influenza from the apical, and vesicular stomatitis (VSV from the basolateral membrane (E. Rodríguez-Boulán and D.D. Sabatini, Proc. Natl. Acad. Sci. USA 75: 5071-5075, 1978; E. Rodríguez-Boulán and M. Pendergast, Cell 20: 45-54, 1980). In the present study, we analyzed whether these viruses affect specific ion-translocating mechanisms located in the plasma membrane. We studied the effect of infection on membrane and transepithelial conductance, passive and active unidirectional fluxes of Na+ and K+, intracellular potentials, cellular content of Na+ and K+, and formation of blisters which, in these preparations, are due to the vectorial transport of fluid. Two main observations are derived from these studies. First, infection with VSV caused an increase in transepithelial electrical conductance, due to the opening of tight junctions, 5 to 6 hr after the start of infection, coincident with the accumulation of envelope protein in the cell surface and with the rise in the curve of virus budding. Infection with influenza, on the other hand, increased the transepithelial conductance only late in the infection (12 to 14 hr) when virus production has already stopped. Second, viruses did affect membrane permeability. Yet, the changes observed may not be ascribed to a perturbation of the specific translocating mechanisms for Na+ and K+ which operate in the same region of the plasma membrane that the viruses use to penetrate and leave MDCK cells. The methods used in the present study are not suitable to decide whether the nonspecific changes in permeability elicited by the viruses occur over the whole cell membrane or are restricted to a given region.
Animals↗
Cell-to-cell communication in monolayers of epithelioid cells (MDCK) as a function of the age of the monolayer.
We explore the existence of cell-to-cell communication in monolayers of MDCK cells plated at high densities so that they form a continuous monolayer in a few minutes. Lucifer Yellow CH is injected in the cytoplasm of a given cell by using a glass microelectrode with a fine tip (ca. 100 M omega) and passing square pulses of current of 1.0 nA that last 10 msec, every 20 msec, during 1 to 3 min. We then examine the monolayer with fluorescence microscopy. In 27 out of 111 cells injected during the first 4 to 15 hr after plating, the dye was transferred to neighboring cells. Electron micrographs of freeze-fracture replicas prepared at this time, show that 20 to 25% of the lateral surfaces present the aggregates of intramembrane particles typical of gap junctions. These early hours correspond to the formation of occluding junctions and polarization into an apical and a basolateral domain of the plasma membrane (Cereijido, Meza & Martínez-Palomo, 1981). Cell-to-cell coupling then decreases sharply and, in the period between the 1st and 3rd day (mature monolayers), only 4 out of 49 injected cells were able to transfer the dye to their neighbors in the monolayers. No image of gap junctions was found in freeze-fracture replicas of mature monolayers. The degree of coupling between cells, as well as the number of cells coupled to the injected one, were highly variable. The lack of coupling between cells in mature monolayers observed in this article with Lucifer Yellow CH and electron microscopy is in keeping with the absence of electrical coupling observed in a previous work (Stefani & Cereijido, 1983). The transient existence of communicating junctions observed in monolayers of MDCK cells is similar to that described in the literature for embryo tissues during development.
Animals↗
[Changes in the soft tissue after functional orthodontic treatment determined by cephalometry--statistical study of Angle Class II division 2 malocclusion].
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Saturation of calcium channels and surface charge effects in skeletal muscle fibres of the frog.
Voltage-clamp and current-clamp experiments were performed to study Ca2+ and Ba2+ permeation through Ca channels in intact twitch skeletal muscle fibres of the frog. Surface charge effects were taken into consideration. Ca2+ (ICa) or Ba2+ (IBa) currents, or Ca2+ and Ba2+ action potentials were recorded in the presence of external tetraethylammonium (TEA+) ions and by replacing C1- for CH3SO3-. To further block K+ outward currents, muscles were incubated in a K+-free, TEA+ and Cs+-containing solution prior to experiments. When 10 mM-Ca2+ was replaced by 10 mM-Ba2+, the I/V curve for the peak inward current shifted by 15-20 mV to more negative potentials and the maximal peak inward current increased from -39 +/- 2 mA cm-3 (5) to -51 +/- 3 mA cm-3 (7). The decay of ICa and IBa followed a simple exponential time course and became faster for large depolarizations. The overshoot of the action potentials changed 29 +/- 3 mV or 32 +/- 3 mV for a 10-fold change in the Ca2+ or Ba2+ concentrations respectively. Ca2+ action potentials were 15-20 mV larger than Ba2+ action potentials. The maximum rate of rise Vmax and the Ca2+ or Ba2+ conductance GC2+ during the plateau tend to saturate as divalent cation concentration was increased. The Michaelis constant (Km) values obtained were respectively: 5.6 and 6.0 mM for Ca2+ and 12.5 and 8.0 mM for Ba2+. When Ca2+ or Ba2+ concentrations were increased, the effective threshold of the inward current Theff and the membrane potential E* at Vmax shifted to more positive potentials along the voltage axis. These shifts were similar for Theff and E* and were more pronounced for Ca2+ than for Ba2+. Voltage shifts could be adequately quantified by the Gouy-Chapman theory with a density of surface charges near Ca channels of 0.20 e nm-2 and including a specific binding constant for Ca2+ of 45 +/- 4 m-1. The fractional increase of the Ca2+ and Ba2+ calculated concentrations at the membrane surface near the channel was smaller than the corresponding one in the bulk solution. This partially explained the reported saturation. Saturation was still present in the Vmax of GC2+ curves corrected for surface concentration. The corrected Km values for the Vmax data were 60 mM for Ca2+ and 350 mM for Ba2+.(ABSTRACT TRUNCATED AT 400 WORDS)
Action Potentials↗
Calcium channel inactivation in frog (Rana pipiens and Rana moctezuma) skeletal muscle fibres.
The decay of the Ca2+ current (ICa) during a maintained depolarization was studied in intact twitch skeletal muscle fibres of Rana pipiens and Rana moctezuma with the three-micro-electrode voltage-clamp technique. ICa was recorded at 23 degrees C, after blocking K+ currents, in TEA methanesulphonate saline with 10 mM-Ca2+ made hypertonic by adding 350 mM-sucrose. In two-pulse experiments, ICa during the test pulse was reduced to about 80% (R. pipiens) or 50% (R. moctezuma) of the control value, without any detectable inward ICa during 7 s conditioning pre-pulses. The experimental points of the steady-state inactivation curve (h infinity) were fitted to h infinity = (1 + exp [Em - Vh)/kh]-1, where Em is the membrane potential and with Vh = -33 +/- 3 mV and kh = 6 +/- 1 mV for R. pipiens, and Vh = -44 +/- 3 mV and kh = 9.5 +/- 1.0 mV for R. moctezuma. The rate constant of decay for inactivated currents (range -8 to -47 mA cm-3) and for control currents (range -23 to -62 mA cm-3), was independent of ICa amplitude. The average rate constant of decay at 0 mV was 1.18 +/- 0.02 s-1 (66). These results indicate that in intact fibres under hypertonic solution ICa decay can be explained by a voltage-dependent inactivation process and not by depletion of tubular Ca2+. The absence of depletion could be due to a large fractional tubular volume or to the presence of a Ca2+ pump in the tubular system.
Animals↗
[Extraction therapy in mixed dentition].
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Bicuspid↗
Electrical properties of cultured epithelioid cells (MDCK).
This is a study of the intracellular electrical potential, membrane resistance, and capacity of MDCK cells (epithelioid of renal origin) cultured in monolayers on a collagen couch. These monolayers have a transepithelial resistance of 256 +/- 12 (22) ohm cm2 (mean +/- standard error, and number of observations), and the cells have 61.6 +/- 6.3 (92) M omega across their plasma membrane. The electrical capacity of the cells is 45.1 +/- 2.9 (63) pF and is much higher than expected for a cell of its size (diameter 14 micrometers, height 5 micrometers) and cannot be attributed to intercellular coupling, as no evidence of this type of connection was found in 20 pairs of neighboring cells. On the contrary, the high capacity is in keeping with previous studies using electron microscopy showing microvilli and a high degree of lateral infolding. The relationship between resistance and capacity was 1981 +/- 177 (61) omega . microF. The cells have an intracellular potential of -40.5 +/- 15 (120) mV. Yet the shape of the distribution curve suggests that the actual value may be somewhat higher (some -50 mV). The current/voltage curve of the distribution curve suggests that the actual value may be somewhat higher (some -50 mV). The current/voltage curve shows a marked asymmetry, and in some cells the voltage becomes time-dependent for large, depolarizing current pulses.
Animals↗
[Movement of the anterior teeth in different directions with functional appliances].
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Calcium action potentials in rat fast-twitch and slow-twitch muscle fibres.
Slow action potentials were evoked in twitch fibres of rat extensor digitorum longus (e.d.l.) and soleus muscles after drastically reducing the Cl and K conductances of the muscle fibres. Cl conductance was eliminated by exposing the muscles to a Cl-free saline in which methanesulphonate replaced Cl. K conductance was reduced by adding tetraethylammonium (TEA) and 3,4-diaminopyridine (3,4-DAP) to the Cl-free saline or by overnight incubation of the muscles in a saline containing Cs and TEA. The delayed rectifier was markedly blocked by TEA and 3,4-DAP. In contrast, the inward rectifier was blocked only by TEA. Depolarization with pulses of increasing amplitude triggered slow responses which had a threshold of -30 to -10 mV and a peak amplitude of 50-60 mV. In e.d.l. muscles the time course of the response was sustained for the duration of the pulses and was not affected by repeated stimulation. In soleus muscles the first evoked response was sustained in about 60% of the fibres and transient in the rest. Transient responses reached a peak amplitude and were followed by a hyperpolarization. Repeated stimulation irreversibly transformed the sustained responses of soleus fibres into transient ones. The responses were blocked when the Ca in saline was replaced by Mg (10 mM) or Co (5 mM) or by the addition of Cd (0.1-1.0 mM) or nifedipine (5-6 microM). Tetrodotoxin did not affect the responses. These results strongly suggest that Ca is the main carrier of current during the response. Nifedipine blocked both the Ca response and the subsequent hyperpolarization, suggesting that the latter is due to the activation of a Ca-dependent K conductance.
4-Aminopyridine↗