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Biomedical subjects

Y Kurachi

Publications and source records attributed to Y Kurachi.

At least 163 records · Page 9Linked to original sources
PubMed1989

[The report of the 12th and 13th clinical practical training of the Tsurumi University School of Dental Medicine].

This report concerns the state of the patients and the progress of the 12th and 13th clinical practical training. A questionnaire was carried out with the trainees of the 13th clinical practical training and their leaders. Consequently it was learned that a trainee was in charge of ten patients on the average a year. He was able to complete the treatments of 3.5 patients, but was obligated to discontinue them for 1.4 patients, while handling over treatments for 5.2 patients to the next year's trainees or doctors. The progress of the clinical practical training was slow during the first 9 months but the pace increased rapidly during the last 3 months. The results of the questionnaire showed 37% of the trainees were satisfied with the present clinical practical training, but 17% of the trainees were not satisfied. On the other hand 15% of the leaders were satisfied with it, but 48% of the leaders were not satisfied.

Education, Dental↗
PubMed1989

Cheilitis glandularis: report of a case affecting the upper lip.

Cheilitis glandularis is a rare disorder characterized by swelling of the lip with hyperplasia of labial salivary glands, typically in the lower lip of adult males. A definitive cause and treatment for this disorder have not yet been established. Herein is reported a case of cheilitis glandularis affecting the upper lip with nodules, treated by surgical excision with good post-surgical results.

Cheilitis↗
PubMed1987

Quinidine inhibition of the muscarine receptor-activated K+ channel current in atrial cells of guinea pig.

Postsynaptic mechanisms underlying the anticholinergic effects of quinidine were examined in single atrial cells, using the tight-seal whole-cell recording technique. The solution in the glass pipettes contained guanosine-5'-triphosphate (GTP) or guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma S, a non-hydrolyzable GTP analogue). In both cases, acetylcholine (ACh), applied to the bath, induced a specific K+ current. In GTP-loaded cells, quinidine in the bath solution depressed the ACh-induced K+ current concentration-dependently. Atropine also blocked the K+ current. On the other hand, in GTP-gamma S-loaded cells, the ACh-induced current was not blocked by atropine and persisted even when ACh was washed out from the bath, indicating that GTP-gamma S causes uncoupling of the K+ channels from the muscarine receptors. Quinidine, however, did depress the increased K+ current concentration-dependently. The percent inhibition curves for quinidine to depress the K+ current were very similar between GTP-loaded and GTP-gamma S-loaded cells. From these observations, we suggest that direct inhibition of the muscarine receptor-activated K+ channel current by quinidine, and not blockade of the muscarine receptor itself, is mainly responsible for the anticholinergic effects of the drug in atrial myocytes.

Acetylcholine↗
PubMed1987

Short-term desensitization of muscarinic K+ channel current in isolated atrial myocytes and possible role of GTP-binding proteins.

The short-term desensitization of the acetylcholine (ACh)-induced K+ channel current was examined in single atrial cells of guinea-pig heart. The tight-seal whole cell voltage clamp technique was used. The solution in the pipettes contained GTP or guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma S, a non-hydrolyzable GTP analogue). In GTP-loaded cells, ACh evoked a specific K+ channel current via GTP-binding proteins (G) in a dose-dependent manner. The K+ current showed agonist-dependent desensitization similar to those reported in other cardiac tissues (Nilius 1983; Carmeliet and Mubagwa 1986). The cellular response to ACh was also desensitized by activation of P1-purinergic receptors with adenosine (Ado). In GTP-gamma S-loaded cells, the K+ current was gradually induced even in the absence of agonists, probably due to direct activation of G proteins by GTP-gamma S. In the early phase of the spontaneous current increase, ACh evoked a large current transiently. As the GTP-gamma S-induced activation of the current progressed, the magnitude of the ACh-evoked current transient became smaller and finally negligible. Similar results were obtained when Ado was used as an agonist instead of ACh to induce the K+ current. Therefore, it is indicated that the agonist-receptor interaction may not be essential for the desensitization of ACh-induced K+ current in atrial myocytes.

Acetylcholine↗
PubMed1986

On the mechanism of activation of muscarinic K+ channels by adenosine in isolated atrial cells: involvement of GTP-binding proteins.

The molecular mechanisms underlying activation of a K+ channel by adenosine (Ado) and acetylcholine (ACh) were examined in single atrial cells of guinea-pig. Whole cell clamp and patch clamp techniques were used to characterize the K+ channel. In the whole cell clamp conditions, Ado and ACh increased the K+ channel current in a dose-dependent manner. The maximum responses and the apparent dissociation constants were different for Ado and ACh activations of the current. Theophylline blocked activation of the K+ current by Ado, while atropine blocked ACh-activation, indicating that two different membrane receptors were involved. Measurements of the conductance and kinetic properties of both whole cell and single channel currents indicate that Ado and ACh regulate the same K+ channels. In "inside-out" patch conditions, GTP was required in the intracellular side of the membrane for activation of the K+ channel by agonists (present in the patch electrode). The A promoter of pertussis toxin inhibited the channel activation only when NAD was also present. Furthermore, GTP-gamma S, a non-hydrolyzable GTP analogue, gradually caused activation of the K+ channel in the absence of agonists. Therefore, it was concluded that Ado and m-ACh receptors link with the same population of K+ channels via GTP-binding proteins Ni and/or No in the atrial cell membrane.

Acetylcholine↗
PubMed1986

Role of intracellular Mg2+ in the activation of muscarinic K+ channel in cardiac atrial cell membrane.

Effects of intracellular Mg2+ in the activation of a muscarinic K+ channel were examined in single atrial cells, using patch-recording techniques. In "cell-attached" patch recordings, acetylcholine (ACh) or adenosine (Ado), present in the pipette, activated a specific population of K+ channels. In "inside-out" patches, openings of the K+ channel by ACh or Ado diminished and did not resume until Mg2+ was added to the perfusate which contained GTP or GTP-gamma S, a non-hydrolyzable GTP analogue. Channel openings caused by GTP faded by removing Mg2+, while GTP-gamma S-induced openings persisted steadily even when both Mg2+ and GTP-gamma S were removed. In contrast to the case of GTP-induced channel openings, the GTP-gamma S-induced openings were not inhibited by the A promoter of pertussis toxin with NAD. From these observations, we concluded: Intracellular Mg2+ is essential for GTP to activate the GTP-binding protein. Deactivation of the N protein may be caused by hydrolysis of GTP to GDP. This process may not require Mg2+. During the activation by GTP analogues, the N protein may be dissociated into its subunits.

Animals↗
PubMed1986

Acetylcholine activation of K+ channels in cell-free membrane of atrial cells.

The activation mechanisms of K+ channels by muscarinic acetylcholine (m-ACh) receptors were examined in isolated atrial cells by use of patch-recording technique. In "cell-attached" patch recordings, ACh, present in the pipette, activated an inwardly rectifying K+ channel. In "inside-out" patches, activation of the K+ channel by ACh diminished with time following excision of the patch, but it resumed when GTP was present in the solution bathing the intracellular side of the membrane. The A protomer of pertussis toxin, together with NAD, inhibited the channel activation in the presence of GTP. Since pertussis toxin specifically ADP-ribosylates GTP-binding proteins Ni and No, which can interact with m-ACh receptors, and inhibits their functions, it was concluded that m-ACh receptors communicate with the K+ channel via GTP-binding proteins, probably Ni and/or No, in atrial cell membrane.

Acetylcholine↗
PubMed1986

Ionic mechanisms underlying the negative slope formation of the inward-rectifying potassium background current in ventricular cell of guinea-pig heart.

Kinetics of the inward-rectifier K+ channel (IK rec), which is the major fraction of the background potassium current (iK1) in cardiac cells, were studied in enzymatically-dispersed cells of guinea-pig ventricle. Currents flowing through IK rec channel were recorded using the cell-attached patch clamp technique with pipettes containing 150 mM or 75 mM K+. Steady state unitary currents and ensemble averaged currents of the channel were analysed. From the analyses, it was indicated that the kinetics of IK rec channel at potentials positive to EK-20 mV are determined mostly by activation gate. The activation gate of the channel follows the first order reaction between one open and one closed states and depends on shift of the membrane potential from the potassium equilibrium potential. The calculated macroscopic current flowing through the channel during the activation process showed prominent inward-reactification and formed a negative conductance region. In conclusion, the properties of iK1 depend on the activation kinetics of IK rec channel.

Animals↗
PubMed1985

Voltage-dependent activation of the inward-rectifier potassium channel in the ventricular cell membrane of guinea-pig heart.

The activation kinetics of the inward-rectifier K+ channel were studied by single-channel recording in isolated single cells of the guinea-pig ventricle with two different extracellular concentrations of K+ ([K+]o 150 and 75 mM). When voltage pulses were applied from a holding potential more positive than the potassium equilibrium potential (EK), to potentials more negative than EK, the probability of the channel being in the open state (Po) increased with time after the onset of the command pulse. The ensemble averaged current increased in its initial phase (activation). When the command potential was more negative than EK-40 mV, the current decreased after rapid activation due to the inactivation of the channel. The averaged current could be divided into an instantaneous and a time-dependent activation component; the latter was fitted by a single exponential function. The time constant of the time-dependent component became shorter, at more negative command potentials. When compared at the same command potential, the instantaneous component became smaller, as the patch membrane was held at more depolarized potential. This indicates that the steady-state Po of the channel decreases with depolarization at potentials more positive than EK. The Po of the activation gate of the channel was estimated by dividing the steady-state Po of the channel by the Po of the inactivation gate at each potential. It was about 0.1 at EK + 20 mV and increased sigmoidally with hyperpolarization. At potentials more negative than EK-40 mV, the Po of the activation gate saturated and was almost 1. The single-channel analysis and the noise analysis of the steady-state current fluctuations revealed that the activation gate of the channel follows first-order kinetics between the open and closed states. The activation kinetics shifted along the voltage axis in a similar way as EK when different [K+]o were used. Thus, the activation of the channel depends not only on the membrane potential but also on EK, when [K+]o is changed. The macroscopic current flowing through the inward-rectifier K+ channel during the activation process was calculated, assuming that the elementary conductance of the channel is not voltage dependent. The calculated current showed a prominent inward-rectifying property in the steady state and formed a negative conductance region at potentials positive to EK. It was, therefore, concluded that the properties of the inward-rectifier time-independent background K+ current (iK1) in the whole-cell current records (Noble, 1979) mainly depend on the activation kinetics of the inward-rectifier K+ channel in the cardiac myocyte membrane.

Action Potentials↗
PubMed1985

Isolation and properties of beta-glucosidase from Ruminococcus albus.

An enzyme active against p-nitrophenyl-beta-D-glucoside was purified from logarithmic-phase cells of Ruminococcus albus cultivated in a medium containing ball-milled cellulose. The purification yielded homogeneous enzyme after an approximately 520-fold increase in specific activity and a 9% yield. The enzyme was identified as a beta-glucosidase because it can hydrolyze cellobiose and cellooligosaccharides to glucose from the nonreducing ends.

Cations, Divalent↗
PubMed1985

Effects of intracellular acidification on membrane currents in ventricular cells of the guinea pig.

The membrane currents of single ventricular cells were measured under whole cell voltage clamp using a giga-sealed patch electrode, and the effects of intracellular acidification were examined by perfusing the electrode pipette with different pH solutions. The plateau of the action potential was shortened when the pH of the pipette solution was lowered from the control of 7.2 to 6, and finally to 5. The pH 6 pipette solution evoked a time-independent outward current at positive potentials and increased the slope conductance near the resting potential. These changes were suppressed by removal of both intra- and extracellular potassium ion, indicating that these currents were carried by potassium ions, but not by protons. Increasing the calcium concentration in the pipette from pCa 8 to pCa 6 induced a time-dependent outward current which had a reversal potential of about -13 mV. This result clearly differed from the changes induced by the acidic pipette solution, suggesting that the calcium-mediated conductance was not involved in the genesis of the acidic effects. The calcium current was not significantly affected by perfusion at pH 6, but was decreased by the more acidic (pH 5) solution. When the calcium current was recorded in sodium- and potassium-free external solution but with a cesium-rich internal solution, however, the calcium current was suppressed even with a weak acidic (pH 6.8) pipette solution. This effect was attributed not to an increased sensitivity of the calcium channel to protons, but to a more extensive intracellular acidification, which might have been caused by a depressed extrusion of proton via a sodium-hydrogen exchange mechanism on the surface membrane.

Action Potentials↗
PubMed1984

Action potential and membrane currents of single pacemaker cells of the rabbit heart.

Single, viable pacemaker cells were isolated from sinoatrial (S-A) and atrioventricular (A-V) nodes by treating with collagenase. In normal Tyrode solution containing 1.8 mM Ca2+, these pacemaker cells had a round configuration and contracted rhythmically at a frequency of about 150-260/min. The amplitude, duration, and maximum rate of rise of the spontaneous action potentials recorded using patch clamp electrodes were similar to those obtained from multicellular preparations. Amplitudes of the recorded membrane current were normalized with reference to the surface area of the cell by assuming the cell shape as a plane oblate spheroid. The membrane resistance of the isolated nodal cells was 14.9 +/- 4.0 k omega . cm2 (n = 12) at about -35 mV and the membrane capacitance was 1.30 +/- 0.24 microF/cm2 (n = 18). The inactivation time course of the slow inward current, isi, was fitted with a sum of two exponentials with time constants of 6.7 +/- 0.6 ms and 46.6 +/- 15.3 ms (n = 4) at +10 mV. The amplitude of isi peaked at 0 approximately +10 mV in the current-voltage relationship and was 18.2 +/- 8.4 microA/cm2. The potassium current, iK, was activated in the voltage range positive to -50 mV and was saturated at about +20 mV. The amplitude of the fully-activated iK at -40 mV was 3.3 +/- 1.4 microA/cm2 (n = 10) and showed an inward-going rectification. The activation of the hyperpolarization-activated current was observed at potentials negative to -70 mV in seven of 14 experiments. The current density and membrane capacitance calculated could be overestimated and the membrane resistance underestimated, because of the presence of caveolae on the cell surface. However, these data give the nearest possible estimates of the electrical constants in the nodal cells, which cannot be measured accurately in the conventional multicellular preparations.

Animals↗
PubMed1984

Resting K conductances in pacemaker and non-pacemaker heart cells of the rabbit.

Currents through the inward rectifier K channel (iK X rec) and the ACh-operated K channel (iK X ACh) were recorded in isolated heart cells of rabbit using the patch clamp technique with electrodes having 0.5-1 micron tip inner diameter. The maximum number of overlaps of open iK X rec channels per patch was measured over 347 experiments. An average of 2.3 was found in ventricular cells and 0.03-0.06 in sinoatrial (S-A) and atrioventricular (A-V) node cells. The estimated total number of the iK X rec channels for each ventricular cell was great enough to supply the resting K conductance of the cell. The iK X ACh channel was present in S-A and A-V node cells, but was never observed in the ventricular cells. The resting conductance of the nodal cells measured with whole cell clamp recordings was about 16 times smaller than that of the ventricular cells, and was hardly decreased at all by the removal of K+ from the bath solution. Thus, the lower membrane potential of the nodal cells compared with that of the ventricular cells was attributed to the smaller K conductance of the resting membrane, which is due to the very low density of the iK X rec channel. On the other hand, the iK X ACh channel, when activated by neural regulation, may play a major role in generating the resting K conductance of the nodal cells.

Animals↗
PubMed1982

The effects of intracellular protons on the electrical activity of single ventricular cells.

Acidic or alkaline solutions were injected into single guinea-pig ventricular cells and the effects of cytoplasmic proton concentrations ([H]i) on their electrical activity were examined. Injections of low pH (3.7-4.7) solutions shortened the action potential and depressed the plateau by decreasing isi and increasing the outward current at the plateau potentials. Injections of high pH (9.3-9.7) solutions had the opposite effects on the action potential and the membrane currents. A decremental oscillatory current, similar to the strophanthidin-induced transient inward current, was generated upon injecting large amount of low pH solutions. Injections of high pH solution abolished this current. Alterations in [Ca]i also mimiced the changes of the action potential caused by H+-injections. Comparison of the effects of high pH and EGTA injections, however, disclosed marked different actions of these agents on the inactivation process of isi. Therefore, it may be concluded that a combination of a direct effect of the alterations in [H]i and an effect due to changes in [Ca]i secondary to proton injections, causes the above electrical changes of single ventricular cells.

Action Potentials↗
PubMed1982

Transient depolarization and spontaneous voltage fluctuations in isolated single cells from guinea pig ventricles. Calcium-mediated membrane potential fluctuations.

Under the influence of cardiotonic steroids, single ventricular cells exhibit transient depolarization after a train of driven action potentials or, in voltage clamp experiments, transient inward current after a depolarizing clamp pulse. Transient depolarization or transient inward current was abolished by an intracellular injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) or by superfusion of 5 mM caffeine. Transient depolarization was elicited even in the control Tyrode's solution by an intracellular injection of CaCl2 or augmented by an injection of adenosine 3',5'-cyclic monophosphoric acid (cAMP). Along with transient depolarization or transient inward current, digitalis intoxication promoted spontaneous oscillatory fluctuations in membrane potential or in membrane current. Their power spectra showed peaks at frequencies ranging from 2 to 7 Hz, which coincided well with the frequency of repetitive transient depolarization or transient inward current. The fluctuations were eliminated by intracellular injections of EGTA and decreased in amplitude by 5 mM caffeine with a shift toward higher frequencies. Depolarization of the membrane caused a shift of the spectrum peak toward higher frequencies. These results suggest that an oscillatory release of Ca from intracellular storage sites is the common basis underlying both the transient events (depolarization or inward current) and the spontaneous miniature fluctuations in membrane potential or current.

Animals↗