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T Kiyosue

Publications and source records attributed to T Kiyosue.

At least 55 records · Page 3Linked to original sources
PubMed1993

Characterization of two cDNAs (ERD11 and ERD13) for dehydration-inducible genes that encode putative glutathione S-transferases in Arabidopsis thaliana L.

Two cDNA clones, designated ERD11 and ERD13, isolated from a cDNA library from Arabidopsis thaliana L. plants dehydrated for 1 h were sequenced and characterized. These clones encoded polypeptides that were homologous to glutathione S-transferases of tobacco and maize. Genomic Southern hybridization suggested that there are a few additional genes showing high similarity to the ERD11 gene in the Arabidopsis genome. The expression of the genes for ERD11 and ERD13 was induced by dehydration, but was not affected by the application of four plant growth regulators, 2,4-dichlorophenoxyacetic acid 6-benzylaminopurine, abscisic acid, or gibberellic acid.

Amino Acid Sequence↗
PubMed1993

Characterization of cDNA for a dehydration-inducible gene that encodes a CLP A, B-like protein in Arabidopsis thaliana L.

Sequence was obtained from a cDNA clone, designated ERD1, isolated from a cDNA library of 1-hour-dehydrated plants of Arabidopsis thaliana L. The clone (3150 bp) contains an open reading frame of 946 amino acid residues with greater than 34% sequence identity to the regulatory subunit of the Clp ATP-dependent protease in Escherichia coli and contains a putative chloroplast-targeting signal at the N-terminus. Southern blot analysis suggested the presence of additional ERD1-related genes in A. thaliana. The expression of ERD1 gene was strongly induced by dehydration-stress but not by heat-, cold-, or heavy-metal-stress. In addition ERD1 gene-expression was not strongly affected by treatment with plant growth regulators, such as auxin, cytokinin, abscisic acid, and gibberellic acid, or by starvation-stress for 10 hours.

ATP-Dependent Proteases↗
PubMed1993

Background inward current in ventricular and atrial cells of the guinea-pig.

Atrial and ventricular myocytes were exposed to Ca(2+)- and K(+)-free solutions containing blockers of gated channel and exchange currents. Replacement of external sodium by large organic cations revealed a background sodium current ib,Na. In atrial cells, the average conductance was 5.0 pS pF-1. In ventricular cells the conductance was 2.3 pS pF-1. Together with previous results, these figures reveal a strong gradient of background current density: sinus > atrium > ventricle. Replacement of sodium with inorganic cations showed that the channel selectivity behaves like an Eisenman group III/IV sequence, in agreement with previous results. The permeability of the channel to TMA was found to be pH dependent, suggesting that protonation of the channel is a factor determining permeation in addition to ionic size. The values of gb,Na obtained from these experiments are very similar to those assumed in computer modelling of cardiac cell electrical activity.

Animals↗
PubMed1993

A comparative study of effects of isoproterenol and dihydroouabain on calcium transients and contraction in cultured rat ventricular cells.

We investigated the effects of isoproterenol, a beta-adrenergic agonist, and dihydroouabain, a Na+,K(+)-pump inhibitor, on Ca2+ transients and contraction of cultured rat ventricular cells and compared the effects with those of altered external ion concentrations, with special reference to the changes in diastolic intracellular free calcium concentration ([Ca2+]i). We measured [Ca2+]i of cultured cell aggregates, stimulated at 1.0 Hz, with the use of dual-wavelength microfluorometry of fura-2, at room temperature (24-26 degrees C). The contraction was measured as a shortening of the aggregates using a photodiode array placed on a video monitor. Isoproterenol increased the magnitude of contraction and the peak amplitude of the Ca2+ transient, in a concentration (10(-9)-10(-6) M)-dependent manner, but did not change the diastolic Ca2+ level. Isoproterenol at 10(-7) M or higher significantly shortened the duration of contraction and half decay time of a Ca2+ transient yet it did not change the time to peak. Dihydroouabain (10(-7)-10(-5) M) increased the contraction and elevated both systolic and diastolic calcium levels but it did not alter the duration of contraction, the time to peak and the half decay time. The effects of dihydroouabain on Ca2+ transients were mimicked by lowering [K+]o (0.4 mM), by lowering [Na+]o (74 mM) or by elevating [Ca2+]o (3.6 or 5.4 mM). Ryanodine (10(-5) M), by itself, decreased systolic Ca2+ transient amplitude, increased diastolic Ca2+ levels and prolonged the time to peak and the half decay time. In the presence of ryanodine, isoproterenol increased both systolic and diastolic [Ca2+]i. Thus, most procedures that increased the systolic Ca2+ transient amplitude increased the diastolic Ca2+ levels as well, and enhanced the contraction. The only exception was isoproterenol that markedly increased the systolic Ca2+ transient amplitude without affecting the diastolic Ca2+ level, a finding in keeping with the observation that isoproterenol stimulates Ca2+ uptake by the sarcoplasmic reticulum.

Animals↗
PubMed1993

cDNA cloning of ECP40, an embryogenic-cell protein in carrot, and its expression during somatic and zygotic embryogenesis.

A cDNA of 1.2 kb was isolated from a cDNA library of embryogenic cells of carrot (Daucus carota L.) by use of nucleotide sequences that encode two internal amino-acid sequences of ECP40 (an embryogenic-cell protein with a relative molecular mass of 40,000). A genomic Southern blot using the cDNA as probe suggested that there are at least two genes for ECP40 in the carrot genome. The cDNA encoded an open reading frame of 306 amino acids, and the deduced amino-acid sequence was found to share two motifs, namely SSSSSSEDDGXGGRRKKGXXXKIKEKLXGG and EKKXXXDKIKXKLPG, with rab16 protein from rice and dehydrins from barley and maize. The level of expression of these proteins has been reported to be high during late embryogenesis and to be induced by a plant hormone, ABA. Accumulation of ECP40-specific transcripts started 18 days after flowering and continued until maturation of seeds, but the levels decreased within 24 h after imbibition. ECP40 and its mRNAs were detected in the endosperm and zygotic embryos of mature seeds by immunohistochemistry and in situ hybridization. Exogenous application of 0.1 mM ABA to carrot seedlings did not induce expression of the gene for ECP40, while drought treatment induced the accumulation of low levels of the mRNAs. During somatic embryogenesis, the mRNAs were found at high levels in embryogenic cells and at low levels in somatic embryos at the torpedo stage. Immunohistochemical analysis and in situ hybridization showed that both ECP40 and its transcripts were preferentially localized in the peripheral cells of the clusters of embryogenic cells. In somatic embryos, application of ABA resulted in increases in levels of mRNAs for ECP40 up to the levels in embryogenic cells, but no such increases were observed in ABA-treated embryogenic cells. The pattern of expression of the gene for ECP40 during somatic embryogenesis was basically the same as that of ECP31, another ABA-regulable embryogenic-cell protein of carrot, the presence of which has been correlated with the embryogenic competence of cultured cells (T. Kiyosue, S. Satoh, H. Kamada and H. Harada, Plant Physiol 95 (1991) 1077-1083). The various results together imply that a group of ABA-inducible genes is expressed in these embryogenic cells.

Amino Acid Sequence↗
PubMed1993

Differential mechanism of block of palmitoyl lysophosphatidylcholine and of palmitoylcarnitine on inward rectifier K+ channels of guinea-pig ventricular myocytes.

We investigated the effect of lysophosphatidylcholine (lysoPtdCho) and palmitoylcarnitine (PamCar), ischemia-induced amphipathic lipid metabolites, on the inward rectifier K+ channel in guinea-pig ventricular cells, under whole-cell and cell-attached configurations with patch-clamp techniques. (a) Both lysoPtdCho (10-50 microM) and PamCar (10-50 microM) depolarized the resting membrane potential (RP), retarded the repolarization of action potential, provoked spontaneous action potential discharges from oscillatory afterpotentials, and eventually caused a sudden rise of the RP to plateau levels. (b) These lysoPtdCho- or PamCar-induced depolarizations of RP were due to a decrease in the inward rectifier K+ current (IK1), and the sudden rise of the RP could be accounted for by a crossover of N-shaped current-voltage relationship on the voltage axis (zero current line) more than once. (c) Single-channel studies in the cell-attached mode revealed that lysoPtdCho (5-100 microM) decreased the conductance of the single IK1 channel with little change in its open probability, whereas PamCar (10-50 microM) did so by decreasing the open probability, with the channel conductance unaltered. (d) A short-chain acylcarnitine, l-propionylcarnitine (PpCar, 100 microM), prevented the depressant effect of lysoPtdCho (50 microM), but not of PamCar (50 microM), on the IK1. (e) Both lysoPtdCho and PamCar produced identical electrophysiological alterations on the membrane potential and IK1 in whole-cell recordings. However, molecular mechanisms involved in the effects of these toxic metabolites on single IK1 channels differ.

Animals↗
PubMed1993

Cibenzoline inhibits diazoxide- and 2,4-dinitrophenol-activated ATP-sensitive K+ channels in guinea-pig ventricular cells.

1. We have investigated the effects of diazoxide (a sulphonamide derivative) and cibenzoline (a class I antiarrhythmic drug) on ATP-sensitive K+ currents in guinea-pig ventricular cells, using whole-cell clamp techniques. 2. Diazoxide (50 microM) produced a marked shortening of action potential duration which was antagonized by 1 microM glibenclamide, an ATP-sensitive K+ channel blocker. 3. Diazoxide (50 microM) increased the quasi-steady state outward current elicited by a ramp voltage protocol (-20 mV s-1) at potentials positive to about -70 mV. This effect was completely prevented in the presence of glibenclamide (1 microM), thereby suggesting that diazoxide opens ATP-sensitive K+ channels. 4. Cibenzoline (5 microM) depressed the diazoxide-induced increases in the outward current and the pretreatment with this agent prevented the development of the diazoxide-induced outward current. 5. Cibenzoline (10 microM) reversed the 2,4-dinitrophenol (50 microM)-induced shortening of the action potential duration partially but significantly. 6. These results suggest that diazoxide activates ATP-sensitive K+ channels of guinea-pig ventricular cells and that cibenzoline, at therapeutic concentrations, inhibits this channel.

2,4-Dinitrophenol↗
PubMed1993

Ionic mechanisms of action potential prolongation at low temperature in guinea-pig ventricular myocytes.

1. We studied the effects of low temperature on the action potentials and membrane currents of guinea-pig ventricular myocytes, using a tight-seal whole-cell clamp technique. 2. The action potential duration at 95% repolarization was prolonged from 146 +/- 33 ms (mean +/- S.D., n = 6) at 33-34 degrees C (control temperature) to 314 +/- 83 ms at 24-25 degrees C (low temperature). 3. In whole-cell clamp experiments, low temperature decreased the calcium current (ICa), the delayed rectifier potassium current (IK), and the inwardly rectifying potassium current (IK1) with 'apparent' Q10 (temperature coefficient) values of 2.3 +/- 0.6 for ICa, 4.4 +/- 1.2 for IK tail current and 1.5 +/- 0.3 for IK1 (n = 7). 4. The effect of low temperature on IK was further studied in the presence of 0.6 microM nicardipine to block ICa. The decay phase of the IK tail consisted of two exponential components. The fast but not the slow component was highly sensitive to the temperature change with an apparent Q10 of 4.5. 5. We found that a component of time-independent current is also sensitive to the temperature. The current had a linear I-V relationship and remained almost unchanged after inhibition of Na(+) -K+ pump in K(+)-free external solution. 6. Using our mathematical model of the ventricular action potential (a modification from the DiFrancesco-Noble model), we simulated the action potential at low temperature by modifying some of the membrane currents, namely IK, IK1, ICa and a component of background current. It was shown that simultaneous changes in these currents could reproduce approximately 75% of the action prolongation induced by low temperature.

Action Potentials↗
PubMed1992

Isolation and characterization of a cDNA that encodes ECP31, an embryogenic-cell protein from carrot.

A full-length cDNA for ECP31, an embryogenic cell protein from carrot (Daucus carota L.) with a M(r) of 31,000 (Kiyosue T, Satoh S, Kamada H, Harada H (1991) Plant Physiol 95: 1077-1083), was isolated from a cDNA library prepared from embryogenic cells using PCR-amplified DNA as a probe. The genomic Southern blot analysis revealed that there are two or three genes for ECP31 in the carrot genome. The transcripts of ECP31 accumulated in the peripheral regions of clusters of embryogenic cells and disappeared in the course of somatic embryogenesis that was induced by transfer of the embryogenic cells to auxin-free media. The cDNA encodes a polypeptide of 256 amino acids, and the calculated molecular weight of this polypeptide is 26,111. The deduced amino acid sequence shows a high degree (62.2%) of similarity to that of a protein that is abundant during late embryogenesis of cotton (LEA D34; Baker JC, Steele C, Dure III (1988) Plant Mol Biol 11: 227-291). The mRNAs for ECP31 started to accumulate in zygotic embryos at a late stage of embryogenesis but were undetectable in mature embryos within 24 h after imbibition of seeds. In dry fruits (seeds), the transcripts were detected only in zygotic embryos by in situ hybridization. The level of ECP31 transcripts increased after treatment with abscisic acid (ABA) in torpedo-shaped somatic embryos but not in seven-day-old seedlings. These results suggest that both embryo-specific factor(s) and ABA are involved in the expression of the gene for ECP31.

Abscisic Acid↗
PubMed1992

Inhibitory effects of palmitoylcarnitine and lysophosphatidylcholine on the sodium current of cardiac ventricular cells.

We investigated the effects of ischemia-related amphipathic compounds, palmitoylcarnitine (PamCar, 0.5-50 microM) and lysophosphatidylcholine (lysoPtdCho, 5-50 microM) on sodium current (INa) of guinea-pig ventricular myocytes. The cells were perfused with low-Na+ (60 mM) Tyrode's solution, and Ca2+ and K+ currents were blocked by external Co2+ (3 mM) and internal Cs+ (140 mM), respectively. INa was elicited by depolarizing voltage steps from a holding potential of -100 mV at a temperature of 33 degrees C. PamCar (5 microM) decreased the peak INa (attained at -20 mV or -30 mV) from 6.1 +/- 2.1 nA to 3.9 +/- 1.4 nA (n = 11), or by 36.1% within 2 min, and shifted the curve of steady-state INa inactivation by 5.4 mV in the positive direction (from -76.3 +/- 4.6 mV, control to -70.9 +/- 4.0 mV, in PamCar, n = 4). Partial restoration of the amplitude and the shift of the steady-state inactivation curve of INa was attained after washout of PamCar. In contrast, lysoPtdCho at concentrations over 10 microM irreversibly depressed the INa within 0.5-3 min and the reduction of INa was followed by cell contracture or cell death (n = 9). The survival time, defined as a period from the start of lysoPtdCho application to the time of the last successful recording of the INa (before evolution of sudden changes in the holding current), depended on the concentrations of lysoPtdCho. Both PamCar and lysoPtdCho retarded the time course of activation and inactivation of INa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Blockade of 2,4-dinitrophenol induced ATP sensitive potassium current in guinea pig ventricular myocytes by class I antiarrhythmic drugs.

OBJECTIVE: The aim was to assess the effects of various antiarrhythmic drugs on 2,4-dinitrophenol (DNP) induced outward current (IDNP), presumably the ATP sensitive K+ current (IK,ATP) of isolated cardiac cells and to discuss mechanisms involved in the hypoglycaemia which occurs in patients on these drugs. METHODS: The quasi-steady state current-voltage relationship from the isolated guinea pig ventricular cells was measured using whole cell voltage clamp techniques with a ramp pulse programme. The effects of seven different antiarrhythmic drugs on IDNP were examined. Action potentials were elicited at a rate of 0.2 Hz by an intracellular current injection. RESULTS: DNP (50 mumol.litre-1) increased the quasi-steady state outward current at potentials positive to about -60 mV. This current (IDNP) was completely inhibited by the subsequent application of glibenclamide (1 mumol.litre-1), thereby suggesting that the IDNP is probably IK,ATP. Cibenzoline (10 mumol.litre-1, class Ia), disopyramide (30 mumol.litre-1, class Ia), and procainamide (100 mumol.litre-1, class Ia) significantly inhibited the IDNP by 95.5(SD 11.3)%, 77.8(21.2)%, and 76.4(23.9)% respectively. Flecainide (class 1c) inhibited the IDNP by 66.9(23.9)% at 10 mumol.litre-1 but not at 2 mumol.litre-1. Mexiletine (30 mumol.litre-1, class Ib), pilsicainide (50 mumol.litre-1, class Ic), and E4031 (10 mumol.litre-1, class III) at concentrations as high as approximately fivefold the clinically effective blood levels, did not suppress IDNP. Except for 10 mumol.litre-1 flecainide, all the concentrations listed above which blocked IDNP were within twofold of the clinical blood concentrations documented to be effective for suppression of arrhythmias. Cibenzoline, disopyramide, and procainamide, but not flecainide, belong to class Ia antiarrhythmic drugs. All these class Ia antiarrhythmic drugs "shortened" the action potential duration of guinea pig ventricular cells, an opposite change to that noted for multicellular preparations, eg, guinea pig papillary muscles. CONCLUSIONS: Class Ia antiarrhythmic drugs (cibenzoline, disopyramide, and procainamide) inhibit IDNP (presumably IK,ATP) in guinea pig ventricular cells within a range of therapeutic concentrations. This inhibitory effect of IK,ATP can probably explain the hypoglycaemia which occurs in some patients receiving these drugs, and the prolongation of the action potential duration alleged to occur in "superfused" papillary muscles.

2,4-Dinitrophenol↗
PubMed1991

Purification and immunohistochemical detection of an embryogenic cell protein in carrot.

An embryogenic cell protein from carrot (Daucus carota L.), designated ECP31 for embryogenic cell protein and with a relative mass of 31,000, was purified by sequential column chromatographies. Its apparent relative mass was estimated to be 120,000 by gel filtration. Immunoblotting and immunohistochemical studies showed that ECP31 was preferentially localized in the peripheral cells of clusters of embryogenic cells in the presence of 2,4-dichlorophenoxyacetic acid (2,4-D) and disappeared during the course of somatic embryogenesis in the absence of 2,4-D. ECP31 began to accumulate on the 33rd day after initiation of cultures of hypocotyl segments on Murashige-Skoog medium with 2,4-D, when callus began to appear on the segments. In dry seeds, lower amounts of ECP31 were located throughout the entire zygotic embryos but not in endosperm. ECP31 was also detected in provascular tissue of malformed somatic embryos.

Journal Article↗
PubMed1990

Two pyridine analogues with more effective ability to reverse multidrug resistance and with lower calcium channel blocking activity than their dihydropyridine counterparts.

Four pyridine analogues and their dihydropyridine counterparts were examined for their ability to reverse drug resistance in a multidrug-resistant human carcinoma cell line, KB-C2. Two pyridine analogues were more able to reverse drug resistance than their dihydropyridine counterparts. The other two pyridine analogues had an effect on drug resistance similar to their dihydropyridine counterparts. The calcium channel-blocking activity of all the pyridine analogues was considerably lower than that of the dihydropyridine analogues. Of the pyridine analogues, 2-[4-(diphenylmethyl)-1-piperazinyl]ethyl 5-(trans-4,6-dimethyl-1,3,2-dioxaphosphorinan-2-yl)-2,6-dimethyl-4 -(3- nitrophenyl)-3-pyridinecarboxylate P-oxide (PAK-104P) was the most effective in reversing multidrug resistance. PAK-104P (1 and 5 microM) completely reversed the drug resistance in KB-8-5 and KB-C2 cells, respectively. The reversing effect of PAK-104P was greater than that of other multidrug resistance-reversing agents, cepharanthine, verapamil, nimodipine, and nicardipine. PAK-104P at 1 microM increased about 10-fold the accumulation of vinblastine in KB-C2 cells, whereas verapamil at the same concentration increased the accumulation about 2-fold. The inhibition of [3H]azidopine photolabeling of P-glycoprotein by the pyridine and dihydropyridine analogues except 2-[methyl(phenyl-methyl)amino]ethyl 4-(2-chlorophenyl)-5-(4-methyl-1,3,2-dioxaphosphorinan-2-yl)-1,4-d ihydro-2,6- dimethyl-3-pyridinecarboxylate P-oxide correlated with the reversing of drug resistance by the analogues. Some newly synthesized pyridine analogues seemed to have lower calcium channel-blocking activity and more potent resistance-reversing ability than verapamil and other calcium channel blockers.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1989

Glucose reverses 2,4-dinitrophenol induced changes in action potentials and membrane currents of guinea pig ventricular cells via enhanced glycolysis.

The precise mechanism involved in the restoration by glucose of action potentials and membrane currents has not been established, so we studied it in single guinea pig ventricular cells under conditions of metabolic inhibition by 2,4-dinitrophenol (DNP). Application of DNP (50 mumol.litre-1) significantly shortened the action potential duration (APD) from 276.3 (SD 47.5) to 43.0(3.9) ms (n = 10). The increase in glucose concentration from 5.5 (control) to 22 mmol.litre-1 significantly restored the APD within 10 min, to 233.2(51.2) ms. In tight seal whole cell clamp studies, we found that DNP increased the steady state outward currents at potentials positive to -60 mV, and that this current was all but suppressed by 22 mmol.litre-1 glucose. The glucose induced recovery in the APD and membrane current was not seen in the presence of 2-deoxyglucose (2 mmol.litre-1), an inhibitor of glycolysis. Insulin (40 mIU.ml-1) reversed the DNP induced shortening of APD and abolished the increase in the outward current in the presence of 11 mmol.litre-1 glucose, though the application of glucose alone at this concentration failed to reverse these changes. Glucose (5.5 to 44 mmol.litre-1) did not directly affect single channel currents of ATP regulated K channels of the excised patch membrane in an outside out mode. These results suggest that the antagonising effects of glucose on the DNP induced alterations in APD and membrane currents are mediated by an increase in intracellular ATP concentration via enhanced glycolysis. Insulin might enhance this effect by facilitating the transport of glucose across the cell membrane.

2,4-Dinitrophenol↗
PubMed1989

Isoproterenol, DBcAMP, and forskolin inhibit cardiac sodium current.

We studied the effects of isoproterenol (ISP), dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), and forskolin on the sodium current (INa) of guinea pig ventricular myocytes using the tight-seal, whole cell voltage-clamp method. The extracellular [Na+] [( Na+]o) was decreased to 60 mM by replacing NaCl with sucrose (temperature, 32-33 degrees C). Ionic currents other than Na+ were suppressed using appropriate channel blockers. Depolarizing clamp pulse (duration, 30 ms) was applied at a rate of 0.2 Hz from a holding potential of -80 mV. ISP (1 microM) decreased the peak INa by 34% from 6.1 +/- 1.9 (SD) nA (control) to 4.0 +/- 1.5 nA (n = 7). The inhibition was more prominent at less negative potentials and disappeared in the presence of a beta-blocker (10 microM atenolol). The effects of DBcAMP (1-5 mM) and forskolin (3 microM) mimicked those of ISP and depressed the peak INa reversibly. DBcAMP (5 mM) shifted the inactivation curve of INa [h infinity-membrane potential (Em) relationship] to a hyperpolarizing direction, by 3.4 +/- 0.8 mV (n = 5). These findings suggest that ISP inhibits the cardiac INa+, probably by altering the gating mechanism of the Na+ channel, and that the effect is secondary to the increased levels of intracellular cAMP, with possible acceleration of cAMP-dependent phosphorylation of the channel.

Animals↗
PubMed1989

Late sodium current and its contribution to action potential configuration in guinea pig ventricular myocytes.

We used the patch clamp technique to study the nature of the late sodium current in guinea pig ventricular myocytes. In a cell attached mode of single channel recording at room temperature (22-24 degrees C) two kinds of late (100 msec or more after beginning of the depolarizing pulse) sodium channel activities were recognized. One is isolated brief openings appearing once for about 120 depolarizations per channel (background type), while the other type is sustained openings with rapid interruptions (burst type) that occurred only once for 2,700 depolarizations per channel. The time constant obtained from the open time histogram of the burst type (1.05 msec) was about five times longer than that of background type (0.18 msec, measured at the potential 10 mV above the threshold). Magnitude of the late sodium current flowing through the entire surface of a myocyte was estimated with tetrodotoxin (60 microM), a specific inhibitor of sodium channels, in whole-cell clamp experiments. The steady tetrodotoxin-sensitive current of 12 to 50 pA was registered at -40 mV (26 +/- 14 pA, mean +/- SD, n = 5), in good agreement with the late sodium current calculated from the single channel recording. Tetrodotoxin produced small (congruent to 10%) but significant decreases in the action potential duration. These results suggest the presence of a small but significant late sodium current with slow inactivation kinetics and that this current probably plays a significant role in maintaining the action potential plateau and the duration in guinea pig ventricular myocytes.

Action Potentials↗
PubMed1989

[Frequency of three-rooted mandibular first molars. Survey by x-ray photographs].

The frequency of three rooted mandibular first molars was surveyed. Subjects were of 1,353 male and female students trained in radiology at Fukuoka Dental College whose average age was 24.3 years old. Dental (complete radiographic survey using 14 films) and panoramic radiographs of their mandibular first molars were taken during a period of 9 years from 1978 to 1986. The results were as follows: 1) The number of the three-rooted mandibular first molars was 440 (18.8%) of 2,331 teeth, including 240 (20.6%) of 1,163 in the right side and 200 (17.1%) of 1,168 in the left. 2) 274 (11.8%) of the three-rooted mandibular first molars were identified by radiographs of the premolar region, 42 (1.8%) by radiographs of the molar region, 124 (5.3%) by radiographs of both the premolar and the molar region. 3) Panoramic radiography identified 70 (15.9%) out of 440 three-rooted mandibular first molars. 4) 136 (12.7%) of 1,070 subjects who had bilateral mandibular first molars had three-roots on both sides 127 (11.9%) of 1,070 had them on one side.

Adult↗