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T Sumi

Publications and source records attributed to T Sumi.

At least 19 recordsLinked to original sources
PubMed1992

Amitriptyline inhibits striatal efflux of neurotransmitters via blockade of voltage-dependent Na+ channels.

Amitriptyline, a tricyclic antidepressant, almost completely inhibited veratridine- or scorpion toxin-evoked efflux of endogenous dopamine (DA) and gamma-aminobutyric acid (GABA) from rat striatal slices without any effects of 30 mM K+ or 4-aminopyridine on basal and evoked efflux. The effects of amitriptyline on glutamate efflux were comparable to those on DA or GABA efflux. These effects of amitriptyline can be well explained by its blockade of voltage-dependent Na+ channels and may be independent of other activities of this drug such as re-uptake inhibition of monoamines and blockade of K+ channels.

Amitriptyline↗
PubMed1992

Estimation of right ventricular volume by modified echocardiographic subtraction method.

To evaluate the accuracy and clinical utility of right ventricular volume estimated by a modified echocardiographic subtraction method versus Krebs' original subtraction method, an experiment was performed on hearts excised from 25 animals (dogs, pigs, and cows) followed by a clinical study of 41 patients with heart disease. Right ventricular volume was measured by subtracting the left ventricular volume from that of the whole heart based on echocardiographic apical two- and four-chamber views by means of the area-length method. In the animal heart study, the coefficient of variation between the right ventricular volume estimated by the modified method and the true volume was +/- 13%. The regression equation was y = 0.94x + 4.15 (r = 0.987, p less than 0.001) and showed good correlation, whereas the right ventricular volume obtained by the original method underestimated the true volume (coefficient of variation = +/- 25%, y = 0.59x + 1.11; r = 0.976, p less than 0.001). In the clinical study, the coefficient of variation between right ventricular volume estimated by the modified echocardiographic method and RV volume estimated by radionuclide ventriculography was +/- 15%. The regression equation was y = 0.80x + 13.3 (r = 0.935, p less than 0.001). This correlation was better than that obtained by the original method (coefficient of variation = +/- 16%), where the regression equation was y = 0.60x + 2.43 (r = 0.888, p less than 0.001). Thus the accuracy of the modified subtraction method was validated, and this method showed a better correlation than the original method both experimentally and clinically.

Adolescent↗
PubMed1992

Expression of c-kit protooncogene is stimulated by cAMP in differentiated F9 mouse teratocarcinoma cells.

Protooncogene c-kit, a transmembrane tyrosine kinase receptor, was recently shown to map to the dominant white spotting locus (W) of the mouse. W mutations affect melanogenesis, gametogenesis, and hematopoiesis during development and in adult life. In order to determine the regulation of the c-kit gene in cell differentiation, we investigated its expression during the differentiation of F9 cells. Undifferentiated F9 cells and F9 cells treated with retinoic acid (RA) alone or dbcAMP alone showed little expression of c-kit mRNA if any. The subsequent addition of dbcAMP to F9 cells treated with RA markedly increased the expression of c-kit mRNA. Furthermore, the effect of dbcAMP on c-kit expression is reversible. In differentiated cells treated with RA, c-kit gene expression is induced by agents such as forskolin or theophylline, which are known to elevate cellular cAMP level. These results indicate that the expression of the c-kit gene is regulated by the level of intracellular cAMP in differentiated F9 cells induced by RA.

Animals↗
PubMed1992

Evaluation of a cholinomimetic drug, 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta [b] quinoline (NIK-247), as an enhancer of endogenous efflux of acetylcholine from brain slices.

Basal and high K(+)-stimulated efflux of endogenous ACh from slices of brain was measured to evaluate the cholinomimetic effect of 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b] quinoline monohydrate HCl (NIK-247) on the central nervous system. The drug NIK-247 dose-dependently accelerated the efflux of ACh from slices of striatum. The maximum increase produced by 1.0 x 10(-4) M of NIK-247 was 329% in basal and 1332% in 30 mM K(+)-stimulated efflux. This drug was nearly twice as potent as THA (9-amino-1,2,3,4-tetrahydroacridine HCl) but had the same potency as physostigmine, in enhancing basal efflux, although there was no significant difference between the efficacy of these drugs in enhancing the K(+)-stimulated efflux. Both basal and 50 mM K(+)-stimulated efflux of ACh were increased by NIK-247, not only from the striatum but also from slices of frontal cortex and hippocampus. The activity was more effective in the striatum than in other tissues, and more effective on K(+)-stimulated than on basal efflux, regardless of the region of the brain. These effects of NIK-247 may be a result mainly of its inhibition of cholinesterase and its other biological characteristics, such as K+ channel blockade, capable of modulating release of ACh, may not be of major importance.

Acetylcholine↗
PubMed1992

c-myc and p53 gene expression in the differentiation of temperature-sensitive mutants of teratocarcinoma F9 cells.

We have previously reported the isolation of several temperature-sensitive (ts) mutants of F9 cells. Further investigations showed that some mutants were induced to differentiate at non-permissive temperature of cell growth, accompanied by changes in the expression of various genes, whereas others were not. During the differentiation induced by shifting up to the non-permissive temperature, a rapid and transient decrease in both c-myc and p53 mRNA levels and rapid induction of c-jun mRNA were observed. These changes were specific in differentiation-inducible mutants and were not observed in a non-inducible mutant. In both types of mutants, the level of c-myc mRNA decreased in association with growth retardation at the non-permissive temperature. The p53 mRNA, however, showed specific increase in the differentiation-inducible ts mutants. These observations suggest distinct roles for p53 and c-myc from proliferation to differentiation in teratocarcinoma stem cells.

Animals↗
PubMed1991

A change in the spontaneous release of endogenous acetylcholine from rat striatal slices after repeated injection of haloperidol.

The spontaneous and 50 mM K(+)-stimulated release of endogenous acetylcholine (ACh) from rat striatal slices was measured to investigate an adaptive change of striatal ACh after a withdrawal period for 24 h from chronic treatment of the rat with haloperidol. The haloperidol injections (2.5 mg/kg/day) for a period of 3, 7 or 14 days all reduced the spontaneous release of ACh significantly by 20-50% without changing tissue levels of ACh. On the contrary, these treatments produced a very small (by about 10%) but significant increase in K(+)-stimulated release except for the treatment of 7 days. These results suggest that the spontaneous ACh release is under the control of a dopaminergic mechanism, which might be different from the mechanism controlling the evoked release of ACh and emerges following withdrawal from chronic haloperidol treatment.

Acetylcholine↗
PubMed1990

Decrease in the evoked release of endogenous dopamine and dihydroxyphenylacetic acid from rat striatal slices after withdrawal from repeated haloperidol.

The release of endogenous DA (dopamine) and DOPAC (3,4-dihydroxyphenylacetic acid) from rat striatal slices was measured after withdrawal from a prior long-term treatment of the rat with haloperidol to investigate adaptive changes in striatal DA and DOPAC release induced by chronic haloperidol treatment. Striatal slices prepared 24 h after the last injection of daily treatment with haloperidol for up to 14 days (2.5 mg/kg per day) were superfused and stimulated for 5 min with K+ (50 mM). Haloperidol treatment for 3 or 7 days decreased K(+)-stimulated DA release by maximally 35%, but a 14-day treatment was not effective. The K(+)-stimulated release of DOPAC, which occurred after the change in DA release, was reduced significantly by the treatment for 7 or 14 days. A higher daily dose of haloperidol (10 mg/kg per day) produced a more pronounced decrease in stimulated DA release after a 14-day treatment without having an effect after 3 days. However, the stimulated release of DOPAC decreased markedly after both 3 and 14 days of haloperidol treatment. The slight reduction in the DA content of the slices after K+ stimulation was seen in some haloperidol-treated tissues, although this change did not always parallel the simultaneous decrease in DA release. These results indicate that the K(+)-induced stimulation of endogenous DA release and the synthesis of DA are impaired after withdrawal from repeated haloperidol treatment.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Release of endogenous acetylcholine from rat brain slices with or without cholinesterase inhibition and its potentiation by hemicholinium-3.

The direct measurement of basal and high K(+)-stimulated release of endogenous acetylcholine from striatum and hippocampus slices was achieved without as well as with a cholinesterase inhibitor, physostigmine. Hemicholinium-3, opposite to its well-known activity as an inhibitor of endogenous acetylcholine release, significantly potentiated both the basal and stimulated release, in particular in the absence of physostigmine, suggesting an involvement of some unknown activity stimulating ACh release in hemicholinium-3.

Acetylcholine↗
PubMed1989

Isolation of mutants showing temperature-sensitive cell growth from embryonal carcinoma cells: control of stem cell differentiation by incubation temperatures.

Embryonal carcinoma(EC) cells, the undifferentiated stem cells of teratocarcinomas, have many properties in common with pluripotent embryonic cells, and thus provide an excellent system for studying the early events involved in embryonic development and stem cell differentiation. We have isolated three novel mutants with temperature-sensitive(ts) cell growth that were able to differentiate at a non-permissive temperature for cell growth. These mutations affect the progression of the cell cycle, leading to the transient accumulation of cells in a specific phase, the S phase, of the cell cycle, which is likely to be the primary cause of stem cell differentiation of EC cells at non-permissive temperature. Isolation of these mutants strongly supports the notion that there is a close association between the inhibition of DNA synthesis and EC cell differentiation.

Animals↗
PubMed1989

Inhibition of DNA synthesis causes stem cell differentiation: induction of teratocarcinoma F9 cell differentiation with nucleoside analogues of DNA-synthesis inhibitors and their inducing abilities counterbalanced specifically by normal nucleosides.

Nucleoside analogues inhibiting DNA synthesis can induce cell differentiation in teratocarcinoma cells. We have examined how their abilities to induce F9 cell differentiation were specifically counterbalanced by their corresponding normal nucleosides. We have also compared the differentiation inducing ability of the wild type F9 cells with that of its thymidine kinase-less mutant using plasminogen activator, as a differentiation marker, which is expressed at a very early stage of endodermal cell differentiation and can be assayed quantitatively. The results obtained were clearly explainable by the conventionally accepted action mechanisms of the nucleoside analogues, thus strongly suggesting that their abilities to induce cell differentiation were direct consequences of the inhibition of DNA synthesis; thus this confirms the notion that a close association exists between the inhibition of DNA synthesis and the induction of teratocarcinoma stem cell differentiation.

Animals↗
PubMed1989

Evoked release of endogenous amino acids from rat striatal slices and its modulation.

The release of endogenous gamma-aminobutyric acid (GABA), glutamate and aspartate stimulated by high K+ was studied by superfusing rat striatal slices. Stimulation with 5 min of 30 mM K+ was applied twice (S1 and S2) at a 20 min interval. The maximum release of GABA following stimulation was 40 (at S1) and 26 (at S2) times greater than the basal release. S1 and S2 each produced a maximum release of almost same magnitude for both glutamate and aspartate (about 2.5 times basal release). The removal of Ca2+ from the perfusion medium reduced the maximum release of these amino acids by more than 80% without affecting basal release significantly. Striatal slices were next stimulated in the same way after the addition of apomorphine or haloperidol to the perfusion medium. Apomorphine, 10 or 100 microM, reduced the K+-evoked release of GABA (by 24% at S1 and 35% at S2 with 10 microM; by 37% at S1 and 47% at S2 with 100 microM) but failed to affect the simultaneous release of glutamate and aspartate. Haloperidol (1 microM) reduced the S1-induced release of GABA but had no significant effect on the subsequent S2-induced release. The evoked release of aspartate or glutamate did not respond significantly to haloperidol, but there was a tendency to a decrease in aspartate release similar to the decrease seen for GABA release, particularly with S1. Based on these results, we discuss the property of GABA, aspartate and glutamate as neurotransmitters and the possible dopaminergic regulation of the release of these amino acids.

Amino Acids↗
PubMed1989

[Study on the radiation effects toward function and vessels of parotid gland in rat].

The effect of irradiation on the parotid gland was determined from 99mTc-pertechnetate (99mTcO4-) uptake and the course of vessels in the parotid gland, by investigating the uptake and excretion of 99mTcO4- in 60Co-gamma ray-irradiated rat parotid gland and ovserving the course of blood vessels and the histological changes. 1. In the uptake test, radiation activity of 99mTcO4- taken into the parotid gland per unit weight was the highest three days after irradiation for both 10 Gy (1.68 x 10(5)cpm/g) and 50 Gy (2.05 x 10(5)cpm/g); however, it began to decrease gradually at 7 days after irradiation. 2. In the clearance test, as in the uptake test, the radiation activity of 99mTcO4- per unit weight remaining in the parotid gland after stimulation of secretion, was high at 3 days after irradiation for both 10 Gy and 50 Gy (0.86 x 10(5), 1.28 x 10(5)cpm/g, respectively) and 7 days (0.88 x 10(5), 1.29 x 10(5)cpm/g) after irradiation, and gradually decreasing thereafter. 3. Stimulation-secretion coefficients determined from the ratio of uptake and clearance of 99mTcO4- were lower in all groups with irradiation than in the group without irradiation, with especially low values at 7 and 14 days after radiation. Thus, parotid function declined after irradiation. 4. With respect to the effect of irradiation on blood vessels, mild dilation was observed at 10 Gy at 3 and 7 days after irradiation, then constriction and meandering were noticed. Such changes were greater at 50 Gy than at 10 Gy. 5. Histological changes appeared 6h after irradiation in the 10 Gy- and 50 Gy-irradiation groups. Derangement of cells in the terminal parts, dilation of conduits, and proliferation of connective tissue were observed from 3 days after irradiation. 6. The periodic aid-Schiff (PAS) reaction was decreased in the 10 Gy- and 50 Gy-irradiation groups, with few PAS-positive cells at 28 days after irradiation. In conclusion, the decline in parotid function after 10 Gy- and 50 Gy-irradiation was related to histological changes in the vascular system and glandular tissues.

Animals↗
PubMed1988

[Comparison of the binding nature of mibolerone to androgen receptor of human prostate with that of R1881].

The authors examined the binding nature of mibolerone in cytosols of hypertrophic prostates from 15 patients to androgen receptor using Dextran-charcoal assay, analyzed it by the method of Scatchard, and compared it with that of R1881. The addition of triamcinolone acetonide into the incubation medium induced specific single binding of mibolerone to androgen receptor with high affinity as well as R1881. The receptor contents obtained with mibolerone were higher than those of R1881, and both of them correlated well. The dissociation constants of both ligands showed good correlation and no significant differences. Mibolerone seems to be as suitable a ligand as R1881 for measuring the androgen receptor.

Estrenes↗
PubMed1988

[In vivo measurements of electrical bio-impedance of breast tumors].

The electrical bio-impedance of 17 breast tumors including 12 breast cancers and 5 fibroadenomas, were measured in vivo with three-electrode method in the frequency range of 0 to 200 KHZ. The three-electrode consists of a coaxial needle electrode inserted into the tumor and a large reference electrode on upper abdominal wall. The tissue can be regarded electrically as a equivalent consisted of extracellular resistance (R1), intracellular resistance (R2), and electric capacitance of the cell membrane (C). These three parameters were calculated from the measured values of electrical bioimpedance. It was found that R1, and R2 of breast cancers were significantly higher than those of fibroadenomas (p less than 0.001), and that C of breast cancers was significantly lower than that of fibroadenomas (p less than 0.001). The measurement of the electrical impedance of breast tumor in vivo may be useful for the differential diagnosis of breast lesions.

Adenocarcinoma, Scirrhous↗