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S Yuasa

Publications and source records attributed to S Yuasa.

At least 163 records · Page 9Linked to original sources
PubMed1987

Na+-dependent transport of taurine by membrane vesicles of neuroblastoma x glioma hybrid cells.

The transport of taurine into membrane vesicles prepared from neuroblastoma x glioma hybrid cells 108CC5 was studied. A great part of the taurine uptake by the membrane preparation is due to the transport into an osmotically sensitive space of membrane vesicles. Taurine uptake by membrane vesicles is an active transport driven by the concentration gradient of Na+ across the membrane (outside concentration greater than inside). The Km value of 36 microM for Na+-dependent taurine uptake indicates a high-affinity transport system. The rate of taurine transport by the membrane vesicles is enhanced by the K+ gradient (inside concentration greater than outside) and the K+ ionophore valinomycin. Taurine transport is inhibited by several structural analogs of taurine: hypotaurine, beta-alanine, and taurocyamine. All these results indicate that the taurine transport system of the membrane vesicles displays properties almost identical to those of intact neuroblastoma X glioma hybrid cells.

Animals↗
PubMed1987

Clinical application of left ventricular assist devices.

In Japan, 32 patients have had application of monoventricular and biventricular assist devices during the past three years. Five of the 32 patients treated by the Fall of 1986 have successfully achieved long-term survival. In this paper we describe our experience with the Tomasu and Pierce VAD in a total of four and two patients, respectively. Four of the six patients could be successfully weaned from the VAD and two of them were long-term survivors. Nonsynchronizing pumping of the VADs was effective, as well as synchronizing pumping. Anticoagulant therapy is highly recommended during the use of the VAD although there was no significant incidence of thromboembolism or thrombus in the devices in this clinical series.

Adult↗
PubMed1987

A long-term follow-up study of schizophrenia in Japan--with special reference to the course of social adjustment.

A 21-27-year follow-up was conducted on 140 schizophrenic patients consecutively discharged from the Department of Neuropsychiatry, Gunma University Hospital, between 1958 and 1962, and 130 patients (93%) were successfully evaluated. Of these patients, 105 were still living, and the longitudinal courses could be fully observed in 98. With regard to the social outcome of the 105 patients, 47% were assessed as 'self-supportive' whereas 31% were 'hospitalised'. As for psychopathological outcome, 31% were 'recovered', 46% were 'improved', and 23% were 'unimproved'. In the studies of the longitudinal courses of the 98 patients, fluctuating courses of social adjustment were the most numerous in the early stages, whereas in the later stages many of the patients showed differentiation in one of two directions, namely the 'stable self-supportive' state and the 'chronic institutionalised' state. However, this form of differentiation was not revealed in the distribution of psychopathological 'end states'.

Female↗
PubMed1987

Suppressive effect of tritoqualine on enzyme leakage induced by D-galactosamine in rat primary-cultured hepatocytes.

Tritoqualine (TRQ) was previously reported to suppress enzyme leakage and lipid peroxidation induced by carbon tetrachloride in isolated hepatocytes. In the present study, we investigated the effect of TRQ on enzyme leakage from rat primary-cultured hepatocytes using D-galactosamine (GalN) which causes hepatic injury without lipid peroxidation. Leakage of GPT and GPT was significantly increased at 18 hr after GalN addition, being saturated at 42-50 hr. This enzyme leakage was suppressed dose-dependently by TRQ at 42 hr, but not by vitamin E. These results suggest that TRQ shows a suppressive effect on enzyme leakage from hepatocytes independently of its inhibitory action on lipid peroxidation.

Alanine Transaminase↗
PubMed1986

Inhibitory mechanism of tritoqualine on histamine release from mast cells.

Tritoqualine (TRQ, (+)-(R*)-7-amino-4,5,6-triethoxy-3-[(R*)-5,6,7, 8-tetrahydro-4-methoxy-6-methyl-1,3-dioxolo[4,5-g]isoquinolin++ +-5-yl] phthalide) strongly inhibited the increased metabolism of [3H]arachidonic acid-labeled phospholipid and 45Ca2+ influx in mast cells stimulated by compound 48/80 (compd 48/80), Concanavalin A (Con A) plus phosphatidylserine (PS), or 2,4-dinitrophenyl-coupled-ascaris extracts (DNP-asc). However, TRQ did not disturb the binding of 14C-labeled compd 48/80 to the mast cell membrane. The activity of calmodulin purified from mastocytoma P-815 cells was inhibited by TRQ at IC50 1.0 microM. From these results, it is concluded that the inhibitory mechanism of TRQ on stimulus-induced histamine release from mast cells may be mediated at least partially by the inhibition of Ca2+ influx and calmodulin activity.

Animals↗
PubMed1986

[Effect of tritoqualine (TRQ) on bile secretion in rats].

An accelerating effect by TRQ-consecutive administration perorally on bile secretion in rats was investigated in comparison with phenobarbital (PB)-administered rats. The bile secretion velocity was increased significantly by administration of TRQ (25, 50, 100 mg/kg/day) or PB (50 mg/kg/day) compared to the control group. A 24% increase in the ratio of the liver weight to body weight was observed in the PB-administered group, but in the TRQ-administered group, a slight increase (5%) was seen compared with the control group. The concentration of excreted bile acid in the bile of rats to which TRQ and PB were administered were lower than that of the control group. However, when excreted bile acid content was represented in terms of wet liver weight, no difference was seen in the TRQ-administered group, but a 17% decrease was observed in the PB-administered group compared with the control group; and also, almost the same results were obtained with regards to the cholesterol and phospholipid in the bile. Though there was no difference of Na+, K+, or Cl- concentration in bile between the TRQ or PB-administered group and the control group, more Na+, K+ or Cl-/g wet liver was excreted in TRQ-treated group than the PB-administered group. TRQ was excreted through the bile duct promptly after an i.v. injection without an increase in the bile secretion, suggesting that the excretion of TRQ and its metabolites were not accompanied by the increase in bile secretion. These results indicate that the accelerating effect of TRQ on bile secretion was presumably derived from bile acid non-dependent bile secretion such as PB; however, a different pharmacological mechanism between TRQ and PB was presumed from the discrepancy of the decomposition in the secreted bile and of drug-metabolizing enzyme induction. Thus, it was suggested that there was a possibility that the accelerating action of bile secretion by TRQ was attributed to the activating effect of TRQ on the hepatocytes.

Administration, Oral↗
PubMed1986

[Suppressive effect of tritoqualine (TRQ) on the acceleration of fibrosis in the liver].

Liver cirrhosis was induced by consecutive CCl4-treatment of rats (0.5 ml/kg, s.c., 2 times/week) to investigate the effect of TRQ on the acceleration of fibrosis in the liver. An increase of hydroxyproline content in the liver of rats began 12 weeks after the CCl4 treatment and a 1.9-fold increase was observed at week 14 compared with non-CCl4 treated rats. Histamine in the liver increased about 2 times at week 14. Increased numbers of mast cells were seen in the area of proliferated collagen fiber in the liver under microscopic observation, and also a good correlation was recognized between the number of mast cells and the progression of fibrosis. An administration of TRQ to the rats for 2 weeks from week 13 resulted in significant suppression of both the increase in hydroxyproline and histamine in the liver dose-dependently compared with the CCl4 control group. Both progression of collagen and increase in mast cell numbers were also suppressed by TRQ dose-dependently under histopathological observation; at the same time the decrease in mast cells was recognized to correspond to the decrease in hydroxyproline and histamine in the liver. Thus, it was suggested that increased mast cells participated in the biosynthesis of collagen. Though the elevated serum transaminases, alkaline phosphatase and leucine amino peptidase were also suppressed by TRQ administration, the protein biosynthesis activity of the liver and lowered serum total cholesterol were not improved as much as the other parameters. From these results, it was shown that TRQ was especially and remarkably effective in suppressing the acceleration of fibrosis, and one of the pharmacological mechanisms of this action may be ascribed to the inhibitory effect of TRQ on the activation of mast cells by some stimulants.

Animals↗
PubMed1986

Suppressive effects of tritoqualine on cell growth and collagen secretion in fibroblasts.

The effects of tritoqualine (TRQ) on established cell lines of fibroblasts, Balb/3T3 and 3T6, were investigated with respect to growth and collagen secretion. TRQ suppressed growth rate in the log phase and inhibited collagen secretion in the stationary phase of both cell lines. However, TRQ was not cytotoxic because of lack of influence on cell maintenance in the stationary phase. These effects of TRQ are thought to be very important as a mechanism of inhibitory action against liver fibrosis in chronic liver injury in rats.

Animals↗
PubMed1986

Suppressive effect of tritoqualine on lipid peroxidation and enzyme leakage induced by carbon tetrachloride in rat hepatocytes.

Since tritoqualine (TRQ) is effective in suppressing the increase of serum transaminases in acute hepatic injured rats induced by some hepatotoxins, protection of the hepatocyte membrane is suggested to be one of the pharmacological effects of TRQ. In the present study, we investigated the effects of TRQ on lipid peroxidation and enzyme leakage caused by carbon tetrachloride (CCl4) exposure in isolated hepatocytes and the liver in vivo, compared with vitamin E. The results were as follows: Hepatocytes isolated from TRQ-administered rats showed less enzyme leakage than those from control rats after CCl4 addition. TRQ displayed strong inhibition of lipid peroxidation in isolated hepatocytes. In comparison with vitamin E, TRQ showed almost the same inhibitory action on lipid peroxidation, but a stronger suppression of enzyme leakage. Vitamin E showed a weaker protection from increase of glutamic oxaloacetic transaminase than TRQ, in spite of its stronger inhibition of lipid peroxidation in vivo. From these results, it is suggested that the membrane protecting action of TRQ is partially derived from its suppression of lipid peroxidation, but "another action" may also play an important role in protecting the fragile membrane.

Alanine Transaminase↗