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Biomedical subjects

S Takehara

Publications and source records attributed to S Takehara.

47 records · Page 3Linked to original sources
PubMed1988

The effect of ceruletide on tardive dyskinesia: a double-blind placebo-controlled study.

1. In a double-blind placebo-controlled study of 37 patients with tardive dyskinesia, the therapeutic effect of ceruletide was evaluated. 2. The patients were assigned at random to two groups that received either intramuscular injections of 0.8 micrograms/kg of ceruletide or placebo once weekly for 4 weeks. Conventional neuroleptic medication was not changed 3 weeks prior to and throughout the study period. Tardive dyskinesia was assessed using the Abnormal Involuntary Movement Scale over an 8-week period. 3. Ceruletide had a more pronounced effect on TD than the placebo however, because of the limited number of subjects examined, the difference between the two groups was not significant. Ceruletide was more effective than placebo in patients under 60 years of age (p less than 0.05) and whose antipsychotic medication was mainly butyrophenones. 4. No serious side effect was noted. 5. The findings suggested that ceruletide therapeutically benefits patients with tardive dyskinesia.

Ceruletide↗
PubMed1987

[Pharmacological studies on Y-8894. (VII). Effects on transient cerebral ischemia-induced amnesia in rats].

The effects of Y-8894 on experimental amnesia in rats induced by transient cerebral ischemia (600 sec) according to the method of Pulsinelli and Brierley were studied using the one trial passive avoidance response and the pole climbing discrete avoidance response. All drugs were administered to the rats immediately after recirculation. The following results were obtained: 1) In the one trial passive avoidance response test, Y-8894 (2.5, 5 and 10 mg/kg, i.p.) improved significantly the decreased latency induced by the ischemia, and it was most effective at 5 mg/kg. Calcium-hopantenate (100, 250 and 500 mg/kg, i.p.) and dihydroergotoxine (5 and 10 mg/kg, i.p.) tended to increase the latency. On the other hand, physostigmine (0.025, 0.05 and 0.1 mg/kg, i.p.), a cholinesterase inhibitor, increased the latency significantly, and it was most effective at 0.05 mg/kg. 2) The pole climbing discrete avoidance response was significantly decreased by the ischemia compared with the sham operated group, and Y-8894 (5 mg/kg, i.p.) tended to improve this decreased avoidance response. 3) Y-8894 (5 mg/kg, i.p.) facilitated recovery from the changes in glycolytic metabolism, and inhibited the accumulation of choline due to the dysfunction of the neuronal membranes induced by the ischemia. These results show that Y-8894 has beneficial effects on experimental amnesia induced by transient cerebral ischemia.

Amnesia↗
PubMed1987

[Pharmacological studies on Y-8894 (VI). The effect on monoamine uptake and turnover in mouse brain].

The effect of Y-8894 (+/-) 2-[[o-(2-thenyl)phenoxy]methyl] morpholine maleate, which has been shown to improve experimentally induced learning and memory deficits, on cerebral monoamine uptake and turnover was studied in the mouse. The following results were obtained: 1) It inhibited in vitro norepinephrine (NE) uptake to the mouse cerebral synaptosomal fractions about 800 and 1250 times more potently than it did those of dopamine (DA) and serotonin (5-HT), respectively. 2) It dose-dependently inhibited in vivo NE uptake, but not DA or 5-HT uptake. 3) It reduced the accumulation of the NE metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), increased that of the 5-HT metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and had no effect on that of the DA metabolite, homovanillic acid (HVA). These effects were compared with those of imipramine, calcium hopantenate (Ca-hopantenate) and dihydroergotoxine. Y-8894 appeared to act by stimulating the noradrenergic receptor, and it acts to a lesser extent by blocking the serotonergic receptor in the brain.

Animals↗
PubMed1987

An antagonistic activity of etizolam on platelet-activating factor (PAF). In vitro effects on platelet aggregation and PAF receptor binding.

The antagonistic effect of etizolam, an anti-anxiety drug, on platelet-activating factor (PAF) was investigated in rabbit platelets in vitro. Etizolam inhibited PAF-induced aggregation in a dose-dependent manner, with an IC50 of 3.8 microM, about one tenth that of triazolam (IC50 = 30 microM). At 300 microM, it inhibited both ADP and arachidonic acid-induced aggregation only slightly, while the other anti-anxiety drugs tested had no effect on PAF-induced aggregation even at this concentration. Etizolam and triazolam inhibited the specific binding of 3H-PAF to PAF receptor sites on washed rabbit platelets with IC50 values of 22 nM and 320 nM, respectively. Diazepam and estazolam were inactive even at 1 microM. These results indicate that etizolam is a specific antagonist of PAF.

Animals↗
PubMed1987

[Clinical study of traumatic cerebellar contusion].

Numerous authors have reported cases of traumatic cerebellar contusion. A few authors have emphasized delayed deteriorations in patients with cerebellar contusion. Since CT scan was introduced into daily clinical practice, it has become obvious that cerebellar contusion were not necessarily associated with severe head injuries. Of 1176 head-injured cases admitted to our department in the past five years, eight (0.7%) were diagnosed by CT scans to have cerebellar contusion. Among eight cases, two of them were deeply comatose on admission because they had concomitant diffuse cerebral contusions and died soon after admission. Remaining six cases had predominantly cerebellar contusion on CT scans and showed minimal neurological deficits on admission. Most of them recovered without any significant disabilities. But two of them deteriorated several hours after injury, showing brain-stem compression for which emergency posterior fossa decompression were carried out without recovery. One of them underwent external decompression which resulted in intracerebellar massive hemorrhage and the other missed the timing of surgery. In conclusion, it is important to prepare for unexpectedly rapid deterioration, for which wide craniectomy and sufficient internal decompression would be required.

Adult↗
PubMed1985

Effects of iminodibenzyl antipsychotic drugs on cerebral dopamine and alpha-adrenergic receptors.

The iminodibenzyl antipsychotic drugs, clocapramine, carpipramine and Y-516 were studied in order to elucidate their mechanisms of action. They all accelerated the accumulation of the dopamine (DA) metabolites, homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), in the striatum and nucleus accumbens of the rat brain. Only Y-516 antagonized in vivo the apomorphine-induced inhibition of DA synthesis as estimated from the accumulation of 3,4-dihydroxyphenylalanine (DOPA) in the decarboxylase-inhibited rat striatum after cessation of nerve impulse flow. All three drugs showed high affinity for DA receptors labelled by [3H]haloperidol and [3H]ADTN in the rat striatum in vitro, with the order of potency Y-516 greater than clocapramine greater than carpipramine. All accelerated the accumulation of the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), in mouse brain. They showed high affinity for alpha 1-adrenoceptors labelled by [3H]WB 4101 and for alpha 2-adrenoceptors labelled by [3H]clonidine in the rat cerebral cortex in vitro. Although they all had the same level of affinity for the alpha 1-adrenoceptors, Y-516 had less affinity for the alpha 2-adrenoceptors than did clocapramine and carpipramine. The above results indicate that these drugs are potent DA antagonists which block alpha 1- and alpha 2-adrenoceptors in the brain.

Animals↗
PubMed1984

A serum factor stimulating cathepsin D-release from erythrocytes or ghosts.

A serum factor preparation extensively purified from bovine serum stimulated cathepsin D-release from the rat blood cells in a concentration-dependent fashion within a range of physiological concentrations of the factor. Among the blood cells only the erythrocytes (or ghosts) were responsive to the factor, and the leucocytes and lymphocytes were unresponsive. The effects of Ca2+-concentrations, SH- blocking reagents, protease-inhibitors, calmodulin-inhibitors, calmodulin or EGTA-pretreatment of the ghosts on cathepsin D-release from the erythrocytes of ghosts in the presence or the absence of serum factor were investigated. The results suggested that the serum factor may first activate the Ca2+-calmodulin system via the mobilization of "Ca2+-pool" and then the calmodulin-dependent SH-protease in the erythrocyte plasma membranes. The activated protease in turn may break the linkage between cathepsin D and the plasma membranes, liberating cathepsin D activity into the incubation medium. The name of "calciferin" was proposed for the serum factor.

Animals↗
PubMed1982

[Congenital Minamata disease accompanied by arachnoid cyst (author's transl)].

A male, born on December 8, 1956, during the period when many Minamata diseases broke out in a district. His parents who ate much fish and shell fish taken in Minamata Bay suffered from the light, incomplete Minamata disease showing sensory disturbance, the constriction of the visual field, muscular weakness, etc. He weighed 3,225 gr. upon the normal birth given 10 months after pregnancy. His abnormalities were noted since his head was not stabilized on the neck even six months after the birth. Because of the delay in the development of the motor function, he became barely able to sit, stand up and begin walking at the ages of 3, 5 and 6 respectively. In 1962 (at the age of 6), his congenital Minamata disease was diagnosed in view of his clinical symptoms and epidemiological conditions. The mercury value in the hair and blood upon the birth is not known because a considerable time had elapsed after the birth when his mercury poisoning was discovered. However, the clinical symptoms included intelligence disturbance, character change, dysarthria, primitive reflexes, strabismus, hypersalivation, ataxia and hyperkinesia, indicating a typical congenital Minamata disease. Until he became 13 years old (1969) or so, his mental and motor function developed, both gradually. In the same year, he was admitted to a special class for the handicapped. EEG examination revealed that there was a slow alpha activity in the basic pattern and that 6 Hz positive spike was found in the sleep EEG. The constriction of the visual field was classified through examination.2+

Adult↗
PubMed1978

Effects of 6-(o-chlorophenyl)-8-ethyl-1-methyl-4H-s-triazolo [3,4-c]thieno[2,3-e][1,4]diazepine (Y-7131) on the metabolism of biogenic amines in brain.

A new derivative of thienodiazepine, 6-(o-chlorophenyl)-8-ethyl-1-methyl-4H-s-triazolo[3,4-c]thieno[2,3-e][1,4]diazepine (Y-7131) decreased the turnover of 5-hydroxytryptamine (5-HT) but not that of dopamine (DA) in the rat brain. The potency of Y-7131 in inhibiting the 5-HT turnover was stronger than that of diazepam. Imipramine decreased the turnover of 5-HT, whereas chlorpromazine increased the turnover of DA. Y-7131 decreased the turnover of norepinephrine (NE) in the mouse brain. With diazepam, such an action was not recognized. Imipramine did not affect the turnover of NE, whereas chlorpromazine increased it. Y-7131 inhibited the uptake of NE in the mouse brain, although it did not inhibit the uptake of 5-HT. Diazepam was devoid of such an action. Imipramine inhibited the uptake of both amines. The increase of the turnover of 5-HT, NE and DA due to foot-shock stress in the rat brain was suppressed by the administration of Y-7131. In this antagonistic effect, Y-7131 was more potent than diazepam. Neither imipramine nor chlorpromazine showed these antagonistic effects. The results obtained suggest that Y-7131 has biochemical profiles similar to diazepam but differs from it in exhibiting inhibitory effect on the NE turnover and its uptake.

Animals↗