Biomedical subjects
M Terai
Publications and source records attributed to M Terai.
Effect of a new potent H2-receptor antagonist 3[[[2-[(diaminomethylene)amino]-4-thiazolyl]methyl]thio]-N2- sulfamoylpropionamidine (YM-11170) on gastric mucosal histamine-sensitive adenylate cyclase from guinea pig.
The effect of 3[[[2-[(diaminomethylene)amino]-4- thiazolyl]methyl]thio]-N2-sulfamoylpropionamidine (YM-11170), a new thiazole H2-receptor antagonist bearing propionamidine at the terminus of a side chain, on histamine-sensitive adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] of gastric mucosa from the guinea pig was studied and compared with that of cimetidine. YM-11170 displaced the concentration-stimulation curve of histamine-sensitive adenylate cyclase to the right with a pA2 of 7.65 (Ki = 2.25 X 10(-8) M). Stimulation of gastric adenylate cyclase by 0.1 mM histamine was competitively inhibited by YM-11170 and cimetidine in a dose-dependent manner, with IC50 values of 5.9 X 10(-7) M and 1.4 X 10(-5) M respectively. Hippocampal histamine-sensitive adenylate cyclase in the presence of 0.1 mM histamine was also competitively inhibited by YM-11170 with an IC50 of 1.1 X 10(-7) M. YM-11170 did not affect Gpp(NH)p-, NaF-, PGE2-stimulated or basal activity of the gastric adenylate cyclase. These data, together with other results, indicate that YM-11170 is a highly selective and potent H2-receptor antagonist which competes with histamine at the receptor site on the histamine-sensitive adenylate cyclase.
Cross-sectional echocardiographic findings of anomalous origin of left coronary artery from pulmonary artery.
Anomalous origin of the left coronary artery and left ventricular myocardial hypokinesis were visualised by cross-sectional echocardiography. Significant dilatation of the right coronary artery was another important finding. Cross-sectional echocardiography appears to be useful for evaluating patients with anomalous origin of the left coronary artery from the pulmonary artery.
Selective binding of YM-09151-2, a new potent neuroleptic, to D2-dopaminergic receptors.
Effects of YM-09151-2 and five other neuroleptics (haloperidol, spiperone, chlorpromazine, sulpiride and clozapine) on the binding of [3H]-ligands to nine different receptors (alpha 1-adrenergic, alpha 2-adrenergic, beta-adrenergic, muscarinic, D2-dopaminergic, H1-histaminergic, 5HT1-serotonergic, 5HT2-serotonergic and opiate receptors) and on dopamine-sensitive adenylate cyclase were determined using brain membranes in the rat, guinea-pig and dog. The affinity of YM-09151-2 for D2-receptors with a Ki value of 0.1 nM was more than 1000-times higher than that for the other receptors and dopamine-sensitive adenylate cyclase, and it was the greatest among the neuroleptics tested.
[Acute renal failure in emergencies].
Explore the source record for details and available documents.
Relaxant actions of PGE2 and its derivative (YPG-209) on canine tracheal smooth muscle and their enhancement of Ca++ uptake by the microsomal fraction.
The spasmogenic action of tetraethylammonium on canine tracheal smooth muscle was dependent on the extracellular Ca++ concentration. Acetylcholine, on the contrary, produced partial contraction for a certain period of time after removal of extracellular Ca++, suggesting the release of Ca++ from intracellular Ca++ stores into the cytosol. PGE2, 16(S)-methyl-20-methoxy-PGE2 (YPG-209), verapamil, and dibutyryl cyclic AMP relaxed the acetylcholine-induced contraction of the trachea. Pretreatment with prostaglandins or dibutyryl cyclic AMP more efficiently suppressed acetylcholine-induced contraction, whereas verapamil blocked the spasmogenic action of tetraethylammonium in a relatively selective manner. The prostaglandins and dibutyryl cyclic AMP also inhibited the spasmogenic action of acetylcholine in a Ca++-free medium. Influx of 45Ca into tracheal smooth muscle which was produced by 83 mM KCl plus 20 mM tetraethylammonium was not significantly affected by prostaglandins as measured by the lanthanum method. In addition, PGE2 increased ATP-dependent Ca++ uptake by the microsomes from tracheal smooth muscle. These results suggest that prostaglandins induce relaxation of the airway smooth muscle mainly through affecting the intracellular Ca++ movement such as by enhancement of sequestration of Ca++ to the microsomes.
Inhibition of calcium influx in rabbit aorta by nicardipine hydrochloride (YC-93).
Explore the source record for details and available documents.
[Carrier-free separation of manganese-54 from iron targets irradiated with fast neutrons (author's transl)].
Explore the source record for details and available documents.
Inhibition of cyclic AMP phosphodiesterase by 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid 3-[2-(N-benzyl-N-methylamino)] ethyl ester 5-methyl ester hydrochloride (YC-93), a potent vasodilator.
Explore the source record for details and available documents.
Oral bronchodilator effect of 16(S)-methyl-20-methoxy-PGE2 (YPG-209) in guinea-pigs.
The bronchodilator activity of synthetic 16(S)-methyl-20-methoxy-PGE2 (YPG-209) was investigated in guinea-pigs. The potency of YPG-209 in relaxing the isolated trachea contracted by histamine was 10 times smaller than that of PGE2, and was not reduced by propranolol, while in the anesthetized animals YPG-209 given by an intravenous route was 230 times as potent in inhibiting an increase in the airway resistance induced by histamine as PGE2. When administered either intraduodenally to the anesthetized animals or orally to the conscious ones, YPG-209 showed a pronounced protection against histamine-induced bronchoconstriction, in contrast to PGE2 which had no significant protecting effect. Neither hypotension nor diarrhea could be observed at the doses of YPG-209 exhibiting a considerable bronchodilator effect. The hydroxyl group at carbon-15 of YPG-209 was little oxidized by 15-hydroxy prostaglandin dehydrogenase which was purified from the lung of guinea-pigs, consistent with the comparably long lasting bronchodilator activity of YPG-209 in vivo.
Partial purification of adenosine 3',5'-cyclic monophosphate phosphodiesterases from rat pancreas in the presence of excess protease inhibitors.
Explore the source record for details and available documents.
Distribution of trace elements in the human body determined by neutron activation analysis.
Neutron activation analysis and instrumental semiconductor gamma-ray spectrometry were used for analysis of 20 trace elements in 10 autopsied human organs and tissues (liver, kidney, cerebrum, cerebellum, heart, muscle, pancreas, spleen, lung, and aorta) from 63 Japanese persons, whose ages ranged from 15 days to 85 yr. Distributions of aluminum, bromine, magnesium, manganese, rubidium, selenium, and vanadium in human body were almost uniform. High concentrations of cadmium were found in kidney and liver samples. There was a high mercury concentration in the liver, kidney, and brain samples. Concentrations of other elements (arsenic, gold, cobalt, chromium, copper, iron, indium, antimony, selenium, titanium, and zinc) in each organ or tissue are also presented in this paper.
Effects of YM-14673, a new TRH analogue, on behavioral and electrophysiological changes in rats subjected to electrical lesion of the internal capsule.
The effects of YM-14673, a new thyrotropin-releasing hormone (TRH) derivative (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]- L-histidyl-L-prolinamide dihydrate), on the pyramidal motor system were studied in comparison with those of TRH in rats subjected to electrical destruction of the left internal capsule, a brain region of the pyramidal motor tract. In this model, neurological deficits such as hemiplegia and decrease of amplitude of electromyographic activity evoked by electrical stimulation of the left sensory motor cortex, were observed on the right legs. Drug administrations were started from 1 day after the surgical operation on and conducted once or several times a day for 13 days. YM-14673 (0.1 mg/kg, i.p., i.v., i.m.; 1 mg/kg, p.o.), unlike its metabolite (M-1) (10 mg/kg, i.p.), accelerated the recovery from neurological deficits. Decrease of evoked EMG activity on the 6th day after surgery was improved by administration of YM-14673 (0.1 mg/kg, i.p.). Intraperitoneal administration of TRH (1-10 mg/kg) once a day did not show any influence on neurological deficits. However, multiple i.p. administrations of TRH seven times in 1 hr accelerated recovery from deficits. These TRH activities are supported by metabolic studies which indicated that a high plasma level of TRH was maintained by multiple administrations of TRH. These results suggest that YM-14673 has a facilitatory effect on the pyramidal motor system which is due, in part, to its TRH-like properties.
Effects of YM-14673, a new TRH analogue, on neurological deficits in rats with experimental cerebral hematoma.
Effects of YM-14673, a new thyrotropin-releasing hormone (TRH) analogue, on neurological deficits were observed in comparison with those of TRH and citidine diphosphate choline (CDP-choline) in rats with an experimental hematoma. Unilateral cerebral hematoma was prepared by injection of 0.25 ml of autologous blood into the region around capsula interna, putamen and caudate nucleus of the left cerebral hemisphere of the rats. The drug was administered once or multiple times a day immediately after the surgical operation for 7 days and measurement of neurological deficits was conducted every day for 7 days. Neurological deficits, such as hemiplegia, were observed maximally on the 3rd day after the operation and then gradually recovered in the saline-treated group. YM-14673 (0.1, 0.3 mg/kg i.p.) accelerated the recovery of neurological deficits. Single i.p. administration of TRH did not affect the neurological deficits; however, multiple administration (7 times a day for 7 days) of TRH accelerated the recovery of neurological deficits. CDP-choline, a cerebral metabolic enhancer, even in a dose of 300 mg/kg (i.p.) did not show any influence on neurological deficits. These results suggest that YM-14673 ameliorated neurological deficits in the cerebral hematoma models, presumably due to TRH-like activity. Possible mechanisms of the pharmacological actions of YM-14673 are also discussed.
Anti-hypoxic and anti-ischemic actions of indeloxazine hydrochloride and its optical isomers: possible involvement of cerebral energy metabolism.
We evaluated the anti-hypoxic and anti-ischemic actions of indeloxazine hydrochloride ((+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054) in comparison with its optical isomers and several selective monoamine uptake inhibitors in mice. The effects of indeloxazine on both cerebral energy metabolism in normal mice and local cerebral glucose utilization in normal rats were also studied. Indeloxazine and its (-)-isomer, with both serotonin and norepinephrine uptake inhibitory actions, and its (+)-isomer, with a serotonin uptake inhibitory action, prolonged the survival time of mice subjected to nitrogen gas and the gasping duration in decapitated mice. Indeloxazine and its (+)-isomer were approximately 3-10 times more potent than the (-)-isomer with regard to their anti-hypoxic and anti-ischemic activities. Selective norepinephrine uptake inhibitors such as maprotiline and viloxazine, and selective serotonin uptake inhibitors such as citalopram, alaproclate and zimeldine, did not show anti-hypoxic properties. On the other hand, amantadine, a selective dopamine uptake inhibitor, and amitriptyline, a tricyclic antidepressant with anticholinergic properties, significantly shortened the survival time in hypoxic mice. In biochemical studies, increases in brain ATP and glucose levels without affecting lactate level in mice and an elevation in local cerebral glucose utilization in 10 brain regions involving the frontal cortex in rats were observed after administration of indeloxazine. These results suggest that indeloxazine and its optical isomers possess anti-hypoxic and anti-ischemic actions distinct from those of typical monoamine uptake inhibitors, and that these effects of indeloxazine may be due, at least in part, to a facilitation of cerebral energy metabolism.