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Biomedical subjects

S Otsuki

Publications and source records attributed to S Otsuki.

At least 73 records · Page 4Linked to original sources
PubMed1990

[A case of malignant thymoma associated with Eaton-Lambert-type neuromuscular transmission block and sensorimotor neuropathy].

The patient is a 73-year-old male. In January 1988, he noticed sensory disturbance and muscular weakness of his extremities. His thymoma was found in July 1988, and in October 1988, he was admitted to our hospital for treatment. Neurological examination showed muscular weakness, muscular atrophy, fasciculation, and distal dominant sensory disturbance of his right upper extremity and his bilateral lower extremities. The immunological examination showed an increase in serum IgG, gamma-globulin, OKT3 and OKT4 lymphocytes. Electromyographic studies showed severe waxing by repeated stimulations (200% by 10 Hz; 330% by 20 Hz), very low M wave amplitude by single stimulation, and post-tetanic exhaustion. An Eaton-Lambert-type neuromuscular transmission block was thus thought to exist. Concentric needle electromyography showed a neurogenic pattern. The sensory and motor nerve conduction velocity was delayed. Microscopic examination of biopsied skeletal muscle showed neurogenic change. A sural nerve biopsy specimen showed a decrease in the number of myelinated fibers (fiber density 4333/mm2), segmental demyelination, remyelination, and mild axonal change. Thymectomy was performed and pathological examination showed invasive thymoma of predominantly the epithelial type. His muscular weakness and sensory disturbance improved gradually after thymectomy. On the postoperative immunological examination, serum IgG, gamma-globulin, OKT3 and OKT4 lymphocytes were normalized. On the other hand, OKT8 lymphocytes were increased and the OKT4 to OKT8 ratio was decreased. The electromyographic studies showed no waxing, normal M wave amplitude, and no post-tetanic exhaustion. Therefore, we consider that an Eaton-Lambert-type neuromuscular transmission block and sensorimotor neuropathy in this case were caused by the immunological abnormality accompanying malignant thymoma.

Aged↗
PubMed1989

Subchronic cocaine treatment enhances cocaine-induced dopamine efflux, studied by in vivo intracerebral dialysis.

Repeated administration of cocaine in animals results in behavioral sensitization. In order to investigate the neurochemical mechanism underlying such behavioral sensitization, we designed the following two experiments. In both experiments, rats were pretreated with cocaine (20 mg/kg i.p.) or saline, once daily for 14 consecutive days. Exp. 1: 7 days after withdrawal from the drug, the stereotyped behavioral response to a challenge of cocaine (20 mg/kg i.p.) was measured. Exp. 2: 7 days after withdrawal from the drug, we measured extracellular dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) after the challenge administration of cocaine using an in vivo intracerebral dialysis technique. The rats pretreated with cocaine (20 mg/kg i.p.) exhibited behavioral augmentation in response to a challenge of cocaine. The challenge administration of cocaine caused an increase in DA and a decrease in DOPAC. The DA level in the striatal perfusates of the cocaine-pretreated rats was significantly greater than that in the saline-pretreated rats. These results suggest that the increased extracellular DA concentration in the striatum plays an important role in the cocaine-induced behavioral sensitization.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Hippocampal kindling enhances excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the hippocampus and amygdala/pyriform cortex.

We recently demonstrated that a long-lasting increase in ibotenate-stimulated polyphosphoinositide (PPI) hydrolysis in the amygdala/pyriform cortex (AM/PC) is associated with seizure susceptibility of amygdala (AM)-kindled rats. The present study examined (1) whether ibotenate-stimulated PPI hydrolysis would be lastingly enhanced in the hippocampus (HIPP) and AM/PC of the HIPP-kindled rats and (2) whether similar changes would be found in the early stage of HIPP kindling. Although ibotenate-stimulated accumulation of [3H]inositol 1-phosphate ([ 3H]IP1) increased significantly in the HIPP 24 h, 5 days, and 15 days after the last seizure of fully developed HIPP-kindled rats, no statistically significant increase was found in the HIPP 30 days after the last seizure. In the AM/PC, 10(-3) M ibotenate-stimulated [3H]IP1 accumulation significantly increased by 91%, 91%, 86% and 90%, 24 h, 5 days, 15 days and 30 days after the last seizure, respectively. There was no significant increase in ibotenate-stimulated [3H]IP1 accumulation 7 days after the last stimulation in the HIPP and AM/PC of rats which had undergone electrical stimulation only 5 times in the HIPP. These results indicate that (1) PPI hydrolysis coupled to excitatory amino acid receptors increases long-lastingly in the AM/PC regardless of the primary kindled site, and (2) these changes do not occur in the early stage of HIPP-kindling.

Amygdala↗
PubMed1989

Lasting increase in excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the amygdala/pyriform cortex of amygdala-kindled rats.

We previously demonstrated that ibotenate-stimulated polyphosphoinositide hydrolysis, determined as the accumulation of [3H]inositol 1-phosphate, significantly increased in the amygdala/pyriform cortex (AM/PC) 24 h and 7 days after the last seizure in AM-kindled rats. The present study examined whether the increase in ibotenate-stimulated polyphosphoinositide hydrolysis in the AM/PC is longer lasting. AM-kindled rats with a tripolar electrode implanted into the left AM and sham-operated controls were decapitated either 1, 2 or 4 weeks after the last seizure. Ibotenate (10(-3) M)-stimulated accumulation of [3H]inositol 1-phosphate significantly increased by 90% (P less than 0.01), 110% (P less than 0.001) and 73% (P less than 0.05) in the AM/PC 1, 2 and 4 weeks, respectively, after the last seizure. Four weeks after the last seizure, there were significant increases of a similar magnitude in the contralateral (right) AM/PC (by 83%, P less than 0.001) and the ipsilateral (left) AM/PC (by 63%, P less than 0.01). There was no change in the hippocampus or limbic forebrain at any of these times. Also 4 weeks after the last seizure, accumulation of [3H]inositol 1-phosphate significantly (P less than 0.05) increased at ibotenate concentrations of 2 x 10(-4) M, 5 x 10(-4) M and 10(-3) M in the kindled AM/PC. In light of the view that the AM/PC are the crucial brain structures for sustaining seizure susceptibility, the marked and lasting increase in the ibotenate-stimulated polyphosphoinositide hydrolysis coupled to excitatory amino acid receptors in the kindled AM/PC may be associated with the development of kindling and long-term maintenance of kindled events.

Amygdala↗
PubMed1989

Subchronic methamphetamine treatment enhances methamphetamine- or cocaine-induced dopamine efflux in vivo.

Intracerebral dialysis was used to study the mechanism underlying behavioral sensitization. Rats were divided into two groups: a control group that received intraperitoneal injections of saline and an experimental group that was given methamphetamine (MAP) (4 mg/kg) once a day for 14 days. Seven days after the last injection, dopamine (DA) and its metabolites were measured in striatal dialysates obtained from awake freely moving rats. A challenge injection of MAP (4 mg/kg) caused a marked increase in the extracellular concentrations of DA, and the extent of the increase was significantly greater in MAP-pretreated rats than in the saline-pretreated controls. A challenge injection of cocaine (20 mg/kg) also caused a significantly greater increase in extracellular DA levels in MAP-pretreated rats than in saline-pretreated rats. These results suggest that an enhancement in striatal DA efflux may play an important role in MAP-induced behavioral sensitization and cross-sensitization to cocaine.

Animals↗
PubMed1989

Ceruletide suppresses endogenous dopamine release via vagal afferent system, studied by in vivo intracerebral dialysis.

Ceruletide, a cholecystokinin-related decapeptide, has been reported to have some therapeutic effects on tardive dyskinesia and other involuntary movement disorders. In order to clarify the effects of ceruletide on dopaminergic activity in the rat striatum, we measured the release of endogenous dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) after intraperitoneal administration of ceruletide (2, 20, 200 micrograms/kg) using in vivo intracerebral dialysis techniques. After administration of ceruletide (200 micrograms/kg), extracellular DA decreased significantly (P less than 0.05) for 0.5-3 h. The maximal reduction of extracellular DA (by 29%) was observed for 2-2.5 h. Extracellular DA was reduced (21%) by 20 but not by 2 micrograms/kg ceruletide. DOPAC and HVA did not change at any dose of ceruletide. We also demonstrated that bilateral subdiaphragmatic vagotomy blocked this inhibitory effect of ceruletide on DA release. These findings indicate that peripherally administered ceruletide suppresses endogenous DA release via the vagal afferent system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Reduction of rat striatal thyrotropin-releasing hormone receptors produced by repeated methamphetamine administration.

It has been reported previously that repeated, but not continuous, administration of methamphetamine (MAP) to animals produces progressive and sustained enhancement of MAP-induced behavior (behavioral sensitization), which may be related to functional changes in central dopamine (DA) systems. To investigate the possible involvement of thyrotropin-releasing hormone (TRH), a neuromodulator of DA, both immunoreactive TRH (IR-TRH) levels and specific TRH binding were examined in rat brain regions after MAP administration either repeatedly (4 mg/kg intraperitoneally once a day for 14 consecutive days) or continuously (about 4 mg/kg/day for 13 consecutive days). Although no significant changes were observed in IR-TRH levels in any regions of the brain following repeated MAP injections, specific TRH binding in the striatum significantly decreased. Scatchard analysis revealed that the decrease was due to a reduction in the maximum number of binding sites (Bmax). Pretreatment with haloperidol prior to each MAP injection prevented this decrease. Continuous MAP administration had no effect on regional specific TRH binding. These results suggest that repeated MAP administration caused lasting dysfunction in the brain TRH system, which may be implicated in the behavioral sensitization.

Animals↗
PubMed1989

Effects of selective D-1 and D-2 dopamine antagonists on development of methamphetamine-induced behavioral sensitization.

The present study examined effects of selective antagonists of D-1 and D-2 dopamine receptors on the development of behavioral sensitization produced by repeated methamphetamine (MAP) administration. Male Sprague-Dawley rats were divided into four groups. Each group received a daily injection of saline (control group), 4 mg/kg MAP (MAP group), 1 mg/kg YM-09151-2 plus 4 mg/kg MAP (YM + MAP group) or 0.5 mg/kg SCH 23390 plus 4 mg/kg MAP (SCH + MAP group) for 14 days. During daily injection for 14 days, the MAP group exhibited a progressive augmentation in locomotor and stereotyped behavior, whereas the progression of such behaviors in the YM + MAP and SCH + MAP group was completely prevented. After an abstinence period of 7 days, all groups received a challenge of 2 mg/kg MAP. The MAP challenge reproduced hyperlocomotion and intense stereotyped behavior only in the MAP group. However, neither the YM + MAP group nor the SCH + MAP group showed stereotypy. The manner in which both groups showed only hyperlocomotion was similar to that observed in the control group. These results indicate that both selective D-1 antagonists and selective D-2 antagonists not only reverse MAP-induced motor effects at each injection but also prevent the development of behavioral sensitization induced by repeated MAP administration.

Animals↗
PubMed1989

Effect of a noncompetitive antagonist (MK-801) of NMDA receptors on convulsions and brain amino acid level in E1 mice.

Anticonvulsant action of MK-801, a novel noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptor, was examined in genetically epileptic E1 mice. Systemic injection of MK-801 (0.1-1.0 mg/kg) potently suppressed generalized tonic-clonic convulsions of in a dose-dependent manner (ED50, 0.17 mg/kg). This anticonvulsant effect of MK-801 appeared at a dose which did not induce any obvious behavioral changes. Following the administration of a fully anticonvulsant dose of MK-801 (1 mg/kg), amino acid analysis revealed a significantly elevated level of glycine in the hippocampus. Levels of other amino acids including glutamate, aspartate, taurine, glutamine, alanine, and gamma-aminobutyrate were not changed either in the hippocampus or in the cerebral cortex. This study suggests that NMDA system may play an essential role in seizure-triggering mechanisms in E1 mouse.

Amino Acids↗
PubMed1989

Platelet 3H-clonidine and 3H-imipramine binding and plasma cortisol level in depression.

Platelet 3H-clonidine (alpha 2-adrenergic agonist) binding and 3H-imipramine binding were measured and the Dexamethasone Suppression Test performed in 17 normal controls and 14 unmedicated depressed patients in order to clarify the relationship among these three biological markers. Increases in the Bmax and the Kd for 3H-clonidine binding and decreases in the Bmax for 3H-imipramine binding of the platelets from depressed patients were observed when compared with controls. There was a significant positive correlation among 3H-clonidine Bmax, the basal (predexamethasone) plasma cortisol levels, and the severity of depression, as indicated by the Hamilton Depression Rating Scale. On the other hand, no significant correlation was observed in 3H-imipramine binding between the Bmax and the severity of depression or between the Bmax and the basal plasma cortisol levels. There was no statistically significant correlation between the Bmax of 3H-clonidine binding and that of 3H-imipramine binding in depression, but there was a trend toward correlation in normal controls.

Adult↗
PubMed1989

Clinical efficacy of carbamazepine in affective, schizoaffective, and schizophrenic disorders.

The therapeutic effects of carbamazepine (CBZ) were evaluated in 103 patients with affective disorders, 54 with schizophrenic disorders, and 26 with schizoaffective disorders by a multi-institutional open study. The rate of marked and moderate improvement was 72.8% in affective disorders, 54.6% in schizophrenic disorders, and 61.5% in schizoaffective disorders. Symptom items of the Clinical Psychopharmacology Research Group rating scale for mania showed significant improvement in the patients with affective disorders as well as in those of the other two groups. In the Brief Psychiatric Rating Scale as applied to patients with schizophrenic or schizoaffective disorders, symptom items related to affect and emotion showed significant improvement. The antimanic efficacy of CBZ was also noted in many poor responders to lithium. Side-effects were observed in 82 patients (44.8%), and abnormal laboratory findings in 37 patients (44.8%), and abnormal laboratory findings in 37 patients. The present study seems to confirm the usefulness of CBZ for the treatment of affective disorders and in some cases, of schizophrenic and schizoaffective disorders.

Adult↗
PubMed1989

A murine monoclonal antibody that recognizes an extracellular domain of the human c-erbB-2 protooncogene product.

A murine IgM monoclonal antibody, designated SV2-61, was generated against human c-erbB-2 gene-transfected NIH-3T3 (SV11) cells. SV2-61 defined a 185-kDa molecule present on the surface of SV11 cells, another line of c-erbB-2 gene-transfected NIH-3T3 (A4-15) cells, and MKN-7 human gastric cancer cell line carrying an amplified human c-erbB-2 gene. The SV2-61-defined antigen was found to show protein kinase activity in vitro. The SV2-61 was reactive with human c-erbB-2 gene-transfected NIH-3T3 cell lines but not with transfectants carrying c-erbB-2 gene mutants which lack a coding region for the extracellular domain. It was reactive with a portion of human epithelial cell lines but not with native NIH-3T3, TGF-alpha-coding gene-, activated c-raf gene- or Ha-ras gene-transfected NIH-3T3 cells, or non-epithelial human cells. These results indicate that the SV2-61 is an antibody which recognizes an extracellular domain of the c-erbB-2 gene product, 185-kDa protein.

Animals↗
PubMed1989

A double-blind study of adjunctive carbamazepine versus placebo on excited states of schizophrenic and schizoaffective disorders.

A multi-institutional double-blind study comparing the therapeutic effect of adjunctive carbamazepine and placebo with standard neuroleptic treatment was performed on 162 patients with DSM-III diagnosis of schizophrenic (n = 127) or schizoaffective disorders (n = 35) who had excited states or aggressive/violent behavior that responded unsatisfactorily to neuroleptic treatment. The patients participated in a 4-week trial of carbamazepine plus neuroleptics (n = 82) or placebo plus neuroleptics (n = 80). The sum of patients with marked and moderate improvement was modestly larger in the carbamazepine group (48 vs. 30%, P less than 0.05). There was no significant difference between the carbamazepine and placebo groups in the changes of total BPRS scores, although the carbamazepine group showed more improvement on the items suspiciousness, uncooperativeness and excitement. The results suggest that carbamazepine, when used in combination with neuroleptics, is a useful drug for the treatment of excited states of patients with schizophrenic and schizoaffective disorders.

Adolescent↗