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Biomedical subjects

K Onodera

Publications and source records attributed to K Onodera.

At least 217 records · Page 12Linked to original sources
PubMed1993

Proconvulsant effect of ketotifen, a histamine H1 antagonist, confirmed by the use of d-chlorpheniramine with monitoring electroencephalography.

Ketotifen produced seizures in a 5-year-old boy with secondary generalized epilepsy (SGE) and allergic rhinitis. To confirm that the seizures were due to histamine H1 receptors blockade, d-chlorpheniramine was administered with monitoring electroencephalography (EEG). Administration of d-chlorpheniramine significantly increased the number of epileptic discharges in the patient, compared with those before administration. Plasma noradrenaline and dopamine levels were not affected by treatment with d-chlorpheniramine. These findings indicate that histamine H1 receptors blockade produced convulsions and increased epileptic discharges on EEG. Recently, several experimental reports have shown that histamine has an inhibitory role on convulsions through histamine H1 receptors. Experimental findings and present results show that histamine H1 antagonists have proconvulsant effects, especially in the developmental period. Thus, it is recommended that centrally-acting histamine H1 antagonists should be avoided in epileptic patients, especially in children of pre-school age.

Child, Preschool↗
PubMed1993

Effect of alpha-fluoromethylhistidine on brain histamine and noradrenaline in muricidal rats.

Rats maintained on a thiamine-deficient diet for 30 days showed mouse-killing aggression (muricide). Once the muricide tendency appeared, it remained during the entire experimental period, even after subsequent administration of thiamine hydrochloride for 30 days. The effect of alpha-fluoromethylhistidine (FMH) on muricide in this animal model was examined, and histamine and noradrenaline levels in several brain regions were measured. One hour after i.p. injection of 200 mg/kg of FMH, muricide was completely abolished. Significant decrease in histamine levels was found in the hypothalamus, thalamus, amygdala, striatum and pituitary of muricidal rats. Thus, the central histaminergic neuron system may be involved in the suppressive mechanism of muricide. On the other hand, it is noteworthy that the noradrenaline level was significantly decreased only in the hypothalamus. In conclusion, it seems likely that the suppression of muricide induced by FMH was attributable to both inhibition of the histaminergic system and activation of the noradrenergic system.

Aggression↗
PubMed1993

MK-801 and dopaminergic system in electrically-induced convulsions in mice.

In this study, the effects of MK-801 and selective dopaminergic agents on electrically-induced convulsions in mice were examined. MK-801 (0.004-0.1 mg/kg, ip) showed significant and dose-dependent anticonvulsive effects, and the anticonvulsive effects of MK-801 (0.02 mg/kg, ip) were not antagonized by dopamine selective antagonists, SCH-23390 (D1, 0.1 mg/kg, sc), sulpiride (D2, 100 mg/kg, sc) and pimozide (D2, 0.5 mg/kg, sc). Apomorphine (0.02-0.5 mg/kg, sc), a D1/D2 agonist, showed proconvulsant effect on electrically-induced convulsions. Dopamine selective antagonists, SCH-23390 (0.02-0.5 mg/kg, sc), sulpiride (5-100 mg/kg, sc) and pimozide (0.1-2.5 mg/kg, ip), also showed proconvulsant effect. However, these effects of dopamine agonist and antagonists were not dose-dependent. These findings suggest that the dopaminergic system neither plays an inhibitory role, at least on electrically-induced convulsions in mice, nor contributes to the anticonvulsant effect of MK-801 in electrically-induced convulsions.

Animals↗
PubMed1993

Association of phenotypic abnormalities of Down syndrome with an imbalance of genes on chromosome 21.

The phenotype of the brain in Down syndrome is different from that of a normal child both in its reduced size and altered gyral configuration. Underlying the mental retardation are neuronal abnormalities, including alterations of cortical lamination, reduced dendritic ramifications, and diminished synaptic formation. However, cholinergic enzymes such as choline acetyl transferase and acetyl cholinesterase have shown no abnormalities in young children with Down syndrome. The pace of dendritic maturation is altered in Down syndrome. In infancy, the normal dendritic tree continuously expands; in Down syndrome, at 4 months of age, the neurons show a relatively expanded tree, but during the first year, the dendrites stop growing and become atrophic relative to control neurons. To relate these phenotypic alterations to chromosome 21, we examined the gene products of several genes localized to chromosome 21. Identification of such genes and determination of their gene product allow the production of specific antibodies and the identification, through immunohistochemical techniques, of the expression of these proteins in both normal development and Down syndrome. Specifically, the localization and appearance during development of proteins such as S100 beta, beta A4-amyloid, superoxide dismutase, and OK-2 are providing links between genotype and phenotype. S100 beta protein is of particular interest because of its effect in vitro on neuritic outgrowth and its increased expression in the temporal lobe in Down syndrome. The brains of transgenic mice bearing multiple copies of the human S100 gene show some comparable changes to those in Down syndrome. These experimental approaches provide the means for better understanding the cellular and molecular basis for the mental retardation in Down syndrome.

Age Factors↗
PubMed1993

Evaluation of LDL subfractions in vascular complications of familial hypercholesterolemia.

The authors attempted to investigate the possibility of estimating modified LDL (acetylated LDL, oxidative LDL and glucosylated LDL) with peroxidized lipid in the native LDL from patients with familial hypercholesterolemia (FH). A group of 7 patients with FH were studied, with age ranging from 18 to 60 years. 10 ml of fasting blood were collected into siliconized syringes with 0.5 ml of 0.05 M ethylene diamine tetraacetic acid 2Na. LDL, LDL1 and LDL2 were separated by sequential ultracentrifugation. Total cholesterol (TC), triglycerides (TG) and phospholipids (PL) were estimated by enzymatic methods. Analyses of lipids in each LDL were done by thin layer chromatography (TCL). The modified LDL in native LDL of the FH patients was estimated by the authors' own method. The cholesterol concentration of LDL was 0.49 +/- 0.28 mmol/L in FH patients and 0.07 +/- 0.04 mmol/L in the healthy persons (P < 0.001). The LDL1 cholesterol concentrations in the patients with FH and the normal controls were similar while that of the LDL2 was of significant difference (P < 0.05). On the TLC plate, the detection of the spot X1 was considered an indicator of the existence of modified LDL. The percentages of spot X1 in LDL of FH patients were higher in all 3 fractions (LDL, LDL1, and LDL2), as compared to the corresponding percentages of spot X1 in the healthy controls. (P < 0.001). Using the authors' own method, the molecular size were found in the order of LDL > LDL1 > LDL2.

Adolescent↗
PubMed1993

[A case of Behçet's disease associated with aortic regurgitation].

A 42-year-old woman was admitted to our hospital because of anterior chest discomfort on exercise. She had already been diagnosed as having a complete form of Behçet's disease. On auscultation, there was a grade 2/6 diastolic regurgitant murmur along the left sternal border. Echocardiogram and pulse doppler led to the diagnosis of aortic regurgitation and mitral fluttering in diastole. Left ventriculography disclosed an enlarged left ventricular chamber, but the ejection fraction was 60% within the normal range. Aortography confirmed the diagnosis of aortic regurgitation (III.) and dilatation of the ascending aorta. The coronary arteriogram was normal. An endomyocardial biopsy of the right ventricular wall revealed mild hypertrophy of the myocardial fibers and interstitial edema. In this report, we discussed a case of Behçet's disease with reference to 28 cases reported in the medical literature in Japan.

Adult↗
PubMed1993

[Coronary vasodilation during intracoronary injection of papaverine and acetylcholine in syndrome X: evaluation by coronary arteriograms and coronary venous oxygen saturation dynamics].

To evaluate coronary vasodilatory reserve in syndrome X, left coronary arteriography and continuous measurement of coronary venous oxygen saturation (CSO2-Sat) were performed during intracoronary injection of papaverine (PAP) and acetylcholine (ACh) in 11 patients of syndrome X and 13 control subjects. Coronary diameter after PAP increased 10.2% in the control group and 9.8% in the syndrome X group, but after ACh decreased 1.7% in the control group and decreased 2.3% in the syndrome X group. These changes in coronary diameter by PAP and ACh in the two groups were not significantly different. However, coronary vasodilatory responses estimated by CSO2-Sat dynamics to ACh and to ACh/PAP were significantly lower in the syndrome X group than those in the control group (p < 0.05), although coronary response to PAP in the 2 groups was not significantly different. These findings suggest that endothelial-dependent vasodilation of coronary microcirculation is decreased in syndrome X.

Acetylcholine↗
PubMed1992

Opioid mu-deficient CXBK mouse and the role of mu 1-receptors in electrically induced convulsions.

Studies were made on the role of mu 1-receptors on electrically induced convulsions in mice. A relatively selective mu 1-agonist, DAGO ([D-Ala2-N-methyl-Phe4-Gly-ol]-enkephalin) decreased the durations of tonic and clonic convulsions in C57BL/6 mice, but not in opioid mu-deficient CXBK mice, indicating that the activation of mu 1-receptors had an anticonvulsive effect on these convulsions in mice. The selective mu 1-antagonists naloxonazine and naltrexonazine promoted the clonic phase of electrically induced convulsion in C57BL/6 mice. Moreover, the duration of the clonic phase was longer in mu-deficient CXBK mice than in C57BL/6 mice. These data for CXBK mice confirmed, at least some proconvulsant effects of mu 1-antagonists in C57BL/6 mice. Thus, blockade of mu 1-receptors has a proconvulsant effect, and mu 1-receptors have at least some protective role against electrically induced convulsions.

Animals↗
PubMed1992

Lethal midline granuloma (peripheral T-cell lymphoma) after lymphomatoid papulosis.

A Japanese woman with an 8-year history of lymphomatoid papulosis (LP) had lethal midline granuloma (LMG) develop at the age of 51 years. There were histologic similarities between LP and LMG seen in this patient. Surface phenotypic studies on nasal and cutaneous lesions demonstrated a population of T-cells expressing CD2, CD4, CD25, CD30, and histocompatibility antigen-DR (HLA-DR). Genotypic analyses of nasal and skin biopsy specimens disclosed a clonal rearrangement of the beta T-cell receptor gene with the same rearrangement pattern. These data indicate that this patient had LMG characterized by clonal peripheral T-cell lymphoma, which probably resulted from progression of the LP.

Adult↗
PubMed1992

Histamine levels and clonic convulsions of electrically-induced seizure in mice: the effects of alpha-fluoromethylhistidine and metoprine.

The purpose of this study was to investigate the possible role of the central histaminergic neuron system in electrically-induced seizure in mice. For this purpose, we examined the effects of intraperitoneal (i.p.) injections of histaminergic agents, such as L-histidine, metoprine, and alpha-fluoromethylhistidine (FMH), on electrically-induced seizure. L-Histidine decreased the duration of clonic convulsion in electrically-induced seizure, but not affected that of tonic convulsion. This effect of L-histidine was antagonized by pretreatment with FMH, indicating that it was due to histamine formed by decarboxylation of L-histidine in the central nervous system. The anticonvulsive effect of L-histidine was also reduced by the H1-antagonist pyrilamine, but not by the H2-antagonist zolantidine, indicating that the effect on electrically-induced seizure is mediated through central H1-receptors. Metoprine, which increased the histamine levels in the cerebral cortex, diencephalon and midbrain of mice, decreased the duration of clonic convulsions dose-dependently. Conversely, FMH, which decreased the brain histamine levels, increased the duration of clonic convulsions. Good inverse correlations were found between the duration of clonic convulsions and brain histamine levels, especially in the diencephalon: the histamine levels were inversely proportional to the duration of clonic convulsions. No correlation was found between the duration of tonic convulsions and brain histamine levels. These results suggest that the histaminergic neuron system is important in inhibition of the duration of clonic convulsion on electrically induced seizure in mice.

Animals↗
PubMed1992

Chemically defined medium for the production of biologically active substances of CHO cells.

A recombinant CHO cell line (GT19) secreting a high level of human growth hormone (hGH) was constructed with amplification of the introduced hGH gene. The cells grew well in the alpha MEM medium supplemented with 5% dialyzed fetal calf serum (dFCS), but not with less than 1% dFCS. Therefore we examined various medium components and obtained an improved medium which supported cell growth at low serum concentrations. The production of hGH by the cells was also enhanced in this medium.

Animals↗
PubMed1992

Effects of (S)-alpha -fluoromethylhistidine and metoprine on locomotor activity and brain histamine content in mice.

We examined the effects of (S)-alpha -fluoromethylhistidine (FMH), an inhibitor of histidine decarboxylase, and metoprine, an inhibitor of histamine N-methyltransferase, on the locomotor activity and the brain histamine content of ICR mice. The brain histamine content was decreased by FMH (12.5 or 50 mg/kg, i.p.) and increased by metoprine (4 mg/kg, i.p.). Under these conditions, the locomotor activity and the number of rearing were significantly decreased and increased by FMH and metoprine, respectively. The higher the brain histamine content, the greater the locomotor activity and vice versa. In a previous paper [Sakai et al., Life Sciences, 48, 2397-2404 (1991)], we showed that thioperamide, a histamine H3 antagonist, which enhances the release of histamine from histaminergic neurons, in doses of 12.5 and 25 mg/kg, i.p. increases the locomotor activity, whereas it decreases the brain histamine content. Taken together, these results support the hypothesis that central histaminergic neurons may be involved in the control of state of locomotion and rearing.

Animals↗
PubMed1992

Crystallization and preliminary X-ray studies of a Bacillus subtilis and Thermus thermophilus HB8 chimeric 3-isopropylmalate dehydrogenase and thermostable mutants of it.

A new type of chimeric 3-isopropylmalate dehydrogenase (2T2M6T) was produced by expressing the fused gene of Bacillus subtilis and Thermus thermophilus. The enzyme shows heat stability intermediate between those of the parents. The crystal of the enzyme belongs to the space group of P3(2)21, with cell dimensions of a = b = 78.9 A and c = 158.9 A. Two thermostable mutants of the chimeric enzyme were prepared by site-directed mutagenesis and then crystallized.

3-Isopropylmalate Dehydrogenase↗
PubMed1992

Induction of DNA synthesis by fibroblast growth factor in temperature-sensitive cell-cycle mutants of rat 3Y1 fibroblasts arrested at restrictive temperature.

Four temperature-sensitive cell-cycle mutants of rat 3Y1 clonal fibroblasts representing separate complementation groups (3Y1tsD123, 3Y1tsF121, 3Y1tsG125 and 3Y1tsH203) are arrested at restrictive temperature, primarily with a G1-phase DNA content (temperature arrest). We examined various factors affecting signal transduction for activity which induces DNA synthesis at the restrictive temperature when added to the temperature-arrested cultures of these mutants. The factors examined were theophylline, dibutyryl cyclic AMP, cholera toxin (CT), dibutyryl cyclic GMP, sodium nitroprusside, phorbol 12-myristate 13-acetate, 1-oleoyl 2-acetylglycerol, bombesin, vasopressin, basic fibroblast growth factor (FGF), platelet-derived growth factor, A23187, monensin, epidermal growth factor (EGF), insulin and fetal calf serum (FCS). None of these factors induced DNA synthesis in 3Y1tsH203. In one mutant (3Y1ts121), FGF, EGF and FCS individually induced DNA synthesis. In the other 2 mutants (3Y1tsD123 and 3Y1tsG125), FGF and CT individually induced DNA synthesis. The FGF-induced DNA synthesis was suppressed by islet-activating protein (IAP) in 3Y1tsD123 and 3Y1tsG125, but not in 3Y1tsF121. The CT-induced DNA synthesis was also suppressed by IAP, as previously shown. When temperature-arrested cultures were shifted to a permissive temperature, all 4 mutants initiated DNA synthesis in the presence of IAP. These results suggest that (1) a cell can prepare for the initiation of DNA synthesis by using several independent signal transduction pathways, and (2) in a given situation, the cell uses a particular pathway because of its availability, which depends on the culture conditions.

Animals↗
PubMed1992

[Abnormal behavior induced by thiamine deficiency in rats: muricide and its behavioral and pharmacological characteristics].

When rats were maintained on a thiamine-deficient diet for 30 days, about 70% of the animals showed a mouse-killing response (muricide). The thiamine-deficient killer-rats do not eat but merely killed the mice. Once this abnormal behavior appeared, the response remained, and could not be suppressed by the administration of thiamine hydrochloride plus thiamine-supplemented diet, regardless of a return to normal feeding, growth and heart rate. Drugs that activate the central serotonergic and noradrenergic systems have suppressive effects on it. Conversely, among the various depletions of brain monoamines, only depletion of serotonin by the drug p-chlorophenylalanine significantly increased the incidence of muricide. Antihistaminergic drugs were potently effective, but atropine, an anticholinergic drug, were ineffective. Various antidepressants and electroconvulsive shock treatment also suppressed muricide to various degrees. Thus, it is expected that the muricide induced by thiamine deficiency may be useful as an animal model of depression, although the usefulness of this abnormal behavior as a working model of depression or for screening new antidepressants remains to be evaluated.

Aggression↗
PubMed1992

The use of bovine anti-PMSG serum in beef cattle after PMSG-superovulation.

Thirteen beef cows were superovulated using 4,000 i.u. of pregnant mare serum gonadotrophin (PMSG) on days 9 to 14 of the estrous cycle, followed by two injections of 500 micrograms prostaglandin F2 alpha analogue (PGF2 alpha) 48 and 55 hrs later. Seven of them were injected intramuscularly with bovine anti-PMSG serum 12 hrs after the first signs of estrus. The remaining 6 cows were served as controls and received no antiserum. Peripheral blood concentrations of progesterone (P) and estradiol-17 beta (E2) were compared in relation to the superovulatory responses. The injection of anti-PMSG serum did not significantly affect the numbers of the corpora lutea (CL), the anovulatory follicles and the transferable embryos at 7 to 8 days after superovulatory estrus, but increased the ratio of embryos classified as excellent or good quality. Although the plasma P concentration showed no significant differences between the anti-PMSG-treated and control cows, the plasma E2 concentration displayed a characteristic difference, suppressing the second E2 peak in the anti-PMSG-treated cows. It is concluded that the use of bovine anti-PMSG serum for PMSG/PGF2 alpha-treated cows at 12 hrs after the beginning of the estrus improves the quality of embryos recovered, probably due to inhibition of high estrogenic environment following ovulation.

Animals↗