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Biomedical subjects

K Onodera

Publications and source records attributed to K Onodera.

At least 343 records · Page 19Linked to original sources
PubMed1983

Lipid droplets containing DNA-histones released in the culture medium of transformed rat fibroblasts (HY1).

Lipid droplets appeared during the growing phase in the culture medium of incompletely transformed rat fibroblasts (HY1) induced by AccI-H fragments of adenovirus 12 DNA. These droplets consisted of neutral lipids, DNA, histones and RNA. Electron microscopic observations showed that the droplets had no lipid-bilayers on their surfaces which accounted for the tendency of the droplets to readily fuse together and become larger, and that the inner structures of the droplets looked like networks of fibrous matter. Experiments with DNA hybridization showed that the droplet DNA was composed of both cellular and adenoviral DNA, and that the cellular DNA in the droplets seemed to be derived from various cell DNA sequences. These results suggest that the droplets were derived from parts of the nuclear components of HY1 cells. The mechanisms for droplet release are discussed.

Adenoviridae↗
PubMed1983

[Clinical estimation of the relation between coronary artery disease and regional myocardial blood flow by continuous thermodilution with the multithermistor catheter].

To evaluate coronary hemodynamics more precisely in ischemic heart disease, great cardiac vein flow ( GCVF ) and coronary sinus flow (CSF) were simultaneously measured before and during atrial pacing by a continuous thermodilution technique with the multithermistor catheter in 10 patients with significant coronary stenosis (narrowing of the left anterior descending artery of 75% or more) (Group 1: CAD) and 12 cases with the normal coronary artery (narrowing of 25% or less) (Group 2: NonCAD ). GCVF reflects the anterior regional flow of the left ventricle and CSF reflects total left ventricular flow. Between the two groups, no significant differences were noticed in either resting GCVF or resting CSF. However, atrial pacing induced a reduction of coronary resistance (CR) and increasing regional myocardial blood flow in both groups in the same way, and the maximal pacing provoked anginal episode in CAD group in which both the percent decrease of coronary resistance (CR) (% delta CRant 25.3% and % delta CRt 23.3%) and the percent increase of regional myocardial blood flow (% delta GCVF 49.6% and % delta CSF 40.6%) were lower than those in NonCAD group (% delta CRant 42.3%, % delta CRt 37.6%, % delta GCVF 80.6%, and % delta CSF 68.3%, respectively). These data imply that resting coronary blood flow may be maintained as normal in patients with angiographically significant coronary stenosis, though coronary reserve probably decreased in these patients. In this respect, the continuous thermodilution technique using the multithermistor catheter may be useful for the clinical estimation of coronary hemodynamics induced by various interventions. This technique can be performed repeatedly for a short time and permits simultaneous assessment of venous blood flow draining from the anterior wall and of total left ventricular flow.

Cardiac Pacing, Artificial↗
PubMed1983

[The involvement of the cholinergic system in the tremor induced by phenol].

The effect of cholinergic drugs on the tremor induced by subcutaneous (s.c.) injection of a 1 v/v% phenol solution was investigated. Male dd-Y strain mice weighing 18-24 g were used in all experiments. Intraperitoneal (i.p.) administration of physostigmine (0.05-0.1 mg/kg) did not alter the tremor. Neostigmine (0.05-0.1 mg/kg i.p.) increased the strength of the tremor weakly and shortened the latency of the tremor. I.p. administrations of methacholine, atropine, methylatropine, and scopolamine did not produce significant effects on the tremor. I.p. injection of nicotine (0.5-1 mg/kg) shortened the duration of the tremor. Intracerebro-ventricular (i.c.v.) infusions of nicotine (4 micrograms/mouse) and carbachol (5 micrograms/mouse) prolonged the latency of the tremor. Furthermore, i.c.v. infusion of nicotine (4 micrograms/mouse) reduced the strength of the tremor slightly. On the contrary, i.p. (10-20 mg/kg) or i.c.v. (20-60 micrograms/mouse) administration of mecamylamine potentiated the strength and prolonged the duration of the tremor in a dose dependent manner. Hexamethonium (10-20 micrograms/mouse, i.c.v.) also potentiated the strength and prolonged the duration of the tremor. These results suggest that a peripheral increase of acetylcholine level may potentiate the tremor induced by phenol, and the tremor may be suppressed by a negative feedback mechanism involving the nicotinic cholinergic system of the central nervous system.

Animals↗
PubMed1982

On the quantal release of endogenous glutamate from the crayfish neuromuscular junction.

1. The abdominal slow flexor muscle was isolated from the crayfish (Cambarus clarkii) and placed in 150 microliters. Harreveld solution. The concentrations of glutamate and aspartate in this solution were measured by mass fragmentography. 2. Application of black widow spider venom (BWSV) produced a marked increase in the frequency of miniature excitatory post-synaptic potentials (m.e.p.s.p.s). During the high frequency discharge of m.e.p.s.p.s, the glutamate content in the solution was significantly increased. There was an approximately linear relationship between the increase in the glutamate efflux produced by BWSV and the variance of the membrane potential fluctuation during high frequency discharge of m.e.p.s.p.s. 3. In most cases, the efflux of aspartate during control rest periods was smaller than that of glutamate. During the discharge of m.e.p.s.p.s produced by BWSV, the increase in the aspartate efflux was very small compared to glutamate. 4. Nerve stimulation caused a significant increase in the efflux of glutamate, but the change in the aspartate efflux was very small and not significant. 5. Application of methylene blue increased the frequency of m.e.p.s.p.s and glutamate efflux, but little, if any, increase was found in aspartate efflux. 6. It is concluded that glutamate is preferentially released from nerve terminals in a quantal fashion.

Animals↗
PubMed1981

Release of glutamate from the crayfish neuromuscular junction.

1. The superficial abdominal flow flexor muscle was isolated from the crayfish (Cambarus clarkii) and placed in a bath solution of 100 microliters. The concentration of glutamate in this solution was measured by mass fragmentography using a gas chromatograph-mass spectrometer. 2. The excitatory post-synaptic potential (e.p.s.p.) of the slow flexor muscle and its sensitivity to L-glutamate were similar to those observed in the opener muscle of the dactyl in the walking leg or claw of the crayfish. 3. The background efflux of glutamate during control rest periods was about 20 p-mole/10 min. Nerve stimulation caused a significant increase in the efflux of glutamate. The net release of glutamate above the background was 11.9 p-mole/100 microliters. at 10 Hz stimulation and 21.1 p-mole/100 microliters. at 20 Hz stimulation. 4. When the amplitude of e.p.s.p. was decreased by streptomycin, thereby reducing the muscle contraction, the net release of glutamate by nerve stimulation was not changed. Streptomycin depressed the e.p.s.p. by its action on the post-synaptic membrane. 5. When the external concentration of Ca was lowered, the amplitude of e.p.s.p. and the net release of glutamate were decreased. 6. It is concluded that L-glutamate is released from the nerve terminals of the crayfish neuromuscular junction.

Animals↗
PubMed1980

Distribution and pharmacological properties of synaptic and extrasynaptic glutamate receptors on crayfish muscle.

1. The distribution of glutamate sensitivity was measured in the opener muscle in the walking legs of the crayfish (Cambarus clarkii). L-Glutamate was ionophoretically applied under visual control. 2. Bundles of a few muscle fibres were isolated and viewed with Nomarski optics. Two axons, presumably excitatory and inhibitory, branched widely over the surface of individual muscle fibres, forming numerous clusters of boutons or varicosities. 3. Glutamate sensitivity was measured from the slope of the dose-response curves obtained by ionophoretic application of L-glutamate and expressed as mV/nC. The highest sensitivities were about 100 mV/nC, obtained at the edge of synaptic boutons. The sensitivity declined to less than 5% about 2 micrometer away from the synaptic terminal. The time course of glutamate potentials was approximately the same as that of spontaneous synaptic potentials. 4. Glutamate depolarization started within 300 microsec after ionophoretic release of glutamate. This time lag was shorter than the synaptic delay of the nerve-evoked synaptic potential measured with an extracellular micro-electrode. This indicates that glutamate depolarization results from a direct action on the post-synaptic receptor. 5. Application of L-alpha-kainic acid decreased the amplitude of the glutamate potential produced at the synaptic region, whereas kainate increased the amplitude of the glutamate potential at the extrasynaptic region. It is suggested that the pharmacological properties of the extrasynaptic receptor differ from those of the synaptic receptor. Possible mechanisms for the different actions of kainate are discussed.

Animals↗
PubMed1980

[The effect of thiamine deficiency on the actions of drugs affecting the central nervous system in rats (author's transl)].

Male Wistar rats, 35-days-old, maintained on a thiamine deficient diet for 30 days showed marked growth inhibition and a heart rate less than 70% of that of control rats. We examined the effect of thiamine deficiency on the action of drugs effecting the central nervous system at this period. In thiamine deficient rats treated with chloral hydrate 200 mg/kg, ketamine 100 mg/kg sodium pentobarbital 50 mg/kg, and hexobarbital 100 mg/kg, the sleeping time increased. Pretreatment with 15 mg/kg of the metabolic enzymes inhibitor, SKF-525A, 30 min prior to the hexobarbital administration resulted in prolongation of sleeping time in all groups. The thiamine deficient rats slept almost 3.5 times longer than did the control group. Pretreatment with 100 mg/kg of the metabolic enzyme inducer, sodium phenobarbital, 48 hours prior to hexobarbital treatment resulted in decreased sleeping time in all groups, as compared with only hexobarbital treatment. In the thiamine deficient rats the catalepsy and ptosis induced by the i.p. administration of tetrabenazine 50 mg/kg was reduced even when the control and pair-fed groups responded to this drug at the drug peak time. The spontaneous neuronal activity of lateral hypothalamus was most sensitive to the administration of 5-hydroxytryptophan in thiamine deficient rats.

5-Hydroxytryptophan↗
PubMed1980

[Studies on the effects of thiamine deficiency on rat testes (author's transl)].

Using male rats fed a thiamine deficient diet from the age of 35-days, an investigation was made of the effects on testicular tissue after 30 days of thiamine deficiency. It was found that: 1) In the thiamine deficient group, the seminiferous tubuli of rats having erections had atrophied and there was a decrease in the number of primary spermatocytes and spermatogonium, but a moderate increase in the number of sertoli cells. Furthermore, spermatids and spermia were rarely seen in tubuli which contained multinuclear giant cells. In the group of rats not having erections, moderate interstitial edema was seen and there was notable degeneration and reduction in the number of primary spermatocytes and spermatogonium. 2) In the group injected with thiamine hydrochloride after 21 days of thiamine deficient feeding, moderate interstitial edema was seen and the seminiferous tubuli were atrophic. 3) In the pair-fed group, there was a marked edema of interstitial tissue and an atrophy of seminiferous tubulus. 4) With regard to the effects of thiamine deficiency on the polyamine contents of the testicles, there was a marked decrease in spermidine content on the 12th day of feeding and a marked increase of spermine content on the 30th day. The spermidine/spermine ratio, which is high during periods of active cell differentiation and proliferation, was found to be significantly decreased in the thiamine deficient animals on both the 12th and 30th days of thiamine deficiency. Thus, it was clarified that thiamine deficiency causes disturbances in cell differentiation and proliferation in rat testes.

Animals↗