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Biomedical subjects

H Ono

Publications and source records attributed to H Ono.

At least 577 records · Page 32Linked to original sources
PubMed1985

[Skull base metastasis of prostatic cancer presenting as exophthalmos--a case report].

A 72-year-old man was admitted to our hospital complaining of diplopia and right exophthalmos. Craniography and CT scan showed thickening of the right orbital roof and no intracranial lesion. Total acid phosphatase and prostatic acid phosphatase were high. Bone scintigraphy revealed high uptake at that lesion and the right pelvis. Unroofing of the right orbit and opening of the optic canal were performed in order to reduce intraorbital pressure. Microscopic examination revealed a metastatic lesion of prostatic cancer. Postoperatively, the patient was treated with "Honvan" and the course has been good.

Aged↗
PubMed1985

Partial purification of the receptor protein essential for import of pre-ornithine aminotransferase into mitochondria.

The isolated mitochondrial outer membrane fraction strongly inhibits the import of pre-ornithine aminotransferase, but other membranes such as rough microsomes did not. This inhibition seems to be caused by a receptor in the isolated outer membrane which binds competitively pre-ornithine aminotransferase. The mitochondrial outer membrane could be solubilized using detergent. And a receptor for pre-ornithine aminotransferase was partially purified by ammonium sulfate fractionation followed by column chromatography on Sephacryl S-300. Liposomes reconstituted from the partially purified receptor and lecithin could inhibit the import of pre-ornithine aminotransferase into mitochondria and bind the precursor.

Animals↗
PubMed1984

Cadmium-induced stimulation of lipogenesis from glucose in rat adipocytes.

Exposure of adipocytes of rats to CdCl2 caused acceleration of [3-3H]glucose incorporation into lipid maximally at 500 microM in Krebs-Ringer bicarbonate buffer, pH 7.4, containing 0.2% albumin. T.l.c. of the lipids extracted from adipocytes showed that Cd2+ increased labelling of di- and tri-[14C]acylglycerols predominantly. With increasing concentrations of glucose the apparent Km value was not affected by Cd2+, but the V value was increased, similarly to the effect of insulin. In the presence of insulin, Cd2+ (5 microM) exerted a consistent additive effect with a stimulatory effect of insulin on lipogenesis at all concentrations of insulin tested (5-50 mu units/ml). The stimulation was observed at a high concentration of glucose, suggesting that Cd2+ accelerated intracellular metabolism of glucose, mimicking insulin. However, although Zn2+ and Mn2+ stimulated the transport at a rate similar to that observed with insulin (200 mu units/ml), Cd2+ had no stimulating effect on the membrane transport of 3-O-methylglucose. The biological potency of Cd2+ and the insulin-like effects of Zn2+, both of which metals belong to the same group in the Periodic Table, are similar towards glucose metabolism, but quite different towards glucose transport.

3-O-Methylglucose↗
PubMed1984

Effect of methamphetamine on rat spinal cord. Dopamine receptor-mediated depression of monosynaptic reflex.

The experiments were performed on spinal rats transected at Cl. Intravenous administration of methamphetamine-HCl (MA-HCl, 2 mg/kg) and apomorphine-HCl (5 mg/kg) reduced the amplitude of the monosynaptic reflex (MSR), while the polysynaptic reflex was increased by methamphetamine. Depression of the monosynaptic reflex by both drugs was antagonized by haloperidol, but not by phentolamine. Depression of the monosynaptic reflex by methamphetamine was not antagonized by pretreatment with reserpine; however, the result was explained by the assumption that methamphetamine releases newly-synthesized dopamine or that methamphetamine may act directly on dopamine receptors. Depression of the monosynaptic reflex induced by methamphetamine was independent of peripheral changes in blood pressure. Oxygen tension in the spinal cord was slightly reduced by methamphetamine in rats treated with phentolamine and a change of pO2 in the spinal cord was ruled out as a possible mechanism of action. These results suggest that dopaminergic neurons in the spinal cord of the rat depress the transmission of monosynaptic spinal reflexes.

Animals↗
PubMed1984

Interaction between saccade and tracking vergence.

Additivity of saccade and tracking vergence was examined. Binocular eye movements were measured photoelectrically while subjects tracked a target moving smoothly on a radial line with an interpolated step change to a new radial line. Examining the abrupt portions of the two eyes' movements, we found the durations were almost the same for the two eyes, but that there were reliable differences in the magnitudes which were too large to be understood by an additivity hypothesis.

Adult↗
PubMed1984

LSD but not methysergide reduces the inhibitory effect of the medullary raphe stimulation on the spinal reflex in rats.

Conditioning stimulation of the nucleus raphe in the rat medulla enhanced the monosynaptic reflex (MSR) and depressed the polysynaptic reflex (PSR) in separate time courses. The PSR decreasing effect was reduced in preparations pretreated with reserpine, PCPA, or 5,6-DHT. The MSR increasing effect was not altered by these three pretreatments. Intravenously administered LSD but not methysergide reduced the PSR decreasing effect with no influence on the MSR increasing effect. These two drugs had similar effects on the unconditioned responses; the MSR was decreased and the PSR was increased. Thus, the PSR decreasing effect seems to be mediated via a serotonergic pathway probably descending from the nucleus raphe.

Animals↗
PubMed1984

Supraspinal tonic influence on spinal reflexes and involvement in the effect of chlorpromazine.

Chlorpromazine (CPZ) depressed mono-(MSR) and polysynaptic reflexes in anesthetized rats. The MSR remained unaltered after spinal transection (C1). After spinal transection, the inhibitory effect of CPZ on the MSR disappeared. After CPZ injection, spinal transection enhanced the MSR to pre-drug level. Reserpine pretreatment abolished the inhibitory effect of CPZ on the MSR. Phenoxybenzamine inhibited the MSR and, when pre-injected, markedly attenuated the effect of CPZ on the MSR. These results suggest that in anesthetized rats, CPZ blocks the alpha-adrenoceptor-mediated facilitatory component of the spontaneous tonic influence on the MSR.

Animals↗
PubMed1984

Exorcising the double-nail illusion: giving up the ghost.

The principles of visual direction explain the double-nail illusion, without the concept of a ghost image. Also, the stimulus arrangement for the illusion is not perceptually ambiguous for the visual system as Krol and van de Grind claim.

Convergence, Ocular↗
PubMed1984

Transport of the precursor for sulfite oxidase into intermembrane space of liver mitochondria: characterization of import and processing activities.

Sulfite oxidase, a soluble enzyme in mitochondrial intermembrane space, was synthesized as a precursor protein larger than the authentic mature enzyme when rat liver total RNA was translated in a cell-free system. When the in vitro translation products were incubated with isolated rat liver mitochondria, pre-sulfite oxidase was recovered in mitochondria and converted to the size of the mature enzyme. The in vitro-processed mature enzyme was recovered in the intermembrane space of mitochondria (Ono, H. & Ito, A. (1981) Biochem. Biophys. Res. Commun. 107, 258-264). Mature sulfite oxidase was not imported into mitochondria, and did not affect the import of pre-sulfite oxidase. When mitochondria were incubated with gel-filtered translation products, the import was dependent on ATP, and the activity restored by the addition of ATP was blocked by valinomycin and K+ ion. These results suggest that the import of pre-sulfite oxidase into mitochondrial intermembrane space requires an electrochemical potential across the inner membrane. When mitochondria were fractionated, most of the processing activity was recovered in the mitoplast, whereas the inner membrane (after being mostly inverted by sonication) exhibited only slight activity. The processing activity was strongly inhibited by some metal chelators including EDTA, GTP, and Zincon. It was not inhibited by phenyl methyl sulfonyl fluoride, aprotinin, or various microbial protease inhibitors including pepstatin, antipain, leupeptin, and chymostatin. The processing enzyme seems to be a metal protease. The processing of pre-sulfite oxidase by mitoplasts was energy-dependent.

Animals↗
PubMed1984

Transport of the precursor for sulfite oxidase into intermembrane space of liver mitochondria: binding of the precursor to outer mitochondrial membrane.

Rat liver mitochondria were incubated with in vitro translation products programmed by liver RNA, then disrupted by sonication and subjected to sucrose density gradient centrifugation. Pre-sulfite oxidase bound preferentially to the outer mitochondrial membrane recovered with the inner membrane. This outer membrane could not be separated from the inner membrane by recentrifugation, suggesting the tight association of both membranes. The binding was not affected by pretreatment of mitochondria with proteolytic enzymes. The mature enzyme and its precursor synthesized in isolated hepatocytes have isoelectric points of 4.2 and 5.5, respectively. The molecular size of the precursor in cytosol was estimated to be about 100,000 daltons (dimer) by gel filtration.

Animals↗
PubMed1984

Mechanisms of depressant action of muscle relaxants on spinal reflexes: participation of membrane stabilizing action.

The participation of local anesthetic action in spinal reflex inhibition produced by mephenesin-type muscle relaxants was examined by comparing the local anesthetic effects (in vitro), the depressant effects on muscle afferent discharges (in situ) and the depressant effects on spinal reflexes (in situ) of the drugs in rats. At doses producing depression of spinal reflexes, mephenesin, tolperisone (mephenesin-type) and lidocaine (local anesthetic) reduced the frequency of afferent discharges from the muscle. The order of reducing afferent discharges by these drugs corresponded to that of their conduction blocking activities in the isolated sciatic nerve of rats. These results suggest the participation of a membrane stabilizing action in spinal reflex inhibition produced by mephenesin-type muscle relaxants. Baclofen (non-mephenesin-type) did not show any local anesthetic action.

Action Potentials↗
PubMed1984

A study on the cardiodepressant action of a beta-blocking agent carteolol in heart-lung preparation of the dog.

Direct cardiodepressant activities of three beta-blockers, carteolol, pindolol and propranolol, were estimated using heart-lung preparation of the dog. Beta-blocking doses of these drugs to inhibit the positive chronotropic effect of isoproterenol by 50% were 2.2 micrograms for carteolol, 4.0 micrograms for pindolol and 21 micrograms for propranolol. Cardiac performance of the preparation was not influenced by up to 1 mg of these three beta-blockers. After 10 mg of these drugs, the cardiac function curves were shifted rightward and downward indicating the heart failure. It was doubtful, however, that this result indicated the cardiodepressant action of beta-blockers, for the preparation showed spontaneous deterioration without beta-blocker treatment. The influences of these beta-blockers on the compromised heart-lung preparations showed essentially similar results. In conclusion, direct cardiodepressant activity of the beta-blocker, if any, was exerted with far more large doses than their beta-blocking doses. The implication of the results in clinical use of beta-blockers, especially in relation to heart failure, was discussed.

Animals↗
PubMed1984

Mechanisms of slow contracture induced by potassium and caffeine in skeletal muscle of the dog.

Effects of diltiazem (3 micrograms-0.3 mg), verapamil (3 micrograms-0.3 mg), tetracaine (30 micrograms-3 mg), MnCl2 (0.1 mg-10 mg) and CaCl2 (0.1 mg-10 mg) on the skeletal muscle contracture induced by KCl and caffeine infusions were studied in the isolated, blood-perfused canine diaphragm preparation. All drugs were injected intra-arterially. Continuous intra-arterial infusion of KCl (50-100 mg/min) produced a biphasic contracture, which was characterized by a fast phasic contracture and a following tonic contracture. All drugs tested in this study except for CaCl2 produced a dose-dependent relaxation in the state of tonic contracture induced by KCl infusion. Dose-response curves for the relaxation of muscle to these drugs were all in parallel. Diltiazem and verapamil were equipotent and were about 10 and 30 times more potent than tetracaine and MnCl2 on a weight basis. Conversely, CaCl2 produced a contractile response in a dose-dependent manner. On the other hand, diltiazem, verapamil and CaCl2 had almost no effect on contracture induced by continuous intra-arterial infusion of caffeine (20 mg/min). MnCl2 produced a slight relaxation in the caffeine-contracture with much higher doses than those against potassium-contracture. However, tetracaine produced a dose-dependent relaxation of caffeine-contracture. Thus, the results suggest that the entry of external calcium plays an essential role in the potassium-induced tonic contracture and that the potassium- and caffeine-contractures were maintained by different mechanisms.

Animals↗
PubMed1984

Estimation of cardiodepressant potency of nadolol, alprenolol, propranolol and pindolol, beta-blocking agents, in heart-lung preparation and blood-perfused excised papillary muscle preparation of the dog.

Direct cardiodepressant potency of nadolol was determined by comparing its effect with those of alprenolol, propranolol and pindolol, in both heart-lung preparation and blood-perfused papillary muscle preparation of the dog. In the heart-lung preparation, mean 50% beta-blocking doses of the beta-blockers to inhibit the positive chronotropic action of isoproterenol were 3.75 micrograms for nadolol, 12.5 micrograms for alprenolol, 9.6 micrograms for propranolol and 1.6 micrograms for pindolol. Alprenolol and propranolol in a dose of 10 mg shifted the cardiac function curves rightward and downward, while nadolol and pindolol in the dose of 10 mg did not shift the cardiac function curves. In the blood-perfused papillary muscle preparation, mean 50% beta-blocking doses of the beta-blockers, administered i.v. to the donor dog, to inhibit the positive inotropic action of isoproterenol were 9.1 micrograms/kg for nadolol, 56.6 micrograms/kg for alprenolol, 68.3 micrograms/kg for propranolol and 8.1 micrograms/kg for pindolol. Nadolol did not depress the contractile force in doses up to 1 mg/kg given i.v. or doses up to 10 mg given intra-arterially (i.a.) close to the preparation. Alprenolol and propranolol exerted the dose-related negative inotropic effects, when larger doses (30-300 micrograms) were injected i.a. Thus, it is confirmed that nadolol virtually possesses no direct cardiodepressant activity and also that the depressant activity is exerted only by large doses of the other beta-blockers.

Adrenergic beta-Antagonists↗