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Biomedical subjects

T Ohashi

Publications and source records attributed to T Ohashi.

At least 397 records · Page 22Linked to original sources
PubMed1978

Brain tumors in owl monkeys inoculated with a human polyomavirus (JC virus).

Owl monkeys were inoculated intracerebrally, subcutaneously, and intravenously with JC, BK, or SV40 virus. Two of four adult owl monkeys inoculated with JC virus, a human polyomavirus, developed brain tumors at 16 and 25 months after inoculation, respectively. A grade 3 to grade 4 astrocytoma (resembling a human glioblastoma multiforme) was found in the left cerebral hemisphere and brainstem of one monkey. The second monkey developed a malignant tumor in the left cerebral hemisphere containing both glial and neuronal cell types. Impression smears prepared from unfixed tissue of this tumor showed cells that contained polyomavirus T antigen. Virion antigens were not detected. Tumor cells cultured in vitro also contained T antigen but were negative for virion antigen. Infectious virus was not isolated from extracts of this tumor.

Antibodies, Viral↗
PubMed1978

Comparative effectiveness of two extracerebral DOPA decarboxylase inhibitors in Parkinson disease.

In four patients with Parkinson disease, we compared carbidopa combined with levodopa (Sinemet) and benserazide combined with levodopa (Madopar). All of these patients had responded to treatment, first with levodopa and then with Sinemet; after 6 years two continued to show a good response, while two developed marked "on-off" phenomena. Clinically, Sinemet and Madopar were similar; however, DOPA levels were higher, but with a shorter half-life, on Madopar. The higher DOPA levels may have been offset by the shorter half-life, resulting in no clinical change. DOPA levels were lower and half-life was shorter in patients with on-off phenomena. These differences may be responsible in part for the on-off phenomena.

Aromatic Amino Acid Decarboxylase Inhibitors↗
PubMed1978

[Pharmacological studies on supersensitization. V. Augmentation of pressor response to catecholamine induced by N, N-dimethylethylenediamines (author's transl)].

Effects of N,N-dimethylethylenediamines on epinephrine-induced pressor response in pentobarbital-anesthetized rats were examined and 3 out of 12 compounds, i.e., tripelennamine, N,N-dibenzyl-N', N'-dimethylethylenediamine (I) and N1, N1-dibenzyl-N2, N2-dimethyl-1,2-propanediamine (II), were found to be more potent as potentiators to epinephrine. In pithed rats, tripelennamine, I, II and cocaine also augmented pressor response induced by epinephrine. In pentobarbital-anesthetized rats or in perfused hind paw of rats, the potentiation induced by cocaine and tripelennamine was more marked to norepinephrine than to epinephrine, but an inverse relation between norepinephrine and epinephrine was observed in the potentiation by I and II. In pentobarbital-anesthetized rats, tyramine-induced pressor responses were decreased or abolished by cocaine and tripelennamine, but these responses were increased by I and II. In pentobarbital-anesthetized rats, isoproterenol-, acetylcholine- and histamine-induced depressor responses were not influenced by cocaine, tripelennamine, I and II. Sensitivity of reserpinized rats to epinephrine was increased about eight times that seen in pentobarbital-anesthetized rats. In reserpinized rats, epinephrine-induced pressor responses were slightly increased by cocaine, tripelennamine and II, but these potentiations were not dose-dependent. These results indicate that one of the sites of action of cocaine, tripelennamine, I and II is localized in the peripheral portion of cardiovascular system. The principal mode of action of cocaine and tripelennamine appears to be the inhibition of amine-uptake mechanism at sympathetic nerve endings. The mode of action of I and II is apparently different from the actions of cocaine and tripelennamine.

Animals↗
PubMed1978

Enhancement of 5-hydroxytryptamine-induced contraction of the guinea pig ileum by a new sulfur compound, tripropylsulfonium bromide.

In the presence of tripropylsulfonium bromide (TPS) (1 X 10(-4) g/ml), a new compound, the phasic contraction of the isolated guinea pig ileum to 5-hydroxytryptamine (5-HT) (5 X 10(-7) g/ml) was consistently enhanced ("TPS effect"). TPS alone increased moderatley the spontaneous movement of the ileum. When the contraction height was calculated as the percentage of that to 5-HT alone, such was observed in the "TPS effect" to be 167.1 +/- 3.6% (mean +/- S.E., n = 80). TPS did not enhance the contraction due to acetylcholine or histamine. The "TPS effect" remained unaffected in the presence of dibenzyline (1 X 10(-7) g/ml), was abolished by morphine(1 X 10(-6) g/ml), tetrodotoxin (2 X 10(-8) g/ml) adenosine (3 X 10(-6) g/ml) and atropine (1 X 10(-7) g/ml) and was not observed under anoxic conditions. Eserine (1 X 10(-8) g/ml) strengthened the "TPS effect" markedly. It is concluded that this effect may be the result of the potentiating effect of TPS on the action of 5-HT through the M receptors, possibly by the facilitation of the acetylcholine-liberation from the nervous tissue.

Acetylcholine↗
PubMed1978

Effects of intraventricular and intraspinal 6-hydroxydopamine on blood pressure of renal hypertensive rats.

6-Hydroxydopamine (6-OH-DA) was administered into the lateral brain ventricle of normal rats and of rats with renal hypertension produced by unilateral clipping of the renal artery, and was also administered into the spinal cord of normal rats. Intraventricular administration of 6-OH-DA prevented the development of renal hypertension in rats, but was ineffective in developed renal hypertension. The development of renal hypertension was not affected by pretreatment with intraspinal injection of 6-OH-DA, which produced a marked reduction only in spinal cord noradrenaline. These data suggest that brain adrenergic neurones may participate in the production of renal hypertension but the noradrenergic projections in the spinal cords are not essential for this process.

Animals↗
PubMed1977

Adrenergic mechanism in cold stored taenia caecum after rewarming.

After cold storage of guinea-pig taenia strips for 4 days at 2 degrees C, structures with specific catecholamine fluorescence were not observed. Upon incubation in Krebs Ringer medium (37 degrees C) the fluorescence in the cold stored tissue reappeared and the density of fluorescence was comparable to that of fresh preparations. The specific fluorescence was affected following reserpine or 6-hydroxydopamine treatment; however, the rewarming process restored fluorescence only in the reserpine-treated tissue. The cold storage treatment (4 and 7 days) also decreased the tissue noradrenaline and dopamine contents and dopamine-beta-hydroxylase activity and inhibited the [3H-noradrenaline release from the tissue, all of which were not restored by the incubation procedure. Moreover, in these cold stored taenia the inhibitory effect to nicotine and perivascular nerve stimulation were not manifested. Therefore, the reappearance of specific fluorescence in the cold stored taenia strips after rewarming does not assure functional recovery of adrenergic nerve activity.

Animals↗
PubMed1977

The interactions of bromocriptine and lergotrile with dopamine and alpha-adrenergic receptors.

Bromocriptine and lergotrile, which are clinically used as antiparkinsonian (AP) agents, compete for the binding of H3-dopamine, H3-apomorphine, and H3-haloperidol to striatal membrane sites. Lergotrile has a higher affinity for the H3-dopamine binding to bovine striatal membranes than bromocriptine. Lergotrile and bromocriptine are almost equipotent in competing for the binding of H3-apomorphine to rat striatal membranes, but bromocriptine is more potent in competing for the binding of H3-haloperidol than lergotrile. These results indicate that lergotrile and bromocriptine are mixed putative agonist-antagonist with respect to the postsynaptic dopamine receptors. Lergotrile and bromocriptine at higher concentrations inhibit synaptosomal tyrosine hydroxylase activity, and reverse the apomorphine elicited enzyme inhibition. Thus, these ergot alkaloids behave as mixed agonist-antagonist also with respect to the presynaptic dopamine receptors. Bromocriptine and lergotrile, as well as other tested DH-ergot alkaloids and neuroleptics, compete for the binding of the alpha-antagonist H3-WB-4101 to rat cerebral cortical membranes. The displacing potencies of the tested DH-ergot alkaloids and of the neuroleptics indicate that they have a high affinity for the alpha-adrenoreceptors in the CNS.

Acetonitriles↗
PubMed1977

The electrical induction of callus formation and external skeletal fixation using methyl methacrylate for delayed union of open tibial fracture with segmental loss.

A case of delayed union of an open tibial fracture with segmental loss is presented in which electricity was applied to the bone defect through two screws that were connected to a methy methacrylate skeletal fixation device. The fracture developed electrically induced callus formation around the cathode, callus extended to the anode, and solid bony union ensued. External skeletal fixation using methyl methacrylate is convenient and is a suitable adjunct to electrical stimulation of fracture healing.

Adult↗
PubMed1977

Electret induced callus formation in the rat.

Wrapping the mid-femoral shaft of the rat with a Teflon film electret produced a bony callus in 9 out of 10 animals. This model of electret-induced callus formation should lend itself to the histo-biochemical study of electrically induced osteogenesis.

Animals↗