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Biomedical subjects

A Sugimoto

Publications and source records attributed to A Sugimoto.

At least 91 records · Page 5Linked to original sources
PubMed1990

Cutaneous reactions caused by experimental exposure to jellyfish, Carybdea rastonii.

Dermatitis caused by contact with tentacles of jellyfish was studied on 25 volunteers. Two tentacles cut from a living jellyfish, Carybdea rastonii, were applied on each of the forearms and skin reactions were observed. All volunteers complained of severe pain, which lasted from 10 min to 8 hrs. Erythema and wheal appeared within 3 to 4 min and enlarged for 15 to 20 min. Erythema subsided within 24 hrs to 3 days in all but two individuals. Seven to 13 days after the application, linear erythema and papulo-vesicular lesions with pruritus were observed on the forearms of 15 out of 25 volunteers tested. These flare-up lesions lasted for one week leaving slight pigmentation. Histological findings from the flare-up lesions corresponded to those of allergic contact dermatitis. The lymphocyte response to the jellyfish venom in the subjects who had recurring lesions was greater than that in either the subjects with no recurring lesions or the control group, who was never exposed to jellyfish.

Adult↗
PubMed1989

[Synthetic studies of substituted quinazolinone].

We re-examined 2-methyl-3-(2-chlorophenyl)-6-ethoxycarbonyl-5,7-dimethyl-4 (3H)-quinazolinone to be hydroxymethylated by means of selenium oxide oxidation, followed by Ca (BH4)2 reduction. Chlorination reaction of 2-hydroxymethyl quinazolinone proceeded effectively by use of PCl5 in anhyd. benzene at room temperature. Thus, we prepared new compounds in respect of substituted quinazolinone.

Quinazolines↗
PubMed1988

Damage of hippocampal neurons caused by cobalt focus in the cerebral cortex of rats.

The relationship between the focus of cobalt seizures in the cerebral cortex and neuron loss in the hippocampus, as well as the CD50 of pentylenetetrazol was examined in rats. Spike activity in EEG frequently appeared 4 days after cobalt application and reached a peak 8-16 days after cobalt application, which was sometimes accompanied by jerks in the limbs. Changes in the CD50 value showed a two-step pattern, i.e., the first decrease in CD50 appeared one day after application of cobalt and continued at the same value until the fourth day. Then a second gradual decrease of CD50 was observed from the fourth day to eighth day and continued at the same value until 20 days after cobalt application. Neuron loss in the CA1 area of the hippocampus was observed as early as two days after cobalt application and the degree of neuron loss progressively increased until the 20th day. These findings suggest that neuron loss in the hippocampus following cobalt-induced seizures is not a result of generalized convulsions.

Animals↗
PubMed1987

Characteristics of primary cultured neurons from embryonic mutant El mouse cerebral cortex.

To elucidate the differences between neurons of epileptogenic animals and those of normal animals, cellular characteristics of neurons of mutant strain El mice which are highly susceptible to seizures were investigated using immunocytochemical techniques. In neurons of 3-day primary cultures, the control ddY mouse neurons showed dividing stages in about 0.2% of neurofilament (NF)-positive neurons, whereas no dividing neurons were observed among the NF-positive El mouse neurons. In 7-day cultures, localization of GD3 ganglioside in the proliferating control ddY mouse neurons was observed, but there was no GD3 ganglioside in the mutant El mouse neuron. The content of GD3 ganglioside detected by high-performance thin-layer chromatography of El mouse cultured cells was ca. 1/4 of that of ddy mice. These findings suggest that neurons of the El mouse are differentiated earlier than those of the control ddY mouse.

Animals↗
PubMed1987

Function of the 30 kd protein of tobacco mosaic virus: involvement in cell-to-cell movement and dispensability for replication.

We have investigated the function of the 30 kd protein of tobacco mosaic virus (TMV) by a reverse genetics approach. First, a point mutation of TMV Ls1 (a temperature-sensitive mutant defective in cell-to-cell movement), that causes an amino acid substitution in the 30 kd protein, was introduced into the parent strain, TMV L. The generated mutant showed the same phenotype as TMV Ls1, and therefore the one-base substitution in the 30 kd protein gene adequately explains the defectiveness of TMV Ls1. Next, four kinds of frame-shift mutants were constructed, whose mutations are located at three different positions of the 30 kd protein gene. All the frame-shift mutants were replication-competent in protoplasts but none showed infectivity on tobacco plants. From these observations the 30 kd protein was confirmed to be involved in cell-to-cell movement. To clarify that the 30 kd protein is not necessary for replication, two kinds of deletion mutants were constructed; one lacking most of the 30 kd protein gene and the other lacking both the 30 kd and coat protein genes. Both mutants replicated in protoplasts and the former still produced the subgenomic mRNA for the coat protein. These results clearly showed that the 30 kd protein, as well as the coat protein, is dispensable for replication and that no cis-acting element for replication is located in their coding sequences. It is also suggested that the signal for coat protein mRNA synthesis may be located within about 100 nucleotides upstream of the initiation codon of the coat protein gene.

Journal Article↗
PubMed1987

Antinociceptive activity induced by tizanidine and alpha 2-adrenoreceptors.

Tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole] is able to increase the pain threshold in the tail-flick test in mice. The effect of tizanidine was investigated after treatment of mice with drugs influencing central monoaminergic and GABAergic mechanisms. A drug that inhibits the synthesis and storage of monoamines and drugs that cause specific lesions of monoaminergic neurons had no consistent effect on the antinociceptive action of tizanidine. The action of tizanidine was antagonized by the alpha 2-adrenoreceptor antagonist, yohimbine, but not by the alpha 1 antagonist prazosin, nor by dopamine, serotonin and GABA receptor antagonists. These results indicate that the antinociceptive action induced by tizanidine may be mediated by alpha 2-adrenoreceptors.

Analgesics↗
PubMed1986

Effect of chronic haloperidol on dopamine release following microinjection of GABA into the substantia nigra zona reticulata in the rat.

To investigate the influence of the striatonigral gamma-aminobutyric acid (GABA) system on the nigrostriatal dopamine (DA) system, the release of DA and/or 3,4-dihydroxyphenylacetic acid in the striatum ipsilateral to the injection side was examined by in vivo voltammetry following microinjection of GABA into the substantia nigra zona reticulata (SNR). The microinjection of GABA (100-300 micrograms/2 microliters) into the SNR produced a dose-dependent increase in the electrochemical signals recorded from the caudate nucleus ipsilateral to the injection side. Following chronic treatment with haloperidol, microinjection of GABA into the SNR produced only a slight (non-significant) increase in the electrochemical signals recorded from the caudate nucleus ipsilateral to the injection side. These results provide additional evidence to support the concept that DA cells in the substantia nigra zona compacta are regulated by the SNR non-DA neurons in an inhibitory manner. It appears, furthermore, that chronic treatment with haloperidol reduces the release of DA in the striatum ipsilateral to the injection side and that this effect may be due to a gradual development of depolarization block of DA cells by chronic administration of haloperidol.

Animals↗
PubMed1986

Comparison of alpha-adrenoceptor involvement in the antinociceptive action of tizanidine and clonidine in the mouse.

The effect of drugs that influence the opioidergic and monoaminergic neuronal systems on the antinociceptive action of tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1, 3-benzothiodiazole] was compared with their effect on the action of clonidine. The potency of the clonidine-induced antinociceptive action was 1.83 and 7.75 times greater than that of tizanidine in the tail-flick and acetic acid-induced writhing tests, respectively. The action of tizanidine and clonidine was completely antagonized by pretreatment with yohimbine, an alpha 2-adrenoceptor blocker, but not by prazosin, an alpha 1-adrenoceptor blocker. Other alpha-adrenoceptor blockers, phenoxybenzamine and phentolamine, also attenuated the action of tizanidine and clonidine but the potency of these drugs was less than that of yohimbine. An opioid antagonist (naloxone), drugs influencing the serotonergic neuronal system (p-chlorophenylalanine, 5,6-dihydroxytryptamine, cyproheptadine), and drugs influencing the catecholaminergic system (alpha-methyl-p-tyrosine, diethyl-dithiocarbamate, 6-hydroxydopamine, haloperidol) showed no effect on the action of tizanidine and clonidine. From these results, it appears that alpha 2-adrenoceptors might be of importance in mediating the tizanidine and clonidine antinociceptive action in the tail-flick test.

Acetates↗
PubMed1986

Comparison of tizanidine and morphine with regard to tolerance-developing ability to antinociceptive action.

The antinociceptive, tolerance-developing and anti-withdrawal activities of tizanidine [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzo-thiadiazole] were investigated by comparing its effects with those of morphine and clonidine in tail-flick-, hot plate-, acetic acid-induced writhing-, and naloxone-precipitated withdrawal jumping-tests. The antinociceptive action of tizanidine was not altered by naloxone, while that of morphine was antagonized. Tolerance to the tizanidine-induced antinociceptive action and to motor incoordination was developed by successive administration of tizanidine. In the tizanidine-tolerant mice, the antinociceptive action of morphine was significantly decreased, but not sleeping time induced by pentobarbital. The action of tizanidine was not modified in the morphine-tolerant mice. Tizanidine failed to induce morphine-withdrawal jumping and to inhibit naloxone-precipitated withdrawal jumping in the morphine-dependent mice. Cross tolerance to the antinociceptive action induced by tizanidine and clonidine was developed. These results suggest that alpha 2-adrenoreceptors may be involved in the action mechanism of tizanidine, but not opioid receptors. Functional tolerance to tizanidine action may be developed by successive administration of tizanidine.

Analgesics↗
PubMed1986

In vivo voltammetric study of dopamine release in the striatum following microinjection of apomorphine into the substantia nigra zona reticulata.

Effect of microinjection of apomorphine into the substantia nigra zona reticulata (SNR) on the dopamine (DA) release in the ipsilateral striatum was examined in the present study. To measure the DA release, we determined DA and/or DOPAC levels in the striatum by using in vivo voltammetry. The microinjection of apomorphine (10 micrograms/2 microliters) into the SNR produced a rapid and prolonged increase in the DA and/or DOPAC peak in the ipsilateral striatum. These results suggest that release of DA from dendrites of DA cells normally plays a physiological role in the SNR neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Antinociceptive action of tizanidine in mice and rats.

The antinociceptive action of tizanidine [5-chloro-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole], a centrally acting muscle relaxant, was evaluated after subcutaneous or peroral administration in mice and rats. Tizanidine strongly inhibited the writhing response induced by acetic acid, phenyl-p-benzoquinone and acetylcholine in mice, and its potency was found to be greater than that of morphine. Tizanidine showed antinociceptive action like morphine not only in tail pressure and electrical stimulation tests in mice but also in tail-flick tests in mice and rats. The antinociceptive action of tizanidine was unaffected by pretreatment with naloxone. These findings suggest that tizanidine develops relatively strong antinociceptive action by a nonopioid mechanism.

Analgesics↗
PubMed1985

Non-Hodgkin's lymphomas in Osaka, Japan.

Six hundred and eight-four cases with non-Hodgkin's lymphomas (NHL) in Osaka, Japan were reviewed, using current histopathological classification to obtain a general feature of Japanese lymphomas. There were no remarkable differences in the distribution of age, sex and the location of primary tumors between Japanese NHL and the disease in Western races. Histologically, however, several differences were present; in particular, the lower frequencies of nodular lymphomas of nodal origin and lymphocytic type of nodal and extranodal origin in the present cases. About 10% of the cases show a peculiar histology characteristic for adult T cell lymphomas. From this study, it appears that the ratio of low-grade malignant NHL in Japan is much lower than in the Western countries.

Adolescent↗
PubMed1984

A great Brunner's gland adenoma of the duodenal bulb.

The occurrence of Brunner's gland adenoma in the duodenum is infrequent. The authors report a case of great Brunner's gland adenoma of the duodenal bulb, which is of interest because of its great size (8.5 X 4.5 cm) and the negative result of the endoscopic biopsy. Endoscopy has improved the diagnosis of the duodenal tumors; however, traditional endoscopic pinching biopsy does not always make a histological diagnosis. In our case, the endoscopic biopsy was negative because the tumor was located completely in the submucosa and the biopsy forceps was unable to reach to the tumor tissue.

Adenoma↗
PubMed1984

7-(Ethoxycarbonyl)-6,8-dimethyl-2-phenyl-1(2H)-phthalazinone derivatives: synthesis and inhibitory effects on platelet aggregation.

7-(Ethoxycarbonyl)-6,8-dimethyl-2-phenyl-1(2H)-phthalazinone derivatives and several analogues were synthesized and their inhibitory effects on platelet aggregation were evaluated. Structure-activity relationships are discussed. All synthesized compounds showed no appreciable effect on platelet aggregation induced by adenosine diphosphate, but most of them inhibited effectively the arachidonic acid induced platelet aggregation. The parent compound, 2-phenyl derivatives, and ortho-substituted 2-phenyl derivatives show the most potent inhibition of all compounds.

3',5'-Cyclic-AMP Phosphodiesterases↗