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Biomedical subjects

T Honma

Publications and source records attributed to T Honma.

At least 217 records · Page 12Linked to original sources
PubMed1980

Cytotoxic antibody in cattle and sheep exposed to bovine leukemia virus.

Sera from bovine leukemia virus-infected cattle and sheep lysed fetal lamb kidney cells in the presence of rabbit complement. This cytolytic activity was removed completely from the sera by absorption with bovine leukemia virus (BLV). Antiserum against surface glycoprotein antigens of BLV contained cytolytic antibody but antiserum against the internal protein p24 did not. The complement-dependent antibody cytotoxicity test employing the trypan-blue dye exclusion method appeared to be suitable for routine diagnosis of BLV infection.

Animals↗
PubMed1980

Structure elucidation of an intermediate of 2-deoxystreptamine biosynthesis.

The structure of a 2-deoxystreptamine (DOS) precursor named S-11-P, which was isolated by using a DOS negative mutant derived from a xylostasin-producing strain of Bacillus circulans B15M, has been elucidated as (1 L)-1,3,5/2,4,-5-aminocyclohexanetetrol by comparison with an authentic specimen, which was synthesized from kanamycin A.

Anti-Bacterial Agents↗
PubMed1979

The involvement of serotonergic neurons in the central nervous system as the possible mechanism for slow head-shaking behavior induced by methamphetamine in rats.

Following the IV administration of d-methamphetamine (MA), rats showed slow head shaking (SHS) and stereotyped gnawing (SG) behaviors in a dose-dependent manner. Methysergide, cyrpoheptadine, and p-chlorophenylalanine given intracerebroventricularly (ICV) or systemically significantly blocked SHS behavior induced by 10 mg/kg MA. Combined administration of L-5-hydroxytryptophan and peripheral decarboxylase inhibitor (Ro 4-4602) enhanced SHS behavior. Tyrosine hydroxylase inhibitor (H44/68) blocked SG behaviors, but dopamine-beta-hydroxylase inhibitors (FLA 63 and U-14, 624) and combined administration of L-3,4-dihydroxyphenylalanine and Ro-4-4602 enhanced it. These drugs did not affect SHS behavior. Phentolamine, phenoxybenzamine, clonidine, isoproterenol, and propranolol given ICV or systemically showed no effect on either SHS or SG behaviors. These results suggest that SHS behavior is produced by the activation of seronergic neurons in the central nervous system and are consistent with the view that SG behaviors are mediated through the release of dopamine. Some neuroleptics inhibited SHS as well as SG behaviors, but the older of inhibitory activity of neuroleptics onSHS behavior was quite different from their effects on SG behaviors induced by MA or apomorphine.

Animals↗
PubMed1979

Role of macrophages in intraepidermic vesiculation in pemphigus vulgaris. Electron-microscopic observations.

The authors made an electron-microscopic observation of intraepidermic vesiculation in pemphigus vulgaris at its early stage, and found that numerous macrophages were invading the cleft located immediately superior to the basal cell layer. They suggest that the formation of cleft, as a preceding stage to the eventual development into intraepidermic vesiculation, is intimately related to the squeezing-in of invasive macrophages among keratinocytes.

Humans↗
PubMed1979

Investigations of source and route of Yersinia enterocolitica infection.

Isolation of Yersinia enterocolitica was performed on healthy humans, animals and food, and growth of Y. enterocolitica on sliced ham at various temperature ranges was also examined. It was noticed that the most prevalent 0 group (03) in human infection was isolated from swine, pork and chopping boards. The storage of food in the refrigerator (5 degrees C) possibly increases the risk of infection since Y. enterocolitica is multipliable at low temperatures more readily than many other pathogenic bacteria. Pork and meat products contaminated with Y. enterocolitica, either primarily or secondarily, are probably the most important source of human infection.

Adult↗
PubMed1978

[Mechanism of methamphetamine toxicity in grouped mice and the effects of centrally acting drugs on its toxicity (author's transl)].

The mortality of ddK mice treated with 40 mg/kg i.p. of methamphetamine (MA) was 85% in grouped conditions (10 mice in a cage) and 3% in individually isolated conditions. This mortality was not altered by the social environments even when other mice in the cage were not treated with MA. The mortality of mice individually isolated in cages with transparent walls was significantly higher than that of completely isolated mice. Almost all neuroleptics dose-dependently antagonized the MA toxicity in grouped mice, in small doses. The antagonizing activity of clozapine was somewhat weak, and sulpiride potentiated MA toxicity. Phentolamine and propranolol antagonized the MA toxicity at higher doses than neuroleptics. Reserpine and tetrabenazine previously given to mice remarkably antagonized the MA toxicity. H44/68 (a tyrosine hydroxylase inhibitor) had a considerable effect in antagonizing the MA toxicity, but diethyldithiocarbamate, U-14, 624 and FLA 63 (dopamine-beta-hydroxylase inhibitors) prevented the MA toxicity to a lesser extent than did H44/68. Apomorphine had no effect on the MA toxicity. The present data show that the MA toxicity in grouped mice (the increase in mortality) was enhanced by the presence of other mice, and suggest that the norepinephrine neurons play an important role in promoting the MA toxicity. Neuroleptics antagonize MA toxicity probably by blocking alpha-receptors in the central nervous system.

Adrenergic alpha-Antagonists↗