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Biomedical subjects

E Kondo

Publications and source records attributed to E Kondo.

At least 163 records · Page 9Linked to original sources

Liposomes-mycobacteria incubation systems as a partial model of host-parasite interaction at cell membrane level.

The multilamellar lecithin-cholesterol liposomes entrapping carboxyfluorescence as a specific marker were prepared to be incubated with mycobacteria. The extent of resulting liposomal lysis was measured by marker release. Mycobacteria were highly active in this respect regardless of the species. Staphylococci were much less active and E. coli was completely inactive. Molecular species of lecithin and their ratio to cholesterol were related with the liposome sensitivity to mycobacteria. Ultrastructural and biochemical study showed that liposomes can be in close contact with mycobacteria and lecithins are degraded so that released fatty acids are incorporated into bacterial lipids, especially in virulent species. Liposomes-mycobacteria interaction was discussed as a partial model of the phagocyte-parasite interaction at the membrane level.

1,2-Dipalmitoylphosphatidylcholine↗

Mechanism of bactericidal activity of lysolecithin and its biological implication.

Lysolecithin exhibited bactericidal effect on mycobacteria and staphylococci, but not on E. coli. The effect on staphylococci was manifested shortly after exposure, but that on mycobacteria was of the delayed type. The mycobactericidal activity was dependent on the fatty acid moiety of the chemical structure reflecting the cytotoxicity of the free form. The activity on staphylococci was not, however, of such fatty acid dependency and showed the same pattern of molecular species in hemolytic activity. These and other collateral findings suggest that the mycobactericidal effect of lysolecithin is due to the free fatty acids released therefrom by the enzymatic activity of the exposed bacterial cells, but that staphylococci are killed by the detergent effect of the whole lysolecithin molecule.

Escherichia coli↗

Effect of strychnine on the contractile response of rat vas deferens.

Strychnine at concentrations of 0.1 approximately 1.0 microM induced supersensitivity of rat vas deferens to alpha-agonists but not to other stimulants. Strychnine-treatment resulted in an increase in the number of alpha-adrenoceptors, determined by measuring the binding of [3H]prazosin. Glycine did not have any significant effect on the contracture and did not antagonize the action of strychnine. Thus, specific supersensitivity of alpha-adrenergic system was induced by treatment with low concentrations of strychnine.

Animals↗

Monoclonal antibodies to hog thyroglobulin recognizing disulfide-dependent conformational structures.

Monoclonal antibodies (MAbs) to hog thyroglobulin (Tg) were obtained by fusion of myeloma cells with B-lymphocytes from mice immunized with the protein. The five MAbs were classified into three groups which recognized different determinants; (1) MAb 4, (2) MAbs 6 and 10, and (3) MAbs 16 and 18. MAb 16 was IgG2b and the others IgG1. The immunoreactivity of Tg to the five MAbs was lost after reduction of the protein under denaturing conditions but remained after limited digestion by proteolytic enzymes. Tryptic fragments were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, electrophoretically blotted and stained by a peroxidase-linked second antibody. Various sized tryptic fragments reacted similarly with the three MAbs which had different determinant specificities. All the MAb-reactable fragments in the tryptic digest completely lost their immunoreactivity after reduction of their disulfide linkages.

Animals↗

Isolation of L-cycloserine from Erwinia uredovora.

An antibiotic which seems to be a cell wall synthesis-inhibitor was isolated from a bacteria strain identified as Erwinia uredovora. The antibiotic was identified with L-cycloserine from its physico-chemical properties. This is the first example for isolation of L-cycloserine as a microbial product.

Cycloserine↗

Decreased resistance to mycobacterial infection in mice fed a trichothecene compound (T-2 toxin).

The effect of T-2 toxin, a trichothecene compound, on bacterial infection was examined in mice infected intravenously with mycobacteria. T-2 toxin dissolved in olive oil was given orally in a dose of 0.1 mg, six to 12 times, at various stages of infection. The resistance-decreasing effect of the toxin was judged by two different criteria, the mouse survival period and the fate of tissue viable counts. This effect was accompanied by a decreased spleen weight. T-2 toxin was found to be a more potent immunosuppressing agent in this model than 5 mg of cortisone given intraperitoneally according to a similar schedule. In view of these observations, the potential importance of this mycotoxin was considered in relation to food hygiene.

Animals↗

beta-Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Simultaneous studies on the secretory response of amylase and the neurotransmitter receptors of rat parotid gland, after brief treatment with agonists, showed selective alteration in beta-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretory response. The beta-adrenergic agonist (+/-)-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration of an alpha-adrenergic or cholinergic agonist. The stimulatory effects of IPR were studied by pre-treating rat parotid tissues with IPR for 10 min and then incubating the tissue in fresh medium for 10 min. Pre-treatment with 10 microM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC50 value of amylase secretion for IPR. This treatment also resulted in selective changes in the number and affinity of beta-adrenoceptors, assessed by measuring binding of [3H]dihydroalprenolol (DHA): the maximal binding sites increased from 286/357 f-mole to mg protein and the IC50 value (the concentration for 50% inhibition of specific [3H]DHA binding) of beta-agonists, not antagonists, decreased significantly. An increase in the period of pre-treatment with IPR to 30 min resulted in a decrease in the maximal binding sites of beta-adrenoceptors and a decrease in amylase secretion during further incubation with IPR. Experiments with other agonists showed that supersensitivity of the secretory response was induced specifically by beta-agonists. Binding studies with [3H]WB-4101 and [3H]quinuclidinyl benzilate showed that alpha-adrenoceptors and muscarinic ACh receptors in rat parotid did not change under the conditions tested. The alteration in beta-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.

Acetylcholine↗

Characteristics of [3H]E-643-binding to alpha adrenoceptors.

Radiolabeled E-643, a newly developed antihypertensive compound, bound specifically to a preparation obtained from rat brain with a maximum of 85 f moles of binding sites per mg protein and a dissociation constant of 0.59 nM. Prazosin markedly inhibited the binding. While yohimbine and clonidine were only weak inhibitors. Other characteristics of the binding of [3H]E-643 to the brain and its specific binding to preparations of peripheral rat organs were also studied. The present findings suggest that [3H]E-643 is useful for labeling alpha 1-adrenoceptors.

Adrenergic alpha-Agonists↗