[A case of non-Hodgkin's lymphoma with huge splenomegaly, pancreatic pseudocyst, and intracystic bleeding (author's transl)].
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Biomedical subjects
Publications and source records attributed to Y Hashimoto.
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The ability of carcinogenic and non-carcinogenic aminoazo dyes to induce unscheduled DNA synthesis (UDS) in primary cultures of hepatocytes of 3 strains of rats and 2 strains of mice was examined by means of microautoradiography. Azo dyes tested were 4-aminoazobenzene (AAB) and 4 of its ring methoxyl (MeO) derivatives, their N-hydroxy (N-OH) derivatives, N-methyl-4-aminoazobenzene (MAB) and its N-bezoyloxy derivative, and N,N-dimethyl-4-aminoazobenzene (DAB). All carcinogenic aminoazo dyes (AAB, 3-MeO-AAB, 4'-MeO-AAB, MAB and DAB), but not the non-carcinogenic dyes (2-MeO-AAB and 2,5-diMeO-AAB), induced UDS in rat hepatocytes as well as mouse hepatocytes. N-Hydroxy derivatives of AAB and its 3- and 4'-MeO derivatives elicited higher levels of UDS than did the corresponding mother aminoazo dyes. N-OH-2-MeO-AAB was as inactive with rat hepatocytes as the mother dye. N-OH-2,5-diMeO-AAB, however, elicited a definite level of UDS, in contrast to the mother 2,5-diMeO-AAB. N-Benzoyloxy-MAB, a prototype compound of the ultimate carcinogenic metabolite of MAB, was as active as the mother MAB. N,-OH-3-MeO-AAB induced UDS more rapidly than did 3-MeO-AAB. The UDS elicited by 3-MeO-AAB was found to end within a few hours after releasing the hepatocytes from the azo dye.
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The responses of interplexiform cells in the dace retina were recorded intracellularly and identified morphologically. The response pattern closely resembles the response of bipolar cells and amacrine cells (on- and off-types). Morphologically, the perikaryon of most of these cells lies in the amacrine cell layer, and is usually large in size. Distal and proximal processes arise from the soma directly. The distal process ramifies and extends widely in the outer plexiform layer, but does not make contact with receptor terminals. The proximal process branches and extends widely in the inner plexiform layer. The majority of these cells resembles the dopaminergic interplexiform cells, but a few resemble the glycinergic interplexiform cells in the goldfish retina.
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Bone remodelling depends on a balance formation and resorption. Little is known of the biological factors involved in bone formation, whereas there is much evidence that physiological factors, such as parathyroid hormone (PTH) and active metabolites of vitamin D3, influence resorption. Cells responsible for osteogenesis and and osteoclasis occur in close proximity, suggesting that both might be controlled by the same physiological factors in the micro-environment of the body fluid. To clarify the factors stimulating bone formation or accelerating osteogenic cell activity, we have examined the effects of vitamin D3 metabolites and PTH on bone formation in vitro. We report here that combinations of those metabolites especially 1 alpha,25-(OH)2D3 and 24R,25-(OH)2D3, directly stimulate calcification on bone synergistically with PTH.
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A simple agglutination microassay is described for studying the presence of antigenic determinants on the surface of liposomal membranes. Antigen-sensitized radioactive liposomes, reacted with specific immune IgG in the wells of a microtest plate, were passed through a glass fiber filter in a multiple cell culture harvester. The amount of agglutinate trapped on the filter as determined by the radioactivity, was proportional to the amount of antigen in the liposomes and to the amount of specific immune IgG in the reaction mixture. The specificity of the agglutination was determined by inhibition with hapten and carrier antigens. Liposomes actively sensitized with hapten-conjugated lipid, and passively sensitized with protein, were used in the assay. A new method of preparing protein-bound liposomes is also described.
A heretofore unknown metabolite of vitamin D3 was isolated from the 1 alpha, 24, 25-trihydroxyvitamin D3 fraction of lipid extracts obtained from plasma of rats which were given intravenous or oral doses of 100 pmol/100 g of either 1 alpha-hydroxyvitamin D3 or 1 alpha, 23-dihydroxyvitamin D3. Doses of 25-250 pmoles of the new metabolite when given to a vitamin D deficient rat were completely inactive in terms of stimulating the classic vitamin D response of bone calcium mobilization. The nature of the metabolism of 1 alpha-hydroxyvitamin D3 or 1 alpha, 25-dihydroxyvitamin D3 to the metabolite is not clear at the present time, but it is probable that neither of these steroids undergo side-chain cleavage to yield the new metabolite.
This paper reports the cleavage maps of ampicillin transposons Tn2601 and Tn2602, for restriction endonucleases BamHI, PvuII, AvaI, HincII, and HaeII. Both of the transposons are very similar to the well-known ampicillin transposon Tn3 in size, endonuclease cleavage sites, and possession of a short inverted repeat sequence at both ends. A slight difference in the cleavage pattern among these three transposons was observed in the region around the BamHI site which was assumed to be a part of the repressor gene for transposition.
S-sulfonated gamma globulin (GGS), newly developed as a safe drug for intravenous use, was studied for its protective effects against some experimental infections in mice. Gamma globulin showed a good protective activity against infections due to Streptococcus pneumoniae and Escherichia coli and was moderately active against infections due to Staphylococcus aureus and Pseudomonas aeruginosa. In most cases, the potency of GGS was almost the same as that of original native gamma globulin. The duration of GGS activity in vivo was found to be comparable to that of native gamma globulin and much higher than that of pepsin-digested gamma globulin. In the control of infection due to E. coli, specific antibody was found to play a central role in the antibacterial action of GGS. When GGS was administered in combination with the antibiotics gentamicin and cefazolin for the control of infections due to S. pneumoniae or E. coli, a clear synergistic effect was observed.
A 24-hour of basal noradrenaline (NA) levels in normal human plasma in the supine position was observed; higher NA levels during daytime and lower NA levels at night, especially early in the morning. This pattern of the 24-hour rhythm of plasma NA levels was similar to that of serum dopamine-beta-hydroxylase (DBH) levels. After oral administration of fusaric acid, a DBH inhibitor, the rhythm changed, and plasma NA levels increased at 3 h and returned to the initial level at 23 h. In contrast, plasma DBH activity was markedly inhibited during 23 h after fusaric acid administration.
Several N-substituted-3-acyl-2, 5-dimethyl pyrrole derivatives were examined for their potency to inhibit aggregation of platelets in vitro and extra vivo in guinea pigs. A structure-activity relationship study showed that the substitution at 3 position of the pyrrole ring affected in vitro activity of inhibiting platelet aggregation. Compounds with 3-benzoyl or 3-thenoyl substituent had greater potency than those with 3-aliphatic acyl substituent. Modification of benzoyl, such as para substitution of phenyl group or reduction of carbonyl group, decreased the activity. There was no clear correlation between that N-substitution of the pyrrole ring and in vitro anti-platelet activity. However, compounds with a longer alkyl chain in the N-substituent had weaker activity. The in vitro inhibitory activity on prostaglandin synthetase of these compounds, though less potent compared with their antiplatelet activity, has a close correlation with the latter. N-substituents of the pyrrole ring had the effect on extra vivo activity. Compounds which have no N-alpha-methyl group and no hetero atoms such as oxygen or sulfur in the N-substituent diminished the extra vivo activity.
Interaction of calcium regulating hormone, active form of vitamin D3, and aspirin (ASA) was studied in rats. One alpha-hydroxyvitamin D3 (1 alpha-OH-D3) produced a hypercalcemia in parathyroidectomized, thyroparathyroidectomized and thyroparathyroidectomized nephrectomized rats. The effect of 1 alpha-OH-D3 was inhibited by treatment with 200, 50 and 20 mg/kg p.o. of ASA. ASA did not stimulate the gut absorption of calcium in vitamin D deficient rats. These data suggest that ASA acts by inhibiting 1 alpha OH-D3 induced bone resorption. This is the first report demonstrating the inhibitory effect of ASA on bone resorption as induced by 1 alpha-OH-D3, although partial inhibition of bone resorption in vitro has been reported.