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S Otani

Publications and source records attributed to S Otani.

At least 289 records · Page 16Linked to original sources
PubMed1989

[A case report of graft-versus-host reaction after aortocoronary bypass--a clinicopathological study].

An immunologically normal 70-year-old male developed fever and disturbance of consciousness after aortocoronary bypass; this was followed by diarrhea, systemic erythroderma and granulocytopenia. He died as a result of sepsis and acute renal failure. The skin biopsy showed basel vacuolar degeneration, epidermal eosinophilic necrosis and invasion of T-lymphocytes. The autopsy showed necrotic small interlobular bile ducts, severely hypoplastic bone marrow and widespread necrosis of lymphoid tissue. Based on these clinicopathological findings, we made a diagnosis of graft-versus host reaction after transfusion.

Aged↗
PubMed1988

Altered production of the active oxygen species is involved in enhanced cytotoxic action of acylated derivatives of ascorbate to tumor cells.

Our previous study shows that 6-O-acyl derivatives of L-ascorbic acid inhibits more markedly cell growth of mouse Ehrlich carcinoma than ascorbic acid. The present study shows that 6-O-palmitoyl ascorbic acid but not ascorbic acid prolongs the lifespan of mice into which tumors such as Meth A fibrosarcoma, MM46 mammary carcinoma, Ehrlich carcinoma and sarcoma 180 are implanted. The potentiated cytotoxicity of 6-O-palmitoyl ascorbic acid is not due to an increase in duration time of the cytotoxic action, because 6-O-palmitoyl ascorbic acid is gradually inactivated during contact with tumor cells and exhibits a similar action time curve to that of ascorbic acid as shown by clonal growth assay. Cytotoxicity of 6-O-palmitoyl ascorbic acid is markedly diminished by combined addition of catalase and superoxide dismutase (SOD), as shown by dye exclusion assay, whereas the cytotoxicity was slightly reduced by either enzyme alone but not by the specifically inactivated or heat-denatured enzymes. In contrast, cytotoxicity of ascorbic acid is abolished by catalyse but not SOD. Autooxidation of 6-O-palmitoyl ascorbic acid was not inhibited by catalase plus SOD. The results indicate that cytotoxicity of 6-O-palmitoyl ascorbic acid is attributed at least partly to both hydrogen peroxide (H2O2) and superoxide (O2-.) generated at the early stage. Cytotoxicity of 6-O-palmitoyl ascorbic acid is also appreciably attenuated by singlet oxygen (1O2) scavengers such as hydroquinone, 1,4-diazobicyclo-2,2,2-octane or sodium azide, but not by hydroxyl radical scavengers including butylated hydroxytoluene, D-mannitol, benzoic acid and ethanol. Thus, in contrast to cytotoxicity of ascorbic acid mediated entirely by H2O2 initially generated, acylated ascorbic acid produces a diversity of active oxygen species including H2O2, O2-. and other species secondarily generated via disproportion, which may be additively involved in the enhanced cytotoxic action.

Animals↗
PubMed1988

Inhibition of ornithine decarboxylase induction of interferon (alpha + beta) and its reversal by dibutyryl adenosine 3',5'-monophosphate.

Interferon (alpha + beta) given to C3H/HeN mice intraperitoneally inhibited increases in the activities of adenylate cyclase and ornithine decarboxylase after partial hepatectomy. The inhibition of ornithine decarboxylase was prevented by administration of dibutyryl cAMP. Core (2'-5')oligo(adenylate), i.e. A2'p5'A2'p5'A or (A2'p)2A, as well as interferon inhibited the increases in these two enzymes caused by partial hepatectomy. The inhibition by (A2'p)2A of ornithine decarboxylase activity was reversed by dibutyryl cAMP. These results suggested that the activity of interferon was similar to that of (A2'p)2A and that the inhibition of ornithine decarboxylase induction caused by these agents resulted from the inhibition of adenylate cyclase activity.

Animals↗
PubMed1988

Synergistic stimulation of S-adenosylmethionine decarboxylase activity by Ca2+ ionophore A23187, cholera toxin and 1-oleoyl-2-acetylglycerol.

The Ca2+ ionophore A23187 induced S-adenosylmethionine decarboxylase in guinea-pig lymphocytes, and cholera toxin stimulated the induction synergistically. The activator of protein kinase C, 1-oleoyl-2-acetylglycerol, did not induce S-adenosylmethionine decarboxylase activity but potentiated the enzyme activity induced by A23187 or by A23187 and cholera toxin. The addition of both A23187 and cholera toxin induced S-adenosylmethionine decarboxylase, but the further addition of 1-oleoyl-2-acetylglycerol or 12-O-tetradecanoylphorbol 13-acetate did not potentiate the enzyme induction in protein kinase-C-down-regulated cells that had been treated with 12-O-tetradecanoylphorbol 13-acetate for 18 h. These results suggest that a Ca2+-dependent pathway, other than that for protein kinase C, is essential for the induction of S-adenosylmethionine decarboxylase and that a cAMP-dependent pathway and also protein kinase C are involved in the potentiation of the induction.

Adenosylmethionine Decarboxylase↗
PubMed1988

Biological activity of 26,26,26,27,27,27-hexafluorinated analogs of vitamin D3 in inhibiting interleukin-2 production by peripheral blood mononuclear cells stimulated by phytohemagglutinin.

Vitamin D compounds suppress the production of interleukin-2 (IL-2) by peripheral blood mononuclear cells (PBMCs) stimulated with phytohemagglutinin in a dose-dependent manner. We used this suppression to test 26,26,26,27,27,27-hexafluorinated analogs of vitamin D3 for their immunosuppressive activity in PBMCs. 26,26,26,27,27,27-Hexafluoro-1,25-dihydroxyvitamin D3 and 26,26,26,27,27,27-hexafluoro-1,24-dihydroxyvitamin D3 were approximately 10 times more potent than 1,25-dihydroxyvitamin D3 in suppressing IL-2 production. 26,26,26,27,27,27-Hexafluoro-1-hydroxyvitamin D3 was 20 to 30 times less potent than 1,25-dihydroxyvitamin D3 in causing this effect. The relative biopotency of each vitamin D3 analog toward PBMC proliferation was roughly similar to that toward IL-2 production by PBMCs. Suppression of PBMC proliferation by vitamin D3 analogs seemed to be a secondary effect of their inhibition of IL-2 production.

Calcitriol↗
PubMed1988

Characterization of liver regeneration stimulatory factor in human portal serum.

Factors capable of stimulating DNA synthesis in rat hepatocytes (stimulating activity) were detected in the portal serum of patients after liver resection. The stimulatory factors were fractionated by gel filtration into four fractions with the molecular weights of 45,000-60,000 (fraction A), 1,500-2,500 (fraction B), 800-900 (fraction C), and about 700 (fraction D). Fraction A was inactivated by trypsin digestion or by being heated at 56 degrees C for 2 h, suggesting that this factor might be a protein. The stimulating activity in fractions B, C, and D was dose-dependent. These stimulatory factors seemed to be different from known hormones such as insulin and glucagon.

Animals↗
PubMed1987

Biological activity of fluorinated vitamin D analogs at C-26 and C-27 on human promyelocytic leukemia cells, HL-60.

Vitamin D compounds added to the culture medium induce HL-60 cells to differentiate into macrophage/monocytes via a receptor mechanism. This system provides a biologically relevant assay for the study of biopotency of vitamin D analogs. Using this system, the biological activity of various fluorinated derivatives of vitamin D3 was compared with that of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). As assessed by cell morphology, nitroblue tetrazolium reduction and nonspecific esterase activity, 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 (26,27-F6-1,25-(OH)2D3) and 26,26,26,27,27,27-hexafluoro-1,24-dihydroxyvitamin D3 (26,27-F6-1,24-(OH)2D3) were about 10 times as potent as 1,25-(OH)2D3 in suppressing HL-60 cell proliferation and inducing cell differentiation. The biological activity of 26,26,26,27,27,27-hexafluoro-1-hydroxyvitamin D3 (26,27-F6-1-OH-D3) was equal to that of 1,25-(OH)2D3 in this system. 1,25-(OH)2D3 and its fluorinated analogs exerted their effects on HL-60 cells in a dose-dependent manner. HL-60 cells have a specific receptor for 1,25-(OH)2D3 with an apparent Kd of 0.25 nM, identical with that of chick intestinal receptor. While the binding affinities of 26,27-F6-1,25-(OH)2D3 and 26,27-F6-1,24-(OH)2D3 for chick intestinal receptor were lower than that of 1,25-(OH)2D3 by factors of 3 and 1.5, respectively, they were as competent as 1,25-(OH)2D3 in binding to HL-60 cell receptor. The ability of 26,27-F6-1-OH-D3 to compete for receptor protein from HL-60 cells and chick intestine was about 1/70 that of 1,25-(OH)2D3. These results indicate that trifluorination of carbons 26 and 27 of vitamin D3 can markedly enhance the effect on HL-60 cells.

Animals↗
PubMed1987

Biphasic effects of dibutyryl cyclic adenosine 3',5'-monophosphate on synergistic stimulation of DNA synthesis by diacylglycerol, and the ionophore A23187 in guinea pig lymphocytes.

When guinea pig lymphocytes were cultured with 1-oleoyl-2-acetylglycerol (OAG) and the ionophore A23187 for 8 h, [3H]-thymidine incorporation into the acid-insoluble fraction of the cells was stimulated synergistically. Further addition of dibutyryl cAMP caused a biphasic effect on the synergistic stimulation. Dibutyryl cAMP augmented the synergistic stimulation when A23187 was at the concentration of 0.075 micrograms/ml, but inhibited it when the ionophore was at 0.25 micrograms/ml. At the higher concentration of A23187, dibutyryl cAMP stimulated the [3H]thymidine incorporation when culture was for 4 h, but inhibited it when culture was for 8 h. The results were the same when 12-0-tetradecanoylphorbol-13-acetate (TPA) was used instead of OAG. Butyrate could replace dibutyryl cAMP for stimulation of [3H]thymidine incorporation in combination with TPA and A23187, but not with OAG and A23187 at the lower ionophore concentration. Dibutyryl cAMP but not butyrate stimulated ornithine decarboxylase induction caused by TPA and A23187. These results suggest that the effect of dibutyryl cAMP on DNA synthesis induced by OAG and A23187 was biphasic and depended on the concentration of A23187 and on the time of culture, and that the stimulation mechanism of butyrate is different from that of dibutyryl cAMP.

Animals↗
PubMed1987

Effects of acute and long-term treatment with amphetamine on evoked responses and long-term potentiation in the dentate gyrus of anesthetized rats.

We examined the effects of D-amphetamine (AMP) on evoked responses and long-term potentiation (LTP) in the dentate gyrus of rats in 4 different conditions: untreated + saline, untreated + acute AMP, long-term AMP-treated + saline, and long-term AMP-treated + acute AMP. Long-term AMP-treatment comprised once daily i.p. injections of 5 mg/kg AMP for 14 consecutive days followed by 7 drug-free days. Acute AMP administration consisted of a single i.p. injection of 5 mg/kg. Acute AMP significantly increased the slope of the synaptic component, the excitatory postsynaptic potential (EPSP), of the evoked response without changing the cell discharge component (population spike), resulting in a significant decrease in the population spike per unit EPSP in the evoked potentials of both untreated and long-term AMP-treated rats. The acute AMP slightly reduced LTP of the population spike in the untreated rats and significantly reduced it in the long-term AMP-treated rats. LTP of the EPSP did not differ between the 4 conditions. The two saline conditions did not differ significantly in their evoked responses or in LTP. It is suggested that AMP has 3 acute effects in the dentate gyrus, and that the effect of reducing the capacity for LTP of the population spike is selectively enhanced following long-term AMP treatment.

Animals↗
PubMed1987

Effect of hyperthermia on spermidine/spermine N1-acetyltransferase activity in Ehrlich ascites cells.

When Ehrlich ascites tumor cells were incubated at 42 degrees C, the activity of spermidine/spermine N1-acetyltransferase, a rate-limiting enzyme of polyamine biodegradation, decreased to 20% of the control level within 1 hr. Protein synthesis, judged from the incorporation of [3H]leucine into the acid-insoluble fraction, was less affected by heat exposure. The decrease in the enzyme activity caused by heat treatment could be reversed by switching the incubation temperature back to 37 degrees C. The reversion of enzyme activity was suppressed by cycloheximide but not by actinomycin D.

Acetyltransferases↗
PubMed1987

Formation of roseoflavin from 8-amino- and 8-methylamino-8-demethyl-D-riboflavin.

A synthesis of roseoflavin (RoF) by Streptomyces davawensis from 8-amino- (AF) and 8-methylamino-8-demethyl-D-riboflavin (MAF) was demonstrated. The lines of evidence are: 1) the RoF formation was increased by addition of AF or MAF to the culture, 2) [2-14C]RoF was formed by addition of [2-14C]AF or [2-14C]MAF to the culture, and the location of the 14C atom at the 2-position was demonstrated by identifying [14C]urea in the hydrolysate of the RoF, 3) [N-methyl-14C]RoF was formed by addition of [methyl-14C]methionine to the culture containing AF or MAF, and the location of the 14C atom was confirmed by the photochemical conversion of the RoF to MAF, the specific radioactivity of which was about half that of the original RoF, and by localization of the 14C atom in 1,2-dihydro-6-methyl-7-dimethylamino-2-keto-1-ribityl-3-quinoxalinecarbo xylic acid (QC), which was formed from the RoF by hydrolysis.

Chromatography, Thin Layer↗
PubMed1987

Polyamine biosynthesis is necessary for interleukin-2-dependent proliferation but not for interleukin-2 production or high-affinity interleukin-2 receptor expression.

DL-alpha-Difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase [EC 4.1.1.17] (ODC), inhibited concanavalin A-induced proliferation of splenic mononuclear cells (SMNC). The inhibition was not reversed by interleukin-2 (IL-2) addition. Although DFMO did not affect the production of IL-2 or the expression of high-affinity IL-2 receptor, IL-2-dependent proliferation of SMNC was inhibited by DFMO, and the inhibition was reversed by exogenous putrescine. The inhibition of IL-2-dependent DNA synthesis appeared to be related to the decrease in intracellular polyamines. When the proliferation of SMNC was induced by IL-2, ODC activity was also increased. A similar result was obtained in the proliferation of an IL-2-dependent T cell line, CTLL. The time course of ODC induction was similar to that of IL-2 production by concanavalin A-stimulated SMNC. These results indicate that polyamine biosynthesis is necessary for IL-2-dependent proliferation, but not for IL-2 production or IL-2 receptor expression.

Animals↗
PubMed1987

Role of protein kinase C in phytohemagglutinin-stimulated induction of spermidine/spermine N1-acetyltransferase.

We studied the involvement of protein kinase C in the induction of spermidine/spermine N1-acetyltransferase, a rate-limiting enzyme of polyamine degradation, in bovine lymphocytes. When phytohemagglutinin (PHA) and H-7, a protein kinase inhibitor, were added simultaneously to lymphocyte cultures, the elevation caused by PHA of spermidine/spermine N1-acetyltransferase activity at 24 h after administration was reduced. In cells treated with a lower concentration of PHA, the acetyltransferase activity was enhanced with 12-o-tetradecanoyl phorbol-13-acetate (TPA), an activator of protein kinase C, and reached the level of cells with a higher concentration of PHA. PHA did not cause maximum induction of the enzyme in cells treated with 160 ng/ml TPA. The induction of this acetyltransferase with PHA is probably mediated by protein kinase C.

Acetyltransferases↗
PubMed1987

Liver regeneration factor detected in human serum after partial hepatectomy.

We obtained blood sera from patients before and after partial hepatectomy, and estimated the activities of the sera in promoting DNA synthesis in a primary culture of rat hepatocytes. The stimulating activity in portal serum from patients without any postoperative complications increased significantly after liver resection; that in portal serum from patients with complications did not. The amount of stimulatory factor transported to the liver, calculated by use of the stimulating activity in portal serum and the portal blood flow, increased after partial hepatectomy. The maximum amount was correlated to the resection ratio (p less than 0.05) and seemed to be correlated to the increase in liver volume. These results suggest that a stimulatory factor or factors are present in portal serum after partial hepatectomy and that such a factor and portal blood flow are important in liver regeneration after surgery.

Animals↗