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Biomedical subjects

S Otani

Publications and source records attributed to S Otani.

At least 199 records · Page 11Linked to original sources

[Two cases of coronary artery fistula with coronary artery aneurysm].

Two cases of coronary artery fistula with coronary artery aneurysm were reported. Coronary angiography showed dilated right coronary artery with the formation of aneurysm drained to the right atrium and to the right ventricle respectively. The inflow ostium from the coronary artery to the aneurysm were closed from inside adding aneurysmorraphy. Postoperative clinical courses were uneventful and residual shunts were not detected by angiography. We reported these cases with literature.

Child, Preschool↗

[Surgical treatment of subaortic stenosis].

We reviewed 10 cases with subaortic stenosis (SAS) who underwent surgical repairs in our hospital. They were divided into 3 groups. Group I-A included patients with discrete SAS which had been detected before the initial operation. Group I-B included patients with discrete SAS which became apparent following the initial operations. Group II patients included SAS except the discrete type. Surgical treatment of each group was discussed. In group IA, there were no early deaths nor late deaths. There was 1 reoperation due to restenosis. Group IB had 3 cases which included VSD with CoA, Taussig-Bing anomaly, and common atrioventricular canal with VSD. In the Taussig-Bing anomaly case, an arterial switch (Lecompte maneuver) was performed 3 years ago. SAS was successfully relieved with the right ventriculotomy and VSD patch incision. Group II had 3 cases. There were 2 operative deaths and 1 late death. SAS was relieved by, in two cases, Stansel anastomosis with BT shunt and, in the last one, palliative arterial switch operation. It was extremely difficult to detect SAS in group II, when SAS had rapidly progressed following PAB in neonate and early infant. Our present policy is that PAB would be performed if there is no apparent SAS before the initial operation. SAS should be relieved as soon as possible if it is apparent at the postoperative period. Either Stansel anastomosis with BT shunt or palliative arterial switch operation would be the best choice in such a difficult case.

Aortic Valve Stenosis↗

Effect of combined alanine and glutamine administration on the inhibition of liver regeneration caused by long-term administration of alcohol.

We studied the effect of administration of a mixture of alanine and glutamine on the inhibition of liver regeneration caused by alcohol in rats undergoing partial hepatectomy 6 weeks after the start of alcohol administration. DNA synthesis was inhibited 24 hr after partial hepatectomy in rats given alcohol, but treatment with alanine and glutamine partially prevented this inhibition. To identify the mechanism of this effect, polyamine metabolism was studied. Administration of alcohol or alanine plus glutamine had no effect on the activity of ornithine decarboxylase, a rate-limiting enzyme of polyamine metabolism. In the liver, of the three polyamines, only the spermine concentration changed significantly. It decreased during long-term administration of alcohol, and this decrease was prevented by treatment with alanine and glutamine. The level of N(1)-acetylspermidine, the acetylated product of spermidine, was increased by alcohol, and its elevation was significantly less when alanine and glutamine were given. Hepatic spermidine/spermine N(1)-acetyltransferase, the key enzyme of polyamine acetylation, was induced by long-term administration of alcohol, and this induction was suppressed by alanine plus glutamine. The results suggest that treatment with alanine and glutamine can help to prevent the inhibition of liver regeneration caused by alcohol by maintaining the spermine level and suppressing the acetylation of spermidine.

Alanine↗

[Right-sided infective endocarditis with ventricular septal defect].

Two patients underwent surgical treatment for right-sided infective endocarditis with ventricular septal defect. In both cases, blood cultures showed Peptostreptococcus, and the operation was performed at non-active phase after antibiotics therapy. The case 1 was a 7-year-old girl who was observed a vegetation on the chorda of the anterior paillary muscle by echocardiography. The defect was directly closed and the vegetation was excised. The case 2 was 22-year-old female who had been diagnosed of VSD in her infancy. A high fever continued and echocardiography revealed a vegetation attached to the septal tricuspid leaflet. Partial excision of the leaflet and autopericard patch plasty was performed, and the VSD was directly closed. Postoperatively intravenous antibiotic therapy was given for periods of 6 weeks, and clinical course were uneventful in both cases. Local excision of vegetation and leaflet repair by autopericard patch plasty should be performed in cases with localized vegetation and minor valvular regurgitation.

Adult↗

Metabotropic receptor stimulation coupled to weak tetanus leads to long-term potentiation and a rapid elevation of cytosolic protein kinase C activity.

We have previously shown that short-term potentiation (STP) inducing weak tetanus induces long-term potentiation (LTP) when it is coupled with activation of metabotropic glutamate (mGlu) receptors by trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (t-ACPD) in rat CA1 slices. In the present study, we examined if this conversion of STP to LTP involves activation of protein kinase C (PKC). Two minutes but not 30 min after coupling, there was a significant increase in the activator-dependent PKC activity in the cytosolic fraction. STP induction or t-ACPD application did not change PKC activity. There was no activity increase in the membrane fraction. STP was also induced by a co-application of gamma-amino-3-hydroxy-5-methyllisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA). Coupling this STP with t-ACPD, however, did not result in an LTP or PKC activity increase, indicating a requirement for synaptic activity. A rapid and transient (< 5 min) increase in cytosolic PKC activity was also seen after the induction of LTP by stronger tetanic stimulation. No LTP tested in the present study was accompanied by activator-independent, persistent increases in PKC activity. STP induction depends on NMDA receptor activation, and the activation of mGlu receptors results in the production of intracellular second messengers. Our results therefore indicate that these separate components may add and bring about PKC activation and LTP.

Animals↗

Biochemical correlates of long-term potentiation in hippocampal synapses.

Figure 2 summarizes biochemical events which are currently known or hypothesized to participate in LTP induction/maintenance. Current evidence strongly suggests that postsynaptic Ca2+, both entered from the outside of cells and released from intracellular stores, is the initial key substance for the induction of LTP. A rise of [Ca2+]i triggers a variety of enzymatic reactions and initiates the enhancement of synaptic transmission. This first step may be achieved by direct/indirect phosphorylations of protein molecules in postsynaptic receptors/ion channels. This would result in an increase in receptor sensitivity. An immediate increase in the number of available postsynaptic receptors by modifications of spine morphology is another candidate. Such modifications may be accomplished by cytoskeleton rearrangements or changes in extracellular environments. A change in spine structure may also cause an increase in spine neck conductance. Although it is unknown to what extent the increase in [Ca2+]i affects cellular chemistry, Ca2+ probably also directly/indirectly stimulates cascades which exert effects more slowly. A delayed increase in metabotropic receptor sensitivity may occur. New synthesis of protein molecules may be involved in late periods of LTP by replacing turnovered molecules and/or by supplying new materials. Some of these chains of biochemical events may also apply to presynaptic terminals, although the existence of retrograde messenger substances must still be confirmed. In addition, interactions between different protein kinases and second messengers appear to occur to bring about final effects.

Animals↗

Effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment.

We studied the effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment after partial hepatectomy (PH) in rats. When rats were dosed i.p. with ethanol at 2 g/kg at the time of PH, DNA synthesis 48 hr after PH was significantly inhibited, but it was completely reversed by the combined use of alanine and glutamine. Although hepatic ornithine decarboxylase (ODC) activity in the alcohol-treated group 4 hr after PH was significantly inhibited, there was a tendency towards recovery of the ODC inhibition in the alanine and glutamine-treated group. The putrescine (PUT) level in liver which was decreased by ethanol was also increased by the administration of alanine and glutamine. However, the levels of spermidine (SPD) and spermine (SPM) in liver were unaffected either by ethanol or by alanine and glutamine. These results suggest that alanine and glutamine show a protective effect on the inhibition of liver regeneration caused by acute ethanol treatment by improving polyamine metabolism, particularly by increasing hepatic PUT levels.

Alanine↗

Severity of promotion by sodium salts of succinic acid in rat urinary bladder carcinogenesis correlates with sodium ion concentration under conditions of equal urinary pH.

Elevation of urinary pH and Na ion concentration induced by feeding high doses of sodium salts plays a crucial role in promotion of urinary bladder carcinogenesis in male rats initially treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). In the present study, urinary bladder carcinogenesis in male F344 rats was promoted by feeding the mono- and di-sodium salts of succinic acid, and the activity was enhanced by varying urinary sodium ion concentration under conditions of equally high pH. In Experiment 1, the rats were given 0.05% BBN in their drinking water for 4 weeks and then fed basal diet containing 5% succinic acid, 5% sodium succinate (Na-Suc) or 5% di-sodium succinate (2Na-Suc) for 32 weeks. The development of carcinomas in the urinary bladder was enhanced by treatment with Na-Suc and with 2Na-Suc. 2Na-Suc induced larger urinary bladder tumors than the Na-Suc. In Experiment 2, 5% Na-Suc and/or 5% 2Na-Suc were fed to the rats for 8 weeks without prior BBN treatment. Induction of simple hyperplasia as observed by light microscopy, was greater in rats fed 2Na-Suc than Na-Suc. Increased 5-bromo-2'-deoxyuridine labeling index and alterations of the urothelial surface observed by scanning electron microscopy of the urinary bladder were similarly greater in rats fed 2Na-Suc compared to Na-Suc. In addition, there was a tendency toward increased spermidine/spermine N1-acetyltransferase activity in the urinary bladder epithelium of rats fed 5% 2Na-Suc. The results of Experiment 2 corresponded to differences in promoting activity for the different chemicals in Experiment 1. Thus, tumor growth was associated with sodium ion concentration level under conditions of equal increase of urinary pH.

Animals↗

The effect of hepatic ischemia-reperfusion on polyamine metabolism in some organs of the rat.

Hepatic ischemia was produced by clamping the portal venous and hepatic arterial blood supply to the left lateral and median lobes of the rat liver. Hepatic ornithine decarboxylase (ODC) and spermidine/spermine N1-acetyltransferase (SAT) activities in ischemic and nonischemic regions were increased and, respectively, peaked by 6 hr and 3 hr after 1 hr of hepatic ischemia. Hepatic putrescine contents in ischemic and nonischemic regions were increased and peaked by 6 hr. However, hepatic spermidine and spermine were not increased. an increase in ODC activity was also observed in the spleen and the kidney after 1 hr of hepatic ischemia. [3H]thymidine incorporation into DNA was observed in the liver and the spleen--however it was not observed in the kidney--after hepatic ischemia.

Animals↗

Effects of ultraviolet-B and PUVA on ornithine decarboxylase activity, DNA synthesis, and protein kinase C activity in mouse skin.

Ultraviolet-B and PUVA share several biological events with phorbol ester tumor promoters. The effects of ultraviolet-B irradiation and topical PUVA treatment on ornithine decarboxylase activity, DNA synthesis, and protein kinase C activity, which are known to be induced or activated by phorbol ester tumor promoter, were investigated in hairless mouse skin. Ornithine decarboxylase activity was remarkably enhanced by ultraviolet-B and PUVA. Although PUVA did not affect DNA synthesis significantly, ultraviolet-B stimulated epidermal DNA synthesis approximately 5-fold over control values at 48 h. However, unexpectedly, neither cytosolic nor membrane-bound protein kinase C activity showed any change during the 2 h after either treatment. These results suggest that the protein kinase C system is not involved in the initial signal transduction system of ultraviolet-B or PUVA, unlike the case with phorbol ester tumor promoter.

Animals↗

Effects of colchicine on the induction of ornithine decarboxylase and its gene expression by the phorbol ester tumour promoter.

The activity and gene expression of ornithine decarboxylase (ODC, an indicator of tumour promotion) were induced by the phorbol ester tumour promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), in mouse skin. In the present study, the effect of colchicine, a microtubule-disrupting agent, on ODC activity and its gene expression were investigated. On administration of colchicine (100 micrograms) intraperitoneally 1.5 h before TPA treatment, ODC activity and ODC mRNA levels stimulated by TPA were suppressed to about 52 and 64%, respectively. These results suggest the involvement of a microtubule or colchicine-sensitive substrate in the signal transduction system for gene expression.

Animals↗

[Pacemaker implantations in children with regard to the site of implantation].

We reviewed thirty eight children, ranged 3 days to 15 years (mean, 7.2 years) of age, who underwent permanent pacemaker implantations in our hospital. Long-term results including the site of generator pocket were discussed. They are alive and well except two early and three late deaths that were not related to the pacemaker implantation. Twenty-seven epicardial and 11 endocardial electrodes were implanted at the initial operations. Thirteen pulse generators implanted in subaxillar position had no complications, otherwise, 12 subcostal implantation resulted 4 skin necrosis and 3 lead fractures. Eleven anterior chest implantations used for relatively older children resulted in one skin necrosis. We recommend subaxillar implantation for children, especially for small infants. The replacements of pulse generators due to battery depletion were done between 1.7 to 5.5 years (mean 4.0 years). Because epicardial implanted electrodes often show higher stimulation threshold than epicardial ones, pacing rate should be as lowered as possible if the patient had no symptom. Stab-in leads placed on the atrial wall sometimes caused the elevation of stimulation threshold and undersensing. We conclude that the development of more reliable and stable electrode is desired to improve the long term results of pacemaker therapy in children although the improvement of pulse generator itself and the operative procedure.

Adolescent↗

[Study of the localization and the concentration of superoxide dismutase in various thyroid disorders].

The localization of Cu/Zn and Mn superoxide dismutase (SOD), which catalyzes the dismutation of superoxide radicals (O2-) to O2 and H2O2, in various thyroid disorders was studied by an immunohistochemical technique in 20% formalin fixed paraffin embedded thin sections using anti-human Cu/Zn and Mn-SOD antibodies. The concentrations of both SODs in those tissues were also measured by a sandwich enzyme immunoassay technique. Cu/Zn SOD was immunocytochemically stained in most of papillary carcinoma, and some of other disorders. In the normal follicular cells it localized in the perinuclear cytoplasm, whereas in the tumor or hyperplastic cells it was in the cytoplasm homogeneously. Mn SOD was strongly stained in papillary carcinoma and papillary growing cells in adenoma and Graves' disease. The concentrations of Cu/Zn and Mn SOD in every thyroid disorder were higher than those in normal thyroid, and it was much higher in the malignant tumors. The ratio of the concentration of Mn SOD against Cu/Zn SOD in the tissues was higher only in papillary carcinoma compared with that in normal thyroid. In conclusion, SOD seems to be relating to the cell proliferation and differentiation in the thyroid since both SODs increased in tumors and hyperplastic disorders, and Cu/Zn SOD changed its localization and Mn SOD existed predominantly in papillary carcinoma or papillary growing cells.

Carcinoma, Papillary↗