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Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 19 recordsLinked to original sources
PubMed1992

[Expandable metallic stent therapy for SVC syndrome--effects on local venous pressure, vascular diameter, symptoms, and these correlations].

To evaluate the efficacy of Z-stent therapy for SVC syndrome, we studied changes in the pressure, the diameter of stenotic lumen and the symptoms in the cases of SVC syndrome with higher pressure than 30 cmH2O at distal to the stenosis. The symptoms were classified and graded to be scored up. Immediately after the Z-stent placement into the stenotic lesions, the venous pressure distal to the stenosis decreased from 36.0 +/- 3.4 cmH2O to 12.0 +/- 12.0 cmH2O (p < 0.001), the diameter of stenotic lumen increased from 3.3 +/- 3.4 mm to 14.0 +/- 3.4 mm (p < 0.01). According to the remarkable symptomatic improvements the averaged score decreased from 6.7 to 1.3 (p < 0.01). The pressure, the diameter and the symptom scores were highly correlated each other (magnitude of gamma not equal to 0.9). Among two cases with the right atrial pressure increase by 2 cmH2O after the placement one suffered transient cardiac in compensation due to overload by reperfusion. Conclusively, the Z-stent therapy was very effective on the SVC syndrome in reducing abnormally elevated venous pressure due to the stenosis, and relieving the symptoms, while the pressure monitor was necessary.

Aged↗
PubMed1992

Exogenous metallothionein and renal toxicity of cadmium and mercury in rats.

The relative tissue distribution and toxicity of cadmium (Cd) and mercury (Hg) in the liver and kidneys of rats when the metals are administered as either inorganic salts or complexed with MT were studied. Male Sprague-Dawley rats were injected (i.v.) with Cd or Hg inorganic salt of chloride or in a complex of MT at a dose of 0.3 mg/kg body weight. The concentration of MT and metals in plasma and urine was monitored for 7 days, at the end of which the rats were killed. Injection of both HgCl2 and Hg-MT induced the synthesis of MT only in the kidney but not in the liver, whereas CdCl2 and Cd-MT injections induced MT synthesis in both liver and kidney, respectively. Plasma MT levels increased 3 days after CdCl2 but not after HgCl2 injection, suggesting that hepatic MT may be an important source of plasma MT under our experimental conditions. Renal toxicity was observed morphologically and by an increase in blood urea nitrogen, plasma creatinine, proteinuria in rats injected with Cd-MT and both forms of Hg. Urinary MT excretion was significantly elevated in Cd-MT injected rats compared with those injected with CdCl2. However, HgCl2 and Hg-MT injected rats showed no significant difference in urinary MT excretion. The magnitude in the renal accumulation of Hg is similar after the administration of Hg-MT or HgCl2, but our findings suggest that the site of epithelial injury may be different. Injury effects of Hg-MT localized mainly in the terminal portions of the proximal convoluted tubule and the initial portions of the proximal straight tubule whereas inorganic Hg caused necrosis in pars recta segments of the proximal tubule.

Animals↗
PubMed1992

Affinity cross-linked delta-opioid receptor in NG108-15 cells is low molecular weight (25 kDa) and coupled to GTP-binding proteins.

The affinity cross-linking of the delta-opioid receptor in neuroblastoma x glioma NG108-15 cells was undertaken using (3-[125I]iodotyrosyl27)human-beta-endorphin ([125I]beta-endorphin) and disuccinimidyl suberate (DSS) or bis(sulfosuccinimidyl) suberate (BS3) in order to estimate molecular size. Following sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis, two radioactive bands were observed. Labeling of a major band of 29 kDa diminished in the presence of unlabeled selective delta-opioid agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE), in a concentration-dependent manner, while labeling of a minor band of 58 kDa was hardly affected. The labeling intensity of the 29 kDa band decreased by addition of guanosine 5'-(3-o-thio)triphosphate (GTP gamma S) or by pretreatment of cells with pertussis toxin. These results, taking the molecular weight of covalently bound beta-endorphin (3.6 kDa) into consideration, suggest that the delta-opioid receptor in NG108-15 cell membrane is a 25 kDa protein which is coupled to pertussis toxin-sensitive guanosine triphosphate-binding proteins (G-proteins).

Cell Membrane↗
PubMed1992

Characterization of alpha 1-adrenoceptor subtypes labeled by [3H]prazosin in single cells prepared from rabbit thoracic aorta.

alpha 1-Adrenoceptor agents with alpha 1-adrenoceptor subtypes sensitive and insensitive to inactivation by chloroethylclonidine were characterized in single cells prepared from rabbit thoracic aorta. WB 4101, 5-methylurapidil and spiperone interacted with high- and low-affinity sites labeled by [3H]prazosin. Chloroethylclonidine 10 microM pretreatment eliminated the low-affinity sites of displacement curves obtained with WB 4101 and 5-methylurapidil but had no effect on the high-affinity site for these agents. The treatment also reduced the site of the displacement curve obtained with spiperone but eliminated only the high-affinity site. Methoxamine and clonidine, alpha-adrenoceptor agonists, interacted with binding sites labeled by [3H]prazosin. The displacement curve for methoxamine was not affected by chloroethylclonidine 10 microM pretreatment, while that for clonidine was partially eliminated by the same type of pretreatment. These results suggest that, in single cells prepared from rabbit thoracic aorta: (1) WB 4101, 5-methylurapidil and spiperone interact with differing affinity at sites labeled by [3H]prazosin; (2) chloroethylclonidine-sensitive and -insensitive [3H]prazosin binding sites correspond to those with low- and high-affinity sites for WB 4101 and 5-methylurapidil, and a high- and low-affinity for spiperone, respectively; and (3) chloroethylclonidine treatment was shown to have no effect on the displacement curve of methoxamine but a partial effect on that of clonidine.

Animals↗
PubMed1992

Carcinoids and endocrine cell micronests of the minor and major duodenal papillae. Their incidence and characteristics.

BACKGROUND: There have been no reports about the incidence and characteristics of carcinoids and endocrine cell micronests (ECM) of the minor and major duodenal papillae. METHODS AND RESULTS: The minor and major duodenal papillae of 78 consecutive autopsy and 117 surgical specimens were examined histologically using mirror-image paraffin-embedded tissue samples. ECM were found frequently in these areas in hematoxylin and eosin-stained sections, and their aggregation patterns were classified into four types: nodular type (Type 1, 2 of 167 in the minor papilla and 1 of 145 in the major papilla), scattered type (Type 2, 39 of 167 and 6 of 145), orifice type (Type 3, 7 of 167 and 0 of 145), and islet-like type (Type 4, 14 of 145 and 0 of 145, respectively). Criteria of neoplastic or nonneoplastic ECM were defined tentatively by histologic and immunohistochemical analyses of the ECM. Type 4 was regarded to be atrophic or regenerating islets of Langerhans. Distinct carcinoids (Type 1), neoplastic ECM (39% of all Type 2 and 3), and nonneoplastic ECM (61% of all Type 2 and 3) were found in 1.2%, 9.0%, and 16.2% of 167 samples of the minor papilla and 0.7%, 1.4%, and 2.8% of 145 specimens of the major papilla, respectively. The endocrine cells composing the carcinoids and the ECM usually were immunoreactive for somatostatin and/or pancreatic polypeptide (PP). They were negative for S-100 beta. CONCLUSION: In duodenal papillae, especially in the minor duodenal papilla, carcinoids and ECM seem to occur more frequently than generally thought, and predominantly consist of somatostatin and/or PP containing cells.

Adolescent↗
PubMed1992

Histologic follow-up of ampullary adenomas in patients with familial adenomatosis coli.

BACKGROUND: The major duodenal papilla is a common site of extracolonic adenoma in patients with familial adenomatosis coli (FAC). However, there have been no reports which have systematically discussed histologic change in atypia of ampullary adenomas with time by their location in the papilla. METHODS AND RESULTS: The major duodenal papillae of 23 patients with FAC were followed endoscopically and histologically for an average of 7.7 years (range, 1 year to 14 years 7 months). Tubular adenomas were detected histologically in 17 of the 23 patients at the first (14) or following examinations (3). They occurred in the orifice and/or ampulla in 11 patients and in the surface of the papilla in 8 patients. Three of the 11 orifice and/or ampulla adenomas contained moderate to severe atypia. There was no histologic change in atypia or malignant transformation during the follow-up period. CONCLUSIONS: In the patients with FAC, the major duodenal papilla had adenoma, i.e., precancerous lesion, at a high incidence (74%), and it is reported that the ampulla of the papilla tended to have extracolonic carcinoma. Therefore, it is necessary to follow duodenal papillae of patients with FAC carefully and take biopsy specimens repeatedly from various sites, especially from the orifice or ampulla even if the papilla seems to be normal.

Adenoma↗
PubMed1992

Bifemelane enhances high K(+)-evoked release of glutamate from mossy fiber synaptosomes of guinea-pig hippocampus.

We have shown that bifemelane augments long-term potentiation in the mossy fiber-CA3 system, but not in the Schaffer collateral-CA1 system. To elucidate the mechanism of action of bifemelane in relation to pathway-specific augmentation of long-term potentiation, we prepared a mossy fiber terminal-rich synaptosomal fraction (P3) from guinea-pig hippocampus and investigated the effect of bifemelane on the release of glutamate from these synaptosomes, using an in vitro superfusion technique. Bifemelane (0.01-1 microM) dose dependently increased the 30 mM K(+)-evoked release of glutamate from the P3 fraction, without affecting glutamate release from a conventional synaptosomal P2 fraction. This stimulatory effect of 1 microM bifemelane was abolished by 100 microM H-7, which also suppressed the increase in K(+)-evoked glutamate release by phorbol 12,13-dibutyrate (1 microM). Bifemelane (1 microM) induced the translocation of protein kinase C activity from cytosol to membrane in the P3 fraction (which contains large and irregular-shaped synaptosomes probably derived from mossy fiber terminals), but not in the P2 fraction. These findings suggest that bifemelane directly acts on mossy fiber terminals to potentiate depolarization-induced glutamate release, which may be at least partly mediated by the translocation (activation) of protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

The involvement of muscarinic, beta-adrenergic and metabotropic glutamate receptors in long-term potentiation in the fimbria-CA3 pathway of the hippocampus.

Possible modulatory actions of endogenous neurotransmitters on long-term potentiation (LTP) were investigated in the fimbria-CA3 pathway of rat hippocampal slices. Bath application of atropine (10 microM), but neither timolol (10 microM) nor D,L-2-amino-3-phosphonopropionate (AP3, 100 microM), significantly attenuated LTP induced by 20 pulses of 50 Hz stimulation. When stronger stimulation (3 trains of 100 Hz, 100 pulses) was used for the induction of LTP, timolol significantly attenuated LTP, but atropine and AP3 did not. These results suggest that, under specified conditions, endogenous acetylcholine through muscarinic receptors, and noradrenaline through beta-adrenergic receptors may modulate the generation of LTP in the fimbria-CA3 pathway. Metabotropic glutamate receptors may be involved not in the generation of LTP but in low-frequency synaptic transmission, since 300-1,000 microM AP3 greatly reduced, or abolished synaptic transmission in this pathway.

Adrenergic beta-Antagonists↗
PubMed1992

Evidence that Caenorhabditis elegans 32-kDa beta-galactoside-binding protein is homologous to vertebrate beta-galactoside-binding lectins. cDNA cloning and deduced amino acid sequence.

We have cloned a full-length cDNA for a beta-galactoside-binding protein with a relative molecular mass of 32 kDa (32-kDa GBP), recently purified from a nematode, Caenorhabditis elegans (Hirabayashi, J., Satoh, M., Ohyama, Y., and Kasai, K. (1992) J. Biochem. 111, 553-555). The clone contained a single open reading frame encoding 279 amino acids, including the initiator methionine. Significant sequence homology to metal-independent beta-galactoside-binding lectins (25-30% identities), which had previously been found only in vertebrates, was observed. Moreover, the nematode 32-kDa GBP proved to have a unique polypeptide architecture; that is, it is composed of two tandemly repeated homologous domains, each consisting of about 140 amino acids. The internal homology was about 32%. Thus, this protein is constructed with a duplicated fundamental unit which is similar to the subunit of vertebrate 14-kDa lectins. In spite of the extreme phylogenic distance between nematodes and vertebrates (divergence greater than 6 x 10(8) years ago), both of the two repeated domains of the nematode 32-kDa GBP retained most of the amino acid residues conserved in vertebrate lectins. This means that members of the metal-independent animal lectin family are distributed much more widely than had been believed: from nematodes to vertebrates. The implication is that proteins belonging to this family have fundamental roles which are not restricted to vertebrates but are common to almost all animals.

Amino Acid Sequence↗
PubMed1992

Involvement of postsynaptic G proteins in hippocampal long-term potentiation.

The possible involvement of postsynaptic guanosine 5-triphosphate (GTP)-binding proteins (G proteins) in long-term potentiation (LTP) was studied in rat hippocampal slices, using whole-cell recording techniques. The inclusion of guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) or guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) in the recording pipette significantly reduced or abolished the baclofen-induced hyperpolarization of pyramidal neurons, which indicates uncoupling of the signal transduction from G protein-coupled receptors by these compounds. Both GDP beta S and GTP gamma S significantly attenuated the magnitude of LTP in the fimbria-CA3 synapses, but not in the mossy fiber-CA3 synapses. GTP gamma S did not attenuate LTP in the Schaffer-CA1 synapses. The effects of guanine nucleotide analogs on fimbrial LTP were reversed by postsynaptic depolarization during high frequency stimulation. These results suggest that postsynaptic G proteins may be involved in the generation of LTP in the fimbrial synapses, possibly by affecting membrane depolarization during high frequency afferent activation.

Animals↗
PubMed1992

Expression of renal organic cation transporter in Xenopus laevis oocytes.

The expression of the organic cation transport system of rat renal proximal tubules has been studied in Xenopus laevis oocytes injected with poly(A)+ RNA from the rat renal cortex. The effectiveness of the technique was confirmed by examining expression of the Na+/D-glucose co-transporter. Compared with water-injected and non-injected oocytes, the injection of total poly(A)+ RNA resulted in about a 3-fold increase in tetraethylammonium (TEA) uptake activity. TEA uptake by poly(A)(+)-RNA-injected oocytes was time-dependent and was inhibited by cimetidine and HgCl2, but not by p-aminohippurate. After size-fractionation on a sucrose density gradient, a 1.4-2.4 kb poly(A)+ RNA fragment was identified that expressed the organic cation transport system in oocytes. These results demonstrate that the renal organic cation transporter was expressed in oocytes and that this expression system can provide an effective assay procedure for cloning of the organic cation transporter.

Animals↗
PubMed1992

Metabotropic responses to acetylcholine and serotonin of Xenopus oocytes injected with rat brain mRNA are transduced by different G-protein subtypes.

To assign the GTP-binding protein (G-protein) subtype involved in the signal transduction from exogenous receptors to phospholipase C in the Xenopus oocyte translation system, antisense DNA complementary to rat G-protein alpha-subunit mRNA was designed and injected together with rat brain poly(A)+ RNA. Current response of mRNA-injected oocytes to acetylcholine (ACh) was suppressed dose-dependently by a co-injection of Gil alpha-antisense DNA, but response of the same oocytes to serotonin (5-HT) was not inhibited. In the oocytes co-injected with Go alpha-antisense DNA, the 5-HT response was more effectively suppressed than the ACh response. These results suggest that Go alpha but not Gil alpha intermediates brain 5-HT1C receptor function, and in contrast, muscarinic receptors derived from rat brain utilize Gil alpha rather than Go alpha to activate phospholipase C.

Acetylcholine↗
PubMed1992

Tumor necrosis factor stimulates DNA synthesis of mouse hepatocytes in primary culture and is suppressed by transforming growth factor beta and interleukin 6.

In a previous study, we revealed that tumor necrosis factor (TNF) was secreted in mouse liver at an early phase of liver regeneration after partial hepatectomy. Here, we investigated direct actions of TNF on the in vitro DNA synthesis of adult mouse hepatocytes in primary culture. TNF enhanced both 3H-TdR uptake and the number of 3H-TdR-labeled nuclei of hepatocytes. Their time courses were similar to those by epidermal growth factor (EGF) with about a 15 h lag period and a peak period of 24-48 h. This action of TNF was abrogated by DNA polymerase alpha inhibitor, aphidicolin and blocked specifically by anti-TNF antibody. The actions of rmTNF and rhTNF were not distinguishable; ED50 was about 7.5U/ml (5ng/ml) and 30U/ml (20ng/ml) for maximal response (about 2-fold or more of control). Other inflammatory monokines showed differential effects on in vitro DNA synthesis of hepatocyte. Neither type of interleukin 1 affected hepatocyte DNA synthesis in the range examined (up to 50 ng/ml). IL-6 markedly inhibited the hepatocyte DNA synthesis stimulated by TNF and EGF. The action of TNF was completely suppressed by transforming growth factor beta, which is known as a potent inhibitor of hepatocyte growth. Interferon gamma also blocked this TNF action when added simultaneously. These results indicate that the activation of tissue macrophages and local secretion of TNF in liver after partial hepatectomy is of physiological importance in liver regeneration, in part by a direct stimulation of hepatocyte DNA synthesis. Cytokines induced by TNF may also participate in the later termination of liver regeneration.

Animals↗
PubMed1992

Effect of coadministration of selenite on the toxicity and antitumor activity of cis-diamminedichloroplatinum (II) given repeatedly to mice.

The effect of selenite coadministration on the toxicity and antitumor activity of repeated treatment with high doses of cis-diamminedichloroplatinum (cis-DDP) was examined in mice. Sodium selenite was injected s.c. into separate abdominal sites of mice together with cis-DDP at a molar ratio of 1:3.5 (selenite to cis-DDP) on day 0. The same amount of selenite was given daily for 4 subsequent days (days 1-4). This fixed administration schedule was repeated weekly for a total of 7 weeks. Under the experimental conditions used, the lethal toxicity, renal toxicity [indicated by an increase in blood urea nitrogen (BUN) and plasma creatinine levels], hepatic toxicity (indicated by an increase in plasma GPT and GOT activity), and myelotoxicity (indicated by a decrease in the numbers of leukocytes and platelets) observed in mice given repeated doses of cis-DDP alone (15 or 25 mumol/kg, s.c.) were significantly depressed by the coadministration of sodium selenite. Treatment with cis-DDP alone (15, 20, or 25 mumol/kg, s.c.) resulted in some dose-dependent prolongation of the life span of mice transplanted either s.c. with colon adenocarcinoma 38 (colon 38) or i.p. with P388 leukemia (P388) but did not completely depress the tumor growth, and the animals died of either progressive disease or cis-DDP-induced toxicity. However, following the coadministration of 7.1 mumol/kg selenite with 25 mumol/kg cis-DDP, all of the mice transplanted either s.c. with colon 38 or i.p. with P388 survived for as long as 4 months after the end of the treatment and showed no evidence of malignancy. These results indicate that selenite coadministration enables the use of increasing doses of cis-DDP and, consequently, enhances the antitumor effect of cis-DDP by depressing its side effects.

Adenocarcinoma↗
PubMed1992

Neutron-capture therapy of murine ascites tumor with gadolinium-containing microcapsules.

Gadolinium-containing microcapsules were evaluated as an agent for gadolinium neutron-capture therapy. Mice were inoculated intraperitoneally with 10(7) Ehrlich ascites tumor cells and gadolinium microcapsules and exposed to thermal neutrons for 12 min (approximately 1.86 x 10(12) neutrons cm-2). Significantly more mice given gadolinium microcapsules than those given placebo microcapsules or control survived for 60 days and considerably longer (P < 0.0001), indicating that gadolinium neutron-capture reactions effectively suppressed the growth of ascites tumor cells in mice. The results suggest that these microcapsules are an effective gadolinium carrier for neutron-capture therapy.

Animals↗
PubMed1992

Effect of preinduction of metallothionein on paraquat toxicity in mice.

The effect of pretreatment with metallothionein (MT)-inducing metals (Zn, Cu, Bi, Co, Cd or Hg) on paraquat (PQ) toxicity was investigated in mice. PQ lethality was remarkably reduced by pretreatment with the above MT-inducing metals. The protective effect of pretreatment with these metals on PQ lethality was significantly correlated with MT levels in the lung, a target tissue of PQ toxicity, in mice administered MT-inducing metals, but not with MT in the liver or kidney. The increase in pulmonary lipid peroxidation in mice treated with PQ was significantly inhibited by Zn pretreatment. Zn was the most effective of the MT-inducing metals used in this experiment in protecting mice against PQ lethality. Of those monitored, the only pulmonary free radical scavenging factor increased by Zn pretreatment was MT. Other free radical scavenging factors (activities of superoxide dismutase, glutathione peroxidase and catalase, and concentration of non-protein thiols level) were not influenced by Zn treatment. These results indicate that the induction of pulmonary MT protects against the lethality and lung toxicity of PQ. Pulmonary MT may scavenge free radicals produced by PQ, thereby protecting against lethal pulmonary toxicity.

Animals↗