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H Satoh

Publications and source records attributed to H Satoh.

At least 739 records · Page 41Linked to original sources
PubMed1988

Rat liver carboxylesterase: cDNA cloning, sequencing, and evidence for a multigene family.

A cDNA clone was isolated from a rat liver lambda gt11 expression library by screening with polyclonal antibodies raised against a rat liver microsomal carboxylesterase. This clone of 1.8 kb contained an open reading frame encoding a mature protein of 531 amino acids with a predicted molecular weight of 58,084. The 5' portion of the clone coded for 9 amino acids of a putative signal peptide. The 3' end of the clone included an untranslated region and a poly (A) tail. Carboxylesterase active site regions, five potential N-linked glycosylation sites, and 2 postulated cystine disulfide bridges were found in the cDNA-deduced amino acid sequence. Sequences obtained from tryptic peptides and the NH2-terminus of the purified native carboxylesterase were aligned with the deduced amino acid sequence, and the overall identity was 84%. Southern blot analysis suggested the presence of multiple genes. Thus it is concluded that we have cloned a rat liver carboxylesterase, and that this enzyme is a member of a multigene family.

Amino Acid Sequence↗
PubMed1988

Kinetic analysis of in vivo receptor-dependent binding of human epidermal growth factor by rat tissues.

Kinetic analysis of the tissue distribution of human epidermal growth factor (hEGF) in rats was performed in vivo. The plasma disappearance half-life of [125I]hEGF was prolonged by coadministration of unlabeled hEGF, indicating saturation of the mechanism for hEGF removal from the systemic circulation. To analyze the contribution of each tissue to the uptake of hEGF, the amount of [125I]hEGF taken up by each tissue was determined after coadministration of various amounts of unlabeled hEGF. Kinetic analysis of the data yielded the following results. (1) Among the tissues examined, the distribution of [125I]hEGF to the liver, kidney, small intestine, stomach, and spleen was much greater than that accounted for by the distribution to the extracellular space of each tissue. (2) The binding (or uptake) of hEGF by these tissues showed remarkable saturation, which may represent the receptor-dependent binding (or uptake) mechanism. (3) The apparent binding (or uptake) clearance per gram of tissue at the low dose (in the range of first-order kinetics), defined with regard to the arterial plasma concentration, was greatest in the kidney, followed by the liver and small intestine. The larger binding (or uptake) clearance of the kidney compared with that of the liver can be attributed to the higher plasma flow rate (per gram of tissue) in the kidney. However, the intrinsic ability to take up hEGF was much greater in the liver than that in the kidney. The hepatic binding (or uptake) of hEGF at the low dose was almost limited by the hepatic plasma flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

On electrophysiological responses to phorbol esters which stimulate protein kinase C in rabbit sino-atrial node cells.

Effects of phorbol esters on spontaneously beating rabbit sino-atrial (SA) node cells were investigated by means of voltage clamp technique. In a small SA node specimen, 12-O-tetradecanoylphorbol-13-acetate (TPA) 10(-7) mol/l lengthened the cycle length (CL) and at over 3 X 10(-7) mol/l prolonged the action potential duration (APD). Action potential amplitude (APA), maximum diastolic potential (MDP) and maximum rate of rise (Vmax) were unaffected. Amiloride 10(-3) mol/l, an inhibitor of Na+-H+ exchange, did not reverse the phorbol ester-induced effects. In voltage-clamp experiments, TPA 1-10 X 10(-7) mol/l slightly increased the slow inward current (Isi) and the time-dependent inward current (Ih) which activates during hyperpolarization. The outward current and the tail current were reduced, although the activation curve was not shifted along the voltage axis. In the presence of 10(-7) mol/l isoprenaline, TPA produced dysrhythmia and a transient inward current in voltage-clamp experiments. In the presence of 5 X 10(-5) mol/l phenylephrine or 2 X 10(-6) mol/l acetylcholine, TPA also elicited dysrhythmia. 4-beta-phorbol-12,13-dibutyrate (PBD) induced similar electrophysiological effects as TPA, but 4-alpha-phorbol-12,13-didecanoate (PDD) never did so even in the presence of isoprenaline. These results suggest that TPA and PDB might mobilize intracellular Ca2+ via protein kinase C activation in the presence of isoprenaline, phenylephrine or acetylcholine, resulting in dysrhythmia due to delayed afterdepolarization.

Acetylcholine↗
PubMed1988

Phorbol ester does not mimic, but antagonizes the alpha-adrenoceptor-mediated positive inotropic effect in the rabbit papillary muscle.

The phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) was used to examine the hypothesis that phosphoinositide turnover is involved in the regulation of myocardial contractility mediated by stimulation of alpha-adrenoceptors in the mammalian cardiac muscle. Exposure of the isolated rabbit papillary muscle electrically driven at a rate of 1 Hz at a temperature of 37 degrees C to TPA in concentrations of 10-1000 nmol/l for 30 min did not affect the basal force of contraction. The concentration-response curve for the positive inotropic effect of (-)-phenylephrine mediated by stimulation of alpha-adrenoceptors in the presence of (+/-)-bupranolol (100 nmol/l) was shifted to the right and downward by TPA in concentrations of 30-1000 nmol/l, while the effect of (-)-phenylephrine mediated by stimulation of beta-adrenoceptors in the presence of prazosin (100 nmol/l) was not decreased, but slightly enhanced by exposure of the muscle to relatively low concentrations of TPA (10-100 nmol/l). Incubation of the membrane fraction isolated from the rabbit ventricular muscle with TPA in vitro under the same condition as employed in the physiological experiments decreased the specific binding of [3H]prazosin but not that of [3H]CGP-12177, while the non-tumor promoting phorbol ester, alpha PDD, was ineffective. These results indicate that activation of protein kinase C by TPA does not mimic the positive inotropic effect of catecholamines mediated by activation of myocardial alpha-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

Effect of alpha 1-adrenoceptor stimulation with methoxamine and phenylephrine on spontaneously beating rabbit sino-atrial node cells.

Effects of methoxamine and phenylephrine on the action potential and the membrane currents in spontaneously beating rabbit sino-atrial node cells were examined by means of a two-microelectrode voltage-clamp technique. Both methoxamine and phenylephrine (10(-4) mol/l) prolonged the cycle length (CL) and the action potential duration (APD), significantly. At concentrations higher than 3 x 10(-4) mol/l, phenylephrine increased the maximum rate of rise of action potential (Vmax) but methoxamine reduced it. Both agents depolarized the maximum diastolic potential (MDP). These changes in the action potential parameters occurred in a concentration-dependent manner. In the presence of phentolamine (10(-5) mol/l), methoxamine (3 x 10(-4) mol/l) did not modify the action potential parameters. Also, phenylephrine did not affect them during exposure to phentolamine (10(-5) mol/l) and pindolol (10(-7) mol/l). In voltage-clamp experiments, at 10(-3) mol/l both methoxamine and phenylephrine slightly increased the slow inward current (Isi), but decreased the time-dependent outward current (Ik). The steady-state activation variable of Ik (p infinity) was unaffected by these agents. The hyperpolarization-activated current (Ih) was suppressed in the presence of methoxamine, but enhanced in the presence of phenylephrine. An additional application of pindolol (10(-7) mol/l) during exposure to phenylephrine (10(-3) mol/l) depressed the action potential amplitude (APA) and Vmax, and prolonged CL slightly. Under the same condition, all the membrane currents (Isi, Ik and Ih) were decreased. In addition, the time courses of decay for Isi were not modified in the absence and the presence of phenylephrine (10(-3) mol/l) and phenylephrine plus pindolol (10(-7) mol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

Effect of acute ethanol administration on noradrenaline metabolism in brain regions of stressed and nonstressed rats.

The effects of ethanol on noradrenaline (NA) metabolism of brain regions in stressed and nonstressed rats were investigated. Male Wistar rats were injected IP with either saline, or ethanol at 0.5 g/kg or 2 g/kg, 5 min before exposure to 1-hr immobilization stress. Levels of NA and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in various brain regions and plasma corticosterone levels were fluorometrically determined. Immobilization stress caused significant increases in MHPG-SO4 levels in all brain regions examined, i.e., the hypothalamus, amygdala, hippocampus, cerebral cortex and locus coeruleus (LC) region. In nonstressed rats, ethanol significantly increased MHPG-SO4 levels in the hypothalamus, hippocampus and cerebral cortex, but not in the amygdala or in the LC region. In stressed rats, ethanol attenuated stress-induced increases in MHPG-SO4 levels preferentially in the amygdala and LC region, but not in the remaining three regions. Although ethanol per se dose-dependently elevated plasma corticosterone levels in nonstressed rats, ethanol at 2 g/kg attenuated the stress-induced elevation of corticosterone. These results suggest that the attenuating effect of ethanol on stress-induced increases in NA turnover in the amygdala and LC region might be related to the stress-relieving properties of this drug.

Animals↗
PubMed1988

Human HST1 (HSTF1) gene maps to chromosome band 11q13 and coamplifies with the INT2 gene in human cancer.

The human HST1 gene, previously designated the hst gene, and now assigned the name HSTF1 for heparin-binding secretory transforming factor in human gene nomenclature, was originally identified as a transforming gene in DNAs from human stomach cancers by transfection assay with mouse NIH 3T3 cells. The amino acid sequence of the product deduced from DNA sequences of the HST1 cDNA and genomic clones had approximately 40% homology to human basic and acidic fibroblast growth factors and mouse Int-2-encoded protein. We have mapped the human HST1 gene to chromosome 11 at band q13.3 by Southern blot hybridization analysis of a panel of human and mouse somatic cell hybrids and in situ hybridization with an HST1 cDNA probe. The HST1 gene was found to be amplified in DNAs obtained from a stomach cancer and a vulvar carcinoma cell line, A431. In all of these samples of DNA, the INT2 gene, previously mapped to human chromosome 11q13, was also amplified to the same degree as the HST1 gene.

Animals↗
PubMed1988

Enflurane metabolism produces covalently bound liver adducts recognized by antibodies from patients with halothane hepatitis.

The existence of a rare syndrome of "enflurane hepatitis" similar to that described for halothane and of a cross-sensitization between halothane and enflurane has been controversial, largely due to equivocal clinical case reports and a lack of a plausible molecular mechanism for the hepatotoxicity. The present study suggests a possible hypersensitivity basis for enflurane hepatitis and the apparent cross-sensitization between halothane and enflurane involving covalently bound liver microsomal adducts. Immunoblotting studies have revealed that antibodies in the sera of six patients with halothane hepatitis recognize liver microsomal antigens of Mr = 100,000, or both 100,000 and 76,000, formed in rats treated with enflurane or halothane. These antigens were not detected in microsomes from isoflurane- or sesame oil-treated rats. The recognition of these antigens could be abolished by preincubation of the sera with microsomes from halothane-treated rats. These data suggest that the difluoromethoxydifluoroacetyl halide metabolite of enflurane, as well as the trifluoroacetyl halide metabolite of halothane, covalently bind to similar hepatic proteins, and may become immunogens in susceptible patients. This mechanism may also account for the apparent cross-sensitization between halothane and enflurane anesthesia, and the development of hepatic necrosis.

Animals↗
PubMed1988

Protection of isolated rat gastric cells by prostaglandins from damage caused by ethanol. Preliminary report.

The direct effects of exogenous and endogenous prostaglandins (PGs) on damage to isolated gastric cells caused by ethanol were assessed in rats. 16,16-Dimethyl-PGE2 (dmPGE2) significantly inhibited cellular damage caused by 15% ethanol in three fractions rich in surface epithelial cells, rich in parietal cells, and rich in chief cells at the concentration of 10(-6) M but it was less effective either at a lower concentration (10(-7) M) or a higher concentration (10(-5) M). The surface epithelial cells synthesized 6-keto-PGF1 alpha and thromboxane (TX) B2 predominantly, and less PGE2. Indomethacin completely inhibited synthesis of these prostanoids. This agent induced cellular damage in a dose-related way and this damage was inhibited by 10(-6) M dmPGE2. Indomethacin alone at the dose of 10(-4) M, at which synthesis of prostanoids was completely inhibited, did not affect the viability of the cells, but made the cells susceptible to damage caused by 15% ethanol. This effect of a minimum dose of indomethacin was inhibited by 10(-6) M dmPGE2. These results suggest that dmPGE2 has a direct protective effect on the isolated gastric cells in rats, and this effect is not limited to a specific cell type. That endogenous prostanoids have a possible role in the maintenance of cellular integrity is also postulated.

Animals↗
PubMed1988

Nucleotide sequence and chromosomal mapping of the human c-yes-2 gene.

We molecularly characterized the second gene, c-yes-2, of two copies of yes-related genes which we previously found to contain in the human genome. First, nucleotide sequence analysis revealed that the c-yes-2 gene is a pseudogene of the c-yes-1 gene. Second, by using two independent methods, hybridization of both DNAs from sorted chromosomes and metaphase spreads with c-yes-2 DNA, we assigned the c-yes-2 gene to chromosome 22q11.2. This chromosomal localization is consistent with that given in our previous report. The failure of proper mapping in our experiment might have been caused by instability of hybrid cell clones.

Base Sequence↗
PubMed1988

Evidence for movement of the alpha-amylase gene into two phylogenetically distant Bacillus stearothermophilus strains.

The gene for an alpha-amylase cloned from strain DY-5 of Bacillus stearothermophilus was used to examine to what extent the corresponding genes are structurally similar in other B. stearothermophilus strains. The structure of the gene itself was almost identical in DY-5 and a group of strains represented by strain 799. The gene was not detected at all in strain DSM2334, which was phenotypically amylase deficient. Comparison of the structure of 5S rRNA and electrophoretic pattern of the ribosomal proteins indicates that strains DY-5 and DSM2334 are closely related to each other, whereas strain 799 is phylogenetically very distant from the two. We estimate that strain 799 separated from DY-5 and DSM2334 some 420 million years ago. Nucleotide sequencing of the region containing the amylase gene from strains DY-5 and 799 revealed the presence of a 3.4-kilobase stretch that was highly similar in the two strains. Furthermore, comparison of the restriction map surrounding the amylase gene of DY-5 with that of a corresponding region in DSM2334 indicated that the former strain contained an extra segment 5.5 kilobases in length, which included the 3.4-kilobase stretch mentioned above. This segment was missing in DSM2334. It thus appears that the alpha-amylase gene was brought into strains DY-5 and 799 from outside despite a large phylogenetic distance.

Base Sequence↗
PubMed1988

Gastric cytoprotection by tetraprenylacetone in human subjects.

We assessed the inhibition by tetraprenylacetone (TPA) of gastric mucosal damage caused by ethanol in human subjects. Seventeen healthy volunteers were given either TPA (a 50-mg capsule) or a placebo 3 times daily for 5 days. Then, 20 ml of 70% ethanol were sprayed onto the gastric antrum and 15 min later, visible mucosal lesions were evaluated with an endoscope, and biopsy specimens were taken from mucosa that looked normal but had been sprayed with ethanol. The specimens were observed by light microscopy and scanning electron microscopy. The gross mucosal damage was significantly less (p less than 0.05) in the subjects given TPA than in those given the placebo. Hyperemia and hemorrhage in the mucosa and surface epithelial damage were also significantly less (p less than 0.05) in the subjects given TPA. The results suggested that TPA protects the gastric mucosa from damage by ethanol as judged not only by the gross appearance of the mucosa but also by microscopic observation.

Adult↗
PubMed1988

Gastric mucosal resistance and prostanoid levels after cimetidine treatment in rats.

We studied the effects of cimetidine administered intraperitoneally to rats at a dose of 20 mg/kg twice daily for 7 days on gastric mucosal integrity and endogenous prostaglandins. Cimetidine significantly (p less than 0.05) reduced the mucosal concentration of prostaglandin E2 and 6-keto-prostaglandin F1 alpha both 30 min and 24 h after the last injection of this drug, and the level had returned to normal 5 days later. Cimetidine significantly (p less than 0.01) enhanced gastric mucosal lesions induced with 0.6 N HCl 24 h after the last injection; this increased vulnerability had disappeared 5 days later. Cimetidine did not affect the synthesis of these prostanoids in isolated gastric mucosa in vitro. Gastric secretion, which was significantly (p less than 0.05) inhibited 30 min after the last injection of cimetidine, returned to control level 24 h after the last injection. The increase in gastric mucosal vulnerability observed 24 h after the last cimetidine injection might be related to a decrease in the prostanoid content and recovery of acid secretion.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Protection of gastric surface epithelial cells of rats by 16,16-dimethyl prostaglandin E2 and sofalcone, a synthetic flavonoid derivative of sophoradin, against ethanol.

We studied the effects of 16,16-dimethyl prostaglandin E2 (dm-PGE2) and sofalcone, a new antiulcer agent developed in Japan, on ethanol damage to isolated surface epithelial cells (SEC) in vitro and gastric mucosa of rats in vivo. Rats were given 5 micrograms/kg dm-PGE2, 30, 100, or 300 mg/kg sofalcone, or the vehicle, intraperitoneally. In the in vitro study, damage of the SEC isolated from rats given dm-PGE2 or sofalcone was significantly less after exposure to 15% ethanol than for the SEC from the control rats. In the in vivo study, the 15% ethanol did not induce gross visible damage, but did cause surface epithelial damage in the control rats as judged by scanning electron microscopy. This damage was inhibited by dm-PGE2 or sofalcone. Damage from absolute ethanol was inhibited by both of the agents as judged by the gross appearance, but the surface epithelium was damaged in all rats. We concluded that dm-PGE2 and sofalcone protect gastric mucosa from gross damage caused by absolute ethanol, and protect SEC both in vivo and in vitro from being damaged by ethanol when the concentration of ethanol is 15%.

16,16-Dimethylprostaglandin E2↗
PubMed1988

Myopathy and encephalopathy in chick embryos experimentally infected with Akabane virus.

Chick embryos infected with Akabane virus by the yolk sac route at 6 days of incubation developed polymyositis and encephalitis. At 3 to 7 days after inoculation, skeletal muscles had myotubule degeneration, clumping of muscle cell nuclei, and infiltration of heterophils; dysplasia and aplasia were evident at 9 to 15 days after inoculation. Changes in the cerebral neostriatum and optic lobes at 2 to 11 days after inoculation included necrosis of primordial nervous tissue, hemorrhages, and hyperplasia of the vascular endothelial cells. Cavities were in nervous tissue subsequent to encephalitis. Hydranencephaly and vascular wall thickening were found 13 and 15 days after inoculation. Embryos infected intravenously at 15 days incubation had foci of encephalitis 3 to 6 days after inoculation, including neuronal degeneration, neuroglial hyperplasia, vascular endothelial proliferation, and heterophil infiltration.

Anencephaly↗