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Biomedical subjects

H Satoh

Publications and source records attributed to H Satoh.

At least 775 records · Page 43Linked to original sources
PubMed1987

Molecular cloning and sequence analysis of two rat major globin cDNAs.

Two cDNA clones for globins of the adult Wistar rat were isolated from a reticulocyte cDNA library and the nucleotide sequences of the inserts were determined. One clone contained a cDNA insert consisting of 556 bp and the other contained one of 577 bp, both covering the entire coding sequences for rat globins. Comparisons of their predicted amino acid sequences with known sequences of rat globins revealed that these cDNAs coded for a rat major alpha- and a major beta-globin, I alpha and II beta, respectively. The cause of diversity of rat globins was discussed in terms of the nucleotide sequences of cDNAs and known amino acid sequences of globins.

Amino Acid Sequence↗
PubMed1987

Actions of antisecretory agents on proton transport in hog gastric microsomes.

The properties of K+-stimulated ATP hydrolysis (K+-ATPase) and vesicular accumulation of H+ (H+ accumulation) in hog gastric microsomes were investigated. The microsomes consisted of smooth surfaced vesicular particles, 70-300 nm in diameter. Both the activities of ATPase and the vesicular accumulation of H+ were stimulated by K+ in the presence of Mg2+, and enhanced by the K+-ionophore, valinomycin. However, there were differences in regulation of K+-ATPase and H+ accumulation by K+ ions, i.e. K+ at concentrations higher than 10 mM decreased K+-ATPase activity but further enhanced H+ transport. This observation suggests that the two reactions are partly independent. The H+ accumulation was inhibited by omeprazole, fenoctimine, spermine, and NaSCN, but not by cimetidine, prostaglandin E2, and atropine. The inhibitory effect of omeprazole on H+ accumulation paralleled the inhibition of K+-ATPase, while fenoctimine, spermine, and NaSCN suppressed H+ accumulation, without inhibiting K+-ATPase, under appropriate concentrations. In addition, the spontaneous diffusion of H+ across the microsomal membrane was markedly enhanced by fenoctimine, but not by the other agents used. These results indicate that omeprazole inhibits H+ accumulation by inhibiting K+-ATPase, fenoctimine suppresses H+ accumulation mainly by increasing the loss of accumulated H+ from the microsomal vesicles, spermine and NaSCN reduce H+ accumulation by inhibiting the transport of H+ into microsomal vesicles.

Adenosine Triphosphatases↗
PubMed1987

Induction of the oscillatory current by low concentrations of caffeine in sheep cardiac Purkinje fibres.

The actions of low concentrations of caffeine (0.5-2 mmol/l) on the transient inward oscillatory current (Ios) and the inward tail current (Iex) were studied in sheep cardiac Purkinje fibres by means of a two microelectrode voltage clamp method. The following results were obtained. Caffeine: induced an Ios when this current was not already present; increased the amplitude (within limits) and consistently decreased the time to peak of an already present Ios; increased Iex upon which Ios may be superimposed; shifted the depolarizing threshold for the appearance of Ios to more negative and the repolarizing threshold to less negative values; increased the effects of strophanthidin of Ios and Iex; exaggerated the effects of high [Ca]o which by itself mimicked some of the actions of caffeine; had a small effect of Ios and Iex in low [Ca]o; 8. reversed the effect of norepinephrine on Iex; enhanced the effects of trains of clamps and of longer clamp steps on Ios and Iex. It is concluded that low concentrations of caffeine facilitate the manifestations of calcium overload thereby inducing or exaggerating the oscillatory and tail currents and that these effects are modulated by the cellular calcium load but are not mediated through adrenergic mechanisms.

Animals↗
PubMed1987

Endogenous prostaglandin E2 in gastric mucosa of patients with alcoholic cirrhosis and portal hypertension.

The amount of prostaglandin E2 in endoscopic biopsy specimens from the mucosa of the gastric corpus and antrum of 10 healthy volunteers and 8 patients with alcoholic cirrhosis (7 of whom had portal hypertension) was measured by radioimmunoassay. The mean prostaglandin E2 level in both corpus and antral mucosa was significantly lower in the cirrhotic patients (p less than 0.025). Release of prostaglandin E2 into the gastric cavity was also significantly less in the cirrhotic patients in the basal state (p less than 0.025) and in that of tetragastrin stimulation (4 micrograms/kg, s.c.; p less than 0.01). There was no significant difference in acid secretion between the two groups of subjects. The histologic findings of biopsy specimens showed no difference in the extent of chronic gastritis between the cirrhotic patients and healthy subjects. Therefore, this deficiency of prostaglandin E2 in the gastric mucosa of cirrhotic patients was not related to acid secretion or chronic gastritis.

Adult↗
PubMed1987

Reverse-transcribed pseudogenes of U1 small nuclear RNA presumably amplified in the rat genome together with the flanking region.

We have examined 25 independent rat genomic clones each of which contains a U1 RNA gene or a pseudogene. We have found five clones whose restriction maps are identical with or overlapping one another. These clones contain sequences which are co-linear with that of U1 RNA except for one or two nucleotides (nt). They also contain 21-23-nt poly(A) stretches immediately after U1 RNA homology. In addition, the U1 RNA-poly(A) regions are surrounded by the same direct repeat sequences. Therefore, they seem to be pseudogenes which have been generated by the reverse transcription of poly(A)-tailed U1 RNA followed by the insertion of the transcript into the genome. Furthermore, conservation of the sequences extends over at least 18 kb of the flanking sequences. This suggests a family of conserved reverse-transcribed pseudogenes, which implies amplification of an original pseudogene. It is also suggested that the target sequence without insertion of a U1 RNA sequence has been amplified. The mechanisms for the amplification and sequence conservation are discussed.

Animals↗
PubMed1987

Binding of mercury to metallothionein-like protein in fetal liver of the guinea pig following in utero exposure to mercury vapor.

After exposure of pregnant guinea pigs to mercury vapor, the soluble fraction of maternal or fetal liver was chromatographed on a Sephadex G-75 column. In the fetal liver, more than 50% of the mercury was bound to metallothionein-like protein having a molecular weight of about 10,000-12,000. On the other hand, the bulk of the eluted mercury in the maternal liver was associated with a high molecular weight protein, with only a small amount associated with metallothionein-like protein. The findings suggest that fetal metallothionein-like protein plays a role in preventing further distribution of mercury after in utero exposure to mercury vapor.

Animals↗
PubMed1987

Noradrenergic function and the dexamethasone suppression test in depression.

We measured the plasma free 3-methoxy-4-hydroxyphenylglycol (MHPG) levels and the serum cortisol levels before and after the oral administration of dexamethasone. There was not a significant difference in the plasma free MHPG levels between the patients with major depression and normal subjects. There was a significant positive correlation between the plasma MHPG levels and postdexamethasone cortisol levels in patients with major depression. This indicates that there exists a certain relation between abnormalities of the central noradrenergic systems and hypothalamic-pituitary-adrenal axis in patients with major depression. The mean total scores of the Hamilton Rating Scale for Depression of the first (MHPG less than 5 ng/ml) and third (10 ng/ml less than or equal to MHPG) groups were significantly higher than those of the second (5 less than or equal to MHPG less than 10 ng/ml) group.

Depressive Disorder↗
PubMed1987

[Host mediated anti-tumor effect of Nocardia rubra cell wall skeleton on syngeneic tumor in mice].

The mode of action of Nocardia rubra cell wall skeleton (N-CWS) on Meth A fibrosarcoma (Meth A) was studied in BALB/c mice. N-CWS suppressed or regressed the intradermal growth of syngeneic Meth A cells in normal BALB/c and athymic BALB/c mice. The intradermally and subcutaneously infiltrated cells harvested from injection sites of N-CWS in normal mice showed in vitro cytotoxic activity against Meth A cells. Pretreatment of normal BALB/c mice with immunosuppressing agents such as hydrocortisone, carrageenan, or silica particles significantly reduced the anti-tumor effect of N-CWS. The growth of Meth A cells, rechallenged into BALB/c mice in which Meth A cells had once been suppressed or regressed by N-CWS treatment, was also inhibited, but not in similarly treated athymic nude mice. This resistant mechanism was shown to be dependent out cellular components but not on humoral components by the Winn Assay. The present results suggest that N-CWS exerts its anti-tumor activity by mediation of the immune system of the host and that the main effector cells in the early stage of tumor rejection are macrophages; T cells may also be involved in the later stage.

Animals↗
PubMed1987

Comparative study of tiapride and neuroleptics with anti-dopamine activity on convulsive seizure in mice.

The effects of tiapride on the convulsive seizures induced by pentylenetetrazole, strychnine, picrotoxin and bemegride, and on electric seizure are reported and compared with those of sulpiride, chlorpromazine, haloperidol and reserpine. The number of deaths and intensity of convulsion increased dose-dependently and also with the increase in amplitude of electric shock. Tiapride and a similar compound, sulpiride, did not affect these seizures, whereas chlorpromazine potentiated strychnine-induced and electric seizure. Haloperidol and reserpine potentiated electric seizure, and chlorpromazine and reserpine tended to potentiate bemegride-induced seizure. Reserpine also tended to potentiate pentylenetetrazole-induced seizure. These results suggest that tiapride would be clinically safer than other drugs with anti-dopamine activity, except for sulpiride.

Animals↗
PubMed1987

Effect of cibenzoline, a class I antiarrhythmic drug, on action potential in canine ventricular muscle.

Effect of cibenzoline, a class I (local anesthetic-type) antiarrhythmic drug, was investigated upon canine ventricular muscle using a conventional micro-electrode method. In the presence of cibenzoline at the concentration of 3 X 10(-6) M or higher, the maximum rate of rise of the action potential was inhibited and the action potential duration was lengthened significantly in a concentration-dependent manner. The effective refractory period was also prolonged. From its effect on the action potential duration, cibenzoline should belong to Ia, according to the Vaughan Williams classification of antiarrhythmic agents. On the other hand, cibenzoline inhibition of the maximum rate of depolarization was greater with an increase in stimulation frequency (a use-dependent block). In the presence of cibenzoline concentrations of 3 X 10(-6) M and 8 X 10(-6) M, which blocked the maximum rate of depolarization by 36% and 67% at 180 beats/min, the rates of onset of inhibition of the maximum rate of depolarization were 0.109 +/- 0.027 and 0.146 +/- 0.070 AP-1 (mean +/- S.D.), respectively. From the kinetics of inhibition of the maximum rate of depolarization, these results suggest that cibenzoline should be classified as an intermediate drug with the prolongation of the action potential duration.

Action Potentials↗
PubMed1987

Effect of long-term dosing with tiapride on brain dopamine receptors and metabolism in rats. Comparative study with sulpiride and haloperidol.

The effects of long-term dosing with tiapride for 21 days on barin dopamine receptors and dopamine turnover were compared with those of sulpiride and haloperidol. Haloperidol caused an increase in both antagonist (3H-spiperone) labeled receptors and agonist (3H-N,n-propylnorapomorphine) labeled ones, whereas tiapride acted on the agonist binding sites and sulpiride acted on the antagonist binding sites. The increases induced by sulpiride were only observed in the striatum, while those induced by tiapride and haloperidol were observed in both the striatum and limbic area. Dopamine and dopamine metabolites in the brain tissues were measured at 2 hr and 3 days after long-term dosing with the drugs as an indicator of dopamine turnover. They were higher at 2 hr and lower at 3 days than those of the saline treated controls; however, the increase at 2 hr was much less than that after single acute dosing with drugs. This suggested that all drugs induced tolerance with regard to dopamine turnover. In these studies, tiapride and sulpiride were less active than haloperidol in the effects on brain dopamine receptors and dopamine turnover. This generally weaker activity of sulpiride and tiapride suggest that the benzamide drugs have fewer side effects such as a tardive dyskinesia, than does haloperidol, even after long-term dosing. Furthermore, a slight difference between the effects of tiapride and sulpiride on the dopamine receptor subtypes in the brain subdivision was suggested.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Wide distribution of rat hepatoma asialo GM1 and its different responses to anti-asialo GM1 antibody-mediated in vitro and in situ cell killing.

By means of TLC immunostaining with anti-asialo GM1 antiserum and conventional structural analyses including exoglycosidase treatment, permethylation and negative ion FABMS, asialo GM1 was found to be widely distributed in rat ascites hepatomas, AH130, AH109A, AH44, AH272, AH41C, AH60C, AH414, AH7974, AH66, AH66 alpha F, AH66F and AH13, and Yoshida sarcoma cells. However, reactivity of asialo GM1, when measured by flow cytometry and complement-mediated cytotoxicity assay with anti-asialo GM1 antiserum, was only observed on AH13 and AH66F, and did not necessarily correspond to the concentration of asialo GM1 on the cells, indicating a cryptic or unreactive nature of glycosphingolipids with respect to their antibodies. On the other hand, although rats injected with 10(7) cells of AH66F died within 7 days, treatment of the rats with anti-asialo GM1 antiserum was found to be effective for their cure or for prolonging their survival, indicating an in situ cytotoxic effect of antiserum. For the in situ cytotoxicity, the timing and period of injection and the dose of antiserum were found to be important.

Animals↗