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Biomedical subjects

T Tanabe

Publications and source records attributed to T Tanabe.

At least 631 records · Page 35Linked to original sources
PubMed1983

Primary structures of beta- and delta-subunit precursors of Torpedo californica acetylcholine receptor deduced from cDNA sequences.

The nicotinic acetylcholine receptor (AChR) from fish electric organ and mammalian skeletal muscle is the best characterized neurotransmitter receptor (reviewed in refs 1-3). The AChR from the electroplax of the ray Torpedo californica consists of five subunits present in a molar stoichiometry of alpha 2 beta gamma delta (refs 4-6); the apparent molecular weights of the alpha-, beta-, gamma- and delta-subunits are 40,000 (40K), 50K, 60K and 65K, respectively. Knowledge of the primary structures of these constituent polypeptides would facilitate the understanding of the molecular mechanism underlying the function of the neurotransmitter receptor. Recently, we have cloned cDNA for the alpha-subunit precursor of the T. californica AChR and have deduced the primary structure of this polypeptide from the nucleotide sequence of the cloned cDNA. Here we report the cloning and nucleotide analysis of cDNAs for the AChR beta- and delta-subunit precursors. The primary structures of the two polypeptides deduced from the cDNA sequences reveal conspicuous amino acid sequence homology among these and the alpha-subunits. The three subunits contain several highly conserved regions which may be essential for the receptor function or inter-subunit interaction.

Amino Acid Sequence↗
PubMed1983

Hepatocyte plasma membrane antigens. II. Characterization of liver-specific membrane lipoprotein (LP-1) and Tamm-Horsfall glycoprotein (THGP) like antigens (hepatic THGP) on the plasma membrane of Chang liver cell.

Radioiodinated cell-surface antigens of Chang liver cells recognized with anti-liver-specific membrane lipoprotein (anti-LP-1) and anti-Tamm-Horsfall glycoprotein (anti-THGP) rabbit antibodies were analyzed by the immunoprecipitation followed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. The analysis revealed that the antigens precipitated with anti-LP-1 were heterogeneous in molecular species consisting of 2 major and 5 minor polypeptides with molecular weights ranging from 36 X 10(3) (36 K) to 250 K daltons. That with anti-urinary THGP was a single polypeptide with a molecular weight of 67 K daltons, which was different from urinary THGP in molecular size, and was designated hepatic THGP.

Antigens, Neoplasm↗
PubMed1983

Unstable angina pectoris--changes in the ST-T segment during daily activities such as bathing, eating, defecating and urinating.

The significance of positive ST-T changes during bathing, eating, defecating and urinating was studied in 103 patients with ischemic heart disease using Holter and 12-lead ECG. The incidence of positive ST-T changes was very high in patients with unstable angina (US) and in those with old myocardial infarction (OMI) associated with unstable angina. However, it was relatively low in angina-free OMI and extremely low in stable angina. Positive ST-T changes during defecation and urination were mostly (70% and 73%, respectively) seen from night to early morning. With regard to showering or eating, the incidence of positive ST-T changes was low during spraying hot water on the body without motion or remaining motionless after eating. It was not until light exertion was added that the incidence increased. However, pressure-rate product after such behavior did not always increase as compared with that before them. Consequently, it is suggested that the mechanism of anginal attack during urination may be similar to that of variant angina. With regard to showering or eating, it is considered that the spraying of hot water or food intake may bring about a change in the cardiac autonomic nerve tone, and that the addition of light exertion can easily induce myocardial ischemia which is not due to an increase in the oxygen demand of the myocardium.

Activities of Daily Living↗
PubMed1983

[Teratogenicity study on ranitidine hydrochloride in rats].

A teratogenicity study was carried out in Crj: CD (SD) rats orally administered ranitidine hydrochloride, a histamine H2-receptor antagonist, at dose levels of 50, 200 and 800 mg/kg/day as base weight for a period of 11 days from day 7 to day 17 of gestation. Two-thirds of the pregnant females in each group were sacrificed on day 20 of gestation and their fetuses were examined. The remaining dams were allowed to litter naturally, and the postnatal development of the offspring was observed. The incidences of external, internal, and skeletal anomalies were not significantly increased in the fetuses of any treated group. Ranitidine treatment caused no effects on parturition, lactation, postnatal growth and reproductive ability of the male and female offspring.

Administration, Oral↗
PubMed1983

[Effects on offsprings induced by oral administration of ranitidine to the female rat in peri- and postnatal periods].

A perinatal and postnatal study was carried out in the Crj:CD (SD) rats orally administered ranitidine hydrochloride, a histamine H2-receptor antagonist, at dose levels of 50, 200, and 800 mg/kg/day as base for a period of time from day 17 of gestation to day 21 after delivery. All pregnant rats were allowed to litter naturally, and the postnatal development of the offsprings was observed. In the 800 mg/kg group, the delivery rate was significantly decreased and offspring mortality during the lactation period showed a tendency to increase as compared with control, but the difference was not significant. No significant differences between the control group and the treated groups were found in postnatal growth and differentiation, behavior and reproductive ability of male and female offsprings.

Administration, Oral↗
PubMed1983

[Chronic toxicity study of ranitidine hydrochloride orally administered in rats].

Chronic toxicity of ranitidine hydrochloride, a new histamine H2-receptor antagonist, was studied using Sprague Dawley rats. Ranitidine was administered orally at dose levels of 30, 100, 300 and 1000 mg/kg/day for 26 or 53 weeks. In the 1000 mg/kg/day group, ten of 31 females died showing acute toxic signs. In the survived animals of this dose group, changes were observed, such as salivation, depression of body weight gain, increase in water consumption, increase in urinary Na and K excretion, increase in serum albumin content, increase in weights of the liver, kidneys and heart. Main histopathological findings were as follows: centrolobular or midzonal fat deposition in liver, increase in s-ER in hepatocytes, increase in foamy cells in lung and some slight degenerative changes occasionally seen in renal tubules. In the 300 mg/kg/day group, the changes similar to those in the 1000 mg/kg/day group were observed, however, the degree of these changes was more moderate. All of the above-mentioned findings were demonstrated to be reversible in recovery period for 8 weeks. In the 100 and 30 mg/kg/day groups, no remarkable changes were observed in both sexes. It was concluded that the maximum nontoxic dose of ranitidine hydrochloride was 100 mg/kg/day in male and female rats.

Administration, Oral↗
PubMed1983

[Fertility study on ranitidine hydrochloride in rats].

A fertility study was carried out in Crj: CD (SD) rats orally administered ranitidine hydrochloride, a histamine H2-receptor antagonist, at dose levels of 50, 200 and 800 mg/kg/day in base weight. Male rats were treated from 60 days before mating until the completion of mating. Female rats were administered ranitidine hydrochloride from 14 days prior to mating up to day 7 of gestation. All pregnant females were sacrificed on day 20 of gestation and all fetuses were examined for abnormalities. Temporary salivation was noted in rats of both sexes given 800 mg/kg/day of ranitidine and in the male rat group given 200 mg/kg/day. No abnormal signs were seen in mating or fertility in the rats treated with ranitidine. No external, internal and skeletal anomalies attributable to ranitidine hydrochloride were observed in the fetuses. It was concluded that ranitidine hydrochloride has no harmful effect on mating, fertilization, implantation, or embryonic development.

Administration, Oral↗
PubMed1983

[Effects of propranolol and atenolol on the rat kidney].

The present experiments were designed to study the renal effects of propranolol and atenolol in rats. Wistar rats were anesthetized with urethane and continuously hydrated with saline solution. In one group of the rats, the drugs were injected into the jugular vein. In the other group of the rats, the drugs were injected into the abdominal aorta through a canula which was inserted from the left carotid artery into the aorta up to the middle between forking points of left and right renal arteries. Intravenous infusion of propranolol and atenolol increased urine volume (UV), urinary sodium excretion, urinary potassium excretion and urinary chloride excretion. Propranolol and atenolol, which were intraaortally injected, produced an increase in UV and sodium concentration in the urine, inducing a more marked increase in total sodium amount excreted from both kidneys by propranolol than by atenolol. However, the natriuretic response was far more marked in the left kidney than in the right kidney in the case of atenolol administration as compared to that in the case of propranolol. It was speculated, therefore, that the natriuresis induced by these drugs was the first pass effect on the rat kidneys. It was also noted that the first pass effect of atenolol on kidneys was more marked than that of propranolol.

Animals↗