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N Takasu

Publications and source records attributed to N Takasu.

At least 163 records · Page 9Linked to original sources
PubMed1979

Effect of gelatin on the cyclic AMP response of primocultured hog thyroid cells to acute thyrotropin stimulation.

The cyclic AMP response of cultured hog thyroid cells to acute thyrotropin stimulation was shown to be under a dual regulatory control by thyrotropin: both positive and negative regulation have been described. When added to the culture medium, gelatin (0.25%) promoted the reorganization of the cells into folicle-like structures, as does thyrotropin. Unlike thyrotropin, gelatin did not induce an increase in intracellular cyclic AMP but enhanced the acute cyclic AMP response to thyrotropin in cells cultured in gelatin-containing medium. When both gelatin and thyrotropin were present, the positive effect of low concentrations of hormone (less than 50 microU/ml) was increased whereas the refractory process observed in the presence of higher concentrations of hormone (greater than 50 microU/ml) was unchanged. These effects of gelatin might be mediated by interaction of the denatured collagen molecules with external proteins of the plasma membrane of thyroid cells.

Animals↗
PubMed1978

Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 1. Negative regulation.

Isolated porcine thyroid cells, cultured in the presence of thyrotropin (greater than or equal to 0.25 mU/ml) or prostaglandin E2 (greater than or equal to 0.1 micron), showed decreased adenosine 3':5'-monophosphate (cyclic AMP) response to further thyrotropin or prostaglandin E2 stimulation, respectively. Kinetics of the refractory process to thyrotropin and prostaglandin E2 are different: (a) maximal refractoriness to prostaglandin E2 was attained after 2--6 h exposure to prostaglandin E2 while refractoriness to thyrotropin was maximal only after 12--24 h; (b) the degree of refractoriness to prostaglandin E2 was much greater than that to thyrotropin. Refractoriness to thyrotropin or prostaglandin E2 is characterized: by specificity for each thyroid stimulator; by dependence upon the dose of thyrotropin or prostaglandin E2 in culture, e.g. induction of high degree of refractoriness with 0.5 mU/ml thyrotropin (or 1 micron prostaglandin E2), which elicits only a small cyclic AMP increase; by time requirement for induction; by partial effect; by changes of maximum activation of cyclic AMP response; by reversibility. This refractoriness of the cyclic AMP response was not induced by dibutyryl adenosine 3':5'-monophosphate. It was not attributed to increased cyclic AMP-phosphodiesterase activity, but to alterations in the receptor-adenylate cyclase system. Prevention of refractoriness to thyrotropin or prostaglandin E2 by incubation of cells in the presence of actinomycin D, puromycin and cycloheximide suggests that new RNA and protein syntheses are required for the development of the refractory state.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Modulation of adenylate cyclase/cyclic AMP response by thyrotropin and prostaglandin E2 in cultured thyroid cells. 2. Positive regulation.

Two different independent processes are operating in cultured thyroid cells to regulate adenylate cyclase/cyclic AMP responsiveness to thyroid stimulators (thyrotropin and prostaglandin E2): firstly, refractoriness or negative regulation [preceding paper], which is specific for each thyroid stimulator, is not mediated by cyclic AMP and is not accompanied by alteration of adenylate cyclase activity; secondly, positive regulation which is characterized by an augmentation of the cyclic AMP response stimulated by thyrotropin and prostaglandin E2. This process is not specific for each thyroid stimulator and is a state of increased susceptibility of cyclic AMP synthesis to stimulation, accompanied by increased activity of the catalytic subunit of adenylate cyclase. Positive regulation is apparently mediated by increased intracellular cyclic AMP levels. It is a time-dependent and dose-dependent process. Very low concentrations (5-50 micronU/ml) of thyrotropin augmented cyclic AMP synthesis stimulated by thyrotropin and prostaglandin E2 whereas higher concentrations (above 0.1 mU/ml) augmented prostaglandin E2 stimulation but induced refractoriness to thyrotropin. Prostaglandin E2 (0.1 to 10 micronM) augmented thyrotropin stimulation and dibutyryl adenosine 3':5'-monophosphate (0.3 to 2 mM) augmented thyrotropin and prostaglandin E2 stimulation. Positive regulation is a slow process which develops within days and increases up to day 5 in culture. Experiments using inhibitors suggested that protein synthesis is required for the full expression of the increase in adenylate cyclase activity induced by the studied thyroid stimulators.

Adenylyl Cyclases↗
PubMed1976

The different modes of action of thyrotropin and prostaglandin E1 on cyclic adenosine 3',5'-monophosphate synthesis in human thyroid, as studied by sequential stimulations.

PGE1 was equally effective in increasing 3H-cyclic AMP in normal and in toxic thyroids, whereas TSH was less effective but over a longer time in the toxic thyroids. Stimulation by a large second dose of TSH could not be elicited after prior stimulation by large doses of TSH. Similar results were obtained with regard to the effect of PGE1. However, stimulation by a large dose of PGE1 was still effective after the slices became refractory to TSH. Similarly, stimulation by a large dose of TSH was still effective after the slices became refractory to PGE1. It is suggested that the site and/or mode of action of TSH is quite different from that of PGE1.

Cyclic AMP↗
PubMed1974

[Thyroiditis].

Explore the source record for details and available documents.

Chronic Disease↗
PubMedDate not supplied

Effects of phospholipase inhibitors and calcium antagonists on the changes in myocardial phospholipids induced by isoproterenol.

To investigate the change in myocardial phospholipids after the administration of isoproterenol and its prevention by pretreatment with phospholipase inhibitors and calcium antagonists, we determined the phospholipid species in the heart of female Wistar rats. Isoproterenol (40 mg/kg) was administered 24 h before excising the heart, and chlorpromazine, mepacrine (phospholipase inhibitors), nifedipine, verapamil (calcium antagonists) and propranolol (beta-adrenoceptor blocker) were injected intraperitoneally 30 min prior to isoproterenol administration. The phospholipid species were quantified using silica gel precoated thin-layer rods and the hydrogen flame ionization method. Isoproterenol induced significant increases in heart/body weight ratio, myocardial protein/heart weight ratio and lysophosphatidylcholine (LPC), and significant decreases in myocardial total phosphorus, creatine kinase (CK) activity, phosphatidylethanolamine and phosphatidylcholine (PC). The significant decrease in PC and increase in LPC indicated the degradation of myocardial phospholipids. Pretreatment with nifedipine (30 mg/kg), verapamil (50 mg/kg) or propranolol (20 mg/kg) completely prevented the occurrence of myocardial injury through the preservation of myocardial phospholipid composition, total phosphorus, CK activity and heart/body and protein/heart weight ratios. On the other hand, chlorpromazine (30 mg/kg) and mepacrine (50 mg/kg) partially prevented myocardial damage through the preservation of myocardial phospholipid composition, total phosphorus and CK activity. Results suggest that not only calcium influx but also phospholipase activation plays an important role in the development of myocardial injury induced by isoproterenol.

Animals↗
PubMedDate not supplied

Chronic neurobehavioral and central and autonomic nervous system effects of Tokyo subway sarin poisoning.

To evaluate delayed (prolonged) neurobehavioral and neurophysiological effects of acute sarin poisoning, nine male and nine female patients of the Tokyo subway sarin poisoning in Japan were examined by neurobehavioral tests, posttraumatic stress disorder (PTSD) checklist, brain evoked potentials, computerized static posturography, and electrocardiographic R-R interval variability, 6-8 months after the poisoning. Their serum cholinesterase activities on the day of the poisoning (March 20, 1995) were 13-131 (mean 72.1) IU/L. The results suggested delayed effects on psychomotor performance, the higher and visual nervous system and the vestibulo-cerebellar system with psychiatric symptoms resulting from PTSD.

Autonomic Nervous System Diseases↗
PubMedDate not supplied

Chronic neurobehavioral effects of Tokyo subway sarin poisoning in relation to posttraumatic stress disorder.

Chronic neurobehavioral effects of acute sarin poisoning were evaluated in 9 male and 9 female patients who were exposed to sarin poisoning in the Tokyo subway incident in Japan. The investigators used nine neurobehavioral tests, as well as a posttraumatic stress disorder checklist, 6-8 mo after the poisoning occurred. Serum cholinesterase activity in patients on the day of poisoning (i.e., March 20, 1995) ranged from 13 to 131 IU/l (mean=72.1 IU/l). The results of analysis covariance, in which age, education level, alcohol consumption, and smoking status (covariates) were controlled in 18 sarin cases and in 18 controls, showed that the score on the digit symbol (psychomotor performance) test was significantly lower in the sarin cases than in controls. Nonetheless, the scores for the General Health Questionnaires, fatigue of Profile of Mood States, and posttraumatic stress disorder checklist were significantly higher in the sarin cases than controls. The investigators added posttraumatic stress disorder to the covariates, and only the score on the digit symbol test was significantly lower in sarin cases. In addition, the results of stepwise multiple regression analysis in 18 sarin cases revealed that scores for the General Health Questionnaires, fatigue of Profile of Mood States (i.e., fatigue, tension-anxiety, depression, and anger-hostility)-together with the paired-associate learning test-were associated significantly with posttraumatic stress disorder. The association did not remain significant for the digit symbol test score. Perhaps a chronic effect on psychomotor performance was caused directly by acute sarin poisoning; on the other hand, the effects on psychiatric symptoms (General Health Questionnaire) and fatigue (Profile of Mood States) appeared to result from posttraumatic stress disorder induced by exposure to sarin.

Adult↗