Decrease in muscarinic acetylcholine receptors in the small intestine of mice subjected to repeated cold stress.
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Biomedical subjects
Publications and source records attributed to T Hata.
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We designed a simple technique for surgical excision of the pineal body in mice. Such can be accomplished in 10 min by a skilled worker and there are no lesions whatever. In pinealectomized El-strain mice the appearance of convulsions was inhibited up to 30 days, while intact El-mice were all fallen into convulsions by being shaken up and down on a flat carton. Pentazole-induced convulsions propagate from one dd-mouse to another in an aggregated state, but such propagation did not occur in pinealectomized animals. Exploratory movements of pinealectomized dd-mice increased as compared to intact animals and the increase was always more extensively observed in El-mice in which, even in the intact animals, the exploratory movements were much more than those of dd-mice. From the above-mentioned experiment, it is considered that the pineal body plays a role not only in initiating but also in propagating convulsions, and that it may have a depressive action on motor activities in mice.
Two angiotensin II analogues, i.e., 1-sarcosine, 8-isoleucine angiotensin II (Sar1, Ile8-AII) and 1-sarcosine, 8-alanine angiotensin II (Sar1, Ala8-AII), are now available in the clinical study. Comparative studies of the antagonistic potency and the agonistic effect of these two AII analogues were made in normal subjects on three sodium balances and in hypertensive patients with various etiologies on sodium depletion. Both AII analogues had an agonistic pressor effect in normal subjects. This effect changed with different sodium balances. In the low sodium state, this agonistic action was minimized. The agonistic pressor effect of Sar1, Ile8-AII was greater than that of Sar1, Ala8-AII in all sodium states. There was found an agonistic activity of both AII analogues not only on blood pressure, but also on renin and aldosterone secretion, and renal vasculature in normal subjects on a regular diet. The antagonistic depressor potency of both compounds was also varied by changing sodium balance, being greatest in the low sodium state. In hypertensive patients on sodium depletion, the blood pressure responses of individual patients to these two AII analogues were significantly correlated (r = 0.8, n = 20). These results indicate taht pretreatment of sodium depletion is necessary to prevent the side effect caused by the agonistic pressor action of AII analogue, and also to predict renin depency in hypertensive patients efficiently.
The structures of enaminomycins A and B were determined by their physico-chemical properties and X-ray crystallographic analyses to be 4-amino-2,5-dioxo-7-oxa-bicyclo[4,1,0]hept-3-ene-3-carboxylic acid and 2-oxo-4-amino-5-hydroxy-5-acetonyl-7-oxa-bicyclo[4,1,0]hept-3-ene-3-carboxylic acid, respectively. The structure of enaminomycin C was also determined by the analysis of NMR spectrum and other physico-chemical properties to be 2-oxo-4-amino-5-hydroxy-7-oxa-bicyclo[4,1,0]hept-3-ene-3-carboxylic acid.
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The substrate specificities of two different molecular sizes of cathepsin A, A,L (large form) and A,S (small form), for synthetic substrates were examined kinetically. Both enzymes showed a similar broad substrate specificity against various acyl dipeptides, amino acid esters, and amino acid amides. Z-Phe-Ala and Ac-Phe-OEt were good substrates. Peptides containing hydrophobic amino acids were hydrolyzed rapidly. The presence of hydrophobic amino acid residues, not only at the C-terminal position but also at the second position and probably the third position from the C-terminal, resulted in an increase in the rate of hydrolysis. Peptides containing glycine and proline were hydrolyzed slowly. Inhibition studies with Z-D-Phe-D-Ala and Z-Phe suggested that the peptidase and esterase activities of the enzymes are both catalyzed by the same site of the enzyme molecule, but it remains to be elucidated whether or not the binding sites for peptides and esters are the same.
A propranolol-glucagon test was evaluated in 24 control normal children, 21 pituitary dwarfs, 15 patients with constitutional short stature, 2 with chromosome aberration and 4 with miscellaneous diseases. The dose of glucagon enough for the stimulation of human growth hormone (HGH) secretion is more than 20 microgram/kg of body weight. During the test in the control subjects the serum HGH level increased from 2.3 +/- 1.2 ng/ml to a maximum level of 30.0 +/- 15.1 ng/ml, when 10 mg propranolol, regardless of body weight and 30 microgram glucagon per kg of body weight are given. The dose of propranolol administered ranged from 0.2 to 1.0 mg/kg of body weight in normal children studied. Serum 11-OHCS also increased significantly from 14.5 +/- 11.2 microgram/100 ml to 30.1 +/- 15.5 microgram/100 ml (P less than 0.01). There was no difference in the maximum level of urinary total catecholamines in propranolol-glucagon test between 7 pituitary dwarfs and 7 control subjects. The mechanism of HGH response to propranolol-glucagon administration is unknown, but propranolol-glucagon administration is a sensitive and reliable provocative test for HGH secretion, since false negative response of HGH are not observed in patients with non-pituitary disease.
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Oligonucleotides and nucleoside phosphoramidates can be synthesized in high yields by a combined use of triphenyl phosphite and 2,2'-dipyridyl diselenide as a coupling reagent.
Central activity, antihypertensive action and antiulcerogenic actions of Neurotropin (NSP), an extract isolated from vaccinia virus-innoculated skin or tissues of rabbits were investigated herein. When actions of NSP were examined in isolated muscle preparations by the Magnus-method, peristalsis and ACh-induced contraction in the small intestine isolated from crayfish were not influenced, peristalsis and ACh-induced contraction in the small intestine from mice were slightly accelerated, but adrenaline-induced relaxation in the small intestine from mice was not affected. Histamine-induced contraction in the small intestine and tracheal muscles isolated from guinea pigs was antagonized slightly, or not at all by NSP in a high concentration. NSP had no direct action nor anti-ACh action on abdominal muscles from frogs. NSP had no influence on E1-mice-convulsions. Both spontaneous motor activities and exploratory movements in mice were depressed. Sleeping time induced by hexobarbital-Na was prolonged in mice. Tremorine-induced tremor in mice was inhibited by NSP, while perphenazine-induced catalepsy in rats was not. Normal blood pressure in Wistar rats was not influenced, but high blood pressure in SHR (spontaneously hypertensive rats) decreased close to normal levels after NSP. NSP had antiulcerogenic effects on Takagi's restraint-plus-water-immersing ulcers in rats and histamine-induced duodenal ulcers in guinea pigs, but no influence on Shay ulcers in Wistar rats. From the data obtained herein, it may be concluded that NSP has many central depressant-like activities.
Four cases of variant angina pectoris with normal findings on coronary arteriogram were experienced. The facts may show that the existence of serious arteriosclerotic lesions in a major branch of coronary artery as pointed out by Prinzmetal is at least not essential for the occurrence of anginal attack in the present disease. But the finding that age and sex distribution of variant angina was nearly the same as that of effort angina seems to still indicate the possibility that arteriosclerotic lesion somehow participates in the mechanism of occurrence of the present disease.