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Biomedical subjects

J Adachi

Publications and source records attributed to J Adachi.

At least 163 records · Page 9Linked to original sources
PubMed1983

Calmodulin-binding proteins that interact with actin filaments in a Ca2+-dependent flip-flop manner: survey in brain and secretory tissues.

Regulatory actions of calmodulin on the contractile apparatus and cytoskeleton of smooth muscle and nonmuscle tissue are mediated by a number of specific calmodulin-binding proteins that bind to F-actin in a flip-flop manner--i.e., they bind to calmodulin or F-actin depending on the presence or absence, respectively, of Ca2+. A survey for such proteins in brain, adrenal gland, and pituitary gland identified six polypeptides on polyacrylamide gels--Mr 340,000 (band 1), Mr 240,000/235,000 doublet (band 2), Mr 150,000 (band 3), Mr 129,000 (band 4), Mr 105,000 (band 5), and Mr 94,000 (band 6)--as flip-flop-regulated calmodulin- and F-actin-binding polypeptides. In addition to these polypeptides, a Mr 58,000 non-flip-flop calmodulin-binding actin-binding polypeptide (band 7) was found in all tissues examined. Band 2 was identified as calspectin (spectrin-related protein; fodrin). The flip-flop regulation of calspectin required the presence of a heat-labile nondialyzable factor contained in a supernatant fraction of brain homogenates. Band 1 was distinct from microtubule-associated proteins (MAPs) 1 and 2. However, when band 1 polypeptide was kept on ice 3 days, it converted to a lower molecular weight doublet that migrated with MAP2 on NaDodSO4 gel electrophoresis. Bands 1 and 2 were found in all tissues examined.

Actins↗
PubMed1983

Acetaldehyde-mediated alcohol sensitivity and elevation of plasma catecholamine in man.

According to the presence and absence of aldehyde dehydrogenase (ALDH) I isozyme which had low Km for acetaldehyde, subjects were divided into two groups: the former, the usual ALDH group and the latter, the unusual ALDH one. Blood alcohol and acetaldehyde levels, plasma norepinephrine and epinephrine levels, and urinary excretion of norepinephrine, epinephrine, dopamine, vanillylmandelic acid (VMA) and 3-methoxy-4-hydroxyphenylglycol (MHPG) were determined; and the differences in these values and cardiovascular symptoms after alcohol intake between the two groups were investigated. Fifty-six healthy male volunteers were studied after they ingested 0.4 g of alcohol per kg of body weight. There was no difference in blood alcohol level between the two groups. In the unusual ALDH group, facial flushing, increase of pulse rate and decrease in diastolic blood pressure associated with accumulation of blood acetaldehyde were shown. In addition, rises in plasma catecholamine and urinary excretion of catecholamine were also observed. However, in the usual ALDH group, in which blood acetaldehyde level scarcely increased, these changes were not significant. The alteration of catecholamine metabolism, decrease in urinary VMA and increase in urinary MHPG was recognized in both groups.

Acetaldehyde↗
PubMed1980

Individual differences in blood and breath acetaldehyde levels and urinary excretion of catecholamines after alcohol intake.

Sixty three male Japanese, aged 20-40 yr were evaluated as to the degree of facial flushing following a controlled dose of ethanol either as Japanese rice wine or ethanol 0.4 g kg body weight. Thirty four subjects responded with overt facial flushing. The acetaldehyde levels in blood and expired air were significantly higher in the flushing group without a change in ethanol elimination rate. Urinary excretion of Vanilmandelic acid (VMA) and 3 methyoxy-4-Hydroxyphenylglycol (MHPG) are reported.

Acetaldehyde↗
PubMed1979

Relationship between facial flushing and blood acetaldehyde levels after alcohol intake.

Normal subjects were divided into two groups, i.e., those showing, and those not showing, facial flushing after consuming a small amount of alcohol. In the flushing group, increases of pulse rate, facial skin temperature and carotid arterial pressure and blood flow rate, as well as changes of digital plethysmogram and electrocardiogram, were found together with a conspicuous rise in blood acetaldehyde levels after the drinking. However, significant changes of the signs as mentioned above and elevation of blood acetaldehyde did not occur in the non-flushing group. The maximum blood alcohol levels and the rate of alcohol elimination showed not difference between these two groups. Furthermore, urinary excretions of epinephrine and norepinephrine increased in the flushing cases after the drinking.

Acetaldehyde↗
PubMedDate not supplied

Polymorphism of aldehyde dehydrogenase and ethanol elimination.

The influence of polymorphism of aldehyde dehydrogenase (ALDH) on ethanol elimination was investigated. Japanese healthy male volunteers were divided into two groups, i.e., a normal ALDH group of 52 subjects with the low Km isozyme of ALDH, and a deficient group of 48 subjects without it. The subjects of the normal group were given 0.4, 0.8, 1.2, 1.6 or 2.0 g/kg of ethanol, while those in the deficient group ingested 0.4, 0.8 or 1.2 g/kg of ethanol. Widmark's factors (beta 60, Co and r) and ethanol elimination rate (ER) were compared between the two groups. In the deficient group, beta 60 and ER were not clearly elevated with the increase of ethanol dose, while those in the normal ALDH group increased depending on the blood ethanol level. Blood acetaldehyde level was elevated with the increase of the ethanol dose in the deficient group, but not in the normal group. In the experiment of the repeated ingestion of ethanol in the deficient group, the second peak of blood acetaldehyde level was lower than that of the first one.

Acetaldehyde↗
PubMedDate not supplied

Effect of acetaldehyde on urinary salsolinol in healthy man after ethanol intake.

The effect of acetaldehyde on urinary salsolinol (6, 7-dihydroxy-l-methyl-1,2,3,4-tetrahydroisoquinoline) after ethanol intake was investigated. Healthy Japanese male volunteers were divided into two groups, i.e., a normal aldehyde dehydrogenase (ALDH) group of 13 subjects with a low Km isozyme of ALDH and a deficient group of 12 subjects. The subjects were given 0.4 or 0.8 g/kg of ethanol. Blood ethanol and acetaldehyde levels, urinary excretions of salsolinol, norepinephrine, epinephrine and dopamine were determined. A significant elevation of salsolinol in urine was found after intake of 0.8 g/kg of ethanol in the two groups, but the increase in the deficient group was greater than that in the normal group, while 0.4 g/kg of ethanol did not affect the excretion of salsolinol in either group. Blood acetaldehyde was highly correlated with urinary salsolinol (r = 0.88, p less than 0.001) and the correlation coefficient was greater than that between blood ethanol and salsolinol.

Acetaldehyde↗
PubMedDate not supplied

Individual difference in urinary excretion of salsolinol in alcoholic patients.

Urinary excretion of salsolinol (6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline) in 30 male alcoholic patients during the withdrawal period was determined. They were divided into two groups, i.e., Group A with 14 subjects had a high level of urinary salsolinol (51.9 +/- 40.8 ng/mg creatinine) on admission to a hospital, and Group B with 16 subjects showed a low level of the substance (3.9 +/- 1.9 ng/mg creatinine). Following a sustained drinking bout, urinary salsolinol in Group A declined to a normal level within a few days. We found that the subjects in Group A showed a greater excretion of urinary dopamine and norepinephrine than those in Group B. There were no differences between the two groups in levels of blood ethanol, serum GOT, GPT and gamma-GTP.

Adult↗
PubMedDate not supplied

Pharmacological features of the coronary, renal, mesenteric, and femoral vascular beds of rats revealed by intra-arterial administration of drugs.

We investigated the effects of 42 drugs on the circulation in the isolated, blood-perfused heart, kidney, small intestine, and hindlimb of rats and compared them with previously reported results in dogs. Single intra-arterial injections of drugs were made into the perfusion system of the coronary, renal, mesenteric, or femoral vascular bed. The most striking qualitative differences between rats and dogs were observed in vascular responses to nicotine, dipyridamole, 5-hydroxytryptamine (5-HT), lobeline, tetraethylammonium (TEA), and procaine. Nicotine constricted all vascular beds except the coronary bed in dogs, but dilated all four vascular beds in rats. Dipyridamole produced a dilatation in all vascular beds of rats, while it specifically constricted the renal vasculature of dogs. 5-HT constricted all vascular beds of rats, but dilated the coronary vasculature of dogs. Lobeline, TEA, and procaine constricted only the renal vascular bed in dogs, but elicited constriction of all vascular beds of rats.

Animals↗