Search PubMed⌕ Search

Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 271 records · Page 15Linked to original sources
PubMed1984

Natural variations in brain phenylethanolamine-N-methyltransferase activity during different phases of the oestrous cycle: effect of chronic dexamethasone treatment.

The activity of phenylethanolamine-N-methyltransferase (PNMT) was studied in the hypothalamus, hypophysis, striatum and the rest of the brain during the four different phases of the oestrous cycle of the rat. The oestrous phase was marked by high level of enzyme activity in all the regions except the hypophysis. The hypophysis showed maximum increase in activity at the metoestrous phase of the oestrous cycle. Chronic treatment of rats with dexamethasone for 10 days led to decreased level of PNMT activity in the hypophysis, hypothalamus and the rest of brain. These decreases were important in the hypothalamus and the hypophysis which represented only 25 and 20% of the control activity after dexamethasone administration.

Animals↗
PubMed1983

The stimulation of macrophage prostaglandin E2 and thromboxane B2 secretion by Streptococcus mutans insoluble glucans.

The effect of insoluble glucan synthesized by Streptococcus mutans on [3H]arachidonate metabolites secretion from peritoneal macrophages was studied. Insoluble glucans stimulated [3H]arachidonate release and secretion of prostaglandin E2 and thromboxane B2 from macrophages. In contrast, commercial soluble glucan (dextran) did not induce [3H]arachidonate release.

Animals↗
PubMed1983

Some properties of prostaglandin E2 receptors in rabbit alveolar bone cell membranes.

[3H]prostaglandin E2 (PGE2) binding receptors exist in rabbit alveolar bone cell membranes. The presence of high (Kd = 3.9 X 10(-9) M) and low (Kd = 8.8 X 10(-8) M) affinity binding sites of [3H]PGE2 was demonstrated. The saturation values of [3H]PGE2 for high and low affinity binding sites were 0.13 pmol/mg protein and 1.22 pmol/mg protein, respectively. The digestion of the membranes with pronase, phospholipase C, D and neuraminidase led to a decrease of [3H]PGE2 binding but phospholipase A2 did not.

Alveolar Process↗
PubMed1983

Vitamin D-mediated decrease of Ca2+-pump activity in the rat parotid gland.

In vitro activities of Ca2+-ATPase and 45Ca2+ uptake in microsomes, which were prepared from vitamin D-deficient rat parotid glands, were decreased in parallel by the oral administration of vitamin D3 as compared with those of control animals (r = 0.83). In vivo 45Ca2+ uptake in the parotid glands of vitamin D-deficient rats was also decreased by the oral administration of vitamin D3.

Animals↗
PubMed1983

Metabolic responses to a new beta-adrenoceptor agonist, ICI 118,587, in conscious rats.

The effect of a new beta-adrenoceptor agonist, ICI 118,587, on the blood levels of cyclic AMP, glucose, lactate, and FFA was studied in conscious rats. ICI 118,587 (200 micrograms/100 g s.c.) increased the cyclic AMP level in the normal and reserpine-pretreated rat, and increased the FFA level in the reserpine-pretreated rat. Adrenaline (10 micrograms/100 g s.c.) increased the levels of cyclic AMP, glucose, and lactate in the normal rat, and increased the FFA level in the reserpine-pretreated rat. The increases in these metabolites induced by this particular dose of adrenaline were inhibited by ICI 118,587. In the normal or reserpine-pretreated rat, ICI 118,587 acts as a beta-agonist on metabolism, and is capable of antagonizing the metabolic effects of adrenaline.

Adrenergic beta-Agonists↗
PubMed1983

Evaluation of selected hypolipidemic agents for the induction of peroxisomal enzymes and peroxisome proliferation in the rat liver.

There is a considerable interest in developing potent and safe hypolipidemic drugs for the prevention and management of coronary heart disease in man. In rodents, many of these hypolipidemic compounds induce hepatomegaly, proliferation of peroxisomes and a polypeptide with an approximate mol. wt. of 80000 in liver cells. In the present study, we have examined 10 hypolipidemic compounds for the induction of peroxisome proliferation associated 80000 mol. wt. polypeptide (polypeptide PPA-80), peroxisomal enzymes and peroxisome proliferation in rat liver, in view of the emerging evidence that hepatic peroxisome proliferators as a class are carcinogenic in rats and mice. All ten compounds, fenofibrate (isopropyl-[4-(p-chlorobenzoyl)2-phenoxy-2-methyl] propionate; LS 2265 (taurine derivative of fenofibrate); bezafibrate (2-(4-(2-[4-chlorobenzamido)ethyl] phenoxy)-methyl propionic acid; gemfibrozil (5-2[2,5-dimethylphenoxy]2-2-dimethylpentanoic acid); methyl clofenapate (methyl-2-[4-(p-chlorophenyl)phenoxy]-2-methyl propionate); DG 5685 (5-[4-phenoxybenzyl]trans-2-(3-pyridyl)1,3-dioxane); DH 6463 (5-[4-phenoxybenzyl] trans-2-(3-pyrimidinyl)-1,3-dioxane); tiadenol(bis[hydroxyethylthio]-7, 10-decane); ciprofibrate (2,-[4-(2,2-dichlorocyclopropyl)-phenoxy]2-methyl propionic acid) and RMI-14,514 ( [5-tetradecycloxy]-2-furancarboxylic acid), produced a marked but variable increase in the activities of peroxisomal enzymes catalase, carnitine acetyltransferase, heat-labile enoyl-CoA hydratase and the fatty acid beta-oxidation system and in the amount of polypeptide PPA-80 as demonstrated by SDS-polyacrylamide gel electrophoresis. The peptide map patterns of polypeptide PPA-80 in liver induced by these compounds were strikingly similar. The ultrastructural studies demonstrate that fenofibrate, ciprofibrate, LS 2265, DG 5685 and DH 6463 can induce proliferation of peroxisomes in liver cells of rats, and further confirm the previous reports of hepatic peroxisome proliferative activity of methyl clofenapate, tiadenol, bezafibrate, gemfibrozil and RMI-14514, as shown morphologically. Whether these structurally unrelated chemicals or their metabolite(s) directly activate the peroxisome specific genes to induce this multi-enzyme system or they exert their action on peroxisomes indirectly by causing fatty acid overload in hepatocytes remains to be elucidated. These chemicals offer a simple and reproducible means of stimulating peroxisomal enzymes in liver and should serve as useful tools, for evaluating the implications of hepatic peroxisome proliferation and in elucidating the mechanism of peroxisome proliferator-induced carcinogenesis.

Animals↗
PubMed1983

Effects of nitroglycerin, dipyridamole and propranolol on myocardial pH and pO2 during regional ischemia in the dog heart.

In dogs anesthetized with pentobarbital, the left anterior descending coronary artery (LAD) was occluded so that the blood flow could be reduced to about 1/3 (partial occlusion). Before partial occlusion, myocardial pH and pO2 were 7.63 (n = 35) and 17.1 mm Hg (n = 30), respectively. Partial occlusion of the LAD decreased the pH and pO2 by 0.68 pH units and 7.4 mm Hg, respectively. In the nonischemic heart, nitroglycerin (20 micrograms/kg, i.v.) did not affect myocardial pH, although it increased the LAD flow. In the ischemic heart, however, nitroglycerin increased the myocardial pH that had been reduced by partial occlusion, without an increase in myocardial pO2. Dipyridamole (250 micrograms/kg, i.v.) did not increase pH and pO2 in both nonischemic and ischemic hearts. Propranolol (1 mg/kg, i.v.) increased both pH and pO2 of the ischemic myocardium that had been reduced by partial occlusion with a decrease in heart rate. It is concluded that propranolol and nitroglycerin restore (though incompletely) the myocardial pH that has been reduced by partial occlusion of the coronary artery, while dipyridamole does not, and that only propranolol increases the ischemic myocardial pO2.

Animals↗
PubMed1983

Effects of 1-(4-nitrophenyl)-2-isopropylaminoethanol (INPEA) and propranolol and their dextro-isomers on hemodynamic and metabolic responses to isoproterenol in dogs.

The effects of dl-propranolol, D-(-)-(4-nitrophenyl)-2-isopropylaminoethanol (INPEA) and L-(+)-INPEA on the hemodynamic and metabolic responses to isoproterenol were investigated in dogs anesthetized with pentobarbital. Isoproterenol (200 micrograms/kg i.p.) was injected 15 min after an i.v. injection of propranolol or INPEA, or their dextro-isomers. Isoproterenol increased heart rate, myocardial contractile force (determined by a strain gauge arch), blood glucose, blood lactate and plasma free fatty acids, and decreased diastolic blood pressure. dl-Propranolol (1 or 3 mg/kg) or D-(-)-INPEA (5 or 15 mg/kg) inhibited all the responses to isoproterenol. d-Propranolol (1 or 3 mg/kg) did not inhibit the isoproterenol-induced responses of heart rate, myocardial contractile force and plasma free fatty acids, but it inhibited the isoproterenol-induced responses of diastolic blood pressure, blood glucose and blood lactate, although the inhibition was small. Similar results were obtained by L-(+)-INPEA; L-(+)-INPEA (5 or 15 mg/kg) did not inhibit the isoproterenol-induced responses of heart rate, myocardial contractile force and plasma free fatty acids, but it inhibited the isoproterenol-induced responses of diastolic blood pressure, blood glucose and blood lactate, although the degree of inhibition was small. These results indicate that dextro-isomers of propranolol and INPEA may have a weak beta-2 adrenoceptor antagonistic action.

Animals↗
PubMed1982

Effect of sotalol on ischemic myocardial pH in the dog heart.

In dogs anesthetized with pentobarbital, the left anterior descending coronary artery (LAD) was occluded partially so that the LAD flow could be reduced to 1/2 to 1/3 the original flow (partial occlusion). Myocardial pH was recorded continuously by the use of a micro glass pH electrode inserted in the area to become ischemic by partial occlusion. Before partial occlusion, myocardial pH was 7.51--7.66. Partial occlusion reduced the pH by 0.63--0.72. Sotalol (5 mg . kg-1, i.v.) increased the pH (by 0.45) that had been reduced by partial occlusion, with a marked decrease in heart rate (about 70 beats . min-1) and a slight decrease in blood pressure (about 10 mm Hg in systolic pressure). Even when the sotalol-induced decrease in heart rate was prevented by pacing the heart, sotalol (5 mg . kg-1, i.v.) increased the pH (by 0.43) of myocardium in which LAD was partially occluded. The pH of the non-ischemic normal heart, however, was not influenced by the injection of sotalol (5 mg . kg-1, i.v.). It is concluded that the effect of sotalol to increase the pH of the ischemic heart is not related to the decrease in heart rate produced by the drug injection.

Animals↗
PubMed1982

Effect of pantethine on lipoprotein profiles and HDL subfractions in experimentally hypercholesterolemic rabbits.

A high-cholesterol diet caused in rabbits a great increase in beta-migrating VLDL and a significant decrease in HDL 2 (43% of normal) and HDL 3 masses (64% of normal), without significant changes in HDL cholesterol values. Chemical analysis of the HDL subfractions indicated an abnormal lipid-protein composition in the hypercholesterolemic rabbits, an increase in cholesterol and a decrease in the contents of triglycerides and phospholipid. When these rabbits were treated for about 1 month with pantethine, and intermediate precursor of coenzyme A, the increase in cholesterol levels was effectively prevented in the beta-VLDL (11%) and LDL fractions (43%) but, conversely, HDL-cholesterol was significantly increased (151%). In a separate experiment, HDL 2 and HDL 3 masses were calculated to be increased to 186% and 193%, respectively, by pantethine treatment, when compared with those in control cholesterol-fed rabbits. Serum apolipoprotein AI antigen levels were also significantly increased by the treatment.

Animals↗
PubMed1982

Alpha-adrenergic activity and urethral pressure in prostatic zone in benign prostatic hypertrophy.

In order to examine to what extent adrenergic mechanism contributes to the urethral pressure in patients with benign prostatic hypertrophy, changes in the intraurethral pressure in the prostatic zone were measured in vivo by both the urethral pressure profile technique and the balloon method before and after administration of alpha-adrenergic stimulants and an alpha-adrenergic blocker. The effect of spinal anesthesia on the urethral pressure was also investigated. It is suggested that 40 per cent of the total urethral pressure in patients with benign prostatic hypertrophy is due to alpha-adrenergic tone, and the remaining 53 per cent is due to static pressure resulting from the hypertrophied prostatic bulk. The in vitro study indicates that the increase in urethral pressure and contraction of the prostate, prostatic capsule and prostatic urethra.

Adrenergic alpha-Agonists↗
PubMed1982

Streptococcus mutans genes that code for extracellular proteins in Escherichia coli K-12.

Chromosomal DNA from Streptococcus mutans 6715 (serotype g) was cloned into Escherichia coli K-12 by using the cosmid pJC74 cloning vector and a bacteriophage lambda in vitro packaging system. Rabbit antiserum against S. mutans extracellular proteins was used for immunological screening of the clone bank. Twenty-one clones produced weak to strong precipitin bands around the colonies, but only after the lambda c1857 prophage was induced by being heated to lyse the E. coli cells. None of the clones expressed enzyme activity for several known S. mutans extracellular enzymes. One of these clones contained a 45-kilobase recombinant plasmid designated pYA721. An 8.5-kilobase fragment of S. mutans DNA from pYA721 was isolated and recloned into the BamHI restriction site of the plasmid vector pACYC184 to construct pYA726. pYA726 contained all, or nearly all, of the gene for a surface protein antigen (the spaA protein) of S. mutans 6715. This was deduced from immunological studies in which extracts of cells harboring pYA726 reacted with antisera against both purified 6715 spaA protein (about 210,000 daltons) and the immunologically similar antigen I/II of serotype c strains of S. mutans. In addition, the S. mutans spaA protein was found to possess at least one antigenic determinant not present on the protein specified by pYA726. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of E. coli clone extracts revealed that pYA726 produced a polypeptide with a molecular mass of about 180,000 daltons which was predominantly found in the periplasmic space of E. coli cells. Antisera to the spaA protein of S. mutans reacted with extracellular protein from representative strains of S. mutans serotypes a, c, d, e, f, and g, but not b.

Antigens, Bacterial↗