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Biomedical subjects

H Takeda

Publications and source records attributed to H Takeda.

At least 523 records · Page 29Linked to original sources
PubMed1987

Evaluation of radiation dose resulting from the ingestion of [3H]- and [14C]thymidine in the rat.

Average doses to rat tissues from the ingestion of 2-[14C]thymidine were compared with those from methyl-[3H]thymidine or 6-[3H]thymidine. Among the three precursors, [14C]thymidine gave the highest dose to spleen and small intestine. The doses to other tissues from [14C]thymidine were almost the same or lower as compared with those from [3H]thymidine, irrespective of the 9 times higher beta-ray energy of 14C than that of 3H. In the case of [14C]thymidine, most of the dose was given by radioactivity incorporated into the organic tissue constituents (non-volatile radioactivity). In the case of [3H]thymidine, however, the dose contributions by non-volatile radioactivity were very small and the major contributions were rather from volatile radioactivity (3HHO), formed by degradation of [3H]thymidine. No significant difference in their total doses was found between the two [3H]precursors, but the dose from non-volatile radioactivity alone was 2-3 times higher with methyl-[3H]thymidine than with 6-[3H]thymidine. Estimates of the dose to cell nuclei in various tissues after the ingestion of [3H]thymidine were also made in order to predict more precisely possible radiation hazards.

Administration, Oral↗
PubMed1987

Mechanism of antianaphylactic action of beta-agonists in allergic inflammation of air pouch type in rats.

Using an experimental model of allergic inflammation of air pouch type in rats, the mechanism of antiallergic action of beta-agonists was examined. In this model an immediate increase in vascular permeability and histamine level in the pouch fluid was observed after injecting the antigen (azobenzene arsonate-conjugated acetyl bovine serum albumin) solution into the preformed air pouch on the back of the sensitized rats. The same type of reaction was inducible by injecting anti-rat IgE into the preformed air pouch, but not IgG2a. This fact indicates that the immediate increase in vascular permeability and histamine level is an IgE-mediated anaphylactic reaction. When beta-agonists such as isoproterenol, procaterol and salbutamol were injected into the air pouch together with the antigen, the anaphylactic increase in vascular permeability was suppressed dose-dependently without concomitant decrease in histamine level in the pouch fluid. In contrast, disodium cromoglycate, an inhibitor of degranulation of mast cells, the anaphylactic vascular permeability increase was suppressed in parallel with a decrease of the histamine level. Propranolol, a beta-antagonist, counteracted the effect of beta-agonists. Serotonin-induced vascular permeability was also suppressed dose-dependently by treatment with beta-agonists. Furthermore, vascular permeability in the postanaphylactic phase of the present experimental model was also suppressed by isoproterenol. These results indicate that beta-agonists exert their antiallergic effect by inhibiting the reactivity of local vasculature to chemical mediators released from mast cells.

Adrenergic beta-Antagonists↗
PubMed1987

Hemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol in relation to plasma norepinephrine levels during exercise in patients with left ventricular dysfunction.

A new cardioselective beta 1-adrenoceptor partial agonist, xamoterol, has been developed for the treatment of heart failure, especially that associated with ischemic heart disease. To investigate the hemodynamic effect of xamoterol in relation to sympathetic nervous activity, hemodynamic variables and plasma norepinephrine (NE) levels were measured at rest and during three graded bicycle exercise tests before and after a single intravenous dose of 0.15 mg/kg xamoterol in 10 patients with mild-to-moderate left ventricular dysfunction. Plasma NE increased with increasing grade of exercise and a linear correlation between plasma NE and heart rate was observed at four time points (at rest and three exercise levels) before and after xamoterol. After administration of xamoterol, the slope of the regression line of plasma NE-heart rate relation was significantly less steep than that before drug. Predose and postdose regression lines crossed at 440 pg/ml of plasma NE. Similar effects were observed on the plasma NE-cardiac index and plasma NE-systolic blood pressure relations (regression lines crossed at 380 and 530 pg/ml of plasma NE, respectively). Thus, xamoterol had a dual agonist-antagonist effect in relation to plasma NE, and the crossover point lay approximately between 400 pg/ml and 500 pg/ml. This level of plasma NE was achieved at a low exercise level and at a heart rate of about 100 beats/min. These results indicate that xamoterol has intrinsic sympathomimetic activity comparable to relatively low sympathetic activity (400 to 500 pg/ml of plasma NE) and therefore acts as a beta 1-agonist when sympathetic nervous activity is below this level and as an antagonist when sympathetic activity is above this level.

Adrenergic beta-Antagonists↗
PubMed1987

Multiple regression analysis of sixteen risk factors including serum apolipoproteins in angiographically documented coronary artery disease.

Multiple regression analysis of 16 risk factors, including serum apolipoproteins in angiographically measured coronary stenosis, was carried out in 239 consecutive patients (159 males and 80 females, ranging in age from 30-80 years and mean 56.4 years) who underwent coronary angiography for suspected coronary artery disease during the past five years (1981-1985). The risk factors (independent variables) were age, total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), HDL-C/TC, apolipoprotein (Apo) A-I, A-II, B, C-II, C-III, E, YRSMOK (average number of packs per day X years of smoking), weight index (WI), glucose tolerance (GT), and blood pressure (BP). Severity of coronary atherosclerosis was scored as the extent of disease seen at arteriography (coronary score: CS). The order of importance of risk factors to CS in the five groups of subjects studied were as follows. (1) All patients: YRSMOK greater than Apo A-I greater than TC greater than GT, (2) Male group: Apo A-I greater than TC greater than Age greater than GT, (3) Female group: TC, (4) Young group (age below 54 years): BP greater than YRSMOK, and (5) Old group (age over 55 years): YRSMOK greater than TG greater than TC greater than GT. The results clearly indicated the importance of Apo A-I but not other apolipoproteins including Apo B in males, and that of blood pressure in the young group of the patients studied.

Adult↗
PubMed1987

Visualization of X-chromosome inactivation mosaicism of Tfm gene in XTfm/X+ heterozygous female mice.

The testicular feminization (Tfm) locus, which produces a deficiency in androgen receptors, is located on the X-chromosome. Steroid autoradiographic techniques were used to demonstrate the mosaicism of the X-chromosome inactivation in two androgen target tissues of XTfm/X+ heterozygous female mice. In the mesenchyme of urogenital sinuses of wild-type female fetuses (X+/X+), more than 95% of the cells were androgen-receptor positive (labelled with [3H]testosterone) while in that of heterozygous fetuses (XTfm/X+), about half of the cells were receptor positive (Tfm gene inactive). Statistical analysis of coherent clone size was applied to the heterozygous mesenchyme of the urogenital sinus and the coherent clone size of receptor-positive cells was estimated to be two or three cells per clone. This small clone size suggests that considerable cell mixing occurred in the tissue during embryonic development. Androgen binding in the mammary gland rudiments was restricted to the mesenchymal cells only in close vicinity to the epithelial mammary bud. In the wild-type rudiments most of the mesenchymal cells beneath the epithelium were receptor positive, while in heterozygous rudiments, receptor-positive and -negative cells intermingled. This observation suggests that in the wild-type mammary gland rudiments the epithelial bud may induce the formation of androgen receptors in adjacent mesenchymal cells rather than attract pre-existing receptor-rich mesenchymal cells.

Androgen-Insensitivity Syndrome↗
PubMed1987

Change of mosaic pattern by androgens during prostatic bud formation in XTfm/X+ heterozygous female mice.

The testicular feminization (Tfm) gene, which is characterized by a deficiency in androgen receptors, is located on the X-chromosome. Using steroid autoradiography, the mosaicism of the Tfm gene has been demonstrated in the androgen target tissues of XTfm/X+ heterozygous female mouse fetuses and the effects of androgens on the mosaic pattern analysed. In the mesenchyme of urogenital sinuses of wild-type female fetuses (X+/X+), more than 95% of the cells were androgen-receptor positive (labelled with [3H]testosterone) while in that of heterozygous fetuses (XTfm/X+), only half of the cells were receptor positive (Tfm gene inactive), and receptor-positive cells and -negative cells formed small irregular patches. When the heterozygous sinuses were cultured in vitro in the presence of androgens, the sinuses underwent male sexual development and formed epithelial buds (prostate gland rudiments) projecting into the surrounding mesenchyme. Autoradiographic analysis revealed that the mosaicism of the mesenchyme disappeared around the developing epithelial buds: almost all the mesenchymal cells in close vicinity to the buds were receptor positive while in the outer layers receptor-positive and -negative cells coexisted. The proportion of receptor-positive cells was greatly increased in the mesenchyme beneath the non-budding area of the sinus epithelium. This androgen-induced increase was observed before the onset of bud formation. The results obtained in the thymidine incorporation experiments suggest that the increase of receptor-positive cells beneath the sinus epithelium might be explained by the migratory behaviour of the androgen-incorporating cells rather than by their selective proliferation.

Androgen-Insensitivity Syndrome↗
PubMed1987

Role of alpha 2-adrenergic receptor in platelet activation during insulin-induced hypoglycemia in normal subjects.

The effects of alpha 2-adrenergic-receptor blocker mianserin on the responses of blood glucose, plasma beta-thromboglobulin (beta-TG), and various counterregulatory hormones to insulin-induced hypoglycemia were studied in nine healthy male subjects. The alpha 2-adrenoceptor-blocking action of mianserin was confirmed by its inhibitory effect on platelet activation in vitro. Mianserin was given orally 90 min before insulin injection; the same study without mianserin was performed on another day as the control study. The time courses of blood glucose and serum C-peptide (0, 20, 45, and 180 min after the insulin injection) were identical in both studies, indicating that mianserin has no effect on these parameters. However, a significant increase of beta-TG at 45 min after insulin injection was completely suppressed by the administration of mianserin (mean +/- SE, 68.5 +/- 6.0 vs. 28.8 +/- 7.6 ng/ml, n = 6, P less than .05). No significant differences were obtained between the two studies in the responses of plasma or serum catecholamines, cortisol, glucagon, growth hormone, thromboxane B2, and 6-ketoprostaglandin F1 alpha. These results suggest that epinephrine is responsible for some, if not all, of the beta-TG release from the platelets during insulin-induced hypoglycemia.

Adult↗
PubMed1987

Detection of antibodies to Sendai virus in mouse sera by enzyme-linked immunosorbent assay (ELISA).

Enzyme-linked immunosorbent assay (ELISA) for diagnosis of Sendai virus infection in mice was evaluated. A large-scale survey of infected mice showed that ELISA is approximately 100 times more sensitive than the hemagglutination-inhibition or complement-fixation test. Although a few SPF mice showed false-positive reactions at a serum dilution of 1:40, further dilution to 1:80 eliminated the non-specific reaction. It was shown that ELISA is a highly satisfactory method for examination of Sendai virus infection in mice.

Animals↗
PubMed1987

Effects of interleukin 2 on estradiol binding capacity of peripheral blood mononuclear cells in asymptomatic HBV carriers.

Peripheral blood mononuclear cells from asymptomatic hepatitis B (HBV) carriers and healthy controls were incubated with or without recombinant interleukin 2 (r-lL2) at 37 degrees C for 24 hours. They were then incubated for another hour with 3H-estradiol and cold estradiol at 37 degrees C, and the estradiol binding capacity was estimated by measuring the radioactivity bound to these cells. As a result, when r-lL2 was not added, the estradiol binding capacity of the mononuclear cells in asymptomatic HBV carriers was lower than that in healthy controls. However, when r-lL2 was added, it increased to about the same level as that in healthy controls. This increase in the estradiol binding capacity of the mononuclear cells in asymptomatic HBV carriers may be due to the differentiation and proliferation of the cells induced by r-lL2.

Carrier State↗