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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 919 records · Page 51Linked to original sources

Comparison of two angiotensin II analogues in normal subjects and hypertensive patients.

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.

Adult↗

Medullary carcinoma of the thyroid. Giant cell type.

This report presents a rare histological variation of medullary (C-cell) carcinoma of the thyroid, referred to as giant cell type, which is similar to that found in anaplastic carcinoma of the thyroid, or choriocarcinoma. The giant cells in this case possessed specific immunofluorescence for calcitonin and secretory granules in the cytoplasm. The giant cells were tumor cells of medullary carcinoma and could be distinguished from anaplastic carcinoma of the thyroid by various histological characteristics, such as nuclear invagination, an intermingled pattern of giant cells with typical small solid cells, infrequency of mitosis, and the existence of amyloid stroma.

Carcinoma↗

[A case of medullary thyroid carcinoma with ectopic ACTH syndrome (author's transl)].

A 53-year-old male with Cushing's syndrome due to ectopic ACTH production from medullary carcinoma of the thyroid was reported. The clinical course and results of detailed endocrinological studies and immunohistochemical findings about the cancer tissue were described. An abnormally high concentration of calcitonin, ACTH and beta-MSH in both plasma and cancer tissue (thyroid, lymph nodes and liver) were documented by radioimmunoassay. Urinary 17-OHCS was as high as 38.4 mg/day and showed no supression following dexamethasone 8 mg/day administration. ORAL METYRAPONE (3 G/DAY) CAUSED NO RESPONSE IN URINARY 17-OHCS. Parallel increments in plasma calcitonin, ACTH and beta-MSH were observed following calcium and gastrin loading. Total thyroidectomy with modified radical neck dissection caused minimal changes of plasma levels of calcitonin, ACTH and beta-MSH and no improvement in the clinical manifestations of Cushing's syndrome. An aortogram revealed metastatic tumors in the liver. A second operation, total adrenalectomy, resulted in an improvement of the clinical and laboratory findings such as hypokalemia, high blood pressure, muscle atrophy and moon face. Immunofluorescent study showed different distribution patterns in calcitonin- and ACTH-positive cells in the primary focus but similar patterns in the liver metastasis.

Adrenalectomy↗

[A simplified radioimmunoassay for serum aldosterone--non-extraction method with 125I-labeled aldosterone (author's transl)].

A simplified direct radioimmunoassay system for serum aldosterone measurement was developed by using radio iodine-labeled aldosterone and highly specific antiserum to aldosterone. 8-anilino-1-naphthalene sulfonic acid(ANS) was used to prevent the binding of aldosterone to serum proteins. Polyethylene glycol was used to separate the antibody-bound aldosterone from the free aldosterone as the precipitant. The minimum measurable concentration of aldosterone is 30pg/ml of serum by short incubation method (at 25 degrees C for 3hr incubation) and 15pg/ml of serum by long incubation method (at 4 degrees C for 20 hr incubation) respectively. Present radioimmunoassay eliminates extraction of the aldosterone from serum and chromatographic separation procedures, and requires only 0.1ml of serum sample for assay. The intra-assay precision was C. V. 6.9% (average of 4 samples) and the inter-assay precision was C. V. 10.7% (average of 4 samples). There is an excellent correlation between the extraction method and this direct method in serum aldosterone value obtained (correlation coefficient, 0.96). The normal value was 36.8+/-25.9pg/ml (recumbent) and 113.6+/-6.15pg/ml (upright).

Aldosterone↗

Blood pressure changes following chronic administration to rats of 3beta,16beta-dihydroxy-5-androsten-17-one, 3beta,17beta-dihydroxy-5-androsten-16-one and 21-hydroxy-4-pregnene-3,20-dione-21-acetate.

The urinary excretion of 3beta,16beta-dihydroxy-5-androsten-17-one (16beta-OH-DHEA) is increased in patients with low renin essential hypertension. This steroid and its isomer 3beta,17beta-dihydroxy-5-androsten-16-one (16-oxo-A) have also been reported to have mineralocorticoid activity in adrenalectomized rats. These findings have led to the postulate that excessive secretion of 16beta-OH-DHEA may be responsible for the production of low renin essential hypertension. In this study unilaterally nephrectomized salt loaded rats injected once a week with 30 mg of 11-desoxycorticosterone acetate per/kg of body weight for 2 month periods developed hypertension. Rats given similar amounts of 16beta-OH-DHEA or 16-oxo-A and rats given no steroids did not develop hypertension. We conclude that it is unlikely that 16beta-OH-DHEA and 16-oxo-A are direct causative factors in the production of low renin essential hypertension.

Androstenediols↗

Enzyme immunoassay of serum testosterone.

An enzyme immunoassay of serum testosterone using the testosterone-glucoamylase complex is described. Testosterone was estimated by the enzyme immunoassay after extraction with hexan: ether (4:1) for serum from men and additional thin layer chromatographic step for serum from women. The within and between assay errors, measured as the coefficient of variation were 11.1 percent (n=8) and 12.0 percent (n=12). The sensitivity of this assay was 0.25 ng. The mean testosterone concentration (+/- SD) in 19 normal men and 4 normal cycling women were 5.3 +/- 1.8 and 0.52 +/- 0.12 ng/ml, respectively. The level of testosterone found by the present assay compared favorably with those obtained by other methods.

Cross Reactions↗

Enzyme-labelled immunoassay for plasma cortisol.

An enzyme-labelled immunoassay for plasma cortisol was developed. For this alkaline-phosphatase was conjugated through 21-hemisuccinate of cortisol using water-soluble carbodiimide. An antibody was raised in rabbits against corisol-21-hemisuccinate bovine serum albumin. Before assay 10 mul samples of plasma were mixed with glutamate buffer, pH 3.3, and boiled to denature endogenous cortisol-binding globulin and alkaline-phosphatase. Separation of "bound and free" cortisol was done by the double antibody method. A linear relationship was obtained between the volume of plasma and the amount of cortisol. The minimal detectable level of plasma cortisol was 1 mug/dl and the coefficients of variation were 2.7%-4.4% (within assays) and 4.7%-6.0% (between assays). Cortisol values determined by the present method correlated well with those determined by radioimmunoassay. The present method of enzyme-labelled immunoassay is suitable for routine clinical analysis of plasma cortisol.

Alkaline Phosphatase↗

A non-chromatographic non-extraction radioimmunoassay for serum aldosterone.

A direct radioimmunoassay for serum aldosterone was developed using a highly specific sntibody and 8-anilino-1-naphthalene sulfonic acid as a blocking agent to inhibit the binding of aldosterone to serum proteins. 125I-labeled aldosterone was used as the labeled antigen and polyethylene glycol was used to separate antibody-bound and free aldosterone. The minimum detectable concentration was 1.5 pg/tube. There were excellent correlations between the present method and other methods, i.e., 1) a method using tritiated aldosterone, 2) a method using dichloromethane extraction before assay, and 3) a commercial kit method. The intra-assay coefficient of variation was 6.9%, and the inter-assay coefficient of variation was 10.7%. The values found in normal human serum were comparable with those reported using other methods. The present radioimmunoassay eliminates both extraction of aldosterone from serum and chromatographic separation and requires only 0.1 ml of serum for assay.

Aldosterone↗