Microautoradiographic distribution of 14C-diltiazem in the dog kidney after renal arterial injection.
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Biomedical subjects
Publications and source records attributed to S Tojo.
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Correlation between ovarian follicular apparatus and hormonal parameters such as serum gonadotropin and urinary estrogen levels was investigated in patients with primary and secondary amenorrhea. Serum gonadotropin levels were elevated in amenorrheic patients without ovarian follicles or with follicles of low developmental stage and pituitary responsiveness to LH-RH in these patients were marked compared with patients with follicles of high developmental stage or normal ovulating women in the follicular phase of the menstrual cycle. The 24-hour urinary excretion of total estrogens was low in patients without follicles or with follicles of low developmental stage and ovarian responsiveness to exogenous gonadotropins was quite low in comparison with patients with highly developed follicles or normal control subjects. Thus, serum gonadotropin and urinary estrogen measurements and LH-RH and gonadotropin loading tests are diagnostic of the presence or absence and the state of development of ovarian follicles in the diagnosis and treatment of primary and secondary amenorrhea.
Dehydroepiandrosterone sulfate (DHAS) is now used for a dynamic test of placental function by many obstetricians. While practicing this test, the authors found that DHAS markedly promoted so-called "cervical ripening". To study this problem, DHAS of 50 or 100 mg in multiple doses were injected into 132 Japanese pregnant women in their 38th--42nd week of gestation. The change in Bishop score was carefully recorded. Bishop score in the injected groups of primiparae (100 mg) began to rise much sooner than the control groups (p less than 0.01 on seventh day and 14th day). However, such significant difference in the rise of Bishop score was not noted in the multiparae and primiparae with 50 mg. Although the rise of score is not significant, the duration (day) from injection to delivery was shorter in the injected group than the control group (t=2.1529, p less than 0.05 in primiparae with 50 mg, t=3.8829, p less than 0.01 with 100 mg, t=2.1029, p less than 0.05 in multiparae with 50 mg). In some of these cases, labor began or delivery was finished within 24 hrs. Among the factors of Bishop score, mainly the effacement, consistency and dilatation of the cervix were remarkably improved by DHAS injection (p less than 0.01 and less than 0.05). Side effects of any type were not seen in the mothers and foetuses. As a conclusion, DHAS injection in considered to produce favorable conditions for delivery in women with "unripe cervix" by softening the soft birth canal. Furthermore, it is suggested that DHAS might play an important role in triggering labor.
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The effect of follicle-stimulating hormone (FSH) and diethylstilbestrol (DES) on ovarian follicle growth was studied in hypophysectomized rats, using histologic, autoradiographic and histochemical techniques. The administration of FSH to immature hypophysectomized rats stimulated the follicle growth with thickening of the theca layer and repair of "deficiency cells". Although DES given to hypophysectomized rats also stimulated the follicle growth, the theca layer was relatively thin compared with that in FSH-treated rats. In order to detect cell division in a growing follicle, the number of labelled granulosa cells with tritiated thymidine as a proportion of the granulosa cells in a growing follicle were counted and the labelling indices of the granulosa cells were calculated. The labelling indices increased by the administration of FSH (p less than 0.05) or DES (p less than 0.05). The uptake of tritiated thymidine and leucine by the theca cells was enhanced only by FSH and was not stimulated by DES. The administration of FSH resulted in an increase of the histochemically demonstrable enzyme activity such as delta5-3beta-hydroxysteroid dehydrogenase (3beta-HSD) or alkaline phosphatase in the theca cells. In contrast, the administration of DES did not stimulate the enzyme activity of the theca cells. Furthermore, FSH stimulated a release of estradiol and estriol from the ovary of hypophysectomized rat, whereas DES did not. Although ovarian follicle growth was stimulated by both FSH and DES, the effect of the two hormones on the theca cells was quite different and the secretion of estrogen was stimulated by FSH. The results suggest that FSH induced follicle growth of the ovary might be mediated by estrogen produced by the theca cells.
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Amenorrhea is a symptom having many possible causes. Since amenorrhea can result from disturbed function anywhere in the hypothalamic-pituitary-ovarian-uterine axis, a specific etiologic diagnosis must be made if treatment is to be effective. For this purpose, a diagnostic scheme for the differential diagnosis of the etiology of primary and secondary amenorrhea is proposed. This scheme includes a progestin test, a cyclic estrogen and progestin test, a luteinizing hormone-releasing hormone (LH-RH) loading test, and a gonadotropin (human menopausal gonadotropin and human chorionic gonadotropin) loading test. A specific pattern of responses to LH-RH and gonadotropins exists in patients with hypothalamic, pituitary, and ovarian amenorrheas, respectively, and the character of the response may facilitate the etiologic diagnosis of amenorrhea. The clinical usefulness and/or value of the scheme in the diagnosis and treatment of amenorrheas is discussed.
A soluble glomerular basement membrane (GBM) antigen was detected in the urines of patients with various glomerular diseases including chronic glomerulonephritis, nephrotic syndrome, chronic renal insufficiency, and lupus nephropathy. The urinary GBM antigen (u-GBM) was immunochemically distinct from other renal antigens and other serum components, but it was cross-reactive with trypsinized human GBM antigen (t-GBM). The molecular size of u-GBM was approximately the same as human serum albumin as estimated by elution patterns on Sephadex G-200. The concentration of u-GBM was estimated quantitatively by a single radial radioimmunodiffusion. Although differed from case to case, a rough correlation with the type and/or stage of nephrotic syndrom existed. It was also demonstrated that the amounts of u-GBM decreased in response to steroid therapy of nephrotic syndrome. It was further shown that in a case of membranoproliferative glomerulonephritis, anti-GBM antibody could be eluted from the kidney removed from the patient. These findings imply that the GBM antigen plays an important role in the pathogenesis of human renal diseases. The pathophysiological significance of urinary GBM excretion in renal diseases is also discussed here.
Sera and fluid in molar vesicles from 4 patients with hydatidiform mole were analyzed for hCG and its subunits. These samples were initially chromatographed through a standardized Sephadex G-100 upward column. Starting materials and each fraction on gel filtration were radioimmunoassay in homologous hCG, hCG-alpha and hCG-beta assays. The specimens obtained from 4 patients contained primarily hCG and little hCG-beta. Immunoreactive hCG-alpha was barely detectable in sera but was clearly demonstrated in vesicle fluid from molar patients. This immunoreactive hCG-alpha was combined with [125I]hCG-beta. The combined protein, [125I]hCG and [125I]hCG-beta recombined with urinary hCG-alpha were concentrated in the superovulated rat ovary in vivo. However, [125I]hCG-alpha and [125I]hCG-beta were not taken up by the ovaries. The biosynthesis of hCG-alpha are discussed.
The uptake of 125I-labelled LH by equal numbers of granulosa cells from small, medium or large follicles was greater by cells from large follicles. In contrast, granulosa cells obtained from small follicles bound much more 125I-labelled FSH per cell than did cells obtained from medium and large follicles. Competition studies with unlabelled hormones indicated that porcine granulosa cells have specific receptors for LH and FSH. The addition of diethylstilboestrol enhanced the binding of 125I-labelled LH and inhibited the binding of 125I-labelled FSH to granulosa cells harvested from small and medium-sized follicles, but had no effect on those from large follicles.
"Minamata disease" was found among the residents along Minamata bay contaminated with the effluent from an industrial plant using mercury. The patients were suffering from various neurologic disorders primarily due to organic mercury poisoning. Evidence is described of renal tubular dysfunction associated with this disease by the immunochemical demonstration or renal tubular epithelial antigen and beta-2-microglobulin in the urine. Nineteen patients with Minamata disease and 35 diseased and healthy control subjects were examined. The contents of urinary renal tubular epithelial antigen and beta-2-microglobulin, and the ratios of these proteins to albumin in individuals with Minamata disease were significantly different from the levels in healthy control subjects (P less than 0.05) were identical to those found in patients with tubular and the values, proteinuria. These results indicate that Minamata disease is associated with renal tubular dysfunction, and also suggest that these procedures would be useful for screening the nephrotoxicity in the environmental exposure of heavy metals.
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Twenty patients with molar pregnancy, ten normal pregnant women and ten healthy non-pregnant women were given 30 g of arginine intravenously. The serum concentration of growth hormone, prolactin and chorionic somatomammotropin (CS) was determined by radioimmunoassay. In addition, serum 17beta-estradiol, estriol and progesterone were also measured. Arginine infusion induced a sharp rise of GH in patients with molar pregnancy and in nonpregnant subjects, but the response in normal pregnancy was blunted. The response of PRL was high in patients with molar pregnancy, blunted in normal pregnancy and very small in nonpregnant subjects. CS did not respond at all to arginine infusion both in normal pregnancy and molar pregnancy. The high response to argine of PRL, normal response of GH and low baseline secretion and no response of CS may be characteristic of molar pregnancy.
Estimations of serum HCT, HTSH, T4, T3, PBI, ETR, Triosorb, TBG-binding capacity, BMR and urinary total estrogen were made simultaneously in 160 women in normal pregnancy. TRH stimulation tests were made in 20 cases in each trimester of pregnancy. HCT was detectable even in early pregnancy, tending to increase gradually toward the terminal stage of pregnancy as serum thyrotrophin bioactivity showed. On the other hand, serum TSH level measured by radio-immunoassay remained essentially the same throughout the course of pregnancy as in the nonpregnant state, moreover, it was suggested by the TRH stimulation test that pituitary TSH secreting function of pregnant women was similar to that of the non-pregnant. These findings suggest that thyroid hyperfunction during pregnancy which is shown by progressively increased T3, T4, and PBI may not be due to high estrogen-high TBG binding capacity-low free thyroxinenegative feed back-high TSH secretion but to HCT originating from placenta. In spite of thyroid hormone increase, it is true that the clinical picture of hyperthyroidism is not manifest among normal pregnant women, and ETR remained within the non-pregnant range throughout the course of pregnancy. We have also demonstrated that Triosorb decreased progressively. This may be interpreted to be due to the increase of TBG binding capacity which is increased progressively and binds more of free thyroxine during pregnancy. Such a change in TBG binding capacity is well known to be caused by the effect of estrogen which is progressively increased during pregnancy. In a word, it is possible to say that there is a placento-thyroidal system in pregnancy; HCT elevates thyroid function and TBG increased by estrogen carries thyroid hormone to target organ.
HCT, TSH, T3, T4, PBI, T3-RSU, TBG binding capacity, BMR and thyroid uptake of radioiodine were measured simultaneously on the volunteers with hydatidiform mole and normal pregnancy. TRH stimulation tests were performed on the two groups. The serum HCT levels were higher in association with molar pregnancy than in normal pregnancy. TSH levels were within the nonpregnant range in the two groups. T3, T4, PBI, ETR, BMR and thyroid uptake of radioiodine suggested thyroid hyperfunction in molar pregnancy with a greater degree than that in normal pregnancy. TBG binding capacity and T3-RSU were similar in two groups. The peak TSH levels of TRH stimulation tests ranged widely in patients with molar pregnancies but were within the nonpregnant range in the subjects with normal pregnancies. These findings suggest thyroid hyperfunction in the molar pregnancy is due to a larger amount of HCT than in normal pregnancy.