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Biomedical subjects

T Tamada

Publications and source records attributed to T Tamada.

At least 181 records · Page 10Linked to original sources
PubMed1986

The acute stimulatory effect of estrogen on gonadotropin release in gonadotropin-releasing hormone-primed women.

In order to prove the acute stimulatory effects of estrogen on pituitary gonadotropin release, we have performed the present experiments in 8 women with a hypergonadotropic state due to surgical castration or primary ovarian failure. They received gonadotropin releasing hormone (Gn-RH) for 12-21 h at the constant rate of 20 micrograms/h. In 5 of the women, estradiol-17 beta was concomitantly administered at the rate of 20 micrograms/h from 6 h after the start of Gn-RH infusion. Blood samples were collected frequently throughout the experiments for the analysis of LH, FSH and estradiol. In response to the sole stimulation of Gn-RH, remarkable and prompt rises in LH (313.5%), but to a lesser degree in FSH (194.2%), were observed within the initial 3 h, and their high levels were maintained throughout the experimental period. However, the additional administration of estradiol brought on a further sudden rise in both gonadotropins levels: 178.3% for LH and 163.5% for FSH within 2 h. These high levels were sustained during estradiol infusions. In 2 of them, blood samples were obtained for several hours after cessation of estradiol infusion. The circulating gonadotropin level dropped precipitously close to the baseline level within 3 h after estradiol infusions. Our data indicate that estrogen has an acute and strong augmentative effect on Gn-RH induced gonadotropin release in addition to its conventional negative and positive feedback effects.

Adult↗
PubMed1986

[Immunohistochemical localization of secretory component and IgA in the normal and cancerous endometrium].

Using normal and cancerous endometrial tissues obtained from climacteric and postmenopausal women as the subjects, localizations of secretory component (SC) and IgA were immunohistochemically investigated. The results were as follows: Similar to cyclic women, in normal endometrial tissues from climacteric and postmenopausal women, SC and IgA localized mainly in glandular epithelia. However, in women over 60 years of age, immunoreactivity of SC and IgA decreased. In cancerous tissues, staining intensity of SC and IgA decreased clearly as compared to normal tissues. Also, the loss of polarity was recognized in the localization pattern of SC and IgA. In relation to the tissue differentiation, a further decline was recognized in the SC and IgA staining intensity in the poorly differentiated carcinoma as compared to the well differentiated type. The above findings suggested that the decline of the local immune system in the endometrium, namely, weakening of the local defense mechanism against infections, took place in women of advanced age. Also it was recognized that weakening of the ability to produce SC was caused by the malignant transformation of endometrium, and it was suggested that SC was a substance which had a close relationship to tissue differentiation.

Adult↗
PubMed1986

[Infant and juvenile gynecology; endocrinological study and present status of juvenile pregnancy].

Three topics were reviewed and our recent study on juvenile menstrual disorders was presented. Endocrinology of puberty and mechanism of onset of puberty: Review. Menstruation and its disorders during puberty. Age of menarche at present was investigated with 7,400 high school girls. No advance of menarche was recognized compared with that of 10 years ago. The rate of irregular menstruation was similar to that of 20 years ago. High occurrence of LH and testosterone increase was recognized among juvenile menstrual disorders. The prognosis of high LH/androgens girls was poor when followed for 5.6 years. Sexual activity among young girls keep increasing. Participation of gynecologist in sexual education was discussed.

Adolescent↗
PubMed1986

[Follicular development in pregnancy and the polycystic ovarian syndrome].

In order to obtain some clues to the mechanism of follicular development, we studied sequential changes in circulatory hormone from spontaneous abortion up to the next ovulation in 11 women. In addition, morphological analysis of the follicles was performed in the ovarian tissue obtained from 4 pregnant women and another 4 women with polycystic ovarian syndrome (PCO). Blood was collected every 2-4 days and the serum samples were analyzed for HCG (LH), FSH, progesterone and estradiol by radioimmunoassay (RIA). Whole ovaries or the tissue obtained by ovarian wedge resection were sectioned serially at 2.5 micrometers. Every 13th slice was stained and examined under a light microscope. The present data were summarized as follows. A dominant follicle started to grow when LH.HCG levels declined to approximately 120 mIU l and FSH increased slightly. The largest nonatretic follicle seen in pregnancy or PCO was comparable with that seen in the late luteal phase of a normal cycle. The atretic rate of middle sized follicles (2.0 less than or equal to approximately less than 4.0 mm in diameter) was significantly higher in PCO than that seen in normal or pregnant women. These data indicate that the hormonal milieu of pregnancy or PCO does not interfere with the follicular development up to the stage of the largest nonatretic follicle seen in the late luteal phase of a normal cycle. This sized follicle grows to a dominant follicle within a short period under a minor stimulus by FSH.

Abortion, Spontaneous↗
PubMed1986

[Estrogen production by epithelial ovarian tumors and dermoid cyst].

The estrogen-producing activity was investigated in subjects with common epithelial tumors and dermoid cysts, which were not included in the category of hormone-producing tumors. Serum estradiol (E2) in peripheral blood of patients with ovarian tumors were assayed pre-and post-operatively. In addition, cytological examinations of vaginal smears and histological examinations of the endometrium were carried out. The results were as follows: The mean of preoperative serum E2 levels in postmenopausal cases (16) was 230.9 +/- 248.5pg/ml, which was significantly higher than the control of the same age group (p less than 0.01). In seven (63.3%) out of 11 cases followed up, a distinct postoperative decline was indicated in the serum E2 level. The mean of preoperative serum E2 levels in 28 cases of premenopause collected in the early follicle phase was 135.6 +/- 148.8pg/ml, which was apparently higher than the level in normal females in the follicle phase. Also, an evident decline was observed postoperatively in the E2 level in 8 (40%) out of 20 cases. The cytological observations of vaginal smears in 44 cases of postmenopausal ovarian tumor provided the following results: The karyopyknotic index was 12-23% on the average in each age group, which was comparatively higher than that of the control. The maturation index also indicated a deviation to the right compared to the control. The following were the results of histological examinations of the endometrium carried out in 23 cases of postmenopausal ovarian tumor: 5 cases (21.7%) of proliferative endometrium; 3 cases (13.0%) of cystic hyperplasia and 2 cases (8.7%) of adenomatous hyperplasia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Reduction in pituitary desensitization and prolongation of gonadotropin release by estrogen during continuous administration of gonadotropin-releasing hormone in women: its antagonism by progesterone.

The present study was designed to elucidate gonadal steroid influences on gonadotropin release and subsequent pituitary desensitization to GnRH. Sixteen women, 10 of whom were normal and 6 of whom had hypogonadism, were infused with GnRH at rates ranging from 0.313-10 micrograms/h via an indwelling iv catheter for 66 h. Blood samples obtained throughout the GnRH infusion were analyzed for LH, FSH, estradiol, and progesterone. A prompt and substantial release of gonadotropin occurred in women with ovarian failure or during the luteal phase in normal women compared with that during the follicular phase of the menstrual cycle. Thereafter, a gradual decrease in gonadotropin secretion occurred due to pituitary desensitization, which was slower in the follicular phase than in other groups. A dose-related increase in integrated LH release occurred during GnRH infusion, but this response tapered off with administration of large doses of GnRH to women with ovarian failure or during the luteal phase. In contrast, it increased linearly up to the maximum dose of GnRH in the follicular phase. These data suggest that 1) basal levels of estrogen suppress the early rapid release of gonadotropin in response to GnRH and reduce subsequent pituitary desensitization, resulting in the prolonged release of LH; 2) estrogen widens the range of dose-related increases in gonadotropin in response to GnRH; and 3) these effects of estrogen are antagonized by progesterone.

Adult↗
PubMed1985

Low serum levels of FSH, LH and prolactin in luteal phase inadequacy.

In order to elucidate the relationship between prolactin (PRL) levels and corpus luteum function in humans, assessment of temporal relationship between levels of PRL, LH, FSH, estradiol and progesterone was made in eleven normal cycling women and six short luteal women. All hormones were determined by specific radioimmunoassay. The mean PRL level in the luteal phase was higher than that in the follicular phase in normal women. On the other hand, no difference mean was seen between the PRL levels of follicular and luteal phases in short luteal women. In addition, follicular and luteal phase secretion of PRL in the short luteal phase (SLP) was lower than that in the normal control. LH and FSH in the follicular and luteal phases, estradiol secretion in the late follicular and early to mid-luteal phases in SLP were also lower than those in the control. These observations were consistent with the hypothesis that SLP is a sequel to aberrant folliculogenesis. In addition, it is inferred that low PRL levels in the SLP might be due to inadequate augmentation by estrogen, rather than giving PRL any positive controlling role in the maintenance of corpus luteum function.

Adult↗
PubMed1985

Biphasic stimulatory effects of estrogen on gonadotropin surges induced by continuous administration of gonadotropin-releasing hormone in women.

The present experiments were performed to study the effects of preovulatory levels of estrogen on GnRH-induced gonadotropin release. Twelve female volunteers in various phases of the menstrual cycle received estradiol infusion for 66 h at a constant rate of 500 micrograms/24 h which is grossly equivalent to its production rate during the preovulatory follicular phase. In 8 of the women, GnRH was administered concomitantly from 6 h after the initiation of estradiol infusion. The administered doses of GnRH were 2.5 and 5 micrograms/h. Blood samples obtained throughout the infusion were analysed for LH, FSH, estradiol and progesterone. The sole administration of estradiol failed to induce the positive feedback effect on gonadotropin release within the experimental period in the early follicular phase (days 3-7) in 4 women. In 5 women treated during the follicular phase, remarkable LH releases were induced after a lag period by the infusion of both GnRH and estradiol. The induced LH surge formed a prolonged biphasic pattern. Although a similar pattern of FSH was observed in some cases, its response was minimal compared with that of LH. In 3 women during the luteal phase, however, a combined administration of estradiol and GnRH induced only a short term release of LH which was terminated in only 12 h. The present data indicate that 1) Preovulatory levels of estrogen affect the late part of the LH surge which is induced by constant administration of low doses of GnRH resulting in a prolonged biphasic release of LH, and 2) These effects of both hormones are not manifest in the presence of high levels of progesterone. These results indicate the possibility of a role of GnRH and estrogen in the mechanism of the prolonged elevation of a gonadotropin surge at mid-cycle.

Adult↗
PubMed1985

Effects of progesterone on prolactin secretion in hypogonadal women.

Although estrogen is known to stimulate the secretion of prolactin, there are only slight differences between the prolactin levels in the follicular and luteal phases in normal women. To test the hypothesis that progesterone is involved in the regulation of prolactin release, 50 mg of progesterone was administered intramuscularly at 0600 h to twelve hypogonadal women and blood samples were obtained at 15 min intervals between 1500 and 2000 h to determine the prolactin levels. The day before progesterone treatment, control blood samples were obtained at 15 min intervals between 1500 and 2000 h. The serum progesterone levels were 28.7 +/- 4.1 ng/ml at 1500 h, 24.2 +/- 3.5 ng/ml at 1730 h and 21.3 +/- 2.9 ng/ml (mean +/- SD) at 2000 h. In eight of twelve hypogonadal women, progesterone lowered circulating prolactin levels significantly. These results indicate that a high level of progesterone in the luteal phase may partly block estrogen-induced prolactin release physiologically.

Adult↗