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Biomedical subjects

A Miyake

Publications and source records attributed to A Miyake.

At least 235 records · Page 13Linked to original sources
PubMed1989

Involvement of extracellular calcium and arachidonate in [3H] dopamine release from rat tuberoinfundibular neurons.

The mechanism of [3H]dopamine [( 3H]DA) release was investigated using primary cultures of dispersed cells from the rat tuberoinfundibular region, which contains tyrosine hydroxylase (TH)-like immunoreactive neurons. The calcium ionophore A23187 at 10 nM and above caused a significant and dose-dependent increase in [3H]DA release. In the presence of 50 microM A23187, [3H]DA release was detectable within 30 s and reached a plateau in 15 min. The induction of [3H]DA release by 50 microM A23187 was abolished by lowering the extracellular calcium concentration with 2 mM EDTA. Maitotoxin, another calcium-channel activator, also increased [3H]DA release at a concentration of 50 ng/ml. Exogenous additions of 100 mIU/ml phospholipase A2 and 10 microM arachidonate caused significant release of [3H]DA. Furthermore, A23187 stimulated [3H]arachidonate release from tuberoinfundibular dopaminergic (TIDA) neurons in a dose- and time-dependent manner. These results suggest that extracellular calcium and arachidonate are involved in the process of [3H]DA release from rat TIDA neurons.

Animals↗
PubMed1989

A new pharmacological testing method--different effects of levamisole and the serum of mice orally treated with levamisole on mitogenic activity of lipopolysaccharide.

The direct addition of levamisole to murine splenic lymphocytes had no effect on the mitogenic activity of lipopolysaccharide. However, the addition of serum of mice orally treated with levamisole increased the mitogenic activity, and this increased activity using serum was similar to the result obtained in an in vivo experiment. These results suggest that the new in vitro experimental method using serum may be able to reproduce the in vivo effect of drugs.

Animals↗
PubMed1989

Suppression of serum immunoreactive human epidermal growth factor by acute increase in prolactin in women.

Epidermal growth factor (EGF) is known to stimulate proliferation of various mammalian cells and secretion of prolactin (PRL) from rat anterior pituitary tumor cells. The effect of an acute increase in serum PRL induced by thyrotropin releasing hormone (TRH) or metoclopramide (MCP) on the serum immunoreactive EGF concentration was examined in nine hyperprolactinemic patients and eight normoprolactinemic women. The basal level of serum EGF in normoprolactinemic subjects was 472.8 +/- 51.1 pg/ml (Mean +/- SEM), which was not significantly different from that in hyperprolactinemic patients (487.8 +/- 22.5 pg/ml). The serum EGF concentration was decreased to 40-50% of the basal level after the abrupt increase in serum PRL induced by the injection of TRH or MCP in normoprolactinemic subjects, but no significant change in serum EGF occurred in hyperprolactinemic patients after MCP injection, in spite of a significant increase in PRL. These results suggest that an acute increase of serum PRL in normoprolactinemic women, but not in hyperprolactinemic patients, suppresses serum EGF.

Adenoma↗
PubMed1989

Studies on GnRH agonist suppression of estrogen production in patients with endometriosis.

The chronic administration of GnRH agonists to women results in the reversible suppression of estrogen production by the ovary. In the present study, the mechanism of the GnRH agonist suppression of estrogen production was investigated in patients with endometriosis. During the treatment with intranasal buserelin spray, the concentration of serum estradiol-17 beta (E2) was suppressed to near-castrate levels. Despite this marked suppression of serum E2, immunoreactive LH and FSH levels in serum were not changed. On the other hand, serum bioactive LH was markedly reduced. It was also observed during the treatment that the pituitary LH pulse disappeared and pituitary response to exogenous GnRH was significantly suppressed. In contrast, ovarian response to human menopausal gonadotropin (hMG) was not altered during the treatment. These findings suggest that the GnRH agonist suppression of estrogen production in the patients with endometriosis is through both suppression of the secretion of biologically active LH and the reduction of the LH pulse, but not through a direct inhibitory effect on ovarian estrogen biosynthesis.

Administration, Intranasal↗
PubMed1989

Estrogen stimulates gonadotropin-releasing hormone release from rat hypothalamus independently through catecholamine and histamine in vitro.

Estradiol is known to stimulate gonadotropin-releasing hormone release from the rat medio-basal hypothalamus. Studies were made in an in vitro perifusion system on whether catecholamine and/or histamine was involved in estradiol-induced GnRH release. Normal cycling female rats were decapitated in diestrus II and their medio-basal hypothalami were combined and, perifused with Earl's balanced salt solution containing 0.01% bovine serum albumin bubbled with 95% O2 and 5% CO2. The levels of norepinephrine, dopamine, and histamine and of GnRH in the effluent were measured by HPLC and radioimmunoassay, respectively. Administration of 10(-6) mol/l estradiol resulted in releases of norepinephrine, dopamine, histamine and GnRH at levels of 98, 70, 91 and 288%, respectively, of initial values. Administration of 10(-6) mol/l norepinephrine or dopamine resulted in no increase in histamine release, and administration of 10(-6) mol/l histamine did not increase release of norepinephrine or dopamine. These data suggest that estradiol stimulates the releases of GnRH, catecholamine and histamine from the rat medio-basal hypothalamus, and that it increases GnRH release independently through catecholamine and histamine. As we found previously that norepinephrine or histamine stimulates GnRH release from the medio-basal hypothalamus, we conclude that estradiol stimulates releases of norepinephrine and histamine, resulting in GnRH release from the medio-basal hypothalamus.

Animals↗
PubMed1988

Mass screening for hyperprolactinemia and prolactinoma in men.

To determine the incidence of hyperprolactinemia and prolactinoma without symptoms in men, the serum levels of prolactin were measured in 4803 men. Of these, 14 had hyperprolactinemia with prolactin level of over 50 ng/ml, and 3 had prolactin levels of more than 500 ng/ml. Of these 3 subjects, 2 were found to have pituitary prolactinoma by computed tomograph scanning and surgery, the other subject, who was highly suspected to have prolactinoma, refused further examinations. The serum prolactin levels of 51-100 ng/ml in 11 subjects may have been induced by drugs (sulpiride) or unknown factors. The present survey suggests that the incidence of prolactinoma in men in the general population might be estimated to be 1:1600, and that mass screening is useful for early diagnosis of asymptomatic prolactinoma.

Adult↗
PubMed1988

Possible involvement of lipoxygenase pathway of arachidonic acid in rat pituitary hormone release in vitro.

The roles of arachidonic acid (AA) and its lipoxygenase products in control of secretion of anterior pituitary hormones were studied in vitro using cultured cells. AA (10(-4)M) and 5-hydroxy-eicosatetraenoic acid (5HETE) (5 x 10(-6)M) significantly (p less than 0.05) stimulated the releases of LH, TSH, GH, PRL, ACTH and beta-endorphin (beta-E). Added leukotriene B4 (LTB4) (5 x 10(-6)M) also caused significant increases in the secretions of LH, GH, ACTH and beta-E. The other lipoxygenase metabolites tested, 12HETE, 15HETE, LTA4, LTC4 and LTD4, had no effect on the releases of anterior pituitary hormones. These results suggest that AA and 5-lipoxygenase metabolites may be involved in the control of the releases of anterior pituitary hormones.

Adrenocorticotropic Hormone↗
PubMed1988

The functional role of sensory inputs from the foot: stabilizing human standing posture during voluntary and vibration-induced body sway.

The functional role of sensory inputs from the foot in the stabilization of upright standing in humans was studied using an ischemic nerve block which was applied bilaterally at the level of the ankle. Subjects were asked: (1) to lean forward or backward by pivoting around their ankle joints; and (2) to hold a standing posture during the bilateral application of vibration (140 Hz) to the Achilles tendons. After 30-40 min of ischemia, the magnitude of maximum body leaning was equally reduced to about 70% of controls for both the "eyes-open" and "eyes-closed" conditions with bare feet. This decrease of body leaning caused by ischemia was not observed when a foot was fixed firmly on a "fixation" board. During vibration, body sway was augmented, and characteristic oscillations of this body sway around 3 Hz were observed under ischemic conditions with eyes closed and with bare feet. We concluded that foot sensation may be an important source of information for controlling the magnitude of body leaning and for stabilizing higher frequency components of body sway.

Adult↗
PubMed1988

Second pregnancy with spontaneous ovulation following clomiphene- or gonadotropin-induced pregnancy.

For investigation of the rates of spontaneous pregnancy following termination of pregnancy induced by treatment with clomiphene or human menopausal gonadotropin-human chorionic gonadotropin (hMG-hCG) and of spontaneous abortion in the second pregnancy, 119 women (58 with an anovulatory cycle and 141 with amenorrhea) who desired another pregnancy were studied. The rate of spontaneous pregnancy following pregnancy induced by clomiphene was 46.6%, which was significantly (p less than 0.001) higher than that following pregnancy induced by hMG (14.9%). The mean (+/- SEM) period between the termination of the first induced-ovulation pregnancy and the second spontaneous pregnancy was 16.6 +/- 1.4 months. The spontaneous abortion rates in the second pregnancies after pregnancies induced by clomiphene and hMG were 7.5% and 9.8%, respectively, which were significantly (p less than 0.001, p less than 0.05) lower than those in the first pregnancy (25.7%, 33.0%). There was no difference between the spontaneous abortion rates following a first pregnancy which terminated in abortion and those following a pregnancy which ended in birth. These data suggest that a first pregnancy in anovulatory women may restore the ovulatory cycle and have a beneficial effect on the rates of spontaneous abortion in the second pregnancy.

Clomiphene↗
PubMed1988

Changes in epidermal growth factor receptor and its messenger ribonucleic acid levels in human placenta and isolated trophoblast cells during pregnancy.

We measured the amounts of epidermal growth factor receptor (EGFR) in plasma membrane fractions purified from early, middle, and term placentas and from isolated trophoblast cells, and the amounts of EGFR mRNA were measured in whole placentas. Binding studies were performed using [125I] human EGF as ligand; two classes (high and low) of binding sites were found in placental and trophoblast cell plasma membranes. Although dissociation constants (Kd) were not significantly different in placental plasma membranes from the three stages of pregnancy, the number of binding sites increased significantly during pregnancy. The mean numbers of binding sites were 0.72 +/- 0.18 (+/- SE), 1.02 +/- 0.10, and 1.89 +/- 0.21 pmol/mg protein (high affinity sites) in plasma membrane fractions from early, middle, and term whole placentas, respectively. A similar significant increase was found when the membranes were prepared from isolated trophoblast cells. At the same time, total cellular RNA was isolated, denatured, and blotted onto nitrocellulose membranes. Then, hybridization with 32P-labeled pE 7, a cDNA of EGFR, or 32P-labeled v-erb-B oncogene, autoradiography, and densitometry were performed. The EGFR mRNA increased proportionally to the changes in EGFR during pregnancy. These results indicate that EGF-binding sites and EGFR production increase in human placentas throughout the gestational period.

Blotting, Northern↗
PubMed1988

Lunch induces an increase in the plasma prolactin concentration, but not vasoactive intestinal peptides or cholecystokinin.

Ingestion of lunch is known to be associated with acute release of prolactin (PRL). The neuroendocrine mechanism of this release was examined by measuring changes in serum vasoactive intestinal peptides (VIP) and cholecystokinin (CCK) after the noon meal in six normal men. The serum PRL concentration was significantly increased (40% above the level before lunch) from 30 min to 1 h 45 min after beginning to eat. However, the ingestion of lunch had no remarkable effects on the plasma immunoreactive concentration of VIP and CCK. Thus the changes in the plasma concentration of these two gut-brain peptides did not coincided with acute PRL release after ingestion of lunch, suggesting either that these two gut-brain peptides are probably not involved in PRL release after lunch, or that the level of these two gut-brain peptides in the general circulation may not represent that in the hypophyseal portal plasma.

Adult↗
PubMed1988

Vasoactive intestinal peptide stimulates gonadotropin-releasing hormone release from rat hypothalamus in vitro.

The effects of vasoactive intestinal peptide (VIP) on the releases of LH and GnRH were examined in a sequential double chamber perifusion system by perfusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in diestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats in series were perifused with VIP (10(-6) mol/l), the concentration of LH in the efflux was increased by 59-181% above that before the injection (P less than 0.05), VIP having a dose-dependent effect. VIP had no effect on LH release from the pituitary perifused alone. Infusion of VIP at 10(-6) mol/l induced a significant release (84-159% increase, P less than 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10(-6) mol/l VIP induced a significant release (41-99% increase, P less than 0.05) of LH in ovariectomized rats. These findings suggest that VIP induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that this process does not require ovarian estrogen.

Animals↗
PubMed1987

Effect of clomiphene citrate administration during the early luteal phase on the luteal function and pregnancy rate of women.

To study the effect of clomiphene citrate (clomiphene) administration during the early luteal phase of the menstrual cycle on the luteal function and the pregnancy rate in women, 75 infertile women who ovulated but did not conceive after clomiphene treatment during the early follicular phase and 6 normal cycling women were chosen. Clomiphene was administered orally to 35 of the 75 infertile women at a dose of 50 mg per day for 5 days from the second day of the rise in the basal body temperature (BBT) as well as during the follicular phase, while 40 control patients received clomiphene only during the follicular phase. In the test patients, the rate of pregnancy (25.7%) was significantly (p less than 0.05) higher than that of control patients (10.0%). On the 7th of the rise of BBT, the mean serum progesterone levels of the test patients and normal cycling women treated with clomiphene were significantly (p less than 0.05) higher than those of the control patients. However, the levels of serum estradiol, LH and FSH, the gonadotropin pulsatilities, and the pituitary responses to LH-RH in the test women were not significantly different from those of the control. These data suggest that, when administered during the early luteal phase, clomiphene may act directly on the ovary, enhancing the secretion of progesterone from the corpus luteum, and thereby increasing the rate of pregnancy in infertile women with clomiphene-induced ovulation.

Adult↗
PubMed1987

Involvement of H1 histamine receptor in basal and estrogen-stimulated luteinizing hormone-releasing hormone secretion in rats in vitro.

For determination of the roles of histamine and its receptors, H1 and H2, in the control of basal and estrogen-induced LH-RH secretion, the mediobasal hypothalamus (MBH) and/or pituitary was excised from normally cycling female rats and perifused in an in vitro sequential double chamber perifusion system. Administration of 10(-7) M histamine caused significant release (90-170% increase, p less than 0.05) of LH from the pituitary in sequence with the MBH, whereas 10(-7) M histamine had no effect on LH release from the pituitary perifused alone; administration of 10(-5) M 2-methylhistamine, an H1 agonist, induced significant release (50-120% increase, p less than 0.05) of LH-RH from the MBH, and addition of 10(-5) M mepyramine, and H1 antagonist, abolished this LH-RH release. The LH concentrations in the efflux were not affected by the administration of the H2 agonist 4-methylhistamine. Estradiol caused significant release of LH-RH from the MBH and LH from the pituitary in sequence with the MBH. The estradiol-induced release of LH-RH and LH were completely abolished by perifusion with medium containing 10(-5) M mepyramine. The H2 receptor antagonist ranitidine did not affect estradiol-induced LH release. Histamine did not change the LH release induced by 20 ng LH-RH. These findings suggest that histamine induces release of hypothalamic LH-RH, and that histamine H1 receptors in the hypothalamus are involved in the basal and estradiol-induced LH-RH release.

Animals↗
PubMed1987

Absence of effect of estrogen on dopamine, norepinephrine and beta-endorphin-like immunoreactivity in human plasma.

The plasma concentrations of immunoreactive norepinephrine (NE), dopamine (DA), beta-endorphin (beta-E), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were determined by RIA and HPLC every 6 h until 72 h after iv administration of conjugated estrogens during the midfollicular phase. The LH level showed a biphasic pattern after the injection of conjugated estrogens, i.e. significant suppression (-50%) for 6-42 h after the injection, followed by a rebound increase with a peak (+85%) at 72 h. The plasma levels of immunoreactive beta-E, NE and DA did not change significantly for 72 h after the injection.

Adult↗