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Biomedical subjects

A Miyake

Publications and source records attributed to A Miyake.

At least 325 records · Page 18Linked to original sources

Ultrastructure of meiosis-inducing (heterotypic) and non-inducing (homotypic) cell unions in conjugation of Blepharisma.

Cells of mating types I and II of Blepharisma japonicum interact with each other and unite in heterotypic (type I-type II) or homotypic (type I-type I, type II-type II) pairs. Heterotypic pairs undergo meiosis and other nuclear changes of conjugation, while homotypic pairs remain united for days without the nuclear changes taking place. We compared cell unions of these two kinds of pairs at the ultrastructural level. In the homotypic union, cell membranes are closely juxtaposed, separated by a distance of about 20 nm. This arrangement is interrupted in some places by vacuoles and small cytoplasmic bridges. Saccule-like structures tend to be more abundant near the united surfaces. Microtubules running at right or slightly obtuse angles with the cell surface (PACM microtubules) are characteristically present at the united region of cells. These structures are very similar to those observed in earlier stages of the heterotypic union. However, in homotypic pairs, cells unite only at the anterior half of the peristome, while in heterotypic pairs cells unite also at the posterior half of the peristome, where the cell membrane totally disappears in later stages. PACM microtubules persist for at least 18 h in homotypic unions, while they disappear within a few hours in heterotypic unions. These differences between the two kinds of cell union are discussed in relation to the initiation mechanism of meiosis and other nuclear changes of conjugation. Similarities between homotypic union and cell junctions in multicellular organisms are also discussed.

Animals↗

Absence of positive feedback effect of oestrogen on LH release in patients with testicular feminization syndrome.

The response of serum LH to exogenous oestrogen administration was studied in 5 patients with testicular feminization syndrome (TFS). The serum LH levels were elevated in all the patients, while serum testosterone levels were within the normal male range. Serum FSH levels were elevated in 4 patients and normal in one patient. Intravenous administration of 100 microgram of LH-RH provoked a further increase in both LH and FSH. Following intravenous injection of 20 mg of conjugated oestrogen (Premarin), the LH levels were serially determined until 120 h in TFS patients, 5 normal males, and 10 normal females during the mid-follocular phase (D7-9). Both TFS patients and normal males showed no LH release following oestrogen injection in contrast to normal females who displayed a significant increase in LH with a peak at 48 to 56 h after the injection. These results seem to suggest that the insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. The possible role of oestradiol conversion from testosterone in the hypothalamus is discussed.

Adolescent↗

The time course change after castration in short-loop negative feedback control of LH by HCG in women.

The time course of change in the suppressive effect of human chorionic gonadotrophin (HCG) on luteinizing hormone (LH) and/or LH-beta following castration was studied by a specific LH-beta radioimmunoassay. At 14-50 days after castration 8 women were given 10 000 IU of HCG in a single intramuscular injection (group 1), 5 women were given 2000 IU of HCG in the same way (group 2), and 5 were injected with saline as controls (group 5). In addition, 5 women 6-15 months (group 3) and 7 women 3-8 years (group 4) after castration were given 10 000 IU of HCG. The serum concentrations of HCG in groups 1, 2, 3 and 4 reached peak levels of 209.4, 44.1, 210.6 and 238.6 uU/ml, respectively, 4 h after the HCG injection. The serum LH concentration in group 1 was reduced significantly (P less than 0.01) by HCG administration, but the reductions in the LH levels in groups 2, 3 and 4 after HCG injection were not significantly different from that of the controls. These findings suggest that the threshold of the short-loop negative feedback control of LH in women changes with time after castration.

Adult↗

Pituitary LH response to LHRH during puerperium.

Forty puerperal women and 15 normally menstruating women used as controls were given 100 microgram of synthetic luteinizing hormone releasing hormone (LHRH) in a single intravenous injection. Serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and human chorionic gonadotropin (hCG) were measured by a specific radioimmunoassay (RIA). The LH-beta RIA method, which is unaffected by hCG at sample levels as high as 500 IU/ml, was used to determine serum LH levels. Basal serum FSH and LH levels determined immediately after delivery were lower than those in the follicular and luteal phases during the normal menstrual cycle. These levels rose gradually after delivery, and finally returned to normal levels during the 16th to 25th days of the puerperal period. Small, but significant, LH response to LHRH was observed 6-10 days after delivery, and gradually returned to normal thereafter, though the response was poor during the first 35 days of the puerperal period when compared with that of the controls. On the other hand, no FSH response to LHRH was observed until 16-25 days after delivery, when the response was greater than that of the controls.

Adult↗

LH concentrations in human maternal and cord serum.

Maternal blood and umbilical cord venous blood were collected immediately after delivery in 32 subjects who had completed normal birth during the 38 to 41 weeks of pregnancy, and the concentrations of human chorionic gonadotropin (hCG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were determined by radioimmunoassay (RIA). The specific LH RIA utilized for the measurement of LH is unaffected by hCG at sample levels as high as 500 IU/ml. HCG concentrations were 10,370 +/- 1,480 mIU/ml (mean +/- SE) in mother's serum and 34.5 +/- 5.2 ml in cord serum, while LH concentrations were 0.729 +/- 0.055 and 0.438 +/- 0.033 ng/ml, respectively. The concentration of all 3 gonadotropins in maternal serum was greater than cord serum and the ratio was markedly high with 302:1 for hCG, while the ratio was smaller for LH, being 1.7:1, while that for FSH was 4.2:1. There was no difference in the levels of LH and FSH in relation to the sex of the fetus.

Adult↗

Responses of serum gonadotrophins to LH-releasing hormone and oestrogens in Japanese women with polycystic ovaries.

In order to define the abnormality in gonadotrophin secretion in Japanese women with polycystic ovaries (PCO) who rarely show virilization and markedly enlarged ovaries, basal levels of LH and FSH, and responses of serum gonadotrophins to LH-releasing hormone (LH-RH) or oestrogens were determined by radioimmunoassay. Eleven patients with PCO diagnosed by laparotomy or laparoscopy and 30 normal women in the follicular phase were studied. The mean (+/- SD) basal level of LH was significantly higher in patients with PCO than in normal controls (PCO 28.6 +/- 2.4 vs. normal 10.9 +/- 3.0 mIU/ml), while the mean FSH level in PCO patients was not significantly different from that in the normal controls (9.7 +/- 0.7 vs. 11.4 +/- 2.6 mIU/ml). The mean LH/FSH ratio in PCO patients was significantly higher than that in normal controls (3.2 +/- 0.9 vs. 1.0 +/- 0.3). Exaggerated response of LH to LH-RH was observed in PCO patients, while the FSH response was comparable with the normal controls. Ten out of 11 patients with PCO showed LH release exceeding the basal level after bolus iv injection of 20 mg conjugated oestrogens (Premarin), and virtually the same mean net increase in LH from the basal level was obtained in both PCO patients and normal controls. Since the abnormalities in gonadotrophin secretion in Japanese women with PCO are not different from those reported in patients with PCO in Europe and USA, it seems likely that lower incidence of markedly enlarged ovaries and virilization in Japanese patients may be caused by the difference in ovarian response to gonadotrophin.

Adult↗

Pituitary responses in LH secretion to LHRH during pregnancy.

Thirty-six pregnant women and 15 normally menstruating women were each given 100 microng of synthetic luteinizing hormone releasing hormone (LHRH) by a single intravenous injection. Human chorionic gonadotropin (hCG), luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels were determined by specific radioimmunoassay (RIA) technics. For the determination of the serum LH levels, the LHbeta-RIA method, which is unaffected by hCG at sample levels as high as 500 IU/ml, was used. Serum concentrations of LH and FSH were lower in pregnant women than in the normal women in the follicular and luteal phases. While the release of LH was observed in pregnant women following the administration of LHRH, the average net increase was less than that seen in both the follicular and luteal phases. During pregnancy, there was a progressive decrease in the LH response to LHRH, but no release of FSH.

Adult↗

Impaired LH release following exogenous estrogen administration in patients with amenorrhea-galactorrhea syndrome.

Serum gonadotropin levels were determined in 10 patients with the amenorrhea-galactorrhea syndrome before and following acute iv administration of synthetic LH-releasing hormone (LHRH) or conjugated estrogens, in order to clarify the hypothalamic derangements in the gonadotropin secretion in patients with hyperprolactinemia. The basal prolactin (PRL) levels were elevated in all the patients, and blunted responses to 500 mug of iv synthetic thyrotropin-releasing hormone (TRH) injection were found in 9 out of the 10 patients. The basal levels of LH and FSH were subnormal in 2 and 3 patients, respectively, while those in the remaining patients were normal or slightly elevated. Normal or excessive responses of gonadotropins to 100 mug of iv LHRH were observed in most patients, 9 for LH and 10 for FSH out of 10 patients. In 10 normal cyclic women at the mid-follicular phase (D7-9) and 10 hypothalamic amenorrhea patients without galactorrhea, LH release was found 48 to 72 h after the iv injection of 20 mg conjugated estrogens (Premarin). This LH release following Premarin injection was completely abolished in the patients with amenorrhea-galactorrhea. These data seem to indicate that in patients with hyperprolactinemia, tonic secretion of gonadotropin is maintained fairly well, while of the positive feedback effect of Premarin on the release of LH is impaired. It is suggested that impaired LH release may be partly responsible for anovulation and amenorrhea in patients with hyperprolactinemia.

Abortion, Spontaneous↗

Suppression of luteinizing hormone in castrated women by the administration of human chorionic gonadotropin.

The suppressive effect of human chorionic gonadotropin (hCG) on luteinizing hormone (LH) and/or LH-beta was studied by specific LH-beta radioimmunoassay following hCG administration. Eight castrated women were each administered 10,000 IU of hCG in a single intramuscular injection and five women in the control group were injected with saline. The serum level of hCG increased after the injection, reaching 217.6 mIU/ml after 8 h. There was a significant suppression of LH levels as compared to those of the control group and the pre-injection levels: 68.2% 1 h after injection, 64.7% after 2h, 65.5% after 4 h, 77.0% after 8 h, 78.6% after 12 h, and 78.2% after 24 h. There was no significant suppression of the follicle-stimulating hormone (FSH) as compared to the preinjection and control values. Serum concentration of estradiol1 was not detectable either before or after the hCG injection. We conclude that hCG has a suppressive effect on LH and/or LH-beta secretion not mediated by estradiol.

Adult↗

Studies on juvenimicin, a new antibiotic. II. Isolation, chemical characterization and structures.

A series of new macrolide antibiotics was isolated from the culture filtrate of Micromonospora chalcea var, izumensis. The fat-soluble basic complex consisted of eight components which were named juvenimicin A1 approximately A4 and B1 approximately B4. Juvenimicin A3 was found to be identical with rosamicin and the structures of four of the other components (JVM A2, A4, B1 and B3) have been elucidated. Juvenimicin A2 has a methyl group at position 6 instead of the formylmethyl group of juvenimicin A3. Juvenimicin A4, B1 and B3 possess a hydroxyethyl group at position 6. Juvenimicin A4 and B1 differ from each other in the nature of the chromophore. Juvenimicin B3 differs from juvenimicin B1 in that a hydroxymethyl group is present at position 14 in the former.

Animals↗