Antisperm antibodies appear to impair reproduction. Follicular fluids, ascites and sera taken at the time of oocyte recovery from patients undergoing gamete intrafallopian transfer (GIFT) were examined for the presence of sperm immobilizing antibodies and their immunoglobulin classes were determined. Three out of ten patients were found to have sperm immobilizing antibodies in their sera. The immunoglobulin classes of the antibodies were IgG and/or IgM, and no IgA class antibodies were detected. The same classes of antibodies found in sera also existed in follicular fluids and ascites in these patients. Furthermore, titers of the antibodies in follicular fluids and ascites were consistent with those of patients' sera.

Adult↗

PubMed1988

[Identification and characterization of a human sperm coating antigen isolated from sperm cell membrane].

An antigenic spermatozoal polypeptide was identified from nonionic detergent solubilized membrane material of sperm cells by using a human seminal plasma specific rabbit antiserum. The radiolabeled sperm cell membrane preparation was subjected to gel filtration and gel fractions were assayed for the binding activity with antiseminal plasma antiserum. The immune complex of the peak fraction of the binding was applied on SDS-PAGE, and the antigen was estimated to be a single polypeptide of approximately 12,000 daltons. The inhibition assay of the binding revealed that the antigen is present in sperm, seminal plasma, and milk, but is absent from any other organs and tissues except male genital tracts. Seminal plasma showed the largest amount of the activity, suggesting that this antigen is a sperm coating antigen. In seminal plasma, the antigen molecule present in a large form with a molecular weight of approximately 50,000 daltons. The antigenicity was stable when treated with heat, acid, alkali and various protein denaturants. The characteristics of the present antigen are very similar to those of lactoferrin and ferrisplan, the other sperm coating antigens common to milk. However, they are quite different in molecular weight, and no cross reactivity was found between the present antigen and lactoferrin or ferrisplan.

Antigens, Surface↗

PubMed1988

[Growth inhibition by progestins in human endometrial cancer cells with progesterone receptors].

The presence of estrogen-independent progesterone receptors (PR) was demonstrated in a subline of a human endometrial cancer cell line, Ishikawa cells. Scatchard plot analysis of cytoplasmic binding data in a subline (IK-90) revealed a high affinity binding site for promegestone (Kd, 1.0 nM) with maximum binding sites of 158 fmol/mg protein. Competition experiments showed a binding specificity similar to that of typical PR. By low-salt sucrose gradient centrifugation, radioactive 8S and 4S peaks were found. The addition of 1 microM progesterone in culture medium resulted in a rapid nuclear translocation of cytoplasmic PR. Accumulation of glycogen in cytoplasm of the cells in response to 0.1 microM promegestone was observed by periodic acid-Schiff staining. Addition of various concentrations (1 nM-1 microM) of promegestone reduced the cell growth in a dose-dependent manner. The growth inhibition by promegestone was totally prevented by the concomitant addition of equimolar RU 486, a progestin antagonist. The other steroids including tamoxifen, cortisol, and testosterone had no significant effects on the growth of the cells. The growth-inhibitory effect of progestin on cultured cancer cells from human endometrial adenocarcinomas obtained by hysterectomy was also investigated. Addition of medroxyprogesterone acetate (1 nM-1 microM) caused a marked decrease in [3H]thymidine incorporation in cultured cancer cells from tumors with PR. From the viewpoint obtained in the present studies using both IK-90 cells and endometrial cancer cells in primary culture, it can be concluded that progestins produce regression of endometrial cancer directly via the PR system.

Cell Division↗

PubMed1988

[Prediction of postpartum relapse of Graves' thyrotoxicosis and the development of neonatal Graves' disease by the highly sensitive TSH immunoradiometric assay].

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Female↗

PubMed1988

Morning sickness and thyroid function in normal pregnancy.

Thyroid function in early normal pregnancy was evaluated with reference to morning sickness using a newly developed free thyroxine (T4) radioimmunoassay and a highly sensitive TSH immunoradiometric assay. A significant increase in serum free T4 and a decrease in serum TSH were observed in early pregnancy relative to the levels in nonpregnant controls. The increased free T4 and hCG and decreased TSH correlated with the severity of morning sickness, and these changes were especially marked in subjects with nausea and vomiting. The individual serum levels of hCG in the pregnant group correlated significantly, directly with the levels of free T4 and inversely with those of TSH. The increased free T4 and decreased TSH in subjects with emesis returned to the normal ranges of nonpregnant controls after improvement of emesis. These data indicate that the thyroid gland is physiologically activated in early pregnancy, possibly by hCG or a related substance, which may induce gestational emesis. On the other hand, an increased level of free T4 and a reduced level of TSH in early normal pregnancy are not indications of thyrotoxicosis and may not necessitate antithyroid drug treatment.

Analysis of Variance↗

PubMed1987

Expression of blood group antigens A, B, H, Lewis-a, and Lewis-b in fetal, normal, and malignant tissues of the uterine endometrium.

Fetal, normal adult, and malignant tissues of the uterine endometrium were examined by immunoperoxidase staining for the blood group antigens (BGA) A, B, H, Lewis-a, and Lewis-b. Antigens A, B, and H compatible with the ABO status of fetuses were detected in 20 of the 22 fetal tissues that were examined. Lewis-b immunoreactivity was also found in 21 fetuses, and Lewis-a was present in a third of the cases. In adult endometrium the expression of BGA H and Lewis-b was considerably lower than in fetal tissues. Malignant endometrial glands extensively reexpressed H and Lewis-b regardless of ABO status. BGA A and B were neither absent nor accumulated in cancer tissues. Thus, H and Lewis-b can be considered as oncofetal antigens since they were frequently expressed in fetal and cancer tissues, but not in normal adult tissues. The increased expression of Lewis-a antigen might be associated with malignant transformation as it was observed only in malignant tissues. However, the functional significance of alterations in BGA expression that may be associated with oncogenesis remains to be investigated.

ABO Blood-Group System↗

PubMed1987

Growth inhibition by progestins in a human endometrial cancer cell line with estrogen-independent progesterone receptors.

The presence of estrogen-independent progesterone receptors (PgR) was demonstrated in a subline of a human endometrial cancer cell line, Ishikawa cells, although the original Ishikawa cells contained estrogen-inducible PgR. Scatchard plot analysis of cytoplasmic binding data in our subline (IK-90) revealed a high affinity binding site for R5020 (Kd, 1.0 nM) with maximum binding sites of 158 fmol/mg protein. Competition experiments showed a binding specificity similar to that of typical PgR. By low-salt sucrose gradient centrifugation, radioactive 8S and 4S peaks were found. The addition of 1 microM progesterone in culture medium resulted in a rapid nuclear translocation of cytoplasmic PgR. In contrast to the original cells, estrogen receptors could not be detected in IK-90 cells, and an addition of 17 beta-estradiol (10 nM) to culture medium failed to increase PgR. Accumulation of glycogen in cytoplasm of IK-90 cells in response to R5020 (0.1-1 microM) was observed by periodic acid-Schiff staining. The addition of R5020 to culture medium (0.1-1 microM) also caused a marked decrease in the growth of IK-90 cells, whereas the other steroids including 17 beta-estradiol, tamoxifen, testosterone, and cortisol had no significant effects. These results demonstrate for the first time the presence of a progestin-responsive human endometrial cancer cell line that contains estrogen-independent functional PgR. IK-90 cells appear to be an ideal model for studying the mechanism of the antiproliferative effect of progestin on endometrial cancer cells.

Cell Division↗

PubMed1987

Growth inhibition by danazol in a human endometrial cancer cell line with estrogen-independent progesterone receptors.

Since we recently found that danazol, an isoxazol derivative of ethinyltestosterone, has a growth-inhibitory effect on human endometrial cancer cells in primary culture, the effects of danazol on a human endometrial cancer cell line (IK-90 cells), which contains estrogen-independent progesterone receptors (PR), were investigated in the present study. The addition of danazol (1 nM-1 microM) in culture medium caused a decrease in the growth of IK-90 cells in a dose-dependent manner. Competitive binding studies showed that danazol effectively binds to PR in IK-90 cells, and the binding affinity for PR was estimated to be 6.0% of that of R5020. The addition of 1 microM danazol in culture medium resulted in a rapid and significant increase in nuclear PR with a concomitant decrease in cytoplasmic PR in the cells. These findings suggest that danazol has a growth-inhibitory effect on human endometrial adenocarcinoma cells directly through PR system in the cells.

Binding, Competitive↗

PubMed1987

Roles of antiestrogen binding sites in human endometrial cancer cells.

Estrogen-noncompatible antiestrogen binding sites (AEBS) as well as estrogen receptors (ER), and the growth-inhibitory effect of tamoxifen were investigated in two human endometrial cancer cell lines, IK-90 and HEC-IA cells. IK-90 cells contained specific AEBS, but no ER was found in these cells. Scatchard plot analysis of AEBS in 12,000 g supernatant from IK-90 cells showed a high affinity binding site for tamoxifen (Kd:5.6 +/- 1.0 nM) with the maximum binding site of 457 +/- 47 fmol/mg protein. However, no measurable ER or AEBS was found in HEC-IA cells. The effect of tamoxifen on the growth of cells was found to be identical in both cell lines; the addition of 10 microM tamoxifen to culture medium was cytocidal whereas tamoxifen at lower concentrations (1 nM-1 microM) did not significantly affect the growth of both IK-90 and HEC-IA cells. These results demonstrate for the first time the presence of AEBS in human endometrial cancer cells. The present results also suggest that AEBS does not play a fundamental role in mediating the growth-inhibitory effect of tamoxifen in endometrial cancer cells.

Adenocarcinoma↗

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

Detection of chromogranin in argyrophil cells of endometrial carcinoma.

Normal and neoplastic endometrial tissues were examined immunohistochemically for chromogranin which was shown to be a specific marker for neuroendocrine cells. All 20 normal endometriums and 20 endometrial carcinomas without argyrophilia were chromogranin negative. Endometrial carcinomas with argyrophilia tested were composed of three groups; 10 with type I argyrophil cells, 20 with type II argyrophil cells, and 10 with both type I and II argyrophil cells. Type I argyrophil cells of 20 endometrial carcinomas were all chromogranin positive. Chromogranin immunoreactivity was also intimately correlated with the Grimelius reactivity in type II argyrophil cells of 19 endometrial carcinomas, 13 with only type II argyrophil cells and 6 with mixed type of argyrophil cells. Chromogranin was absent in type II argyrophil cells of 11 endometrial carcinomas, 7 with type II argyrophil cells and 4 with mixed type of argyrophil cells. Chromogranin negativity was related to the disappearance of argyrophilia after diastase digestion in 5 of these 11 tumors, and also partly to mucinous substances in the remaining 6 tumors. In conclusion, the results obtained suggest that some of type II argyrophil cells are neuroendocrine in nature as well as type I argyrophil cells.

Carcinoma↗

PubMed1987

Relationship between the methods of treatment for prolactinomas and the puerperal lactation.

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Adult↗

PubMed1987

Effect of a soluble factor secreted from cultured human trophoblast cells on in vitro lymphocyte reactions.

The immunoregulatory role of trophoblast cells in cell-mediated immunity was investigated. Trophoblast cells were obtained from 8-10-week human placentae by treatment with collagenase followed by differential centrifugation. The cells were cultured for 48 hr, and the culture supernatant was examined for immunosuppressive activity in vitro. The supernatant when added to cultures of peripheral blood lymphocytes from healthy donors suppressed both their reactivity to different lectins (PHA and PWM) and their activity in one-way mixed lymphocyte reaction. The degree of suppression was dose-dependent. Furthermore, the supernatant was able to reduce the natural killer cell activity against K562 target cells. On the other hand, the supernatant had no inhibitory effect on the effector phase of lymphocyte-mediated cytotoxicity activity against tumor cell lines RPMI 8866 and Daudi. In all cases, the suppression observed was not due to lymphocytotoxicity or tumor cell mortality. The results indicate that trophoblast cells release a soluble suppressive factor that is a potent inhibitor of cell-mediated immunity.

Cytotoxicity, Immunologic↗

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↗