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Results for “PLACENTAL HORMONES”

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At least 991 records · Page 55Linked to original sources
PubMed1977

[Attempts at biotechnical induction of puberty in female young pigs. 1. Estrus and ovulation induction with Suigonan (Vemie) or FSH plus HCG mixtures in animals at the age of approximately 200 days].

64 prepuberal gilts in 4 groups were treated with 400 PMS + 200 HCG (Suigonan - Vemie) (I), 100 FSH + 100 HCG) (II), 200 FSH + 200 HCG (III) ("international units") or served as untreated controls (IV). One halve of the groups laparotomized at the 12th day p.i. had ovulated 100, 25, 75 and 12,5% resp., the other halve slaughtered at the 36th day p.i. had ovulated to 83, 43, 88 and 50% resp. Sexual cycle was registered in 50, 29, 43 and 12.5% of the animals. Zystic ovaries (greater than or equal to 11 mm) developed only in a few cases in I and III.

Animals↗
PubMed1973

Radioreceptor assay for prolactin and other lactogenic hormones.

A radioreceptor assay with a sensitivity of 5 nanograms per milliliter has been developed for mammalian and avian pituitary prolactin, placental lactogenic hormones, and humnan growth hormone, using a membrane receptor preparation isolated from rabbit mammary glands. Prolactin preparations inhibited the binding of [(125)I]prolactin to receptors in direct proportion to the biological potency of these preparations. Thus, the radioreceptor assay provides a convenient and simnple assay for hormones which have lactogenic activity.

Adrenocorticotropic Hormone↗
PubMed1987

[A study on the role of DNA methylation within hCG and hPL genes in trophoblastic disease].

It has been shown that the extent of methylation of cytocine in DNA is inversely correlated with gene expression in many cases. The DNAs extracted from placental tissue, hydatidiform mole and choriocarcinoma tissue were examined to see whether the extent of cytocine methylation is correlated to the gene expression of placental peptide hormones and the transformation of trophoblast. First of all we measured the amount of methylated cytocine per total DNA with HPLC. We then examined cytocine methylation in hCG alpha,beta and hPL genes using methylation sensitive (Hha I, Hpa II) and non sensitive (Msp I) restriction enzymes and molecular hybridization. During pregnancy the total amount of methylated cytocine measured with HPLC increases gradually from 0.72 mol.% at first trimester to 0.92 mol.% at term. The DNA of WBC showed a higher level of methylated cytocine than placental DNA. The extent of DNA methylation in the peptide hormone genes increases during placental development. Hypomethylation in the hCG alpha gene was also seen in molar tissue which expresses a high amount of hCG. Therefore it is inversely correlated that gene expression of hCG alpha,beta and the extent of DNA cytocine methylation. Furthermore some restriction polymorphisms were observed with Msp I in hCG alpha and hPL genes which might be related to malignant transformation of the trophoblast.

5-Methylcytosine↗
PubMed2000

[Pathology of gestational trophoblastic tumors].

Gestational trophoblastic tumours result from an abnormal proliferation of different types of trophoblasts. The morphological pattern, together with the immunohistochemical aspect, the cytogenetic data and the clinical profile, helps identify each pathological entity. Hydatiform moles represent malformed placentas caused by genetic aberrations of the villous trophoblast. A complete hydatiform mole displays an hydropic degeneration of all the chorionic villi with a more or less marked proliferation of trophoblasts. A partial hydatiform mole is made up of molar vesicles interspersed with normal chorionic villi. In an invasive hydatiform mole or chorioma destruens, molar vesicles penetrate the myometrium giving rise to a mass distorting the uterine wall. A choriocarcinoma is a malignant proliferation of atypical villous trophoblasts without villi formation. Necrosis, haemorrhage, vascular invasion and distant metastases strongly compromise its outcome. A trophoblastic implantation site tumor, clearly less frequent, results from a proliferation of extravillous trophoblasts, particular for their secretion of human placental lactogen hormone (hPL). This tumour, exceptionally malignant, should be differentiated from the exaggerated placental site and its variants. Except for the placental site trophoblastic tumour, and whatever the outcome (benign or malignant), all gestational trophoblastic tumours secrete the beta-subunit of the chorionic gonadotropic hormone (beta-hCG) more or less abundantly. The serum or urinary level of this unit is proportional to the tumour volume and represents a fundamental basis for the follow-up of these tumours. Multidisciplinary care of high-risk cases allows us to cure the disease, and helps the patient recover her reproductive uterine function.

Chorionic Gonadotropin, beta Subunit, Human↗
PubMedDate not supplied

Low serum estradiol and high serum progesterone concentrations characterize hypertensive pregnancies at high altitude.

OBJECTIVE: Intrauterine growth retardation and preeclampsia are more common at high than at low altitude. Because altered hormonal profiles have been linked with these disorders, we asked whether placental steroid hormone concentrations were altered during pregnancy at high altitude. METHODS: We measured progesterone, unconjugated estradiol, and estriol (by radioimmunoassay) at weeks 20, 30, and 36 of pregnancy in 18 women at low altitude (1600 m) and 40 women at high altitude (3100 m). RESULTS: Women at 3100 m compared with 1600 m had lower serum estradiol concentrations at week 36 of pregnancy, and lower estriol and higher progesterone concentrations throughout pregnancy. As a result, the progesterone/estradiol ratio was greater in the high- versus the low-altitude women. Estradiol fell between weeks 30 and 36 in women who developed transient hypertension or preeclampsia. The fall in estradiol was accompanied by a marked increase in progesterone concentrations among the preeclamptic women. At 3100 m, estradiol correlated negatively (r = -0.37, P < .05) and progesterone positively (r = 0.46, P < .05) with mean arterial pressure at week 36 of pregnancy. CONCLUSIONS: We speculate that reduced placental oxygen pressure (PO2) at high altitude may decrease placental aromatase activity and thereby lower estradiol and estriol concentrations. The factor(s) responsible for the rise in progesterone is unknown. Possibly, high progesterone relative to estradiol concentrations contributes to the development of preeclampsia at high altitude.

Adult↗
PubMed1999

Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta.

The influence of maternal hypothyroxinemia on the expression of the glucose transporters, GLUT1 and GLUT3, in rat fetal brain and placenta was investigated. Fetal growth was retarded in hypothyroxinemic pregnancies, but only before the onset of fetal thyroid hormone synthesis. Placental weights were normal, but placental total protein concentration was reduced at 19 days gestation (dg). Immunoblotting revealed a decreased abundance of GLUT1 in placental microsomes at 16 dg, whereas GLUT3 was increased. Fetal serum glucose levels were reduced at 16 dg. In fetal brain, the concentration of microsomal protein was deficient at 16 dg and the abundance of parenchymal forms of GLUT1 was further depressed, whereas GLUT3 was unaffected. Northern hybridization analysis demonstrated normal GLUT1 mRNA levels in placenta and fetal brain. In conclusion, maternal hypothyroxinemia results in fetal growth retardation and impaired brain development before the onset of fetal thyroid function. Glucose uptake in fetal brain parenchyma may be compromised directly, due to deficient GLUT1 expression in this tissue, and indirectly, as a result of reduced placental GLUT1 expression. Though corrected by the onset of fetal thyroid hormone synthesis, these deficits are present during the critical period of neuroblast proliferation and may contribute to long term changes in brain development and function seen in this model and in the progeny of hypothyroxinemic women.

Animals↗
PubMed2000

[Failure of differentiation of the trophoblast in trisomy 21].

The syncytiotrophoblast is the major component of the human placenta as it is involved in the feto-maternal exchanges and the secretion of pregnancy-specific hormones. In normal placenta, the multinucleated syncytiotrophoblast is formed by fusion of mononuclear cytotrophoblast cells. In trisomy 21-affected placenta, we show that it exists a defect (or a delay) in the syncytiotrophoblast formation and a decrease of the production of pregnancy-specific hormones. We show that it is related to the over expression of the SOD-1 located on chromosome 21. These results will be of help for the understanding of maternal hormonal markers of fetal trisomy 21 and the consequences of the placental defects on the fetal development.

Biomarkers↗
PubMed2000

Tissue- and site-specific gene expression of type 2 17beta-hydroxysteroid dehydrogenase: in situ hybridization and specificenzymatic activity studies in human placental endothelial cells of the arterial system.

Progesterone and estradiol are the most potent human sex steroid hormones of placental origin and are essential to the maintenance of pregnancy, the timing of parturition, the maturation of many fetal organs, and the preparation of the maternal reproductive system. Naturally, regulatory mechanisms must be in place to coordinate the synthesis and inactivation of these two hormones. We have previously shown that the highest levels of type 1 and type 2 17beta-hydroxysteroid dehydrogenase (17betaHSD) messenger ribonucleic acids (mRNAs) occur in the placenta, particularly in the villi. However, in contrast to type 1 17betaHSD mRNA, type 2 17betaHSD mRNA was not detectable in cell cultures of human cytotrophoblasts or syncytiotrophoblasts. Using in situ hybridization, we unequivocally identified endothelial cells as the only cell type expressing the type 2 17betaHSD gene in fetal villi. Moreover, type 2 17betaHSD mRNA was specifically detected in the endothelial cells of the arterial system, and at higher levels in the villi compared with endothelial cells of the cord arteries when the two tissue sections were cohybridized. In fact, both mRNA levels and enzymatic activity are at their highest levels in arterial endothelial cells. In conclusion, the endothelial cells of the villous arterioles are the primary site of type 2 17betaHSD gene expression. This suggests a regulatory role for these cells in the control of progestin, androgen, and estrogen levels during pregnancy, thus opening a whole new way of viewing regionalization and localization of steroidogenesis in the human villi.

17-Hydroxysteroid Dehydrogenases↗
PubMed1987

Effects of betamethasone on maternal plasma corticotropin releasing factor, ACTH and cortisol during pregnancy.

Corticotropin releasing factor immunoactivity (CRFi) has been identified in the plasma of women in the second half of gestation. There are several lines of evidence supporting a placental source for this hormone. Regulation of placental CRFi is poorly understood. In this study, the effect of a long-acting glucorticoid on the release of placental CRFi was investigated. Eleven women in the third trimester of pregnancy had plasma samples measured for CRFi, ACTH and cortisol before and after receiving 12 mg betamethasone. There was a significant decrease in ACTH (p less than 0.05) and cortisol levels (p less than 0.01) but no change in CRFi. It is concluded that the secretion of CRFi by the placenta is not inhibited by the administration of betamethasone while maternal levels of cortisol and ACTH are lowered. These results suggest that the acute regulation of placental CRFi is distinct from the regulation of hypothalamic CRF.

Adrenocorticotropic Hormone↗