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PubMedDate not supplied

[Combined test in the first trimester of pregnancy in 3,316 unselected pregnant patients for diagnosing Down syndrome].

UNLABELLED: The high detection rate (DR) for Down syndrome pregnancies which can be achieved by measuring fetal nuchal translucency (NT) early in pregnancy can be improved by combining it with placental hormones (PAPP-A, f beta hCG) and maternal age ("combined test"). In this study we wanted to assess the DR using the "combined test" in an unselected population of self-referred pregnant women at a false positive rate (FPR) of about 5%. MATERIALS AND METHODS: NT, PAPP-A, f beta hCG and maternal age were measured in all women with singleton pregnancies who booked for delivery in our hospital from 1.12.97 to 31.12.99 and who were between 10 and 13 completed weeks of gestation (crown-rump-length 35-70 mm). Calculation of the specific Down risk was done with the computer program Alpha, Version 5aa (Logical medical systems, London). RESULTS: A total of 3316 women were tested. Out of 10 Down pregnancies, which occurred in this period of time 9 could be detected with the test. 137 women had a positive test result but a non-Down pregnancy (FPR 4.1%). CONCLUSIONS: The combined test is an excellent test for the detection of Down syndrome pregnancies in a low-risk population. DISCUSSION: The constant increase in maternal age at the time of delivery can also lead to an improved DR if a simple age dependant protocol for Down-detection is used, but only at the price of a much higher number of amniocenteses and subsequent abortions. The DR for Down syndrome can be increased much more markedly using the "combined test" at a much lower FPR (approximately 5%).

Abortion, Eugenic↗
PubMed2001

Reactivation of proliferin gene expression is associated with increased angiogenesis in a cell culture model of fibrosarcoma tumor progression.

Proliferin (PLF) is an angiogenic placental hormone. We now report that PLF gene expression can also occur in a progressive fibrosarcoma mouse tumor cell model. PLF mRNA and protein are detectable at very low levels in cell lines derived from the mild noninvasive stage of tumor development. Expression is greatly augmented in cell lines from the aggressively invasive stage of development, a stage at which the tumor becomes highly angiogenic, and PLF expression remains high in cell lines from the end stage of fibrosarcoma. Activator protein 1 factors present at high levels in the more invasive stages of the tumor may in part allow for increased PLF expression, as cells from the mild stage in which c-jun and junB are stably expressed secrete levels of PLF comparable to that of the advanced stages. Secreted PLF protein is functionally important in tumor cell angiogenic activity, as demonstrated by the reduction of angiogenic activity in fibrosarcoma cell culture medium by immunodepletion of PLF. These results suggest that an extraembryonic genetic program, which has evolved to support fetal growth, may be reactivated in certain tumors and contribute to tumor growth.

Cells, Cultured↗
PubMed1990

Effect of human chorionic gonadotropin on mammary gland differentiation and carcinogenesis.

The observation that mammary carcinogenesis is inhibited in rats which completed a pregnancy prior to exposure to the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA) led us to determine whether the protective effect of pregnancy could be mimicked by treatment with the placental hormone chorionic gonadotropin (hCG). We also studied the effect of this treatment on mammary gland structure and differentiation, and determined whether hCG exerts toxic or collateral effects on body weight and endocrine organs. The systemic effect of hCG on body wt and endocrine organs and mammary gland was studied in outbred virgin Sprague-Dawley rats which at the age of 50 days started receiving 100 IU hCG i.p. daily for 21 days. The animals were subdivided into nine groups of five animals each; one group was killed on the first day of and the others at 5, 10, 15 and 21 days of injection and 5, 10, 15 and 21 days post injection. The effect of the hormonal treatment on the estrous cycle was determined by studying the vaginal smears taken during and after the injection period. The following parameters were determined: body wt, weight and morphology of pituitary gland, adrenals, ovaries and uterine horns. Mammary glands were processed for histology, autoradiography for determination of DNA labeling index (DNA-LI) and whole mount preparation for morphometric studies. The effect of hCG on mammary carcinogenesis was studied in two groups of virgin rats; group I, which at the age of 50 days started receiving a daily i.p. injection of 100 IU hCG for 21 days; 21 days after the last injection they were given 8 mg DMBA/100 g body wt. Group II animals received DMBA only. hCG treated animals gained weight as a function of age at the same rate as controls. Treatment did not modify the weight of adrenal glands. The weight of ovaries, uterus and pituitary gland were transitorily increased by the 15th day of treatment, but had returned to the same values of controls by the time of DMBA administration. Treatment stimulated mammary gland differentiation, measured as a progressive reduction in number of terminal end buds and increase in the number of alveolar buds and lobules. The DNA-LI was significantly depressed in all terminal structures in the glands of treated animals. In group I animals hCG treatment decreased incidence of adenocarcinomas to 6.15 from 43.8% in group II animals.(ABSTRACT TRUNCATED AT 400 WORDS)

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Antiphospholipid antibodies in obstetrics: new complexities and sites of action.

The antiphospholipid syndrome, the cause of which remains unknown, is characterized by severe pregnancy complications. Fetal losses have been attributed to thrombosis of the uteroplacental vasculature and placental infarction. Polyclonal and monoclonal antiphospholipid antibodies seem able to recognize a 'plasma cofactor' on the endothelial and trophoblast cell surfaces and to affect cell function, inducing a procoagulant state. Although thrombosis is observed frequently in the decidua and placentas of patients with antiphospholipid antibodies, this observation was not universal, nor present in a sufficient degree to account for the pregnancy loss associated with this syndrome. Recent observations have suggested that antiphospholipid antibodies decreased placental hormone production and trophoblast intercellular fusion and invasion, suggesting that many of the obstetric complications observed in the syndrome may be due to antiphospholipid antibody-induced trophoblast dysfunction. However, the complex antigens on the trophoblast surfaces are still to be characterized and correlated with clinical manifestation. It is clear that successful pregnancies with the syndrome are more likely to occur after maternal treatment. Although prednisone may still be needed to treat manifestations associated with autoimmune disorders, the use of heparin, together with low-dose aspirin, has replaced prednisone for treatment of pregnant women. Maternal treatment and careful monitoring of fetal well-being are mandatory in the management of these high-risk pregnancies.

Abortion, Spontaneous↗
PubMedDate not supplied

The metabolic effect of antenatal corticosteroid therapy.

The use of antenatal dexamethasone to mature the fetal lung in pregnancies likely to deliver before 34 weeks is almost universal. It reduces the incidence of respiratory distress syndrome in the newborn and results in an overall improvement in neonatal morbidity and mortality. Although considered to be generally safe, there are concerns about adverse maternal and fetal effects. In a series of studies, we have found that antenatal dexamethasone administration is associated with reduced placental hormone production and maternal bone formation, impaired glucose tolerance and altered function of the hypothalamic-pituitary-adrenal axis. In this article, we have compared our data with other reports in the human and reviewed the relevant animal data. We conclude that further studies on the long-term effects of antenatal dexamethasone therapy in the human are warranted with particular emphasis on the long-term effects on the fetus.

Adrenal Glands↗
PubMed1990

Human chorionic gonadotropin and rat mammary cancer prevention.

The observation that mammary cancer induced by 7,12-dimethylbenz[a]anthracene (DMBA) in young, virgin, Sprague-Dawley rats is abolished by pregnancy led us to test the possibility of protecting the mammary gland from chemically induced carcinogenesis by using the placental hormone human chorionic gonadotropin (hCG). Fifty-day-old, outbred, virgin, Sprague-Dawley rats were utilized in two different experimental protocols. In protocol 1, four groups of virgin rats received either no hCG (group I) or a daily intraperitoneal injection of hCG at 1 IU (group II), 10 IU (group III), or 100 IU (group IV) for 21 days; group I and groups II-IV, at 21 days after the last injection, were given a single intragastric dose of 8 mg of DMBA per 100 g of body weight. In protocol 2, 50-day-old rats were treated with a single intragastric dose of 8 mg of DMBA per 100 g of body weight; 21 days later, they were separated into groups V and VI. Group V rats remained undisturbed, except for palpation twice a week for detection of tumor development. Group VI rats received a daily intraperitoneal injection of 100 IU of hCG for 60 days. Tumorigenesis was evaluated 24 and 30 weeks after carcinogen administration in animals in protocols 1 and 2, respectively. In protocol 1, in which animals (with the exception of the control group) were treated with hCG prior to carcinogen administration, the incidence of adenocarcinomas decreased in a dose-dependent manner, from 43.8% in the controls (group I) to 34.4%, 18.2%, and 6.15% in groups II-IV treated with 1, 10, or 100 IU of hCG, respectively. Among animals in protocol 2, hCG treatment significantly reduced the incidence of adenocarcinomas, from 100% in DMBA-treated rats (group V) to 45.5% in rats treated with DMBA plus hCG (group VI). These data indicate that hCG can prevent both initiation and progression of mammary carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Only three of the seven human chorionic gonadotropin beta subunit genes can be expressed in the placenta.

Human chorionic gonadotropin (hCG) is a placental hormone essential for the maintenance of pregnancy. While the alpha subunit of this hormone is encoded by a single gene, the beta subunit is encoded by a complex family of seven very similar genes or pseudogenes. Two approaches have been taken to establish which of these genes are functional. First, we have used two restriction enzyme site polymorphisms to correlate 15 independently isolated beta hCG cDNA clones with their corresponding genes. Second, we have used transient expression in COS cells to assay for correctly-initiated transcription from six of the seven beta hCG gene promoters. From these data, we conclude that, at most, only three of the seven beta hCG genes are expressed in the placenta. Comparison of the sequences of a functional and a non-functional beta hCG gene reveals no obvious differences, such as promoter changes, that could account for this differential expression.

Animals↗
PubMed2002

An activator protein-1 complex mediates epidermal growth factor regulation of equine glycoprotein alpha subunit expression in trophoblast cells.

Equids and primates are the only species known to express the placental hormone chorionic gonadotropin (CG). CG is a member of the heterodimeric glycoprotein family and is composed of an alpha subunit linked to a hormone-specific beta subunit. Previously, we have reported that epidermal growth factor (EGF) regulates the equine glycoprotein hormone alpha subunit promoter through a protein kinase C (PKC)/mitogen-activated protein kinase (MAPK) signal transduction pathway in trophoblasts. The current study investigates the regulatory element/factors involved in the induction of equine glycoprotein alpha subunit gene expression by EGF. Using 5' deletion mutagenesis, we have delineated the primary EGF/PKC responsive region of the equine alpha subunit gene to be located between -2039 to -2032 base pairs upstream of the transcriptional start site. The sequence within this region contains an activator protein 1 (AP-1)-like response element (TGAATCA) and is similar to a consensus AP-1 (TGAC/GTCA) response element. This element appeared to preferentially interact with a c-fos/JunD heterodimer. Stimulation by EGF induced the binding of c-fos and JunD to this element and subsequently elevated promoter activity. In conclusion, an EGF/PKC/MAPK signal transduction pathway regulates equine glycoprotein alpha subunit gene expression through a distinct regulatory element(s) that lies between -2039 to -2032 of the equine glycoprotein alpha subunit promoter in trophoblasts and involves an AP-1 complex.

Animals↗