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[Observation on HPL derived from ciliated tumors].
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Endocrine assessments of fetal-placental well-being.
Continued advances in perinatology and neonatology and the introduction of biochemical and biophysical methods for evaluating pregnancy have substantially improved the perinatal outcome. Biochemical evaluation of placental function appears to play an important role in the management of complications of early and late pregnancy. Improvements in methodology and increased experience in the application of the various techniques have enhanced our ability to diagnose normal and abnormal pregnancy. The various new placental proteins recently described have not yet found their place in modern obstetrics and thus far they do not seem to offer distinct advantage over more established methods for assessing fetoplacental function.
Microvascular architecture of the pregnant rabbit oviduct.
Methyl-methacrylate vascular corrosion casts of the oviducts were prepared in 7 rabbits which were 2-3 weeks pregnant. Scanning electron microscopy of the acrylic casts revealed little change in tubal microvascular connections when compared with control oviducts. Venous distension in the isthmic subserosal venous plexus, ampullary subserosal vasculature and in the fimbrial core was substantially greater than that observed in controls. These changes are interpreted as indicating a sensitivity of tubal microvasculature to the increased levels of circulating placental hormones in pregnancy. The implications of this interpretation in the role of tubal microvasculature at the time of ovulation are discussed.
[Effect of abdominal decompression on placental function].
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Clinical correlations of morphologic trophoblast findings: a contribution to the pathologic anatomy of placental insufficiency.
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[Hormone content of fetoplacental origin in the blood of newborn infants].
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[Placental histo-hormonology].
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[Advances in effect of epidermal growth factor on reproductive endocrinologic system].
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c-Jun represses transcription of the human chorionic gonadotropin alpha and beta genes through distinct types of CREs.
Chorionic gonadotropin (CG) is a heterodimeric placental hormone encoded by separate alpha and beta subunit genes that is essential for the maintenance of pregnancy. The production of CG is stimulated by DNA synthesis inhibitors and by cAMP. The present study demonstrates that the proto-oncogene c-jun represses transcription of the human CG alpha and CG beta promoters. c-Jun repressed the CG alpha promoter through a canonical cAMP response element (CRE) that is known to bind c-Jun and other members of the B-Zip transcription factor family. In the CG beta promoter, two adjacent sites, CRE1 (-299 to -289) and CRE2 (-240 to -219), conveyed cAMP responsiveness via sequences that are distinct from the canonical element, TGACGTCA. Mutations within CG beta CRE1 or CRE2 reduced or abolished, respectively, c-Jun-mediated repression. Although the CG beta CREs do not contain consensus sequences previously described to bind c-Jun, CRE2 bound c-Jun and c-Fos in electrophoretic mobility shift assays. Supershift assays, using anti-JUN antibody, demonstrated that Jun formed part of the native complex that binds the CRE2 in JEG-3 cells. A series of c-Jun mutants were used to analyze the transcription factor domains required for repression of the CG subunit promoters. The DNA binding and leucine zipper domains of c-Jun as well as the amino terminus, were required for repression of both subunit promoters. Thus, both the CG alpha and CG beta genes are repressed by c-Jun through promoter regions that convey cAMP-induced transcription, although these DNA sequences are unrelated.
Toward a physiological approach to breast cancer prevention.
Breast cancer is one of the most frequent malignancies in women, and its incidence is increasing. No reduction in the mortality rate has resulted from advances in early diagnosis and new therapeutic modalities; therefore, new approaches to the understanding of this disease are required. The observation that, in an experimental animal model, full-term pregnancy prior to exposure to a carcinogenic agent protects the mammary gland from malignant transformation led us to study the mechanisms underlying this phenomenon. The protective effect observed after pregnancy did not depend upon gestational or lactational hyperplasia of the mammary gland, but upon structural changes induced in the mammary parenchyma by those processes. Those changes are permanent, since the protective effect is maintained after pregnancy and consists in the complete differentiation of terminal end buds to lobules. The protective effect exerted by pregnancy can be mimicked by treating young virgin rats with a single placental hormone, chorionic gonadotropin. Since the possibility of preventing breast cancer by treating young nulliparous females with hormones that mimic a fullterm pregnancy that results in complete differentiation of the gland is of practical interest to the human female population, we undertook the study of the human breast. The breast of postpubertal nulliparous women is composed of lobular structures reflecting different stages of development. Lobules type 1 (lob 1) are the most undifferentiated ones. Lobules type 2 evolve from the previous ones and have a more complex morphology, being composed of a higher number of ductular structures per lobule. They progress to lobules type 3 and 4, which are present in the pregnant and lactational periods of the mammary gland. In nulliparous women the structure most frequently found at all ages is the lob 1, whereas in parous women, lob 3 is the most frequent one. Lob 1 are considered to be the site of origin of ductal carcinoma in situ, which progresses to invasive carcinoma. Lob 2 originate lobular carcinoma and lob 3 originate adenomas, fibroadenomas, sclerosing adenosis, and apocrine cysts. These observations led us to test if the degree of lobular development influences the transformation of human breast epithelial cells exposed in vitro to chemical carcinogens. We found that primary cultures derived from breast tissues composed of lobules type 1 and 2 express phenotypes of cell transformation which were not observed in cells derived from lobules type 3.(ABSTRACT TRUNCATED AT 400 WORDS)
[Pregnancy induced DNA synthesis in parenchymatous organs of the rat. Autoradiographic investigations following permanent infusion of 3H-thymidine (author's transl)].
Autoradiographic investigations, after permanent infusion of 3H-thymidine during the whole course of pregnancy in 3 to 5 months old white Spraque-Dawley rats of 220-305 g body weight demonstrate an enhanced DNA synthesis in all cell systems tested. 1. In the liver the mean value of the proliferation index in the hepatocytes increases from a control value of 0.7% to 10.4%, in the epithelia of the portal ducts from 6.7% to 42.4% and in the sinus cells from 3.7% to 23.9% at the end of pregnancy. The corresponding values in the pancreas run up to 6.3% (3.4%) in the acinus parenchyma and 19.6% (8.8%) in the islet cells of Langerhans. In the duct epithelia no significant increase of labelled cells can be found. In the kidney, the number of DNA synthesizing tubular cells depends on their localization within the nephron: in the epithelia of the proximal tubulus the proliferation index amounts to 2.7% (0.6%), in that of the distal tubulus to 4.5% (1.4%). The highest percentual increase in comparison with the control animals results in the proximal tubular epithelia of pregnant rats. The cells of the glomerula are practically uninvolved. 2. The enhanced proliferation may rest on the influence of hypophysial or placental hormones--especially of somatotropins--as well as on an intensified function of the organs during pregnancy. Both hormonal and functional stimuli are closely mixed up in their significance for the pregnancy-induced DNA syntheses, accordingly their effect cannot be separated exactly. The hormones seemingly represent the inducing factor for the increased DNA syntheses during pregnancy which is realized in a variable amount within the organs depending on their different functional enhancement. 3. The increase of the proliferation indices ranges considerably from individual to individual, but within one single animal all cellular systems are afflicted in the same way. The individual ranges of the proliferation rates within the organs are directly proportional to the weight of the offsprings and indirectly proportional to the weight of the mother. The only exception of this is in the proximal tubular epithelium of the kidney. The important influence of adaptation drocesses to the enhanced function of an organ during pregnancy is emphasized by this fact.
Quantitation of human choriocarcinoma spheroid attachment to uterine epithelial cell monolayers.
Adhesive interactions of trophoblast cells with endometrium are essential for embryo implantation in the uterus. Choriocarcinoma cells, the malignant counterpart of trophoblast, show pronounced invasiveness and are of interest for model studies. We describe here an in vitro model system for the study of adhesion of human JAR choriocarcinoma multicellular spheroids to different human endometrial epithelial cell lines (RL95-2, HEC-1A, KLE, AN3-CA) grown as monolayers. Cell characterization showed JAR spheroids to s++ecrete the placental hormones human chorionic gonadotropin and progesterone into the culture medium; distinct patterns of keratin, vimentin, and uvomorulin expression were seen in the endometrial cell lines. Spheroid attachment to endometrial monolayers was quantified using a centrifugal force-based adhesion assay, and morphology was examined by light and electron microscopy. Results showed the JAR spheroids to attach to three of the endometrial monolayers (RL95-2, HEC-1A, KLE) progressively over a 24-h period (by which time > or = 80% of the spheroids attached). Significant differences in spheroid attachment were most pronounced at 5 h (RL95-2 > HEC-1A > KLE and poly-D-lysine control, i.e. 90:45:17:17% attached). JAR spheroids did not attach to the endometrial cell line AN3-CA. Morphology revealed choriocarcinoma cells to begin to intrude between the uterine RL95-2 epithelial cells at 5 h. At 24 h, this intrusive type of penetration continued to be seen only with the RL95-2 monolayer. The assay system thus identifies differences in attachment properties between choriocarcinoma cells and various endometrial cell lines and forms the basis for further studies on the molecular interactions involved.
[Diagnosis of the placental function with special reference to the pregnancy-specific protein SP-1].
Following a description of the three different functions of the placenta (respiratory, nutritive, endocrine) and their failures the most common function tests are presented. Special emphasis is put on the evaluation of a recently described pregnancy-specific protein (SP1) in the maternal serum. The amount of the substance produced by the placenta correlates well with the fetal weight and well-being in cases of EPH-gestosis and idiopathic placental insufficiency; correlation was not as well in mild EPH-gestosis, diabetes and RH-incompatibility. The validity of measuring SP1-production seems to be similar to that of HPL. The method of quantitative determination is simple and possible even in a smaller hospital.
[Endocrine and nephro-urologic changes in hypertensive and toxemic pregnancy].
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[Status and developmental trends of immunologic contraceptive technics].
The development of contraceptive vaccines is matter of international research. Among antigens possible unique to the reproductive process, sperm antigens, antigens of seminal plasma and of the ovum, antigens of placental hormones and of placenta specific proteins appear suitable targets of the production of fertility regulating vaccines. High specifity of these vaccines can prevent cross reaction with other body cells.
[The early placental trophoblast. I. Normal development and endometrial and non-tumor-induced disorders].
The development of the hemochorial placenta requires, that the trophoblast invades the endometrium, penetrating into its deep layers and blood vessels. Placental tissue includes components from two haplodifferent organisms, the mother and the fetus. Early steps in trophoblastic development are the adhesion and apposition. Invasion is an active process and correlations are observed between cellular invasivness and proteinase production, like uPA, tPA and its inhibitors, for example PAI-1. The process of trophoblast invasion is based on a complex interaction between the trophoblastic cells, various types of matrices and decidual as well as endometrial cells. Immunologic processes, like the production of blocking factors, paraimmune mechanisms and other HLA-dependent processes play an important role. During implantation a differentiation of trophoblastic cells takes place. The syncytiotrophoblast is the active cell of the invasive previllous trophoblast. The intermediate trophoblast plays this role concerning the villous trophoblast. The different trophoblastic cells are characterised by distinct morphologic and immunohistochemical features.