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At least 649 records · Page 36Linked to original sources

PubMed1996

Apoptosis: programmed cell death in fetal development.

Controlled death of cells is as much a part of embryonal development as is cell proliferation and differentiation. This cell suicide is controlled by cell genes involved in induction or prevention of programmed cell death (PCD). During embryogenesis PCD implicates cell elimination, necessary in fashioning of the body, moulding of tissues. PCD is often used synonymous with the designation apoptosis, which indicates an endogenous cell suicide program by which useless or crippled cells are eliminated. Apoptosis occurs in normal tissue turnover, in organ involution after withdrawal of trophic hormones, in distinct cells after deprivation of growth factors or specific stimuli and in cells which have undergone sublethal damage. During PCD the nucleus breaks up into DNA fragments of 180-200 kD and the endoplasmic reticulum transforms into vesicles, which are released as apoptotic bodies into the extracellular space. The apoptotic bodies, containing cell organelles and nuclear fragments, are phagocytosed by neighboring cells. Electron micrographs of embryos have revealed the presence of numerous cells with the characteristic features of apoptosis. Experiments, in which small tissue fragments were explanted to other regions, have proven that focal apoptosis is under control of genetic, hormonal and local tissue factors. Morphological analysis has shown that most of the ovarian follicles undergo during development apoptosis, resulting in follicle atresia. Only a small proportion escapes PCD. Growth factors and estrogens have been identified as follicle survival factors, androgens and gonadotropin releasing hormones are potentiating apoptosis of the follicle. An exaggerated PCD or a defective apoptosis during embryogenesis may cause developmental abnormalities. Certain viruses can inhibit apoptosis, while metabolic stress or damage of cell structures can induce apoptosis. Therefore not only viral infections, also drugs and chemical or physical injuries during embryogenesis may interfere with the balanced PCD and thus induce malformations. Drugs and therapy designs directed to modulate the apoptotic process will offer new approaches to the prevention of congenital malformations.

Animals↗

PubMed1995

Altered specificity of IGF2 promoter imprinting during fetal development and onset of Wilms tumour.

The specificity of IGF2 promoter imprinting was examined in embryonal tissues and Wilms tumour. In several fetal tissues of approximately 12 weeks gestation, IGF2 was found to be monoallelically expressed from all IGF2 promoters i.e. P1, P2, P3 and P4. However, in tissues of slightly older gestation age (15-17 weeks) relaxation of imprinting at the P1 promoter was evident, although the P2-P4 promoters remained imprinted. These data indicate that early in embryogenesis a population of cells exists in which all IGF2 promoters are imprinted, but that as development proceeds the imprinting of the P1 promoter is relaxed. The pattern of IGF2 promoter imprinting was also analysed in Wilms tumour. In some tumours, the pattern of promoter imprinting was identical to that found in early fetal kidney, indicating that this tumour originates within early embryonic kidney tissue. In contrast, in tumours in which relaxation of imprinting had occurred, imprinting relaxation affected all IGF2 promoters. This aberrant pattern of promoter imprinting, which was not detected in fetal kidney, provides further evidence that pathological relaxation of IGF2 imprinting is involved in the genesis of Wilms tumour.

Adult↗

PubMed1997

Somatic instability of the myotonic dystrophy (CTG)n repeat during human fetal development.

Myotonic dystrophy is characterised by the striking level of somatic heterogeneity seen between and within tissues of the same patient, which probably accounts for a significant proportion of the pleiotropy associated with this disorder. The congenital form of the disease is associated with the largest (CTG)n repeat expansions. We have investigated the timing of instability of myotonic dystrophy (CTG)n repeats in a series of congenitally affected fetuses and neonates. We find that during the first trimester the repeat is apparently stable and that instability only becomes detectable during the second and third trimesters. In our series repeat instability is apparent only after 13 weeks gestational age and before 16 weeks. The appearance of heterogeneity shows some tissue specificity, with heart most commonly having the largest expansion. The degree of heterogeneity is not correlated with initial expansion size as gauged by chorionic villus and blood (CTG)n repeat sizes.

Embryonic and Fetal Development↗

PubMed1998

C-pathway polysialogangliosides are transiently expressed in the human cerebrum during fetal development.

Gangliosides are assumed to play a crucial role in processes of cellular recognition and interaction important for neural development. They are designated as cytochemical markers of neuronal maturation, as striking changes in the ganglioside pattern parallel the nervous system development. Of particular interest to us are numerous studies that reported during migration of postmitotic neurons and axon formation in developing avian and mammalian brains a transient accumulation of highly sialylated c-pathway gangliosides. However, it has thus far been thought that c-pathway gangliosides do not appear in the human cerebrum; their absence could be somehow interpreted in the light of an evolutionary trend in the pattern of brain gangliosides: by increasing the phylogenetic scale this pattern changes by an accretion of less sialylated gangliosides and switches from c- via b- to a-series, respectively. The present study presents both biochemical and immunocytochemical evidence for the existence of c-pathway gangliosides in the human cerebrum during prenatal life, and their localization in discrete neuronal populations and growing axonal pathways.

Aging↗

PubMed1992

Toxicology of maternally ingested trichloroethylene (TCE) on embryonal and fetal development in mice and of TCE metabolites on in vitro fertilization.

Trichloroethylene (TCE), an industrial solvent, is a soil and ground water contaminant found across the United States. The metabolism and carcinogenic potential of TCE have been studied extensively in the past 15 years yet there is little information on the chemical's possible effects on reproduction. No reference to the reproductive effects in mice of TCE by oral administration exists in the literature. In this study, female B6D2F1 mice were gavaged from Days 1 to 5, 6 to 10, or 11 to 15 (Day 1 = vaginal plug) with TCE in corn oil at 0, 1/10, and 1/100 of the oral LD50. Weights of mice were recorded and the livers and kidneys were weighed and preserved in 10% buffered formalin. Litters were counted, sexed, weighed, and measured for crown-rump length until weaning on Day 21 and some animals were allowed to develop to 6 weeks of age. At this time, a minimum of two litters from each dose were killed and gonads removed, weighed, and preserved in Bouin's fixative. Litters were also assessed for developmental abnormalities. No maternal or reproductive effect of TCE was seen at either dose level. TCE, administered consecutively on Days 1 to 5, 6 to 10, and 11 to 15 of pregnancy, does not appear to be a potential reproductive toxicant up to 1/10 the oral LD50. In a second series of studies, TCE and its metabolites dichloroacetic acid (DCA), trichloroacetic acid (TCAA), and trichloroethanol (TCOH) were added to culture media to assess the toxic effects on in vitro fertilization (IVF) in mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

[Pregnancy and fetal development in smoking and nonsmoking women].

In the second stage of the European longitudinal study of pregnancy and childhood (ELSPAC) detailed anamnestic data on the mother were assessed, and objective data on the health status during pregnancy, delivery and on the neonate were assembled. Numerous partial results of the ELSPAC study confirmed that smoking during pregnancy has an adverse effect on the course of pregnancy and foetal development. During pregnancy in smokers proteinuria as well as the diagnosis of suspect foetal retardation were significantly more frequent. During delivery placenta previa and placental abnormalities were recorded more often. The mean duration of gestational age was similar in smokers and non-smokers. The mean birth weight of newborns of women who smoked during pregnancy was on average by 107 g lower as compared with non-smokers. Significant differences were also found in the mean length and head circumference, always to the disadvantage of smokers. Smokers reported significantly more frequently greater fear and restlessness at the onset of labour pains and after return from the maternity home. They get frequently more excited without any reason and are more tense.

Birth Weight↗

PubMed1989

Physical work load, fetal development and course of pregnancy.

The effects of physical work load during pregnancy were analyzed in connection with a nationwide case-referent study that screened for associations between selected structural malformations and occupational exposures. The strain of the occupational activities of 1475 mothers of malformed infants and an equal number of mothers of noncase babies was assessed from a description of the work tasks by an expert using a standardized method reflecting energy expenditure. The noncase mothers' experience revealed a relation between physical load and growth retardation that has also been suggested by other epidemiologic studies. No relation was found between an increase in mean physical load and the occurrence of threatened abortion; yet work involving much standing had an increased risk. Mothers whose work included occasional high physical loads had more pregnancy-induced hypertension. The data showed unexpected associations between physical load and structural malformations.

Abortion, Threatened↗

PubMed1987

[Effect of a static magnetic field (3.5 T) on the reproductive behavior of mice, on the embryo and fetal development and on selected hematologic parameters].

To investigate possibilities of magnetic resonance imaging at high magnetic fields in humans, a whole-body magnet with a magnetic field density of 4 T was developed. Due to the few data that are available at present on biological effects and side effects of such high fields, a reproduction experiment with NMRI mice was performed using a crossover design. The mice were allowed to mate during a 7-day period within the field or after their stay in the field. The number of pregnant mice and foetuses were recorded and compared to the controls. Another group was held within the magnetic field during the whole period of pregnancy until day 18, one day before delivery. In all groups, development of the foetuses was studied. Additionally, haematological parameters of the males and females were estimated and necroscopy was performed. Brains, lungs and optical nerves were investigated using pathohistological techniques. It could be shown that in case of mating within the magnetic field, the number of pregnant mice was considerably reduced. This effect was, however, completely reversible if mating occurred after the stay in the field. Malformations, retardations or an increased number of resorptions were never found. The haematological parameters were, in general, not changed. Necroscopy as well as pathohistological investigations showed no pathological alterations. Therefore, it appears that whereas high magnetic fields reduce the activity of mating behaviour, they do not exert any influence on physiological parameters.

Animals↗

PubMed1989

Shift work, fetal development and course of pregnancy.

Information on 1475 mothers of infants with selected structural malformations and an equal number of mothers of "normal" babies was analyzed for a possible relationship between shift work and adverse pregnancy outcome or a complicated course of pregnancy. The primary data were obtained from the Finnish Register of Congenital Malformations supplemented by special interviews on the mothers' work conditions. No signs of a teratogenic risk were observed. The relationship between course of pregnancy and outcomes other than malformations was determined from the noncase mothers' experience. Threatened abortion and pregnancy-induced hypertension were not associated with rotating shift work alone, but in a noisy work environment moderate risks could not be ruled out. Rotating shift work was associated with a slight excess of babies small for their gestational age independently of noise exposure. The results suggest that further studies on the effects of different work schedules on pregnancy are worth consideration.

Adult↗

PubMed1983

Fetal development of primate chemosensory corpuscles. I. Synaptic relationships in late gestation.

Fetal macaque chemosensory corpuscles during the last part of gestation contained chemosensory, sustentacular, and undifferentiated basal cells. Sustentacular cells had apical secretory granules and no specialized contacts with axons. Chemosensory cells contained basal collections of 80-100 nm dense core granules, and specialized axonal contacts of three types--afferent synapses, efferent synapses, and subsurface cisternae. Afferent synapses were commonly present on electron opaque cells with many 80-100-nm granules, typical 40-60-nm synaptic vesicles, and a few cisternae of smooth or granular endoplasmic reticulum. Cells with subsurface cisternae and/or efferent synapses were usually electron lucent, lacked vesicles and granules, and contained numerous intracytoplasmic cisternal elements. A continuum of intermediate forms was observed. It is postulated that transition of synaptic arrays accompanies the maturation of individual chemosensory cells.

Animals↗

PubMed2005

Estrogen receptors and estrogen-metabolizing enzymes in human ovaries during fetal development.

Estrogen action plays a crucial role in many processes throughout the human life span, including development. Estrogens are pivotal in the regulation of female reproduction, but little is known about their role during ovarian development. To better understand estrogen action during ovarian development, the expression of estrogen receptors (ERs)-alpha and -beta and key enzymes regulating estradiol production, 17beta-hydroxysteroid dehydrogenases (17HSDs) types 1, 2, and 7, were analyzed in human fetal ovaries. The expression of ERs was related to the development of ovarian follicles. Before the 26th week of fetal life ERalpha was only occasionally detected, but from then onward, its expression was detected in ovarian follicles. Consistent expression of ERbeta was seen from the 20th week until term. Both ERalpha and ERbeta were localized to the granulosa cells and oocytes. Expression of 17HSD1 and 17HSD7 enzymes, catalyzing the conversion of estrone to more active estradiol, was detected as early as at the 17th week of fetal life. The expression of 17HSD1 displayed a pattern similar to that of ERs and increased toward term, whereas that of 17HSD7 decreased and was negative by the 36th week. 17HSD1 was localized to the granulosa cells, whereas 17HSD7 expression was more diffuse and was found in both granulosa and stromal cells. 17HSD2, converting estradiol to less potent estrone, was negative in all samples studied. The simultaneous appearance of estrogen-converting enzymes and ERs at the time of follicle formation indicates that the machinery for estrogen action exists in fetal ovaries and suggests a possible role for estrogens in the developing ovary.

17-Hydroxysteroid Dehydrogenases↗

PubMed1996

Congenital metatarsus adductus in early human fetal development: a histologic study.

Two feet with congenital metatarsus adductus from fetuses at early development (16 and 19 weeks of gestation) were studied by making serial histologic sections in the horizontal plane of the foot. It was observed that the shape of the medial cuneiform was altered and the first cuneometatarsal joint tilted toward the medial and dorsal directions. The first metatarsal appeared normal, whereas the other metatarsals were deformed in slight adduction at the metaphyseal level. Subluxation at the other cuneometatarsal joints and naviculocuneiform joint was not observed, and the navicular showed no signs of medial or lateral displacement in relation to the head of the talus. No histologic abnormalities of the joint capsules, ligaments, or tendons were observed. On the basis of these pathologic findings, the possibility of a developmental abnormality of the medial cuneiform as a pathogenic factor for the congenital metatarsus adductus deformity should be considered.

Embryonic and Fetal Development↗

PubMed1999

[New aspects in the evaluation of risk factors for fetal development].

Much knowledge concerning the effects of xenobiotics on prenatal development derive from experimental studies, which are generally performed on laboratory animals according to standardized protocols. Conventional in vivo studies should be integrated by other models within a scientifically-based risk assessment strategy. The paper reviews a few in vitro and/or in vivo approaches: identification of critical effects through the characterization of the pathogenesis as well as the use of dose-response relationships; alternative models to identify reproductive risks from single substances and/or mixtures present in the environment; interactions between in vitro and in vivo studies in the risk assessment of solvents: embryonic metabolism in teratogenicity; interactions between experimental and epidemiological studies to understand the pathogenesis of embryolethality; risk assessment of the effects of prenatal exposure to ionizing radiations.

Animals↗

PubMed1995

Noradrenaline is essential for mouse fetal development.

Catecholamines such as noradrenaline and adrenaline have been implicated in numerous physiological processes but, although catecholamine synthesis begins at mid-gestation, previous studies have provided little evidence for any role in early development. Furthermore, there are several case reports of humans with noradrenaline deficiency. To investigate this, we use gene targeting to produce mice lacking dopamine beta-hydroxylase and therefore unable to synthesize noradrenaline or adrenaline. We report here that in heterozygous mothers, most homozygous embryos died in utero, and only about 5% reached adulthood. Survival probably depends on catecholamine transfer across the placenta because, in homozygous mothers, all embryos die in utero. Mortality was due to lack of noradrenaline in utero because it could be prevented by treatment with dihydroxyphenylserine, a precursor that can be converted to noradrenaline in the absence of dopamine beta-hydroxylase. Mutant embryos had a histological phenotype similar to that of embryos deficient in tyrosine hydroxylase, suggesting that death might be due to cardiovascular failure.

Animals↗

PubMed2005

Failure of the emergency contraceptive levonorgestrel and the risk of adverse effects in pregnancy and on fetal development: an observational cohort study.

OBJECTIVE: To determine pregnancy and neonatal outcome after the failure of levonorgestrel as an emergency contraceptive. DESIGN: A retrospective observational cohort study. SETTING: Telephone consultations concerning reproductive risk factors conducted by Telefono Rosso-Teratology Information Service, Catholic University of Sacred Heart, Rome, Italy. PATIENT(S): Women exposed to levonorgestrel (36 cases) compared with a control group (80 cases). INTERVENTION(S): Teratological counseling. MAIN OUTCOME MEASURE(S): The rate of congenital anomalies, the prepartum or peripartum complications, and the pregnancy outcomes. RESULT(S): Twenty-five exposed newborns with length and weight identical to that of the control group were shown to be without increased risk of congenital malformation. No statistical differences were observed in terms of spontaneous or legal abortion and pregnancy and neonatal complications, and there was no ectopic pregnancy in either group. CONCLUSION(S): Although the sample size was small, in our experience, the failure of levonorgestrel as an emergency contraceptive was not associated with an increased risk of major congenital malformations, prepartum or peripartum complications, or an adverse pregnancy outcome.

Adult↗

PubMed1989

Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats.

Pregnant rats were exposed to 0, 100, 200, 400 or 800 ppm of carbon disulfide (CS2), 100 ppm of hydrogen sulfide (H2S) alone or in combination with 400 and 800 ppm CS2, 6 h/d during days 6-20 of gestation. Maternal reproduction and fetal parameters were evaluated on gestational day 21. Treatment with 100 or 200 ppm CS2 or with 100 ppm H2S caused no maternal toxicity or adverse effects on the developing embryo or fetus. Exposure to 400 or 800 ppm CS2 resulted in a low incidence of club foot and in a significant reduction of maternal weight gain. Significant increases in unossified sternebrae occurred at 800 ppm CS2 and reduction of fetal body weight at 400 and 800 ppm CS2. The latter effect was enhanced by combination with 100 ppm H2S. These results support the conclusion that, at levels of exposure associated with maternal toxicity, CS2 leads to an increase in incidence of club foot and to fetal toxicity which is enhanced by simultaneous exposure to H2S.

Administration, Inhalation↗

PubMed1985

[Pregnancy and fetal development after therapy of Hodgkin's disease].

The post-therapeutic pregnancy data of 122/244 women aged until 40 years who had been treated primarily in Freiburg i. Br. for Hodgkin's disease between 1949 and 1981 were obtained by an inquiry based on questionnaires. All of the 122 patients of the questionnaire group were in remission. 39 out of them (32%) became pregnant one or more times; 38/94 (40%) of these had been irradiated down to the promontory and 1/17 (6%) had been submitted to an irradiation including the pelvis with ovariopexy. The resulting 63 post-therapeutic pregnancies leaded to 41 normal births (65%), three premature infants (5%), two viable children suffering from malformations (3%) and five spontaneous abortions (8%). An interruption was performed in twelve cases (19%). There were no significant divergences from distributions of normal populations with regard to the percentages of normal births and negative variants, even under consideration of comparable literature reports. Neither in the questionnaire group nor in the group of 122 patients whose gynecologic data could only be evaluated by means of the medical records available, there was any indication suggesting an increased risk of morbidity or mortality.

Adult↗

PubMed1995

Expression of the heparin-binding cytokines, midkine (MK) and HB-GAM (pleiotrophin) is associated with epithelial-mesenchymal interactions during fetal development and organogenesis.

Midkine (MK) and heparin binding-growth associated molecule (HB-GAM or pleiotrophin), constitute a new family of heparin-binding proteins implicated in the regulation of growth and differentiation (T. Muramatsu (1993) Int. J. Dev. Biol. 37, 183-188). We used affinity-purified antibodies against MK and HB-GAM to analyze their distribution during mouse embryonic development. From 9 to 14.5 day post-coitum (dpc), both proteins were detected in central and peripheral nervous systems, facial processes, limb buds, sense organs, respiratory, digestive, urogenital, and skeletal systems. MK and HB-GAM were often localized on the surface of differentiating cells and in basement membranes of organs undergoing epithelial-mesenchymal interactions. The level of MK protein decreased considerably in the 16.5 dpc embryo, whereas HB-GAM staining persisted in many tissues. Our in situ hybridization results revealed a widespread expression of MK transcripts that was not always consistent with the distribution of MK protein in developing tissues. In many epithelio-mesenchymal organs MK and HB-GAM were codistributed with syndecan-1, a cell surface proteoglycan. In limb buds and facial processes, MK, HB-GAM, and syndecan-1 were localized to the apical epithelium and the adjacent proliferating mesenchyme. Both MK and HB-GAM bound syndecan-1 in solid-phase assays in a heparan sulfate-dependent manner. The biological effects of MK and HB-GAM on limb and facial mesenchyme were studied in vitro by application of beads preloaded with the proteins. Neither MK nor HB-GAM stimulated mesenchymal cell proliferation or induced syndecan-1 expression. Taken together these results indicate that MK and HB-GAM may play regulatory roles in differentiation and morphogenesis of the vertebrate embryo, particularly in epithelio-mesenchymal organs, and suggest molecular interactions with syndecan-1.

Animals↗