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PubMed1995

Implication of inhibin and related proteins in fetal development.

Initial studies on inhibin, activin and follistatin focussed on their role as regulators of adult gonadal function via feedback regulation of anterior pituitary hormones and via intragonadal control of steroid hormones. The discovery of isoforms of follistatin which are either secreted or retained on the cell surface and which bind activin and, to a lesser extent, inhibin adds a further dimension to the regulation of these peptides. More recently, the cloning of inhibin and activin, and the observation of their close homology to the transforming growth factor-beta family of peptides, has led to an interest in their possible role as growth and differentiation factors. Activin, inhibin and follistatin are expressed in embryonic and fetal tissues, as well as in the placenta. However, although activin is a potent regulator of growth and differentiation in a number of cell types, their role in embryonic and fetal development has yet to be established. High concentrations of inhibin have been observed in the fetal gonads, particularly the testes, and in the fetal adrenals of a number of species and a sex difference in fetal plasma concentrations has also been observed. Although the stimulus for high concentrations of inhibin in the fetus is not know, they are associated with decreased testicular testosterone and a decrease in the concentration of circulating follicle-stimulating hormone (FSH); this suggests that, as in the adult, inhibin may be involved in the regulation of fetal testicular androgen and pituitary FSH secretion during late gestation. The recent reports of elevated concentrations of inhibin and, particularly, activin in amniotic fluid during late gestation and its ability to stimulate the production of prostaglandin E2 by fetal membranes provides yet another potential role for this hormone in the regulation of events leading to parturition.

Activins↗
PubMed1978

Escherichia coli infection in mice and impaired fetal development.

Investigations were undertaken, using the mouse as an animal model, to study the effect of Escherichia coli on fetal development. The i.v. injection of 7.5 X 10(6) bacteria, originally obtained from a suspected case of human pyelonephritis, caused only a mild and transient disturbance of maternal health but caused severe fetal wastage. Groups of mice were examined 4, 7 and 11 days after infection and the numbers of organisms were determined in the spleen, liver, kidneys, placentas and resorptions. From the findings obtained, it was concluded that the Esch. coli grew preferentially in the placentas. By the 7th day the placentas showed marked degenerative and necrotic changes and the bacteria could be recovered from the majority of fetuses at this time. Histologically, no significant changes were seen in the spleen, liver and kidneys. As a result of these findings in an animal model, and taking into consideration the observations of other workers, it is suggested that coliform bacteraemia in human pregnancies may also cause infections of the placenta and bring about abortion or premature delivery.

Animals↗
PubMed1992

Intrinsic factor receptor during fetal development of the human intestine.

Intrinsic factor receptor activity was observed in mucosal homogenates from whole small intestine and colon of 10-19-week fetuses, whereas it was only detected in the distal part of the small intestine of a 25-week fetus. The receptor-intrinsic factor-cobalamin complex was eluted into the void-volume position when ileum mucosal extract was assayed for receptor activity by gel filtration after incubation with either fetal gastric extract or human gastric juice. The intrinsic-factor-binding capacity of intestinal mucosal extracts ranged from 2.6 to 30.5 fmol/mg and was correlated with the gestational age of six fetuses. The dissociation constant of the receptor for the intrinsic factor-cobalamin complex was estimated at 0.24-0.36 nM at pH 7.4. In conclusion, intrinsic-factor-receptor activity was detected in the whole intestine in 10-19-week fetuses, whereas it was only present in the distal ileum at the end of fetal development.

Chromatography, Gel↗
PubMed2005

Essential fatty acid transfer and fetal development.

Docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6) are important structural components of the central nervous system. These fatty acids are transferred across the placenta, and are accumulated in the brain and other organs during fetal development. Depletion of 22:6n-3 from the retina and brain results in reduced visual function and learning deficits: these may involve critical roles of 22:6n-3 in membrane-dependent signaling pathways and neurotransmitter metabolism. Transfer of 22:6n-3 across the placenta involves specific binding and transfer proteins that facilitate higher concentrations of 22:6n-3 and 20:4n-6, but lower linoleic acid (18:2n-6) in fetal compared with maternal plasma, or in the breast-fed or formula-fed infant. However, human and animal studies both demonstrate that maternal diet impacts fetal 22:6n-3 and 20:4n-6 accretion. After birth, parenteral lipid, human milk and infant formula feeding all result in a marked decrease in plasma 22:6n-3 and 20:4n-6 and an increase in 18:2n-6. Estimation of fetal tissue fatty acid accretion suggests that current preterm infant feeds are unlikely to meet in utero rates of 22:6n-3 accretion. Consideration needs to be given to whether fetal plasma 22:6n-3 and 20:4n-6 enrichment and the low 18:2n-6 facilitates accretion of 22:6n-3 and 20:4n-6 in developing tissues.

Animals↗
PubMed1993

Fetal development in the rat following disruption of maternal renal function during pregnancy.

Pregnant Sprague-Dawley rats received subcutaneous injections of mercuric chloride (1-4 mg/kg) on either gestation day 7, 9, 11, or 13 to determine effects of altered maternal renal function on embryonic and fetal development. Maternal renal function, assessed by urinalysis, was markedly disrupted for at least 48 hours after treatment and resulted in decreased maternal body weight gain. Residual effects on maternal kidney weight were evident on GD 21 when the females were killed and the fetuses removed and examined for visceral and skeletal development. We did not observe an increased incidence of malformations in the offspring for exposure on any day of gestation. Maternal exposure to mercuric chloride slightly impaired fetal growth over several gestational exposures periods and changed the pattern of rib formation when exposure occurred early in organogenesis. The extent of the changes could not, however, be related to the immediate degree or duration of altered maternal renal function. Rather, we found correlations between lasting effects of exposure as measured by maternal renal weight on GD 21 and super-numerary lumbar rib induction on GD 7 and 9; while for the relationship with fetal weight, the strongest correlation with maternal kidney weight occurred following exposure on GD 9 (P < 0.01), with weaker correlations (P < 0.10) for GD 7 and 13 exposures. Maternal serum urea was negatively correlated with fetal weight from the GD 7 exposure. This study supports the concept that some specific forms of maternal toxicity may be associated with limited manifestations of developmental toxicity, but, in general, embryonic development was observed to proceed normally in the presence of marked disruptions in maternal renal physiology. Maternal toxicity, especially as routinely measured in developmental toxicity studies, cannot be looked upon as a single disease. Instead, each manifestation must be examined for what it signifies to the physiology and well being of the female and for cause-and-effect relationships with fetal observations. Maternal toxicity and developmental toxicity should not be etiologically linked solely because of their concurrent appearance on the dose-response curve.

Acute Kidney Injury↗
PubMed1982

Reproduction and fetal development in mice chronically exposed to nitrous oxide.

The effects of exposure to nitrous oxide on reproductive indices, fetal development, and male fertility were examined in Swiss/ICR mice. In experiment I, female mice were exposed for 4 hours per day on days 6-15 of pregnancy, to 0.5% (5,000 ppm), 5.0% (50,000 ppm), or 50% (500,000 ppm) nitrous oxide. Control mice were untreated, exposed to compressed air, or treated with retinoic acid on day 8 of gestation. In experiment II, male mice were treated, as above, for 9 weeks and then mated nightly for 7 nights to untreated, virgin females. In experiment I, 1,761 fetuses from 154 dams were examined and found to be without evidence of adverse nitrous oxide treatment effects. In experiment II there were no differences among the groups in the ability of males to impregnate females or in litter size, fetal wastage, or fetal size. When we compare nitrous oxide with other inhalation anesthetics we have studied employing a similar protocol, we find the order of reproductive toxicity to be: halothane greater than enflurane greater than methoxyflurane greater than nitrous oxide. None of the agents were toxic, however, at the trace concentrations usually found in operating rooms.

Abnormalities, Drug-Induced↗
PubMed1997

Monitoring of early human fetal development in women exposed to large doses of chemicals.

The toxicological in-patient hospital in Budapest is responsible for the care of chemically poisoned persons from a population of 3 million. A population-based prospective epidemiological study of all pregnant women admitted from 1985 to 1993 was used to evaluate effects of large doses of chemicals on human fetal development. Of 559 self-poisoned pregnant women identified, two died from the poisoning. A total of 213 fetuses were in the first month of their postconception development. Of these, 126 had evaluated pregnancy outcomes: 111 ended in very early loss, 3 ended in clinical miscarriage, and 12 survived to delivery. (In addition 73 pregnancies were terminated and one pregnant woman died.) The 12 liveborn infants had two congenital abnormalities that were probably not related to their mother's self-poisoning. Though based on small numbers, these findings are consistent with an "all-or-nothing" effect of chemical poisoning very early in human gestation.

Abortion, Spontaneous↗
PubMed1987

Differentiation of tracheal mucociliary epithelium in primary cell culture recapitulates normal fetal development and regeneration following injury in hamsters.

Hamster tracheal epithelial cells were grown in primary culture for 8 days on a collagen gel substrate, in hormone-supplemented serum-free medium (Ham's F-12). On Days 1-3 in culture, the colonies were composed of a monolayer of poorly-differentiated flattened cells. Most of these were large cells which appeared to be altered secretory (mucous) cells. On Days 4 and 5, many of the epithelial cells were cuboidal. The rough endoplasmic reticulum was moderately developed, and mucous granules were seen at the cell apices. Preciliated and newly formed ciliated cells were observed on Day 6, and a differentiated mucociliary epithelium was established by Day 7 in culture. The study shows that in the hamster tracheal epithelium, the stages of normal fetal development and regeneration following injury, which have been characterized previously in vivo, are recapitulated in vitro. Formation of a mucociliary tracheal epithelium occurs within 7 days in vito and in vitro.

Animals↗
PubMed1987

Effects of acute alcohol administration on maternal calcium metabolism and fetal development in mice.

Pregnant C57Bl/10J mice were treated intraperitoneally with alcohol (Group A) or saline (control) on Day 7 of gestation. On Day 7, at 0 hour and again at 4 hour, Group A received 0.020 ml/GM body weight of 25% (v/v) alcohol, while control mice received 0.020 ml/GM body weight of physiological saline. The injection schedule specified corresponds to a specific stage of fetal development, namely gastrulation. On Day 13 of gestation, all animals were placed in individual metabolic cages to monitor both food and water intake and urinary output. The animals were sacrificed on Day 14. Blood was withdrawn and the serum was used for analyses. In addition, resorption sites within the uterine horns were recorded and fetuses examined. Group A animals had significantly lower serum calcium (Ca) than the controls (6.1 +/- 0.7 mG% versus 9.6 +/- 1.6 mG%, P less than .01). By contrast, the same alcohol injected mice had higher serum phosphate (P) than the controls (18.2 +/- 5.9 mG% versus 12.3 +/- 4.0 mG%, P less than .05). Urinary Ca levels were lower (P less than .05) while urinary P values tended to be higher in alcohol injected mothers. Furthermore, Group A mice had litters which were smaller in size, lower in average fetal body weight and had a higher incidence of resorption (18%) than control mice. Examination of the viable fetuses showed that 53% of those from alcohol treated mothers had facial abnormalities while only 12% of the fetuses from the controls looked abnormal. The results indicate that exposure to acute alcohol in this early stage of pregnancy creates disturbances in maternal Ca metabolism, which may be ultimately related to the observed fetal abnormalities.

Abnormalities, Drug-Induced↗
PubMed1988

An immunocytochemical study of the germinal layer vasculature in the developing fetal brain using Ulex europaeus 1 lectin.

The characteristics of the germinal matrix vasculature were studied in the developing fetal brain using immunocytochemical methods. A preliminary comparative immunocytochemical study was made on six fetal brains to compare endothelial staining by Ulex europaeus I lectin with that of antibody to Factor VIII related antigen. Ulex was found to stain germinal layer vessels better than Factor VIII related antigen. Subsequently, the germinal layers of a further 15 fetal and preterm infant brains ranging from 13 to 35 weeks' gestation were stained with Ulex europaeus I to demonstrate the vasculature. With increasing gestation, there was a gradual increase in vessel density, particularly of capillaries. This was not a uniform process. A plexus of capillaries was prominent immediately beneath the ependyma while the more central parts of the germinal matrix contained fewer, but often larger diameter, vessels. The variation in vessel density which was a feature of the later gestation brains may have implications for local blood flow and may be a factor in haemorrhage at this site.

Antigens↗
PubMed2004

Fetal development of vomeronasal system in the goat.

Our previous study morphologically revealed that the adult goat vomeronasal (VN) system was different from the rodent and opossum one, and at least two types of VN systems exist in mammals. However, it remains unknown whether the developments in both types of VN systems are ontogenetically distinct and when the goat VN system is established. In this study, we morphologically observed the fetal development of the goat accessory olfactory bulb (AOB) and VN neuron. In the fetus, Gi2-expressing VN terminals terminated at glomeruli throughout the AOB, and no immunoreactivities for Go were detected in the nerve terminals reaching into AOB. The layer structure of AOB rapidly developed in the latter half of gestation. In the VN organ (VNO), at the middle stage of gestation, the dendritic processes of VN neuron were exposed in the VN lumen, and scattered and thin microvilli existed on the protrusion of the VN neuron. In the apical part of dendritic processes, no clear vesicle existed. However, the immunohistochemistry of an olfactory marker protein (OMP) revealed that a few VN neurons with OMP exist in VN sensory epithelium (VSE) before birth, although marked immunoreactivities were detected in adult VSE. Fetal VN neurons appeared to be underdeveloped. These results suggest that the goat VN system is ontogenetically distinct from the rodent and opossum VN systems, and is underdeveloped before birth. The goat VN system will develop and mature during the early postnatal period similar to the rodent and opossum VN systems.

Age Factors↗
PubMed1997

Understanding human sexuality--specifically homosexuality and the paraphilias--in terms of chaos theory and fetal development.

This paper considers human sexual orientation, specifically homosexuality and some paraphilias, to occur as a result of intrauterine development, itself a mathematically chaotic process. Parameter space, an example of state space in the phase diagram, has been used to illustrate different phenotypes. The crossing of a bifurcation boundary by the developing fetus is proposed as a mechanism by which it may be changed from one sexual orientation to another, e.g. from heterosexuality to homosexuality. The factors which push the fetus over a bifurcation boundary, which include a Y-chromosome, specific hormone administration, the lying contiguous to an opposite-sex fetus in multiple pregnancies, maternal stress and immune factors are described. The syndromes congenital renal hyperplasia and the androgen insensitivity syndrome and their relevance to this model are also discussed. Finally, chaos theory is used to encompass the complex interactions between fetal development and cultural factors in human sexuality.

Bisexuality↗
PubMed1988

Differences in the kinetics of the mineralization process in endochondral and intramembranous osteogenesis in human fetal development.

About 300 samples of bone tissue from femoral diaphyses and from parietal bones of calvaria were collected from human fetuses aged from 6-8 to 40-41 weeks in order to compare the kinetics of the mineralization process in endochondral and intramembranous bone formation. The crystallinity of bone mineral was evaluated by the method based on electron spin resonance (ESR) spectrometry, and mineral content was measured after ashing of the samples. Highly significant differences in the kinetics of deposition of mineral (ash content) and maturation of deposited mineral (crystallinity coefficient) were found between parietal bones and femoral diaphyses in the course of fetal development. In the early stages of development (6-8 to 10-12 weeks), the content of mineral and its crystallinity in parietal bones were significantly lower than in femoral diaphyses. In the parietal bones a gradual increase in both values was observed until they reached a plateau at the age of 30 weeks. On the other hand, in femoral diaphyses of 6-8-week-old fetuses mineral content was high and deposited mineral showed a high degree of crystallinity. Both these values did not change significantly until birth. The differences in kinetics of the mineralization process between the weight-bearing bones and bones that are not exposed to the influence of strong external forces are most probably genetically conditioned. The collected data supply embryological information and might be used in the future for evaluation of pathologic changes in skeletal development.

Embryonic and Fetal Development↗
PubMed1997

Calcification of the lumbar vertebrae during human fetal development.

The calcification rate of the human fetal vertebrae has not been previously documented. In bridging this gap in knowledge, this report will specifically provide reference values for mineral content in predominantly trabecular bone during its formation in the prenatal period. Such information would facilitate early detection of ossification defects which become apparent in the fetal spine as early as 20 weeks of gestation [1]. Lumbar vertebrae were obtained at autopsy from 33 human fetuses aged 17-41 weeks of gestation. Vertebral demineralization was effected using an acid-alcohol solution. The extracted concentrations of calcium and phosphorus were determined spectrometrically from the solutions. Atomic absorption spectroscopy was used to determine calcium concentration and phosphate concentration was assessed by ultraviolet colorimetry. Mineralization could be described by a linear relationship over the age range studied. Calcium was taken up by the fetal vertebrae at twice the rate of phosphorus (0.2% per week). When the fetuses were classed according to similar gestational ages, the Ca/P weight ratios increased from 1.7 in the youngest group to 2.2 in the oldest group. The time of onset of calcification, calculated by extrapolation of the calcium data, appeared to be earlier than ultrastructural studies by other investigators suggest, but was subject to many uncertainties.

Calcification, Physiologic↗
PubMedDate not supplied

Effects of ethanol and maternal nutritional status on fetal development.

This study investigated the interactive effects of alcohol and nutritional status of the pregnant female on fetal growth and development. Three liquid diets were formulated ranging in protein content from suboptimal to supraoptimal: diet I provided 18% kcal as protein and 1.0 kcal/ml; diets II and III provided 25 and 32% kcal, respectively, as protein and 1.2 kcal/ml. In all cases, alcohol provided 36% of total calories. Both pair-fed and ad libitum fed control groups were included. We found that blood alcohol levels were consistently high in all three diet regimens throughout gestation. Alcohol intake suppressed weight gains and increased adrenal weights and placenta weights in pregnant females. Both body weights and brain weights were reduced in alcohol-exposed fetuses. However, relative brain weights were found to be increased in alcohol fetuses, indicating "brain sparing." Maternal nutritional status had no major effect on developmental outcome. Thus, with alcohol administered as a high proportion of total daily calories, increasing dietary protein levels did not attenuate the major adverse effects of alcohol on fetal development.

Adrenal Glands↗
PubMed2000

Effects of lead exposure before pregnancy and dietary calcium during pregnancy on fetal development and lead accumulation.

Millions of women of child-bearing age have substantial bone lead stores due to lead exposure as children. Dietary calcium ingested simultaneously with lead exposure can reduce lead absorption and accumulation. However, the effects of dietary calcium on previously accumulated maternal lead stores and transfer to the fetus have not been investigated. We studied the effects of lead exposure of female rats at an early age on fetal development during a subsequent pregnancy. We gave 5-week-old female Sprague-Dawley rats lead as the acetate in their drinking water for 5 weeks; controls received equimolar sodium acetate. This was followed by a 1-month period without lead exposure before mating. We randomly assigned pregnant rats (n = 39) to diets with a deficient (0.1%) or normal (0.5%) calcium content during pregnancy. A total of 345 pups were delivered alive. Lead-exposed dams and their pups had significantly higher blood lead concentrations than controls, but the concentrations were in the range of those found in many pregnant women. Pups born to dams fed the calcium-deficient diet during pregnancy had higher blood and organ lead concentrations than pups born to dams fed the 0. 5% calcium diet. Pups born to lead-exposed dams had significantly (p<0.0001) lower mean birth weights and birth lengths than controls. There were significant inverse univariate associations between dam or pup organ lead concentrations and birth weight or length. The 0.5% calcium diet did not increase in utero growth. Stepwise regression analysis demonstrated that greater litter size and female sex were significantly associated with reduced pup birth weight and length. However, lead exposure that ended well before pregnancy was significantly (p<0.0001) associated with reduced birth weight and length, even after litter size, pup sex, and dam weight gain during pregnancy were included in the regression analysis. The data demonstrate that an increase in dietary calcium during pregnancy can reduce fetal lead accumulation but cannot prevent lead-induced decreases in birth weight and length. The results provide evidence that dietary nutrients can influence the transfer of toxins to the fetus during pregnancy. If these results are applicable to women, an increase in diet calcium during pregnancy could reduce the transfer of lead from prepregnancy maternal exposures to the fetus.

Animals↗