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PubMed1999

Expression patterns of complex glycoconjugates and endogenous lectins during fetal development of the viscerocranium.

Experimental evidence suggests that carbohydrates and their corresponding receptors (endogenous lectins) decode biological information. Therefore, the expression of complex oligosaccharides--the potential ligand part of this recognition system--during chondrogenesis and osteogenesis was determined in the viscerocranium of fetal rats by mapping the staining patterns of exogenous lectins. Results were compared with the expression of bone- and/or cartilage-specific core proteins and the binding profiles of neoglycoconjugates. These synthetic tools make possible the localization of sugar-ligand-binding sites. The spatial and temporal distribution patterns of glycoconjugates were highly dynamic and demonstrated a clear correlation with characteristic morphological modifications. The glycobiological characterization of precartilage mesenchymal cells revealed distinct differences compared to prospective bone anlagen. Especially the binding of the exogenous lectin from Griffonia simplicifolia II, that selectively visualized prechondral aggregations, reveals that regulation of early chondral growth is at least phenomenologically correlated with a relatively atypical oligosaccharide composition terminating with N-acetylglucosamine.

Animals↗
PubMed1973

Regulation of hepatic glycogen synthesis during fetal development: roles of hydrocortisone, insulin, and insulin receptors.

In fetal rat liver in utero, an increase in glycogen and the glycogen synthetic enzyme glycogen synthetase (EC 2.4.1.11) occurs between gestational days 17 and 19. We used an organ culture system for finding the stimulus for increased enzyme activity and defining the relationship of this increase to glycogen synthesis. In fetal-liver explants from an earlier period (gestational day 16), hydrocortisone causes an elevation in total glycogen synthetase activity. This effect, which can be blocked by actinomycin D, is strikingly similar in time course and magnitude to the normal increase in utero. However, in order for glycogen synthesis to proceed after hydrocortisone increases glycogen synthetase levels, insulin is required. Unlike hydrocortisone, insulin does not increase total glycogen synthetase; it appears to act by converting the b or phospho form of synthetase to the a or dephospho form. Insulin alone does not stimulate glycogen synthesis in explants from 16-day fetal liver, although no defect in insulin binding was demonstrable. These findings support the hypothesis that the increase in liver-glycogen synthesis during the last trimester requires glucocorticoids for the developmental induction of glycogen synthetase and insulin for activation of the enzyme.

Animals↗
PubMed1991

Effect of epidermal growth factor on the fetal development of the tracheobronchial secretory apparatus in rhesus monkey.

Fetal rhesus monkeys were treated with recombinant human epidermal growth factor (EGF) to determine if EGF can induce maturation of the tracheobronchial secretory apparatus. At 75% of gestation, EGF was administered simultaneously into both the amniotic fluid and fetal abdominal cavity at an average dose of 66 micrograms/kg body weight, by each route over a 7-d period. At the end of the treatment period, the fetuses were delivered and either euthanized immediately or after maintenance on ventilatory support for 6 h. The lungs were removed, and the trachea and one lobe of the right lung was fixed and embedded for light microscopy. The left lung was lavaged with saline, and the collected fluid was used to quantify released secretory product. Secretory product was also measured in amniotic fluid as well as in situ on histologic sections of tracheal epithelium. When the tracheas of EGF-treated monkeys were examined, the epithelium was found to be taller and to contain a greater proportion of secretory cells and a smaller proportion of intermediate cells than the control group. However, there was no significant change in the total number of cells per millimeter of basal lamina or in the proportion of the epithelial population made up of basal or ciliated cells. There was more secretory product stored in the epithelium and submucosal glands and increased quantities of respiratory secretions in both lung lavage and amniotic fluid of EGF-treated monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of toxins 544 and 514 from Karwinskia humboldtiana (buckthorn) plant upon fetal development of the mouse.

The teratogenic effect of toxins 544 and 514 from K. humboldtiana upon the mouse embryo was evaluated. One half of the LD50 dose for the mouse was administered at day 8 of gestation. At the end of pregnancy, reproduction and fetal data were recorded. Dams treated with toxin 544, but not with toxin 514, showed a higher incidence of reabsorptions, malformations, as well as lower fetal length compared to the control group.

Animals↗
PubMed1988

Intestinal mucosa of celiacs in remission is unable to abolish toxicity of gliadin peptides on in vitro developing fetal rat intestine and cultured atrophic celiac mucosa.

Subfraction 2R of fraction 9 from a peptic-tryptic-pancreatic digest of wheat gliadin is known to be toxic in vivo to celiac patients. We have found that fractions 9 and 2R inhibit the in vitro development of fetal rat intestine and the increase of enterocyte height occurring in organ culture of atrophic celiac mucosa (0.1-0.5 mg/ml medium). Other peptide fractions of the gliadin digest are devoid of such in vitro effects. Subfraction 2R, after incubation with morphologically normal small intestinal mucosa of celiacs in remission and ultrafiltration, was still very active in both culture systems at low concentration (0.1 mg/ml); on the contrary, subfraction 2R was inactivated after incubation with normal mucosa. These results are compatible with the hypothesis that there is a mucosal defect in handling gliadin peptides in celiac disease, and suggest that there is either a primary (or secondary) enzyme deficiency or some other mechanism operating in the intestinal mucosa of celiac patients in remission.

Animals↗
PubMed1998

Embryonic and fetal development of structures associated with the cerebro-spinal fluid in man and other species. Part I: The ventricular system, meninges and choroid plexuses.

Little is known about the development of the central nervous system (CNS) in humans. Ethical considerations preclude experimental studies in this field, and as a result most available data on human ontogenesis are descriptive. Comparative anatomic and embryologic studies have demonstrated that the main developmental milestones are conserved across species, and their results can be used to suggest a likely scenario for human development. The development of the ventricles, meninges, and choroid plexuses are discussed in this article. The central cavity of the neural tube is formed during neurulation, which occurs during the fourth gestational week. The first milestone is occlusion of the spinal neurocele (the central canal in the neural tube) shortly after neurulation. This prevents free communication between the ventricular system and the amniotic cavity. The second milestone is development of the meninges, which separate the central nervous system from the rest of the body. The embryonic origin of the meninges varies across species. In birds (and probably in mammals), the spinal meninges are derived from the somitic mesoderm, the brainstem meninges from the cephalic mesoderm, and the telencephalic meninges from the neural crest. Differentiation of the meninges, which involves formation of the subarachnoid space, occurs early, before the cerebrospinal fluid (CSF) begins to flow around the CNS. During ontogenesis, the meninges play a key role in regulating the growth of underlying nervous structures. They induce the formation of the superficial glial limiting layer and stimulate the growth of precursors located in the superficial blastemas of the cerebellum and hippocampus. The choroid plexuses are complex specialized structures that produce most of the CSF. Their epithelium derives from the neural tube epithelium and their mesenchyma from the meninges. Of the many enzymes produced in the choroid plexuses, some reflect the pivotal metabolic role of these structures (alkaline and acid phosphatases, magnesium-dependent ATPase, glucose-6-phosphatase, thiamine pyrophosphatase, adenylate cyclase, oxidoreductase, esterases, hydrolases, cathepsin D, and glutathion S-transferase). The two enzymes that are crucial to the production of CSF are Na+/K+ ATPase and carbonic anhydrase. Inactivation of catecholamines is mediated by catechol-O-methyltransferase and by the monoamine oxidases A and B. The morphology and synthesis profile of the choroid plexuses changes during development, although little is known about these changes in humans.

Animals↗
PubMedDate not supplied

Fetal development in rhesus monkeys exposed prenatally to cocaine.

Using a timed-breeding protocol, one group of female rhesus monkeys was implanted subcutaneously with osmotic minipumps containing 0.3 mg/kg/h cocaine (N=18) or saline (N=18) from day 24 postconception through gestation. Another group received cocaine (N=12) or saline (N=8) from conception through day 42 of gestation. Mean levels of cocaine in maternal serum were approximately 150 ng/ml during pregnancy. A total of 56 pregnancies were documented in 42 adult monkeys, and 39 pregnancies completed full-term. Maternal food consumption and body weight increased during pregnancy, and there were no significant differences among experimental groups. Although both groups with a history of cocaine exposure had lower survival rates compared to pair-fed controls, of the fetuses that survived, fetal heart rate, fetal biparietal diameter, and mean gestational length were in the normal range for all experimental groups. Similarly, body weight, biparietal diameter, body length, and modified Apgar scores at birth did not differ significantly among experimental groups. The results indicate that surviving fetuses exhibited normal growth.

Animals↗
PubMed1993

Negative regulation of antioxidant enzyme gene expression in the developing fetal rat lung by prenatal hormonal treatments.

Prenatal administration of thyrotropin-releasing hormone (TRH) or TRH plus dexamethasone (DEX) to pregnant rats accelerates lung surfactant system development in late gestation, but paradoxically depresses the normal late gestational elevation in fetal lung antioxidant enzyme (AOE) activities (Pediatr Res 30:522, 1991). In these present studies, we tested whether both prenatal hormonal treatments act to depress normal fetal lung AOE development by negative regulation of AOE gene expression. We used solution hybridization to quantitate the concentration of AOE mRNA. Results of the developmental studies revealed significantly decreased lung mRNA concentrations of copper-zinc superoxide dismutase, manganese superoxide dismutase, catalase, and glutathione peroxidase in late gestation as a result of prenatal TRH treatment. The addition of DEX administration did not reverse the lowered expression of lung AOE genes due to TRH treatment, but instead resulted in significant additional decreases in pulmonary AOE mRNA levels at both 21 and 22 d of gestation. The tested AOE mRNA half-lives (stabilities) revealed no significant differences between controls (8.0-10.5 h) and TRH-treated (8.2-9.5 h) and TRH-plus-DEX treatment (7.8-10.7 h) groups. These findings suggest that prenatal treatment with TRH and with TRH plus DEX acts to depress the normal late fetal lung AOE activity elevations by (direct) negative regulation of AOE gene expression, and the decreased AOE expression is likely regulated at the level of gene transcription rather than posttranscriptionally.

Animals↗
PubMed2001

Culture of preimplantation mouse embryos affects fetal development and the expression of imprinted genes.

Culture of preimplantation mammalian embryos and cells can influence their subsequent growth and differentiation. Previously, we reported that culture of mouse embryonic stem cells is associated with deregulation of genomic imprinting and affects the potential for these cells to develop into normal fetuses. The purpose of our current study was to determine whether culture of preimplantation mouse embryos in a chemically defined medium (M16) with or without fetal calf serum (FCS) can affect their subsequent development and imprinted gene expression. Only one third of the blastocysts that had been cultured from two-cell embryos in M16 medium complemented with FCS developed into viable Day 14 fetuses after transfer into recipients. These M16 + FCS fetuses were reduced in weight as compared with controls and M16 fetuses and had decreased expression of the imprinted H19 and insulin-like growth factor 2 genes associated with a gain of DNA methylation at an imprinting control region upstream of H19. They also displayed increased expression of the imprinted gene Grb10. The growth factor receptor binding gene Grb7, in contrast, was strongly reduced in its expression in most of the M16 + FCS fetuses. No alterations were detected for the imprinted gene MEST: Preimplantation culture in the presence of serum can influence the regulation of multiple growth-related imprinted genes, thus leading to aberrant fetal growth and development.

Animals↗
PubMed2001

Maternal antiepileptic drug use and effects on fetal development.

Many pregnant women take antiepileptic medications, and concern has arisen about the risks this poses to the fetus. It has been debated whether the causative agent is the medication or the underlying maternal disorder. Review of the recent literature indicates that the effects seem to be from the medications themselves. The frequency of malformations is about two to three-fold above the background rate and is dose-related for some of the medications. There seem to be effects on birth weight, length, and head circumference caused by at least some of the medications. The risks are greater when more than one medication is used. Cognitive effects from the medications have been shown, although these effects are of lower magnitude than previously reported. More investigation needs to be done to determine the exact risks of each individual medication, especially the newer ones. Studies on underlying mechanisms indicate potential genetic susceptibility and altered developmental gene expression patterns.

Abnormalities, Drug-Induced↗
PubMed1995

Transfer of bovine embryos produced in vivo or in vitro: survival and fetal development.

The objectives of the present experiment were to compare survival after transfer of bovine embryos produced in vivo with those produced in vitro and to examine the physical characteristics of fetuses produced from these transfers. Embryos produced in vivo (Holstein x Angus) were recovered from uterine flushings of superovulated heifers 7 days after first artificial insemination, and embryos produced in vitro (Holstein x beef breeds) were collected 7 days after insemination. Embryos were paired by source (in vivo, in vitro), stage (compact morula, blastocyst), and quality grade (excellent = 1, good = 2), and transferred nonsurgically to recipient heifers on Day 7 (+/- 1 day) of the estrous cycle. Pregnancy status was monitored by determination of serum progesterone concentrations, ultrasonography, and palpation through 7 mo of gestation, at which time fetuses were recovered. In comparison with grade 1 embryos produced in vivo, the risk of embryonic death after transfer was similar for grade 2 embryos produced in vivo (p = 0.56) and for grade 1 embryos produced in vitro (p = 0.88). By contrast, grade 2 embryos produced in vitro were at greater (p = 0.04) risk of embryonic death. Embryo loss was associated (p = 0.01) with increased serum concentrations of progesterone in recipients at the time of transfer. At 7 mo of gestation, fetuses from embryos produced in vitro were heavier (p = 0.02) than fetuses from embryos produced in vivo and had skeletal measurements that were disproportionate (p < or = 0.04) to body weight.

Animals↗
PubMed1998

Training in pregnant women: effects on fetal development and birth.

OBJECTIVE: The effects of high- and medium-intensity exercise on the fetus and on the onset and length of labor, birth weight, and Apgar score were studied in healthy athletes who performed a high level of exercise before conception. STUDY DESIGN: Forty-two women were recruited to the study by newspaper ads and through acquaintances. They elected to follow either a high- or a medium-intensity exercise program throughout pregnancy until 6 weeks after delivery. Documentation of their intensity of activity before conception (retrospectively), during pregnancy, and after delivery was obtained. RESULTS: There were no differences between the high- and medium-intensity exercise group in duration of labor, birth weight, or 1- and 5-minute Apgar scores. The higher level of exercise correlated with a significantly greater maternal weight gain during pregnancy and significantly earlier onset of labor for those women who gave birth to girls but not for those who gave birth to boys. CONCLUSION: Our results indicate that healthy and well-conditioned women may take part in exercise during pregnancy without compromising fetal growth and development as judged by birth weight or complicating the course of pregnancy or labor.

Adult↗
PubMed1987

A murine model for the assessment of placental and fetal development in teratogenicity studies.

During normal pregnancy in the mouse, maternal serum levels of the analogues to human schwangerschaftsprotein-1 and alpha-fetoprotein correlate significantly with the growth of the placenta and fetus respectively. This relationship has been utilized in the analysis of the effect of sodium selenite on placental and fetal growth in mice. Moderate doses of sodium selenite did not affect the growth of the placenta and fetus significantly, whereas high doses of selenite resulted in a large percentage of abortions. The protein markers were found to be useful in the prediction of placental and fetal growth, and they are suggested to be of general use in the study of the impact of teratogenic substances, since they reflect the status of the fetoplacental mass during gestation.

Abnormalities, Drug-Induced↗
PubMed1994

Differential expression and tissue distribution of type I and type II neurofibromins during mouse fetal development.

Mutations in the NF1 gene may cause developmental abnormalities and the formation of a variety of tumors of neural crest origin in humans. The NF1 gene codes for a large protein, neurofibromin (nf), which is structurally and functionally related to yeast and human ras-GTPase-activating proteins (ras-GAPs). Recently, two transcripts coding for type I and type II nf with different ras-GAP activity have been identified. Since ras proteins do not appear to be significantly regulated during mouse development, we examined if differential expression of neurofibromins may provide evidence for a role of nfs in regulating ras-mediated cell proliferation and differentiation. Nfs were expressed as early as E8. At E11 a marked increase of NF1 transcripts occurred and was associated with expression of nfs in all tissues. Type I and type II nfs each showed a different time course of expression and tissue localization, with type II nf present mainly from E8 through E10, although in the heart type II nf was present at E12. In some tissues such as heart and dorsal root ganglia rapid increases and decreases of nfs were detected related to differentiation of these tissues. These results are consistent with a role of nfs in regulating ras-mediated cell proliferation and differentiation during development and support distinct functional roles for type I and type II nfs.

Animals↗
PubMed1984

Tracheal morphogenesis and fetal development of the mucociliary epithelium of the rat.

In the rat, tracheal development begins at mid-gestation (Day 11) with the formation of the tracheal groove, a longitudinal diverticulum of endodermal epithelium that evaginates from the floor of the pharynx and tubular foregut. At this stage the tracheal groove and developing foregut share a common lumen. Paired primary bronchial buds (lung buds), surrounded by lung bud mesenchyme (splanchnic mesoderm), arise from the caudal end of the tracheal groove. The formation of a longitudinal tracheoesophageal septum divides the combined tracheal groove and developing foregut into two structures, the trachea and esophagus. The trachea and esophagus grow apart, surrounded by independently organized populations of mesenchymal cells. Near this time (Day 12-13), the primary bronchial buds give rise to secondary (lobar) buds of pulmonary epithelium. This establishes the lobar pattern of the right and left lungs and marks the formation of extrapulmonary bronchi. The development of smooth muscle and cartilage within the tracheal mesenchyme precedes the differentiation of the mucociliary epithelium. Smooth muscle forms transversely oriented fascicles in the dorsal tracheal wall (pars membranacea), while pre-cartilage rings surround the remaining ventral and lateral walls (pars cartilagina). Epithelial differentiation is first evident at Day 17, with the formation of ciliated cells in the epithelium of the pars membranacea. Differentiation in the pars cartilagina trails development in the dorsal epithelium. Cell surface characteristics of the tracheal epithelium indicate that secretory cells differentiate about Day 19-20. The precise time and sequence of differentiation of mature cell types of the tracheal epithelium is yet to be determined. It is clear, however, that the development of the mucociliary epithelium in the rat is not completed at birth, but continues into the neonatal period.

Animals↗