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PubMed1988

Skin lipid content during early fetal development.

Although little is known about changes in the lipid composition of the skin during fetal development, information regarding the developmental sequence of fetal skin lipid content could be important for understanding the emergence of epidermal barrier function, as well as providing baseline criteria for prenatal diagnosis of certain inherited disorders of cornification. In these studies, epidermis was separated from dermis in fetal skin samples ranging from 50 to 140 d, estimated gestational ages (EGA), and its lipid composition was analyzed by quartz rod microchromatography/flame-ionization and thin layer chromatography. Lipid biochemical data were correlated with developmental milestones observed by electron microscopy (morphologic studies). The lipid composition of epidermal and dermal fractions from skin samples between 50 and 110 d EGA was similar, with both tissues exhibiting a predominance of free sterols and phospholipids. After 110 d EGA dermis became enriched in triglycerides, corresponding to the progressive development of adipocytes after this time. EGA epidermis after 110 d was enriched not only in triglycerides, but also sterol esters. Moreover, ceramides and glycosphingolipids also became increasingly prominent, changes that were greatest in epidermis from older fetuses and from cephalad regions. These changes in epidermal lipid composition corresponded morphologically to the progressive emergence of both folliculocentric epidermal cornification and sebaceous gland development.

Cholesterol↗
PubMed2004

C-type natriuretic peptide in reproduction, pregnancy and fetal development.

C-type natriuretic peptide (CNP) belongs to the natriuretic peptide family that consists of three structurally related peptides with a 17-amino acid ring linked by a disulfide bond. In contrast to atrial and brain natriuretic peptides that are mainly cardiovascular hormones, CNP acts predominantly in an autocrine/paracrine fashion, is commonly considered to be an endothelial hormone with antimitogenic properties, and is characterized as a regulator of endochondral ossification. Its biological effects are mediated by an intracellular cGMP accumulation via specific membrane-bound guanylyl cyclase B (GC-B) activation. There is growing evidence that this peptide is also involved in various reproductive processes as well as in embryonic and fetal development. In rodents, CNP and its receptor are highly expressed in the uterus and ovaries with specific regulation during the estrous cycle. During pregnancy, CNP mRNA is detectable in mice embryos and shows an organ-specific expression in maternal reproductive tIssues with the highest concentration in the placenta. This could indicate a defined biological function of the CNP/GC-B/cGMP axis in gestation e.g. antagonizing vasoconstrictive peptides like angiotensin II. In humans, besides a postulated fetal de novo synthesis of CNP, both the peptide and its receptor are expressed in the placenta and myometrium with opposite regulation of CNP in pregnancies complicated by pre-eclampsia or intrauterine growth retardation. Since the maternal plasma levels do not reflect these alterations, one can conclude that this part of the natriuretic peptide system acts locally suggesting that CNP-stimulated cGMP release exhibits organ-specific effects. Importantly, CNP has also become a peptide with a distinct role in male reproductive processes, since endocrine function of the testis and the regulation of penile erection are regulated by the CNP/GC-B axis. This review gives a comprehensive overview of the multiple functions of CNP in reproduction and pregnancy as well as in embryonic and fetal development.

Animals↗
PubMed1986

Maternal phenylketonuria-chronology of the detrimental effects on embryogenesis and fetal development: pathological report, survey, clinical application.

Maternal phenylketonuria (PKU) is likely to have detrimental effects on embryogenesis and fetal development. Manifestations in the offspring include spontaneous abortion, various congenital malformations, intrauterine growth retardation, and microcephaly. The time at which the metabolic abnormalities induce pathologic embryogenesis can be documented by knowing the time of the development of specifically damaged organ systems. This review reveals that, while the most recognized congenital malformations occur in the heart, the most common abnormality is growth inhibition occurring throughout pregnancy. The organ system most commonly affected by this growth inhibition is the brain, resulting in a high incidence of micrencephaly. It appears that maternal phenylketonuria interferes with appropriate fetal growth and that this effect occurs during the entire course of pregnancy and has no tissue specificity. This information can be both informative to pathologists and useful to clinicians.

Embryonic and Fetal Development↗
PubMed1995

Cutaneous lipid synthesis during late fetal development in the rat.

Lipid synthesis in fetal skin may be important both for the development of a mature epidermal permeability barrier and for growth. In these studies, we measured cutaneous cholesterol, sphingolipid and fatty acid synthesis during the critical period of epidermal barrier development in fetal rats to determine whether barrier function influences synthetic rates. In addition, the activities of HMG CoA reductase, serine palmitoyl transferase and acetyl coenzyme A carboxylase were evaluated. In whole skin, synthesis of cholesterol, ceramide, sphingomyelin and fatty acid decreased from day 17 to day 21 of gestation, as did the activity of HMG CoA reductase, serine palmitoyl transferase and acetyl coenzyme A carboxylase. In both the epidermis and dermis, a decrease in cholesterol, ceramide, sphingomyelin and fatty acid synthesis was measured over days 19-21 of gestation. Epidermal HMG CoA reductase activity also decreased over this same time period. In summary, epidermal and dermal synthetic rates and enzyme activity were highest early in gestation when the barrier was least competent and decreased as competence was achieved. Since other studies with mature animals have revealed that epidermal synthetic rates and enzyme activity are highest when barrier disruption is maximal, enhanced epidermal lipid synthesis precedes the establishment of a competent barrier in both fetal and mature rodents.

Animals↗
PubMed2005

Fluoxetine during pregnancy: impact on fetal development.

Women are at greatest risk of suffering from depression during the childbearing years and thus may either become pregnant while taking an antidepressant or may require a prescription for one during pregnancy. The antidepressant fluoxetine (FX) is a selective serotonin reuptake inhibitor (SSRI), which increases serotonin neurotransmission. Serotonin is involved in the regulation of a variety of physiological systems, including the sleep-wake cycle, circadian rhythms and the hypothalamic-pituitary-adrenal axis. Each of these systems also plays an important role in fetal development. Compared with other antidepressant drugs, the SSRIs, such as FX, have fewer side effects. Because of this, they are now frequently prescribed, especially during pregnancy. Clinical studies suggest poor neonatal outcome after exposure to FX in utero. Recent studies in the sheep fetus describe the physiological effects of in utero exposure to FX with an 8 day infusion during late gestation in the sheep. This is a useful model for determining the effects of FX on fetal physiology. The fetus can be studied for weeks in its normal intrauterine environment with serial sampling of blood, thus permitting detailed studies of drug disposition in both mother and fetus combined with monitoring of fetal behavioural state and cardiovascular function. Fluoxetine causes an acute increase in plasma serotonin levels, leading to a transient reduction in uterine blood flow. This, in turn, reduces the delivery of oxygen and nutrients to the fetus, thereby presenting a mechanism for reducing growth and/or eliciting preterm delivery. Moreover, because FX crosses the placenta, the fetus is exposed directly to FX, as well as to the effects of the drug on the mother. Fluoxetine increases high-voltage/non-rapid eye movement behavioural state in the fetus after both acute and chronic exposure and, thus, may interfere with normal fetal neurodevelopment. Fluoxetine also alters hypothalamic function in the adult and increases the magnitude of the prepartum rise in fetal cortisol concentrations in sheep. Fetal FX exposure does not alter fetal circadian rhythms in melatonin or prolactin. Studies of the effects of FX exposure on fetal development in the sheep are important in defining possible physiological mechanisms that explain human clinical studies of birth outcomes after FX exposure. To date, there have been insufficient longer-term follow-up studies in any precocial species of offspring exposed to SSRIs in utero. Thus, further investigation of the long-term consequences of in utero exposure to FX and other SSRIs, as well as the mechanisms involved, are required for a complete understanding of the impact of these agents on development. This should involve studies in both humans and appropriate animal models.

Animals↗
PubMed2000

The relationship between the lumbosacral enlargement and the conus medullaris during the period of fetal development and adulthood.

The spinal cord is situated within the vertebral canal by the third month of intrauterine life. The spinal cord possesses two symmetrical enlargements, which constitute the segments of the plexuses: the cervical enlargement for the brachial plexus and the lumbosacral enlargement for the lumbar and sacral plexus. In our study, we aimed to investigate the relationship between the termination level of the lumbosacral enlargement (TLLE) and that of the conus medullaris (TLCM) during the period of fetal development and adulthood. We used a total of 75 cases: 25 fetuses (male: 16, female: 9) whose crown-rump length ranged between 90-190 mm, 25 premature and full-term neonates (male: 17, female: 8) whose post-menstrual ages ranged between 33-55 weeks, and 25 adults (male: 12, female: 13) aged between 22-72 years. The dissection technique for fetuses, ultrasonography for premature and full-term newborns, and magnetic resonance imaging (MRI) for adults were used to determine lumbosacral enlargement and TLCM. The differences between the TLCM and the termination level of the largest part of the transverse diameter of the lumbosacral enlargement were investigated. The differences between the TLLE and TLCM were found in different ratios from the period of fetal development to adulthood. Therefore, during medical treatment and surgical procedures this should be taken into account to avoid complications.

Adult↗
PubMed2001

Cytogenetic analysis of trophoblasts by comparative genomic hybridization in embryo-fetal development anomalies.

Cytogenetic studies of spontaneous abortions or intrauterine fetal death depend on conventional tissue culturing and karyotyping. This technique has limitations such as culture failure and selective growth of maternal cells. Fluorescent in situ hybridization (FISH) using specific probes permits diagnosis of aneuploidies but is limited to one or a few chromosomal regions. Comparative genomic hybridization (CGH) provides an overview of chromosomal gains and losses in a single hybridization directly from DNA samples. In a prospective study, we analyzed by CGH trophoblast cells from 21 fetuses in cases of spontaneous abortions, intrauterine fetal death or polymalformed syndrome. Six numerical chromosomal abnormalities including one trisomy 7, one trisomy 10, three trisomies 18, one trisomy 21 and one monosomy X have been correctly identified by CGH. One structural abnormality of the long arm of chromosome 1 has been characterized by CGH. One triploidy and two balanced pericentromeric inversions of chromosome 9 have not been identified by CGH. Sexual chromosomal constitutions were concordant by both classical cytogenetic technique and CGH. Contribution of trophoblast analysis by CGH in embryo-fetal development anomalies is discussed.

Abortion, Spontaneous↗
PubMed2001

Ontogenesis of prolactin receptors in the human fetus: roles in fetal development.

The lactogenic hormones prolactin (PRL) and placental lactogen circulate in human fetal plasma during mid and late gestation. To explore potential roles for the lactogens in fetal development, we examined the cellular distribution and changes in expression of PRL receptors (PRLRs) during ontogeny, and the metabolic effects of PRL signalling and PRLR dysregulation. PRLRs are expressed in diverse tissues of the human fetus by 7.5 weeks of gestation. In fetal bone, adrenal gland and lung, the receptor is expressed first in mesenchymal cells and subsequently in maturing chondrocytes, adrenocortical cells and bronchiolar epithelial cells. That the lactogens play roles in fetal chondrogenesis is suggested by studies in PRLR-deficient mice, which show a delayed ossification of the calvarium. In the central nervous system, the PRLR is detected initially in periventricular neuroepithelium and later in mature neurons of the hypothalamus and olfactory bulb. Finally, in the pancreas, the PRLR is detected first in exocrine tissue and ductal epithelium. Later in gestation and in the postnatal period, PRLRs predominate in pancreatic beta-cells. The lactogens regulate beta-cell proliferation and insulin production in pancreatic islets, and the insulin secretory response to glucose is blunted in PRLR-deficient mice. These observations suggest roles for the lactogens in pancreatic development and function during pregnancy and postnatal life.

Animals↗
PubMed2004

Effect of Ascaris chymotrypsin inhibitor on fetal development of mice.

BALB/c mice were given daily doses of 40-80 mg of Ascaris chymotrypsin inhibitor /AChI/ per kg body weight from 12th until 15th day of gestation (stage of fetal development). It has been found that injection of AChI disturbed the course of pregnancy (bleeding from uterus, abortions, decreased body weight gain as compared to control /p < 0.05/). AChI exhibited embryotoxic effects (a high rate of intrauterine deaths, decreased number of living fetuses and mean fetal weight, delayed skeletal ossification, induced pathological changes of fetal organs and tissues). Congenital malformation (hydronephrosis) was noted in fetuses after injection of higher doses of the chymotrypsin inhibitor from Ascaris.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Effect of ginger tea on the fetal development of Sprague-Dawley rats.

This study investigated the effect of ginger, a common morning sickness remedy, on fetal development. Pregnant Sprague-Dawley rats were administered, from gestation day 6 to 15, 20 g/liter or 50 g/liter ginger tea via their drinking water and then sacrificed at day 20. No maternal toxicity was observed, however embryonic loss in the treatment groups was double that of the controls (P<0.05). No gross morphologic malformations were seen in the treated fetuses. Fetuses exposed to ginger tea were found to be significantly heavier than controls, an effect that was greater in female fetuses and was not correlated with increased placental size. Treated fetuses also had more advanced skeletal development as determined by measurement of sternal and metacarpal ossification centers. The results of this study suggest that in utero exposure to ginger tea results in increased early embryo loss with increased growth in surviving fetuses.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Myelographic study of the spinal cord ascent during fetal development.

To assess the length of the spinal cord relative to the vertebral column during fetal development, we performed translumbar myelograms on 340 spontaneously aborted fetuses. Of these, 146 were selected for study. There were 76 males and 70 females, with fetal age ranging from 7 to 33 weeks. Significant variation in the level of spinal cord termination was found in fetuses between 12 and 25 weeks gestational age. In fetuses between 25 and 33 weeks gestational age, the cord ended at or above the third lumbar vertebra.

Embryonic and Fetal Development↗
PubMed1998

Human TIMP-3 is expressed during fetal development, hair growth cycle, and cancer progression.

We studied the expression and regulation of TIMP-3, a recently cloned member of the tissue inhibitor of the metalloproteinase family, during human fetal development and in various human tissues, with emphasis on epithelial structures. Expression of TIMP-3 mRNA was detected by in situ hybridization in developing bone, kidney, and various mesenchymal structures. At 16 weeks of gestation, ectoderm-derived cells of hair germs expressed TIMP-3 mRNA, and beginning from the twentieth week consistent expression was detected in epithelial outer root sheath cells of growing hair follicles. In normal adult human skin, expression of TIMP-3 mRNA was limited to hair follicles, starting at the early anagen (growing) phase and vanishing at the catagen (regressing) phase. TIMP-3 mRNA was not detected in benign hair follicle-derived tumors but was present in tumor cells of infiltrative basal cell carcinomas and in surrounding stromal cells in squamous cell carcinomas. Human primary keratinocytes in culture expressed TIMP-3 mRNAs, the levels of which were upregulated by transforming growth factor-beta (TGF-beta), whereas interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) had no effect. Our results suggest a role for TIMP-3 in connective tissue remodeling during fetal development, hair growth cycle, and cancer progression.

Adult↗
PubMed2006

Genes regulating implantation and fetal development: a focus on mouse knockout models.

Timely and efficient regulation of blastocyst implantation and fetal growth are essential for the successful reproduction of viviparous mammals. Disruptions in this regulation can result in a wide variety of human gestational complications including infertility, spontaneous abortion, fetal growth restriction, and premature delivery. The role of several groups of factors, including cytokines, hormones, transcription factors, extra-cellular proteinases, and angiogenic factors has been suggested in both implantation and regulation of fetal growth. Due to the inherent difficulties of studying implantation and fetal development in humans, much of our knowledge of the genes involved in these processes has been derived from animal models. The critical genetic loci involved in blastocyst implantation and fetal growth will be discussed with a focus on those genes with available mouse knockout models.

Animals↗
PubMed1987

Effects of chronic cadmium administration on placental and fetal development.

Cadmium was administered subcutaneously to pregnant Wistar rats: 0.49 mg/kg as CdCl2 in saline daily, starting at the day of conception. Placentas and fetal livers were collected on day 14, 16, 18, 19 and 20 of gestation. Livers and thymuses from the newborns were collected 5 hours after delivery (day 22) and 1, 2 and 5 weeks after delivery. In these tissues concentrations of cadmium and zinc were determined by solid sampling ETA-AAS. Furthermore, the effect of cadmium administration on the glycogen content of the trophoblastic labyrinth and the fetal liver was studied. The concentration of cadmium in the placenta increased with time of exposure, indicating accumulation of cadmium in this organ. In the fetal liver, cadmium was present in a very low concentration, which slightly increased with longer exposure. The concentration of zinc in the placenta tends to decrease between day 14 and day 20. This decrease was observed both in control and in cadmium-exposed animals. Zinc levels increased in fetal livers from control dams, whereas this rise was markedly reduced in fetuses from cadmium-exposed animals. Placentas from cadmium-exposed animals had a changed glycogen pattern as compared to the controls, namely higher glycogen contents of the labyrinth at the end of pregnancy. However, notwithstanding lower zinc levels in the fetus and changed glycogen deposition in the placenta, it is not quite clear whether cadmium affects fetal development. No changes were observed in fetal weights or birthweights, nor in glycogen deposition of the fetal liver. Indications were obtained for reduced neonatal thymic weights.

Animals↗
PubMed1993

Pure FSH alone induces ovulation and subsequent pregnancy in the mouse resulting in fetal development.

The role of FSH in inducing folliculogenesis is well established. Recently, the availability of pure FSH has led to a reevaluation of its role in the process of ovulation. Previously, these functions have been examined separately, usually with pregnant mares' serum gonadotropin (PMSG) followed by FSH for ovulation or FSH for folliculogenesis followed by hCG for ovulation. To determine if FSH alone can induce both folliculogenesis, ovulation and establish a functioning corpus luteum without exogenous LH, we injected sexually mature intact mice (CD-1) with either ovine FSH (oFSH, 5 micrograms; < 0.2% LH contamination) or recombinant FSH (RCFSH, 1 IU; devoid of any LH activity) to stimulate folliculogenesis, followed forty-eight hours later by a second injection of the same preparation (oFSH, 15 micrograms; RCFSH, 1 IU, respectively) to induce ovulation. Injected female mice were mated individually with a fertile male. On days 15-17, pregnancy rates and fetal development were obtained for each animal and were compared with controls, mice injected with PMSG (1 IU) followed by hCG (1 IU). oFSH/oFSH and RCFSH/RCFSH results were combined since no statistical significant differences were detected between these groups. The pregnancy rate for the group receiving FSH/FSH (78.3%, n = 23) was higher than that of the PMSG/hCG group (48.3%, n = 27; p = .02). The number of fetuses produced per mouse in animals receiving FSH alone (8.5 +/- 1.1; mean +/- S.E.) also was greater than the controls (4.5 +/- 99; p = .01). We conclude that the ability of these animals to proceed beyond ovulation to implantation with fetal development demonstrates FSH's ability to cause not only follicular maturation and rupture, but also granulosa cell luteinization, further identifying the potentially important role of FSH in the ovulatory process.

Animals↗
PubMedDate not supplied

[Morphologic features of immune interrelationships in the feto-placental system in development of a large fetus and in retardation of intrauterine fetal development].

Indirect criteria of the value of the immune placenta barrier in case of a large foetus are distinguished: relatively small volume of the fibrinoid substance, moderate synthesis by the syncytial epithelium of glucosaminoproteoglycans (GAPG), slight lymphoplasma cell infiltrates with a marked suppressor influence, the lack of antigens HLA = Dr on the trophoblast and formation of the adequate interrelation ship between the immune dependent placental structure and the thymus of the large foetus this allowing to retain the foetus up to 38-40 weeks or even more. In case of delay in the intrauterine foetus development there is a sharp increase of the fibrinoid substance, focal enhancement of GAPG production by the syncytial cells, decrease of the suppressor activity and the appearance in some cases in the trophoblast of antigens to HLA=Dr this being probably the manifestation of a premature exhaustion of compensatory-adaptive reactions in the placenta.

Chorionic Villi Sampling↗
PubMed1989

5 alpha-reductase, aromatase, and androgen receptor levels in the monkey brain during fetal development.

To elucidate the metabolic fate and possible role of androgens and their derivatives during primate fetal development, aromatase (AROM), 5 alpha-reductase (5 alpha R), and androgen receptor (AR; cytosolic) levels were assessed in the brain, heart (HRT), lung (LNG), and skeletal muscle (MUS) of fetal rhesus monkeys. Analyses were performed on tissues taken on days 100 and 160 postconception. Five male and four or five female fetuses were examined at each stage. Brain tissues analyzed included medial basal hypothalamus (MBH), amygdala (AMG), cerebellum (CB), corpus callosum (CAL; splenial region), cerebral cortex (CTX), and cingulate cortex (CNG). In the following, enzyme activities are reported as picomoles per mg protein/h, while receptor levels are femtomoles per mg protein. 5 alpha R activity was measurable in all tissues. Analysis of variance revealed significant tissue differences [P less than 0.001, combined stages and sexes; CAL (2.05) greater than MBH (1.08) greater than AMG (0.63) greater than CB (0.4)-CNG-CTX-LNG-HRT-MUS (0.02); -indicates not significantly different]. A significant age x tissue interaction (P less than 0.001) was noted which could be explained by higher MBH and CAL levels in older vs. younger fetuses and higher AMG levels in younger vs. older fetuses. There was also a significant sex x tissue interaction which was attributed to higher female values in the MBH and CAL. AROM activity was detected in all tissues. Levels varied significantly among tissues [P less than 0.001, combined stages and sexes; MBH (0.80)-AMG (0.76) greater than CAL (0.4)-CNG-CB-CTX-LNG-HRT-MUS (0.07)]. Significant age (P less than 0.001) and age x tissue (P less than 0.001) effects were noted, which were due to higher MBH and AMG levels in younger vs. older fetuses. No sex difference in AROM levels was evident in any tissue. AR was measurable in all cases. Although stage and sex differences were not significant, tissue levels varied significantly [P less than 0.001; LNG (2.8)-MUS (2.6)-MBH (2.2) greater than HRT-AMG-CB-CTX-CAL-CNG (0.9)]. These findings indicate that neural and nonneural fetal primate tissues have the potential for transforming androgens to products that could have greater or lesser biological activity. AR were also noted through which dihydrotestosterone or testosterone could effect a genomic response. Since stage, tissue, and sex differences were evident in neural tissues, metabolic and receptor activities may be important for the normal differentiation of sexually dimorphic behavioral systems in monkeys as well as for potential teratogenic changes under abnormal metabolic or physiological conditions.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗