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PubMed2006

[Health-related problems in adopted children].

International research shows that the standard of health among children adopted from abroad, especially those adopted by single parents, is not as good as that of other children. Danish studies indicate similar problems. The causes could be several, such as poor development in the embryonic and fetal stages, low birth weight, starvation, neglect, infections, and the lack of the natural bonds between mother and child. Surveys indicate that many adoptive parents, single parents in particular, receive children with health problems. There is no Danish research available, but it is important to be aware of these issues in order for both adoptees and adoptants to receive the most support.

Adoption↗
PubMed1982

[Embryotoxic and teratogenic effect of Pharmachem tetramisole].

Studies were carried out to establish the effect of high rates of Tetramizol Pharmachim on the embryonal and fetal development in rats. The preparation was administered orally to pregnant animals under the form of a 1 per cent solution at the rate of 1/5 LD50 (=200 mg/kg), on the fourth and the thirteenth day of gestation. It was found that the amount of the preparation applied on the fourth day after conception took place led to rise of the preimplantation loss of embryos. The rate of the total embryonal mortality also rose. Accordingly, it was concluded that in high doses Tetramizol Pharmachim could produce an embryotoxic effect on rats. The application of the preparation later during pregnacy (the 13th day) did not have an adverse effect on the normal course of gestation. No abnormal effects were demonstrated on the growth and development of fetuses during all stages of investigation, which might point to the teratogenic action of Tetramizol.

Animals↗
PubMed2005

The role of oxygen tension in the regulation of embryonic lung development.

BACKGROUND/PURPOSE: Oxygen tension is an important physiologic mediator of embryonic and fetal development. In vitro studies have demonstrated that the proper embryonic development is dependent upon low oxygen tension and even short exposure to normoxic environments (21%) can be detrimental to embryonic development. We hypothesized that low oxygen tension promotes lung growth in embryonic organ culture and therefore designed this study to investigate embryonic lung growth in normoxic and hypoxic conditions using simple closed chamber. METHODS: Fetal rat lungs were harvested on day 13.5 and placed in organ culture containing serum-free Dulbecco's modified Eagle's medium with antibiotics. The lung cultures were divided into normoxic group, with a 21% oxygen concentration (n = 15), and hypoxic group (n = 15). Hypoxic condition (6% oxygen) was achieved using Oxoid Campygen in a closed chamber. The lungs were placed in 5% carbon dioxide, 37 degrees C incubator for 48 hours. Media were not changed during the incubation period. The morphometric analysis was measured at 0 hour and at 48 hours by counting total terminal buds and entire epithelial contour using Image J software. The fold increase in branching was calculated as the ratio of buds present at 48 hours minus the buds present at 0 hour divided by the number of buds at 0 hour. The increase in entire epithelial contour over 48 hours was calculated in exactly the same way as described above. RESULTS: There was no significant difference in the increase in total terminal buds count in the hypoxic group (2.06 +/- 0.19) compared with the normoxic group (2.59 +/- 0.21), and no significant difference in the increase in entire epithelial contour in the hypoxic group (1.45 +/- 0.11) compared with the normoxic group (1.63 +/- 0.11). CONCLUSIONS: Although hypoxia has been reported to be an important regulator of murine vascular development, our data show that the embryonic lung growth in whole lung organ culture under hypoxic condition is not significantly different from that in normoxic condition.

Animals↗
PubMed1992

What is the role of growth hormone and related peptides in implantation and the development of the embryo and fetus.

The role of growth hormone (GH) and the related placental lactogens in implantation and subsequent embryonic and fetal development is an enigma. Firstly, these peptides are abundant in both the fetal and maternal circulation. The variant growth hormone (hGH-V) is expressed by the placental syncytiotrophoblast and is released into the maternal circulation. It is not detectable in fetal blood. Fetal pituitary (GH) is abundant but is not a primary stimulus to human fetal musculoskeletal growth, since hypopituitary newborn infants have near-normal birth size. However, pituitary hGH has been shown to stimulate pancreatic islet growth and insulin release in vitro, and to be a mitogen for fetal hepatocytes obtained in late first trimester. This selectivity of action is confirmed by the immunohistochemical localization of hGH receptor in the human fetal kidney, endocrine pancreas, liver, skin and brain during the first and second trimester, and their absence from the musculoskeletal system, gut and lung. High-affinity human placental lactogen (hPL) receptors are abundant in animal and human fetal tissues, and hPL can attain concentrations of 10 nM in the human fetal circulation. In vitro data strongly suggest anabolic and mitogenic actions for PL on fetal tissues, including amino acid transport, hepatic glycogenesis, protein synthesis, and stimulation of insulin-like growth factor and insulin release. The PL axis in the fetus is influenced by maternal nutrition. Despite these findings, definitive evidence is still lacking that PL contributes to fetal growth and development in utero.

Embryo Implantation↗
PubMed1998

Comparison of lectin binding patterns in malformed and normal human embryos and fetuses.

Altered glycosylation in the course of disease detectable by changes in lectin binding patterns has been well established for adult tissues, but only a few authors have described carbohydrate entities during normal human embryonic and fetal development. Whether alterations in carbohydrate patterns occur in human embryonic and fetal tissues, affected by malformations, remains to be investigated. We, therefore, examined human embryos and fetuses at corresponding developmental stages with and without malformations (spina bifida, exencephaly, cleft lip and cleft palate, and dysmelia) with respect to their lectin binding patterns for the lectins RCA I, PNA, WGA, SBA, SNA, Con A, and LTA. Our results demonstrated that during the development of malformations, the affected tissue sites exhibited a different carbohydrate pattern from normally developed specimens. Furthermore, tissues known to be sites of secondary malformation, accompanying the primary defect, although displaying a histologically normal appearance, also showed an altered carbohydrate pattern. This might indicate a possible general alteration in the carbohydrate pattern in the course of development of malformations in man.

Binding Sites↗
PubMed1993

Expression of the developmental I antigen by a cloned human cDNA encoding a member of a beta-1,6-N-acetylglucosaminyltransferase gene family.

The blood group i/I antigens were the first identified alloantigens that display a dramatic change during human development. The i and I antigens are determined by linear and branched poly-N-acetyllactosaminoglycans, respectively. In human erythrocytes during embryonic development, the fetal (i) antigen is replaced by the adult (I) antigen as a result of the appearance of a beta-1,6-N-acetylglucosaminyltransferase, the I-branching enzyme. Here, we report the cDNA cloning and expression of this branching enzyme that converts linear into branched poly-N-acetyllactosaminoglycans, thus introducing the I antigen in transfected cells. The cDNA sequence predicts a protein with type II membrane topology as has been found for all other mammalian glycosyltransferases cloned to date. The Chinese hamster ovary cells that stably express the isolated cDNA acquire I-branched structures as evidenced by the structural analysis of glycopeptides from these cells. Comparison of the amino acid sequence with those of other glycosyltransferases revealed that this I-branching enzyme and another beta-1,6-N-acetylglucosaminyltransferase that forms a branch in O-glycans are strongly homologous in the center of their putative catalytic domains. Moreover, the genes encoding these two beta-1,6-N-acetylglucosaminyltransferases were found to be located at the same locus on chromosome 9, band q21. These results indicate that the I-branching enzyme represents a member of a beta-1,6-N-acetylglucosaminyltransferase gene family of which expression is controlled by developmental programs.

Adult↗
PubMed1998

Epigenetic toxicology as toxicant-induced changes in intracellular signalling leading to altered gap junctional intercellular communication.

Communication mechanisms [extra-, intra-, and gap junctional inter-cellular communication (GJIC)] control, from the fertilized egg, through embryogenesis to maturity and aging, whether a cell proliferates, differentiates, dies by apoptosis, or if differentiated, adaptively responds to endogenous and exogenous signals. From the egg to the 100 trillion cells in the human body, health is maintained when these communication processes between stem, progenitor and terminally differentiated cells are integrated. Each cell choice involves 'epigenetic' mechanisms to alter the expression of genes at the transcriptional, translational or post-translational levels. Disruption of the communication mechanisms can be either adaptive or maladaptive. Modulation of extra-cellular communication, either by genetic imbalances of growth factors, hormones or neurotransmitters or by environmental, exogenous chemicals can trigger signal transducing intra-cellular mechanisms. These intra-cellular signals can modulate gene expression at the transcriptional, translational or post-translational levels while also modulating GJIC. Untimely or chronic disruption of GJIC during embryonic or fetal development could lead to embryonic lethality or teratogenesis. By modulation of GJIC, homeostatic control of cell growth, differentiation or apoptosis could lead to specific diseases, such as neurological, cardiovascular, reproductive or endocrinological dysfunction. Chemical modulation or oncogene down-regulation of GJIC in initiated tissues has been shown to lead to tumor promotion. Genetic syndromes carrying a mutated gap junction gene, together with some transgenic and knock-out gap junction gene mice, provide evidence for the importance of this organelle found only in metazoans. Implications for 'thresholds' to toxicants and for risk assessment are evident.

Animals↗
PubMed1987

Molecular approaches to developmental genetics and pathology.

New insights into gene structure and expression and the observation that homeobox-containing genes, the t-complex, and oncogenes are expressed also in humans contribute to the understanding of normal and pathobiological mechanisms of embryonal and fetal development.

Animals↗
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↗
PubMed1993

Effects of low-frequency magnetic fields on fetal development in rats.

We studied effects of alternating magnetic fields on the embryonic and fetal development of rats. Mated females of the Han:Wistar-strain were sham exposed or exposed continuously to a 50-Hz field or to a 20,000 pulse-per-second (pps) sawtooth magnetic field from day 0 to day 20 of pregnancy for 24 h/day until necropsied on day 20. The respective peak-to-peak intensities of the fields were 35.6 microT (sinewave) and 15.0 microT (sawtooth). Each treatment group contained 72 bred females. Control animals were kept under the same conditions without the magnetic field. No adverse effects were seen in the dams. The mean numbers of implantations and living fetuses per litter were statistically significantly increased in the 50-Hz group. There were, however, three total resorptions of litters in dams of the control group, which contributed to the difference in the number of living fetuses. The corrected body-mass gains (gains without uterine content) of dams were similar in all groups. Pregnancy rates, incidences of resorptions, late fetal deaths, and fetal body masses were similar in all groups. The incidence of fetuses with minor skeletal anomalies was statistically significantly increased in both exposed groups. Only one serious malformation (anophthalmia, sawtooth-exposed group) and a few minor visceral malformations were found. In conclusion, the magnetic fields used in this study did not increase the incidence of major malformations or resorptions in Wistar rats. The increased number of skeletal anomalies and implantations we observed indicates, however, that some developmental effects in rats may attend exposure to time-varying magnetic fields.

Abnormalities, Radiation-Induced↗
PubMed1998

Effect of copper deficiency on prenatal development and pregnancy outcome.

Copper deficiency during embryonic and fetal development can result in numerous gross structural and biochemical abnormalities. Such a deficiency can arise through a variety of mechanisms, including low maternal dietary copper intake, disease-induced or drug-induced changes in maternal and conceptus copper metabolism, or both. These issues are discussed in this article along with the use of in vitro embryo culture models to study the mechanisms underlying copper deficiency-induced teratogenesis. Current data suggest that changes in free radical defense mechanisms, connective tissue metabolism, and energy production can all contribute to the dysmorphogenesis associated with developmental copper deficiency.

Animals↗
PubMed2002

[Genetic view of the development of the human embryo--the importance of chromosome abnormalities].

Normal embryonic and fetal development requires a diploid chromosome set consisting of a haploid maternal and a haploid paternal chromosome set. Chromosome abnormalities in the zygote are not a rare event, however. Moreover postzygotically different types of aberrations can occur, with different effects on embryonic development. As a consequence embryonic development can be arrested at a very early stage. Other consequences are the impairment of the implantation rate, early spontaneous abortions and developmental abnormalities in newborn children. The results of the analysis of the chromosomal constitution of early embryos show the impact of specific chromosome abnormalities on embryonic development. Normal development on the basis of a normal chromosome set seems to be only one of several possible developments after fertilization.

Chromosome Aberrations↗
PubMed1999

Preimplantation access to maternal insulin and albumin increases fetal growth rate in mice.

Provision of the maternal factors, albumin and/or insulin to embryos in vitro restores preimplantation morphological development and cell proliferation to that seen in vivo. The hypothesis that the preimplantation effects of insulin or albumin would be reflected in increased fetal growth rate was examined. Two-cell embryos were cultured 48-50 h in medium supplemented with 0.17 micromol/l, 15 micromol/l albumin or 0.17 micromol/l insulin and the resultant blastocysts transferred to pseudopregnant recipients. Fetal and placental mass and skeletal development were determined at E19 or E20 (day 19 or 20 of embryonic development). Preimplantation access to insulin or albumin increased fetal growth by 4-6%. Combining insulin and albumin did not produce a further increment in fetal growth. The fetal growth achieved by providing preimplantation access to insulin, albumin or both was equivalent to that of in-vivo developed blastocysts. The conclusions are that: (i) preimplantation access to maternal insulin and albumin is required for normal fetal growth rates in the mouse and (ii) the increments in inner cell mass cell number and metabolic rates induced by insulin (and possibly albumin) reflect a requirement for maternal growth factors during preimplantation stages to optimize fetal development.

Animals↗
PubMed1996

Primary structure and tissue distribution of FRZB, a novel protein related to Drosophila frizzled, suggest a role in skeletal morphogenesis.

Articular cartilage extracts were prepared to characterize protein fractions with in vivo chondrogenic activity (Chang, S., Hoang, B., Thomas, J. T., Vukicevic, S., Luyten, F. P., Ryba, N. J. P., Kozak, C. A., Reddi, A. H., and Moos, M. (1994) J. Biol. Chem. 269, 28227-28234). Trypsin digestion of highly purified chondrogenic protein fractions allowed the identification of several unique peptides by amino acid sequencing. We discovered a novel cDNA encoding a deduced 36-kDa protein by using degenerate oligonucleotide primers derived from a 30-residue peptide in reverse transcription polymerase chain reactions. Its N-terminal domain showed approximately 50% amino acid identity to the corresponding region of the Drosophila gene frizzled, which has been implicated in the specification of hair polarity during development. Hydropathy and structural analyses of the open reading frame revealed the presence of a signal peptide and a hydrophobic domain followed by multiple potential serine/threonine phosphorylation sites and a serine-rich C terminus. Cell fractionation studies of primary bovine articular chondrocytes and transfected COS cells suggested that the protein is membrane-associated. In situ hybridization and immunostaining of human embryonic sections demonstrated predominant expression surrounding the chondrifying bone primordia and subsequently in the chondrocytes of the epiphyses in a graded distribution that decreased toward the primary ossification center. Transcripts were present in the craniofacial structures but not in the vertebral bodies. Because it is expressed primarily in the cartilaginous cores of developing long bones during embryonic and fetal development (6-13 weeks) and is homologous to the polarity-determining gene frizzled, we believe that this gene, which we named frzb, is involved in morphogenesis of the mammalian skeleton.

Amino Acid Sequence↗
PubMed1996

Comparative investigations on water-soluble crystallins of the embryonic, fetal, and postnatal human lens during development and ageing.

To compare the crystallin composition of embryonic and fetal human lenses with those of postnatal and adult lenses, we investigated the crystallins of lenses of various ages (from the 5th gestational week to 55 years) by gel chromatography, isoelectric focusing, immunodiffusion, and immunoelectrophoresis. Age-related changes were calculated as relative percentages of the different classes and subclasses of crystallins. During prenatal lens development the percentages of both high- and low-molecular-weight alpha-crystallins as well as gamma-crystallins gradually increased, whereas the percentage of beta-crystallins decreased. A considerable change in crystallin composition was found immediately after birth: the relative percentage of beta-crystallins increased, whereas that of gamma-crystallins decreased. Gel-filtration analysis of crystallins from juvenile and adult lenses showed a high-molecular-weight peak, which was not found in extracts from fetal and new-born lenses.

Adolescent↗
PubMed1995

Studies on reproductive toxicity of iloprost in rats, rabbits and monkeys.

A reproduction toxicological test program was performed with the carbaprostacyclin derivative iloprost, an analogue to the endogenous prostacyclin PGI2, in order to detect possible effects on fertility and reproductive performance, on preimplantational, embryonal and fetal development, on delivery as well as on lactation and postpartum development. While in humans iloprost is administered as an i.v. infusion for 6 h/day, it was administered i.v. to rats, rabbits and monkeys by continuous infusion with a subcutaneously implanted pump. No influence on mating or reproductive parameters was found after treatment of male or female rats during the premating phase up to day 7 post coitum (p.c.). Embryonal and fetal development were not remarkably impaired in rabbits or monkeys after treatment throughout the period of organogenesis. The only remarkable observations in the embryotoxicity and peri-/postnatal studies in the rat were defects on the digits (reductions of phalangeal structures) in single individuals. These malformations were interpreted as resulting from a compound-related hypotonia with subsequent change in the regional blood flow and the consequence of temporary impairments of placental blood supply leading to hypoxia in the affected structures.

Animals↗
PubMed1998

Developmentally regulated expression of the novel cancer anti-apoptosis gene survivin in human and mouse differentiation.

Inhibitors of programmed cell death (apoptosis) may regulate tissue differentiation and aberrantly promote cell survival in neoplasia. A novel apoptosis inhibitor of the IAP gene family, designated survivin, was recently found in all of the most common human cancers but not in normal, terminally differentiated adult tissues. The expression of survivin in embryonic and fetal development was investigated. Immunohistochemistry and in situ hybridization studies demonstrated strong expression of survivin in several apoptosis-regulated fetal tissues, including the stem cell layer of stratified epithelia, endocrine pancreas, and thymic medulla, with a pattern that did not overlap with that of another apoptosis inhibitor, bcl-2. A sequence-specific antibody to survivin immunoblotted a single approximately 16.5-kd survivin band in human fetal lung, liver, heart, kidney, and gastrointestinal tract. In mouse embryo, prominent and nearly ubiquitous distribution of survivin was found at embryonic day (E)11.5, whereas at E15 to -21, survivin expression was restricted to the distal bronchiolar epithelium of the lung and neural-crest-derived cells, including dorsal root ganglion neurons, hypophysis, and the choroid plexus. These data suggest that expression of survivin in embryonic and fetal development may contribute to tissue homeostasis and differentiation independently of bcl-2. Aberrations of this developmental pathway may result in prominent re-expression of survivin in neoplasia and abnormally prolonged cell viability.

Animals↗