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PubMed1995

Consecutive appearance of coagulation factor XIII subunit A in macrophages, megakaryocytes, and liver cells during early human development.

Thirty embryonic and fetal samples were investigated to study the appearance and characteristics of factor XIII subunit A (FXIIIA)-containing cells in the course of human development. Samples were either vacuum-embedded in paraffin for staining FXIIIA by a sensitive biotin-streptavidin system or snap-frozen for double-labeling studies to characterize FXIIIA-containing cells. FXIIIA appeared as early as the fifth gestational week in yolk sac samples in stellate-shaped cells. Nonparenchymal cells in liver samples showed intense labeling for FXIIIA from the sixth week of gestation. The relative amount of FXIIIA-containing cells rapidly diminished up to the 13th gestational week. When characterized, the majority of these cells proved to be KiM7-positive macrophages, while GPIb (CD42b)-labeled cells accounted for less than 10% of FXIIIA-positive cells. Liver cells did not show any staining for FXIIIA in first trimester samples. The earliest liver specimen showing FXIIIA was at the 20th week, when FXIIIA appeared in some liver cells, particularly in those surrounding the central veins. In bone marrow smears, FXIIIA-positive cells started to appear at week 10 in the clavicles and increased in number in subsequent stages of development. Intracellular FXIIIA was distributed between GPIb-, RFD7-, and KiM7-positive cells. The results indicate that, apart from liver cells, at least three different cell populations (KiM7+ RFD7+ GPIb-, KiM7- RFD7- GPIb-, and KiM7- RFD7- GPIb+) contain FXIIIA in the early phase of human development. We conclude that FXIIIA appears very early during human development and is detectable in both extra- and intraembryonic hematopoietic organs. Intracellular FXIIIA in early human development is distributed between different macrophages and megakaryocytes, and by week 20, it appears in liver cells as well.

Antigens, Differentiation↗
PubMed1990

Prenatal development of the human nucleus ambiguus during the embryonic and early fetal periods.

The ontogenetic development of the nucleus ambiguus was studied in a series of human embryos and fetuses ranging from 3 to 12.5 weeks of menstrual age (4 to 66 mm crown-rump length). They were prepared by Nissl and silver methods. Nucleus ambiguus neuroblasts, whose neurites extend towards and into the IXth and rostral Xth nerve roots, appear in the medial motor column of 4-6-week-old embryos (4.25-11 mm). These cells then migrate laterally (6.5 weeks, 14 mm) to a position near the dorsal motor nucleus of X. At 7 weeks (15 mm), nucleus ambiguus cells begin their migration, which progresses rostrocaudally, into their definitive ventrolateral position. The basic pattern of organization of the nucleus is established in its rostral region at 8 weeks (22.2-24 mm) and extends into its caudal region by 9 weeks (32 mm), when its nearly adult organization is evident. Cells having the characteristics of mature neurons first appear rostrally in the nucleus during the 8.5-9-week period (24.5-32 mm), gradually increase in number, and constitute the entire nucleus at 12.5 weeks (65.5 mm). Definitive neuronal subgroups first appear at 10 weeks (37.5 mm) in the large rostral nuclear region. These features suggest that the human nucleus ambiguus develops along a rostrocaudal temporospatial gradient. Evidence indicates that function of nucleus ambiguus neurons, manifested by fetal reflex swallowing, occurs after the cells migrate into their definitive position, establish the definitive nuclear pattern, and exhibit mature characteristics.

Accessory Nerve↗
PubMed1991

Myoblasts, myosins, MyoDs, and the diversification of muscle fibers.

Distinct types of muscle fibers form and become innervated by appropriate motor neurons during development. Though the activity pattern of the innervating motor neuron affects fiber type in the adult, it is now clear that innervation is not required for the initial formation of fast and slow muscle fibers during embryonic and fetal development. In addition, multiple types of intrinsically different myoblasts are found at different stages of development and motor neurons may preferentially innervate specific types of muscle fibers at relatively early stages of myogenesis. Thus, at least some of the information required for the formation of specific motor units must be carried by muscle cells. Cellular and molecular analyses of the multiple types of myoblasts, myosin heavy chain isoforms, and myogenesis regulating proteins of the MyoD family are leading to a new understanding of the events that choreograph the formation of fast and slow motor units.

Animals↗
PubMedDate not supplied

Proto-oncogene c-fos expression in growth regions of fetal bone and mesodermal web tissue.

The phylogenic conservation of the proto-oncogene c-fos suggests that this gene product is required for normal metabolic processes. Investigations into the transcription pattern of c-fos in normal tissues and cells have revealed expression during development, differentiation and growth which is dependent to a large extent on external signals transferred by growth factors. The complex pattern of stage and tissue-specific expression has raised the hypothesis that the c-fos gene product might function in the control of either proliferation or differentiation. However, no detailed analysis is yet available concerning the normal expression of c-fos during embryonic and fetal development. Interestingly, recent data derived from studies in transgenic mice reveal that the biological effect of overexpression of exogenous fos is restricted to the developing bone tissue and T-cell development of the mice, perhaps signifying that these cells represent a physiological target tissue of the proto-oncogene fos. Thus, to gain deeper insight into the functional role of the c-fos gene product during physiological processes, it is a requirement to carry out a detailed analysis of the localization and cell-type specificity of c-fos expression in normal mouse embryos. Using the technique of in situ hybridization, we demonstrate here that stage-specific expression of the proto-oncogene c-fos in mouse embryos is restricted to the perichondrial growth regions of the cartilaginous skeleton. Moreover, we found strong c-fos transcription in web-forming mesodermal cells, which are also characterized by a stage-specific high growth capacity. Our results suggest a tissue-specific regulatory role of c-fos during differentiation-dependent growth processes of fetal bone and mesodermal web tissue.

Animals↗
PubMed1988

An immunoassay to detect human embryonic epsilon globin chains by a murine monoclonal antibody.

Human embryonic epsilon globin chains were isolated from lysates of cultured human leukemic K562 cells induced with hemin. Mice were immunized with epsilon globin chains, and a murine hybridoma cell line was established that secreted monoclonal anti-epsilon globin antibody. A sensitive and specific slot blot immunoassay for epsilon globin chains has been developed. epsilon Globin chains were shown to be present in hemolysates from fetuses of 20 weeks' gestation but were not detected in normal cord blood hemolysates. This immunoassay is useful for the study of epsilon globin ontogeny during embryonic and fetal development as well as for searching for inappropriate epsilon globin chain expression in hematologic disorders resulting from genetic abnormalities or neoplastic processes.

Animals↗
PubMed1979

Embryotoxicity of inhaled benzene in mice and rabbits.

The effect of inhaled benzene on embryonal and fetal development was assessed in mice and rabbits. CF-1 mice and New Zealand white rabbits were exposed to 0 or 500 ppm of benzene for 7 hr per day from days 6 through 15 (mice) and 6 through 18 (rabbits) of gestation. Little evidence of maternal toxicity was seen in either species. Although some signs of embryonal toxicity were observed in both mice and rabbits, a teratogenic effect was not discerned in either species inhaling 500 ppm of benzene.

Aerosols↗
PubMed1996

Fetal brain sparing is associated with accelerated shortening of visual evoked potential latencies during early infancy.

OBJECTIVE: Our purpose was to assess the effects that fetal growth restriction exerts on the myelination of the developing brain. STUDY DESIGN: Fetal haemodynamic centralization, an adaptive strategy to growth restriction caused by placental insufficiency, was determined by Doppler ultrasonography. Infants with a raised ratio between umbilical artery pulsatility index and cerebral artery pulsatility index are severely growth restricted. Visual evoked potentials give information on the degree of brain myelination. Shortening of visual evoked potential latencies is a normal feature of myelination. In a consecutive series of 105 Neonates, visual evoked potentials were recorded at the corrected ages of 6 months and 1 years. Correction for possible confounders, such as cranial ultrasonographic findings, gestational age, and head circumference, was performed. RESULTS: At 6 months, infants with a raised umbilical artery/cerebral artery pulsatility index ratio have shorter visual evoked potential latencies. Opposite of neonates with a normal umbilical artery/cerebral artery ratio, they show no postnatal maturational shortening of visual evoked potential latencies. CONCLUSION: Accelerated neurophysiologic maturation, found in infants with a high umbilical artery/cerebral artery ratio, might be the result of a beneficial adaptive process to severe fetal growth restriction.

Brain↗
PubMed1996

[Effect of fetal and neonatal growth on the occurrence of some diseases in adults].

The findings of many authors show that reduced fetal growth is followed by increased mortality from cardiovascular disease in adult life. They are further evidence that cardiovascular disease originates, among other risk factors, through programming of the bodies structure and metabolism during fetal and early post-natal life. Wrong maternal nutrition may have an important influence on programming.

Adult↗
PubMed1991

Developmental regulation of gap junction gene expression during mouse embryonic development.

The expression of products from three different gap junction genes (alpha 1, beta 1 and beta 2) was studied in pre- and postimplantation mouse embryos, during organogenesis, during differentiation of F9 teratocarcinoma cells, and in cultured embryonic stem (ES) cells. In this analysis, the following results were obtained. 1) Pre- and postimplantation mouse embryos. The alpha 1 transcript was the earliest gap junction RNA detected (in the 4 cell stage embryo) and its abundance increased significantly throughout subsequent development. 2) Organogenesis. Evidence was obtained for developmental expression of these three different gap junction genes during early embryogenesis and throughout the late stages of organogenesis. The expression patterns for these genes may be related to differences in gap junctional communication requirements for fetal organ development versus neonatal and adult organ function, or the utilization of different genes by different cell types during organogenesis. 3) During the differentiation of F9 cells in culture, expression of these three genes was modulated. Thus, this is the first evidence for modulation of gap junction gene expression during the differentiation of a single cell type in culture. 4) In an ES cell culture line, alpha 1 was the only gap junction gene product detected. This is consistent with the findings of alpha 1 expression in the embryonic inner cell mass region and in undifferentiated teratocarcinoma cells.

Amino Acid Sequence↗
PubMed2000

The fetal lung. 1: Developmental aspects.

A literature survey is presented on normal fetal development during the embryonic, pseudoglandular, canalicular, saccular and alveolar stages in the human fetus. Normal anatomical and physiological aspects of fetal lung development including the fetal pulmonary circulation are described. Factors which may influence fetal lung growth and consequently may play a role in the development of pulmonary hypoplasia are discussed, such as intrauterine and intrathoracic space, lung fluid, fetal breathing movements, normal balance of volume and pressure in the lung and interference with the blood supply.

Body Fluids↗
PubMed2001

Stress and mood disorders during pregnancy: implications for child development.

Recent research suggests that stress, anxiety, and depression during pregnancy may have an impact on how the child develops. In this article, the central literature supporting this hypothesis is reviewed. Next, studies from our laboratory showing that differences in fetal heart rate patterns are associated with women's anxiety and depressive symptomatology are reviewed. The data indicate that we can detect fetal markers associated with alterations in women's mood that also are linked to differences in the neurobiological substrate of the fetus' emerging emotion regulation system. Identifying such fetal characteristics someday may contribute to the early detection and prevention of predispositions to childhood risk for emotional problems and even psychopathology.

Child↗
PubMed1985

Toxic effects of chemicals on mouse post-blastocyst development--a trial to establish a testing system for embryotoxicity.

We established a new testing system to assess embryotoxic chemicals using cultured preimplantation mouse embryos. Randomly bred Crj:CD-1 (ICR) mice were used. Late blastocysts collected on Day 4 of pregnancy (plug day:Day 1) were exposed for 24 hrs. to various chemicals at varying concentrations. Morphological embryonic development, structural chromosome aberrations and sister chromatid exchanges (SCEs) were examined as the parameters of embryotoxicity. Treated embryos were then transferred to pseudopregnant foster mice for the evaluation of in vivo development. Of the morphological developmental endpoints in vitro, the formation of two-layer ICMs (inner cell masses) was the most sensitive to the toxicity of chemicals, followed by ICMs and trophoblast outgrowth. Threshold limit values were confirmed regarding morphological growth. However, exposure of embryos to lower concentrations than threshold enhanced the frequency of chromosome aberrations and SCEs. Transfer of embryos treated with the lower concentration of 4-nitroquinoline 1-oxide induced not only fetal wastage but also developmental retardation. 4-nitroquinoline 1-oxide was the most embryotoxic in mouse blastocysts, followed in order by mitomycin C, bleomycin, methylmercuric chloride, diethylstilbestrol, mercuric chloride and ochratoxin-A. This new testing system appears to be a sensitive method of measuring the direct effects of toxic chemicals which yields results in a short term.

4-Nitroquinoline-1-oxide↗