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PubMed1999

Expression of apoptosis in the developing human cephalic region during the embryonic and early fetal period.

The aim of our work was to study the expression of apoptosis in the cephalic region in human embryonic and fetal material. Twelve human embryos and fetuses were processed by routine histological technique and then studied using the Boehringer-Mannheim Company kit for TUNNEL technique. Rich appearance of apoptotic cells was typical for mesenchyme and for tissues of the mesenchymal origin. Dispersed or focal occurrence of apoptotic cells was described in nervous system and some orofacial structures during the embryonic period. During the early fetal period occurrence of apoptosis decreased and only rare apoptotic nuclei were visible in studied areas. Often they failed at all.

Apoptosis↗
PubMed1975

Human globin gene expression and linkage in bone marrow and fetal liver.

During embryonic development there is a transition from embryonic and fetal to adult beta-type globin chains. The high-molecular-weight RNA found in nuclei from embryonic and adult human erythropoietic tissues, fetal liver, and bone marrow, have been investigated for the presence of gamma(fetal)- and beta(adult)-globin messenger RNA sequences by molecular hybridization. Unlike alpha- and beta-globin mRNA sequences, gamma-globin mRNA sequences are absent from both total and high-molecular-weight nuclear RNA isolated from adult bone marrow. The amount of cytoplasmic gamma-globin mRNA is proportional to the level of gamma-chain synthesis, demonstrating that translational control is not a major control mechanism in the expression of globin genes. Since the gamma-, delta-, and beta-globin genes are known to be closely linked genetically, transcriptional control can discriminate between similar gene sequences that are spatially adjacent to one another.

Bone Marrow↗
PubMed1996

Competence of oocytes from the B6.YDOM sex-reversed female mouse for maturation, fertilization, and embryonic development in vitro.

When the Y chromosome of a Mus musculus domesticus mouse strain is placed onto the C57BL/6J (B6) inbred genetic background, the XY (B6.YDOM) progeny develop ovaries or ovotestes, but not normal testes, during fetal life. At puberty, while some of the hermaphroditic males become fertile, none of the XY sex-reversed females produce litters. We have previously demonstrated that the eggs ovulated from the B6.YDOM ovary undergo fertilization efficiently, but cannot develop beyond the 2-cell stage either in vivo or in vitro. In the present study, we collected oocytes directly from the XY ovary, and examined their maturation, fertilization, and embryonic development in vitro. The results show that the juvenile XY ovary yielded far more fertilizable oocytes by direct collection and in vitro maturation than through in vivo ovulation, but the majority of fertilized eggs failed to reach the blastocyst stage. Hence, developmental incompetence of oocytes in the XY ovary appears to be programmed during oocyte differentiation or growth. Nonetheless, in vitro matured oocytes showed a higher potential of embryonic development than the ovulated eggs, suggesting that fertility of the XY female may be impaired by multiple factors. We hypothesized that poor responsiveness of the XY ovary to gonadotropins, as we have previously demonstrated in testosterone production, may impair follicular development or proper recruitment of oocytes for ovulation. In the present study, we compared 125I-hCG binding in XX and XY ovaries, but did not find a significant difference. Hence, LH activity appears to be impaired after receptor binding in the XY ovary. On the other hand, the pattern of 125I-hCG binding indicated that the majority of antral follicles in the XY ovary failed to undergo normal preovulatory phases, which may explain the lower developmental capacity of eggs after ovulation.

Animals↗
PubMed1999

Maternal caffeine consumption during pregnancy does not affect preimplantation development but delays early postimplantation growth in rat embryos.

Models for studying prenatal drug-induced intrauterine growth retardation (IUGR) have, without exception, measured growth-related factors in the postimplantation embryo, fetus or neonate. Therefore, it is not known whether effects of drug exposure on growth and metabolism begin early in the preimplantation embryo, or whether IUGR is exclusively a postimplantation phenomenon. The present study investigates whether caffeine, a drug known to induce a dose-dependent fetal IUGR, affects embryo development before and/or after implantation or is exclusively a fetal phenomenon. Preimplantation embryo assessment (with treatment from Days 2 to 4 of pregnancy) included glucose utilization, cell number evaluation and stage of development (morula to hatched blastocyst); whereas, postimplantation embryo assessment (treatment from Days 2 to 10, 10.5 or 11 of pregnancy) included somite number evaluation and extent of neural tube closure, as seen using scanning electron microscopy. Comparing control preimplantation embryos with those exposed to 30 and 60 mg kg(-1) caffeine did not reveal any effects of caffeine exposure, as assessed on Day 5 of gestation. However, postimplantation embryo development assessed on Day 12 of gestation revealed that caffeine exposure of 15 and 30 mg kg(-1) significantly reduced, at both dosage levels, somite number and the extent of neural tube closure. In addition, comparisons of control and experimental groups revealed that in the high-dose caffeine group the forebrain cavity was significantly enlarged and bounded by a reduced, irregularly aligned neuroepithelium. The findings suggest that IUGR is a phenomenon first identifiable during late postimplantation embryogenesis and continues in fetal life.

Animals↗
PubMed1988

Effects of acute doses of ethanol administered at pre-implantation stages on fetal development in the mouse.

The objective of the present study was to investigate the effects of maternal administration of acute doses of alcohol at preimplantation stages of pregnancy on the fetus and fetal membranes. Single doses of 0.02 ml and 0.03 ml/g body wt. of 25% v/v of absolute alcohol in saline were administered to groups of MF1 mice on one of days 1-6 of gestation. Controls were either pair-fed and pair-watered or saline-treated. Fetuses and placentae were collected on day 15. Resorption and fetal death were increased in most of the alcohol treatment groups. The reduction in fetal body weight was significant in the 0.03 ml group. Compared to the saline controls, most experimental groups exhibited a rise in placental weight. The reduction in cord length was significant in comparison to untreated controls. Craniofacial and systemic abnormalities appeared to correlate with retardation of fetal growth. Hence, following treatment of 0.03 ml/g body wt. of alcohol solution on days 2 and 6, fetuses were collected on days 14, 16 and 18. Most fetuses were found to recover gradually from anomalies associated with growth retardation but the 'catch up' growth was not adequate enough to compensate for the reduction in body weight. These observations indicate that the pre-implantation stage of mouse embryo development is susceptible to the deleterious effects (fetal death and intrauterine growth retardation) of acute doses of alcohol.

Animals↗
PubMed1999

Cytokeratin 19 expression in human gastrointestinal mucosa during human prenatal development and in gastrointestinal tumours: relation to cell proliferation.

Cytokeratin (CK) immunohistochemistry revealed changes in the CK19 immunoreactivity in human gastrointestinal epithelium during embryonic and fetal development. These changes were particularly marked in the jejunum and ileum. CK19 immunoreactivity was strong up to the 11th week of pregnancy, but was absent between weeks 12 and 17, and reappeared weakly from week 18 to week 24. This temporal pattern correlated with that of cell proliferation investigated by immunohistochemical detection of proliferating cell nuclear antigen. Marked CK expression was associated with a low proliferative rate and vice versa. To test whether these results were relevant to the assessment of intestinal metaplasia and the risk of malignant transformation with poor cell differentiation, adenomas and adenocarcinomas of the colon, intestinal metaplasia of the stomach, and two types of gastric carcinoma were also examined by CK19 immunohistochemistry. Substantial CK19 immunoreactivity was found in well-differentiated cancers and low-grade dysplasias with low cell proliferation, whereas only weak CK19 immunoreactivity was found in poorly differentiated carcinomas and high-grade dysplasias with a high proliferation rate.

Adenocarcinoma↗
PubMed1986

The developmental program of fast myosin heavy chain expression in avian skeletal muscles.

We have examined the types of fast myosin heavy chains (MHCs) expressed in a number of different developing chicken skeletal muscles by combining peptide mapping and immunoblotting to identify fast MHC-specific peptides among the total mixture of MHC digestion products. Using this technique, we have identified three different fast MHC patterns among the different fast and mixed (i.e., fast and slow) fiber type muscles of the adult. While the different muscles all underwent sequential changes in fast MHC isoform expression during their development, the exact sequence of these changes and the isoform patterns expressed varied from muscle to muscle. During late embryonic or fetal development, all muscles expressed a similar fast MHC pattern (designated here as the fetal pattern) which was replaced shortly after hatching with a different fast MHC pattern (the neonatal pattern). During the transition from the neonatal to the adult state that occurred sometime in the first year after hatching, many of the muscles underwent additional changes in fast MHC isoform expression. In muscles such as the pectoralis major and pectoralis minor, a new fast MHC isoform pattern was seen in the adult so that the developmental program of isoform switching in these muscles involved the sequential appearance of distinct fetal, neonatal, and adult fast MHCs. Other muscles, such as the sartorius and posterior latissimus dorsi, underwent a qualitatively different program of isoform switching and expressed as an adult a fast MHC pattern that was indistinguishable from that expressed during fetal development. Finally, in some muscles, such as the superficial biceps, no change in isoform pattern was detected during the neonatal to adult transition--in these muscles, expression of the neonatal MHC isoform pattern apparently persisted into the adult state. These data indicate that no single scheme or program of fast MHC isoform switching can describe all the developmental changes that occur in fast MHC isoform expression in the chicken and that at least three different programs of isoform switching and expression can be identified.

Animals↗
PubMedDate not supplied

The effect of ethanol upon early development in mice and rats. XV. The late effect of chronic preconceptional and preimplantational consumption of beer and wine in rats.

The late effect upon fetal development of chronic preconceptional and preimplantational consumption of beer and wine was investigated in rats. Both beverages applied showed a noxious fetal effect, manifested by an increased number of resorptions and the partial retardation of skeletal development. The correlation of experimental blastopathy with late fetal effects is discussed.

Alcohol Drinking↗
PubMed1988

A retrospective study on the safety of prenatal ethanol treatment.

Present data on the harmful fetal effects of maternal alcohol use have seriously questioned the safety of ethanol treatment, as once prescribed for arresting premature uterine contractions. Therefore, we analyzed retrospectively the fate of infants whose mothers took ethanol for threatened first- or second-trimester abortion in 1968-1973. One hundred thirty-six patients were given an average of 38 g of ethanol (10-120 g) per day for two to 34 days, whereas 103 comparable patients received no ethanol treatment. The immediate and long-term effects on each woman's offspring were followed from birth to age 14. No infant had typical fetal alcohol effects. Fetal growth and the rates of fetal/neonatal deaths and anomalies were similar in both groups. Furthermore, there was no difference in postnatal growth and development. Thus, ethanol treatment as once prescribed for threatened abortion evidently did not cause fetal damage.

Abortion, Threatened↗
PubMed1984

Teratology and reproduction studies with triclopyr in the rat and rabbit.

Triclopyr (3,5,6-trichloro-2-pyridyloxyacetic acid), being developed as a new herbicide for use on brush and weeds, was evaluated for its potential effects on reproduction, and embryonal and fetal development. Pregnant Sprague-Dawley rats were given doses of 0, 50, 100, or 200 mg/kg/day by gavage on Days 6 through 15 of gestation. Dose-related signs of maternal toxicity were observed during the treatment period. No teratogenic effects were observed at any dose level, though slight fetotoxicity, possibly secondary to maternal toxicity, occurred at the high dose level (200 mg/kg/day). Pregnant New Zealand White rabbits were given doses of 0, 10, or 25 mg/kg/day by gavage on Days 6 through 18 of gestation which produced transient, dose-related decreases in maternal body weight gain. However, there were no indications of any treatment-related effects on fetal growth and development among rabbits. Male and female Sprague-Dawley rats maintained on diets supplying 0, 3, 10, or 30 mg/kg/day over three generations exhibited no consistent treatment-related effects on reproductive performance, pregnancy, parturition, or neonatal survival. These data indicated that triclopyr had little or no potential for teratogenic or reproductive toxicity even when the level of exposure approached that which elicited maternal toxicity.

Abnormalities, Drug-Induced↗
PubMed1989

The mouse Hox-1.4 gene: primary structure, evidence for promoter activity and expression during development.

This study reports the structure of the mouse homeobox-containing gene Hox-1.4 of the HOX-1 cluster, as well as its expression pattern during embryonic and fetal development. The overall structure of this gene includes two major exons, the second of which encodes the homeo-domain. The putative Hox-1.4 protein displays similarities with products of homologous genes located at the same relative positions in other HOX clusters. A fragment extending 360 base pairs (bp) upstream of a transcriptional start site was shown to be able to promote transcription in transfected cells. This fragment is GC-rich and contains binding sites for the Sp1 transcription factor. In situ hybridization studies revealed the Hox-1.4 expression pattern during development. As already reported for several other murine Hox genes, Hox-1.4 is expressed in the fetal central nervous system (CNS), in structures derived from somitic mesodermal condensations (sclerotomes, prevertebrae) as well as in several mesodermal components of various organs and structures such as lungs, gut, stomach, intestine and meso- and metanephros. This expression pattern is in good agreement with recent proposals concerning the involvement of such genes in the establishment of the vertebrate body plan as well as the relationship between the positions of these genes within their clusters and the anteroposterior restriction of their expression domains.

Amino Acid Sequence↗
PubMed1995

Apoptosis in the nervous system: morphological features, methods, pathology, and prevention.

For nearly 70 years apoptosis has been known to be a form of cell death distinct from necrosis as well as an important regressive event during the normal development of the nervous system. For example, in the chick, mouse, rat and human approximately 50% of postmitotic neurons die naturally during embryonic or fetal development. It is generally accepted that neurons die during this period by apoptosis. After the period of naturally occurring cell death, the surviving neurons may undergo degeneration and death due to injury or disease later either during development or in adulthood. Recently, apoptosis has been suggested to be involved in the abnormal neuronal death that occurs following axonal injury or in neurodegenerative diseases such as amyotrophic lateral sclerosis and Alzheimer's. Although little is known about the etiology of these diseases, progress is steadily being made toward understanding their underlying mechanisms. For diseases of spinal motoneurons, during the past two years gene mutations have been identified in patients with familial amyotrophic lateral sclerosis or spinal muscular atrophy. Furthermore, a number of in vitro, in vivo, and mutant animal models have been developed in order to study the factors which control motoneuron survival and/or death. Here, we review the morphological differences between necrotic and apoptotic cell death and some of the methods used to differentiate the two pathways. We also discuss motoneuron cell death during development, following injury and in disease, and its prevention by different agents, including neurotrophic factors.

Animals↗
PubMed1999

Restricted spatiotemporal expression of lactoferrin during murine embryonic development.

Lactoferrin is a member of the transferrin family of iron-binding glycoproteins. Lactoferrin is induced by estrogen in the mouse uterus during early pregnancy. However, the expression and function, if any, of lactoferrin in the preimplantation embryo during this developmental period has not been investigated. In the current study, the spatiotemporal expression of lactoferrin during murine embryogenesis was examined using in situ hybridization and immunohistochemical analyses. Lactoferrin expression was first detected in the 2-4 cell fertilized embryo and continued until the blastocyst stage of development. Interestingly, at the 16-cell stage, coinciding with the first major differentiation step in the embryo, lactoferrin messenger RNA (mRNA) is synthesized by the inner cells, whereas the protein is selectively taken up by the outside cells. This differential pattern of lactoferrin messenger RNA and protein localization continues until the blastocyst stage, with expression almost absent in the hatched blastocyst. Lactoferrin expression does not resume in the embryo until the latter half of gestation, where it is first detected in neutrophils of the fetal liver at embryonic day 11.5 and later in epithelial cells of the respiratory and digestive systems. Our results show that lactoferrin is expressed in a tightly regulated spatiotemporal manner during murine embryogenesis and suggest a novel paracrine role for this protein in the development of the trophoectodermal lineage during preimplantation development.

Animals↗
PubMed2006

Maternal dietary (n-3) fatty acid deficiency alters neurogenesis in the embryonic rat brain.

Docosahexaenoic acid [22:6(n-3)] is enriched in brain membrane phospholipids and essential for brain function. Neurogenesis during embryonic and fetal development requires synthesis of large amounts of membrane phospholipid. We determined whether dietary (n-3) fatty acid deficiency during gestation alters neurogenesis in the embryonic rat brain. Female rats were fed diets with 1.3% energy [(n-3) control] or 0.02% energy [(n-3) deficient], from alpha-linolenic acid [18:3(n-3)], beginning 2 wk before gestation. Morphometric analyses were performed on embryonic day 19 to measure the mean thickness of the neuroepithelial proliferative zones corresponding to the cerebral cortex (ventricular and subventricular zones) and dentate gyrus (primary dentate neuroepithelium), and the thickness of the cortical plate and sectional area of the dentate gyrus. Phospholipids and fatty acids were determined by HPLC and GLC. Docosahexaenoic acid was 55-65% lower and (n-6) docosapentaenoic acid [22:5(n-6)] was 150-225% higher in brain phospholipids at embryonic day 19 in the (n-3) deficient (n = 6 litters) than in the control (n = 5 litters) group. The mean thickness of the cortical plate and mean sectional area of the primordial dentate gyrus were 26 and 48% lower, respectively, and the mean thicknesses of the cortical ventricular zone and the primary dentate neuroepithelium were 110 and 70% higher, respectively, in the (n-3) deficient than in the control embryonic day 19 embryos. These studies demonstrate that (n-3) fatty acid deficiency alters neurogenesis in the embryonic rat brain, which could be explained by delay or inhibition of normal development.

Animals↗