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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↗
PubMed1993

A new mouse model for embryos with a hatching deficiency and its use to elucidate the mechanism of blastocyst hatching.

OBJECTIVE: To develop an experimental model for embryos with a defect specific to hatching, with the purpose of clarifying the mammalian embryo hatching mechanism. DESIGN: A microneedle was inserted under the zona pellucida (ZP) of mouse embryos, and either 1/2 or 1/4 of the blastomeres were mechanically destroyed. The remainder of embryos that developed into blastocysts were compared for hatching to controls wherein a microneedle was inserted and withdrawn without harming the embryo. Experiments were done to increase pressure within the perivitelline space to decrease the amount of ZP material to study the hatching mechanism. SETTING: University-based basic research laboratory. RESULTS: When 1/2 or 1/4 of the embryo was destroyed and the remaining cells developed into healthy blastocysts within the intact zona, hatching was significantly impaired, and zona thickness was markedly increased relative to controls. When a mineral oil droplet was inserted under the zona to enhance a possible mechanical component of hatching, manipulated embryos were not restored to normal hatching, and hatching of unmanipulated blastocysts was not improved. However, when the zona was circumferentially thinned by application of acid Tyrode's solution, the hatching defect in manipulated "3/4 embryos" was corrected. CONCLUSION: Because it is known that embryos with cells reduced by 1/2 or 1/4 have normal developmental potential, we conclude that the inability of such embryos to hatch from an intact zona constitutes a mouse model for a defect specific to hatching. Moreover, results from mineral oil droplet insertion and circumferential thinning of the zona indicate that normal hatching is accomplished predominantly, if not entirely, by zona lysis, not by pressure exerted against the zona by the expanding blastocyst.

Animals↗
PubMed1999

Blastomere development after embryo biopsy: a new model to predict embryo development and to select for transfer.

One of the most important and unsolved problems in in-vitro fertilization is to decide which embryos are more suitable to implant and therefore should be transferred. We analysed the in-vitro development of isolated biopsied blastomeres and compared it to the development of the original embryo, in order to find a relationship that could show the embryo's potential future development and so increase implantation rates. A total of 66 normally fertilized human embryos were biopsied at the 6- to 10-cell stages. At day 6, blastomeres were counted by nuclear labelling. A total of 33 embryos (50%) reached the blastocyst stage. Of the isolated blastomeres, 63% divided and 53% cavitated over 3 days in culture. Of the blastomeres taken from embryos that developed to the blastocyst stage, 88% divided, 79% cavitated, 76% divided and cavitated and 9% neither divided nor cavitated. In those from arrested embryos, 39% divided (P < 0.001), 21% cavitated (P < 0.001), 15% divided and cavitated (P < 0.001) and 55% neither divided nor cavitated (P < 0.001). Blastomeres biopsied from embryos that reached the blastocyst stage showed a significantly higher proportion of division and cavitation than those originated from arrested embryos. Culture of the isolated blastomeres can demonstrate those embryos more likely to develop to the blastocyst stage and that are probably more suitable to implant. Cryopreserving biopsed embryos and culturing blastomeres would increase implantation rates. Embryos can then be selected according to the blastomere development and thawed for transfer in a future cycle.

Biopsy↗
PubMedDate not supplied

Development and validation of a herring gull embryo toxicokinetic model for PCBs.

A toxicokinetic model was developed to describe polychlorinated biphenyl (PCB) accumulation by herring gull (Larus argentatus) embryos during development. The model consists of two components, a bioenergetics model that predicts the lipid mass balance of embryo and yolk compartments with time and an empirical toxicokinetic model that describes PCB partitioning between lipid compartments in the egg. The model was calibrated using data on PCB and lipid partitioning between embryo and yolk + albumen at four time points during incubation in herring gull eggs injected with a PCB mixture, combined with data sets on herring gull embryo growth rates and bioenergetic demands with time. The model was validated using independent data consisting of maternally exposed, field-incubated Lake Superior herring gull eggs that varied in incubation ages over the range of 8.5 d to pipping age (26-28 days). PCB concentrations in 6-9 d embryos were nearly an order of magnitude less than predicted by equilibrium lipid partitioning between the embryo and yolk + albumen compartments of the eggs. PCB concentrations in embryos were adequately predicted by equilibrium partitioning, however, for eggs incubated for 23-28 d. An empirical relationship was developed to account for the apparent nonequilibrium behaviour of PCBs during early development. The model was sensitive to the mass of yolk lipids and the mass of PCBs deposited to fresh eggs and much of the variability in embryo PCB concentrations could by explained by accounting for variability in these input parameters. Consistent with experimental data for other avian species, the model predicts that the highest PCB concentrations in the embryo/chick occur during pipping or soon after when yolk lipids have been completely resorbed by the embryo.

Animals↗
PubMed2001

The effect of amnio-allantoic fluid pH on the intestines: an experimental study in the chick embryo gastroschisis model.

BACKGROUND/PURPOSE: Prolonged exposure to amniotic fluid causes the intestinal changes such as serosal edema, thickening, fibrous coating, and adhesions in gastroschisis. The effect of amnio-allantoic fluid (AAF) pH on intestines was evaluated using a chick embryo gastroschisis model. METHODS: Seventy fertile eggs were divided into 5 groups: preliminary study (PS, n = 20), AAF control (AAC, n = 10), just gastroschisis (JG, n = 10), gastroschisis pretreated with placebo (GPP, n = 15), and gastroschisis pretreated with sodium bicarbonate (GPS, n = 15). The PS group was also divided into 2 subgroups to determine the biochemical differences between the amniotic and the allantoic fluid. Gastroschisis was created surgically at the 14th day of incubation. In GPS group, 8.4% NaHCO(3) solution (0.1 mL/100 mg/d) was instilled into the AAF for 4 days. RESULTS: A significant decrease in intestinal damage was observed both macroscopically and microscopically in the group GPS compared with the JG and GPP groups. CONCLUSIONS: Pretreatment with alkalization of AAF prevented intestinal damage because of gastroschisis. Alkalization could be a simple alternative for pretreatment with amniotic fluid exchange for human fetuses with gastroschisis.

Alkalies↗
PubMed2004

The effect on the intestines of continuous release of methylene blue from a drug delivery system: an experimental study in a chick embryo gastroschisis model.

Increased small bowel nitric oxide synthase (NOS) activity has been suspected as a cause of postnatal intestinal dysmotility in gastroschisis. The effect of continuous delivery of methylene blue loaded polymer (MBLP) hydroxy-propyl methyl cellulose-ethyl cellulose (HPEC-MC) and daily injection of methylene blue (MB) on the intestinal damage (ID) was evaluated using a chick embryo gastroschisis model. Fourteen-day-old fertilized chick eggs were divided into five groups. In the control (C) group, no intervention was performed. In the sham (S) group, the allantoic and amniotic membranes were opened to create a common cavity that resembles the amniotic cavity in human. In the gastroschisis only (GO) group, a defect in the abdominal wall of the embryo was made, and intestinal loops were exteriorized following connection of amniotic and allantoic cavities. In the gastroschisis plus methylene blue (G+MB) group, gastroschisis was created and MB administered into the amnioallantoic cavity (AAC) by daily injections for 5 days. In the gastroschisis plus methylene blue loaded polymer (G+MBLP) group, MBLP was placed into AAC after gastroschisis was created. At the end of the 19th day of incubation, intestinal morphological changes were investigated macroscopically and microscopically. Although the survival rates were decreased in the chick embryos with creation of gastroschisis compared with C and S groups ( p<0.001), the survival rates were increased in G+MBLP group (76.92%) when compared with the GO group (41%) ( p<0.001). Because of multiple intervention of embryos, higher mortality was observed in the G-MB group (75.61%). Macroscopic and microscopic scores of ID and mean intestinal wall thickness were significantly higher in the GO group when compared with C, S, G+MB, and G+MBLP groups ( p<0.001). The mean score of intestinal ganglia morphology was significantly increased and the total number of ganglion cells was significantly decreased in the GO group when compared with C, S, G+MB, and G+MBLP groups ( p<0.001). It is possible to decrease intrauterine intestinal morphological changes in gastroschisis by inhibiting NOS. As a first preliminary study, we believe that use of MBLP may be an alternative for fetal treatment by eliminating the harmful effects of multiple interventions or amniotic fluid exchanges.

Administration, Topical↗
PubMed1998

A chicken embryo eye model for the analysis of alphaherpesvirus neuronal spread and virulence.

We describe use of developing chicken embryos as a model to study neuronal spread and virulence of pseudorabies virus (PRV). At embryonic day 12, beta-galactosidase-expressing PRV strains were injected into the vitreous humor of one eye, and virus replication and spread from the eye to the brain were measured by beta-galactosidase activity and the recovery of infectious virus from tissues. The wild-type PRV strain, Becker, replicated in the eye and then spread to the brain, causing extensive pathology characterized by edema, hemorrhage, and necrosis that localized to virally infected tissue. The attenuated vaccine strain, Bartha, replicated in the eye and spread throughout specific regions of the brain, producing little to no overt pathology. Becker mutants lacking membrane proteins gE or gI replicated in the eye and were able to spread to the brain efficiently. The pathology associated with replication of these mutants in the brain was intermediate to that induced by Becker or Bartha. Mixed infection of a gE deletion mutant and a gI deletion mutant restored the pathogenic phenotype to wild-type levels. These data indicate that the replication of virus in embryonic brain tissue is not sufficient to induce the characteristic pathological response and that the gE and gI gene products actively affect pathological responses in the developing chicken brain.

Alphaherpesvirinae↗
PubMed1997

[Surgical approach on rabbit embryos. A model trial of bladder exstrophy].

We describe herein a new model of surgical approach of an early mammalian embryo. Indeed the developmental mechanisms of numerous congenital anomalies, such as bladder exstrophy, remain obscure, and progresses in their knowledge must be achieved to propose better treatments. But up to now all the successful reports in experimental models of early produced malformations concerned birds or batracians, whose development is very different from human. We used the rabbit. Twenty-five time matted does were operated at 12.5 days of gestation. Out of their 247 embryos, 99 underwent a surgical procedure. Forty-eight were injured in order to produce an exstrophy. In 18 cases, the embryo extruded from the uterine cavity and could not be reintegrated, and 2 sacs were found empty. The remaining 31 were only exteriorized. Nine additional does received intravenous teratogen at 12.5 days of gestation. In the group of operated embryos we obtained 6 full-term fetuses, one of whom had a cloacal exstrophy. No exstrophy was noted among the intact embryos, neither in the 87 fetuses submitted to the teratogen. We conclude that: it is possible to operate on an early mammalian embryo, and to obtain further growth until term and that the exstrophy we observed in one case resulted from the surgical specific procedure.

Animals↗
PubMed1990

Spina bifida: a chick embryo experimental model.

Neural Tube Defects (NTD) can be induced in the chick embryo with relative ease in order to provide an experimental tool for investigation of such disabling malformations. Domestic hen (Gallus gallus) eggs were incubated at 37.5 degrees C and 80% humidity for 24 h. At that moment, 5 ml of albumen were aspirated by sterile puncture of the shell, and the incubation was resumed. The embryos were recovered and studied at the 8th, 10th and 14th days. Almost half (45%) of the 602 treated embryos survived and 73 of them (12%) had various malformations. Thirty-six (6%) suffered NTD of which 30 were open myelomeningocele, 2 meningocele and 4 encephalocele. The anatomy of the defects was astonishingly similar to that of the human malformation. Whether these experimental NTD are induced by mechanical or nutritional modifications of the internal environment of the egg is unknown, but the similarity of the lesion with those in humans make them suitable for further investigation of these issues. We believe that this relatively simple and inexpensive model is a suitable tool for research on spina bifida.

Animals↗
PubMed1992

Unilateral renal agenesis in chick embryos: a model for chronic renal insufficiency.

Although renal agenesis and dysgenesis are relatively common and significant birth defects, no animal model to date has been utilized to adequately study these developmental pathologies. Blockage of the migration of the mesonephric duct in Day 2 chick embryos results in unilateral renal agenesis (URA) on the operated side, thus providing a model of chronic renal insufficiency. Embryos with URA respond with an increase in the rate of growth of the remaining meso- and metanephric kidney. The allometric scaling of single (left) kidney weight to total body weight in control embryos is KM = 3.48M0.98 compared to KM = 3.02M1.16 in embryos with URA. In addition, embryos with URA exhibit a progressively polycystic mesonephros with distinct glomerulonephritis and expansion of the renal tubules. These renal changes are insufficient for normal urine (allantoic fluid) production and oliguria persists throughout incubation. While mortality is unaffected by URA in embryos up to Day 14 of incubation, there is a steady increase in mortality after Day 14; no chick embryo with URA lives beyond Day 18 of the 21-day incubation period.

Animals↗
PubMed2006

Failure of homocysteine to induce neural tube defects in a mouse model.

BACKGROUND: Folate deficiencies have been associated with many adverse congenital abnormalities. It is not clear, however, whether these defects are due to a folate deficiency or to an increase in homocysteine. Homocysteine has been shown to be teratogenic in the chicken-embryo model and it has been suggested that homocysteine-induced defects are mediated by inhibiting the N-methyl-D-aspartate (NMDA) receptor on neural crest cells. The majority of the teratology studies have been carried out using the chicken embryo model. In an effort to develop a murine model of homocysteine-induced neural tube defects, several inbred mouse strains were treated with homocysteine or the NMDA inhibitor MK801 and the fetuses examined for any induced-NTD. METHODS: Several in-bred mouse strains were administered homocysteine once on gestational day (GD) E8.5 or once daily on GD 6.5-10.5. Additionally, because homocysteine was been reported to mediate its effects through the NMDA receptor, the effect of MK801, an antagonist of this receptor, was also investigated. RESULTS: Regardless of the mouse treatment time, homocysteine failed to induce neural tube defects in our in-bred mouse strains. Homocysteine also failed to increase the number of neural tube defects in the splotch strain, regardless of the genotype. CONCLUSIONS: Irrespective of the mouse strain or treatment, homocysteine failed to induce neural tube defects in our mouse models, which is in contrast to what has been reported in the chicken embryo models.

Animals↗
PubMed2000

[Establishment of in vitro serum-free embryo implantation model].

OBJECTIVE: To observe the growth and implantation of mouse embryos in vitro. METHODS: In order to establish a serum-free coculture system, the whole components of decidual tissue was collected and cultured in vitro. Then 4-day-mouse embryos were added to the well-developed decidual cells, and the following changes of the above system were closely observed under microscope. RESULTS: Mouse embryos were successfully hatched, adhered, implanted and outspreaded under the coculture system. The extraplacental cone and amniotic sac were formed as well. Decidual cells kept stable during the following 4-day coculture. CONCLUSIONS: Decidual cell is an ideal feeder cell for coculture. Our results showed that the modified method of decidual cell culture and the establishment of implantation model were simple, practical and reliable.

Animals↗
PubMed2000

The use of whole rat embryo culture as a technique for investigating potential serum toxicity in recurrent miscarriage patients.

Previously, the rat embryo model has been used as an experimental technique in investigations of the aetiology of idiopathic recurrent miscarriage. The aim of the present study was to validate it as a tool in the investigation of the aetiology of this condition. Subjects (n = 36) with a history of recurrent miscarriage were recruited from two dedicated recurrent miscarriage clinics and compared with control women with at least one previous pregnancy resulting in a live birth (n = 23). Serum from each woman was used as culture medium in the rat embryo model. Cultured embryos were scored for growth and differentiation. No statistical difference was found in any parameter between the two groups. Furthermore, patients from the recurrent miscarriage group whose serum demonstrated a trend towards lower scores, subsequently conceived and underwent uncomplicated pregnancies.

Abortion, Habitual↗
PubMed2003

A study of teratogenicity of hydrosalpinx fluid using a whole rat embryo culture model.

BACKGROUND: Hydrosalpinx fluid may be toxic to sperm and early embryo growth. Information concerning the effect of hydrosalpinx fluid on embryo development during organogenesis is lacking. METHODS: Rat embryos at gestational day 9.5 were cultured for 48 h with 80% rat serum and 20% of either hydrosalpinx fluid (study group) or lactated Ringer's solution (control group). Embryos were scored for growth and development at the end of the culture period. RESULTS: Hydrosalpinx fluid, collected from 10 patients, was tested for embryotoxicity individually. Median total morphological scores were significantly lower in embryos exposed to hydrosalpinx fluid from three of the 10 patients (43.0 versus 47.0, P = 0.01; 36.0 versus 45.0, P < 0.001; 36.0 versus 46.5, P = 0.003). This was accompanied by a significant reduction in median yolk sac diameter (4.0 versus 5.2 mm, P < 0.001 and 4.0 versus 5.0 mm, P < 0.001) and somite number (17.5 versus 22.5, P < 0.001 and 17.0 versus 21.5, P = 0.008) in the latter two patients. CONCLUSIONS: Hydrosalpinx fluid in some patients may contain toxin(s) that is potentially teratogenic.

Animals↗
PubMed1977

Mammalian embryo: a model for congenital prolonged QT syndrome.

The QT interval has been studied in ECG in mouse and rat embryos during two stages of development. The QT interval during the early stage of development is prolonged and an ST segment clearly exists. Both disappear during fetal development and do not exist in adult animals in which the T wave immediately follows the QRS. Mammalian embryos have therefore been proposed as a model for the study of QT prolongation. It is suggested that the origin of the QT prolongation in the young embryos is caused by the prolonged duration of the action potentials of the primordial cardiac tissue. During embryonic development this tissue becomes organized as a conductive system surrounded by "neomyocardial" tissue with a shorter duration of action potential, which causes the shorter QT interval at this stage. Our working hypothesis is that the pathogenesis of the prolonged QT syndrome in children could be interpreted as an incomplete or delayed differentiation between the primordial or primordial-like myocardium retaining prolonged action potential duration, and "neomyocardium" with short duration.

Animals↗
PubMed2004

Nitrofen-induced congenital diaphragmatic hernia in rat embryo: what model?

PURPOSE: The aim of this study was to investigate the natural history of congenital diaphragmatic hernia (CDH) in rat embryos with special attention to the pathomorphologic changes of diaphragm, liver, intestines, and lungs at various stages of embryonic development. METHODS: Pregnant Sprague-Dawley rats were given, via a gavage tube, 100 mg nitrofen (Wako Chemicals, Neuss, Germany) on day 10.5 of gestation. Fetuses were harvested by laparotomy on day 15.5, 16.5, 18, and 21. Anatomic study of the diaphragm, herniated viscera, and lungs was performed under stereoscope with special attention to the diaphragmatic defect. RESULTS: CDH occurred in 44 embryos on right, in 10 on the left, and in 34 bilateral. In the youngest embryos, the small defect was located in the dorsomedial portion of the diaphragm very close to the aortic hiatus. During pregnancy, the defect enlarged progressively to occupy more than half of the affected hemidiaphragm on day 21. In all animals, regardless of their age and side of the defect, the liver was found inside the chest. The intrathoracic mass was formed by ingrown hepatic tissue originating from the dorsal surface of the intraabdominal liver. It appeared as an accessory liver lobe. The amount of intrathoracic liver increased rapidly. From around day 18, the thoracic portion of liver, when examined in sagittal plane, was bent forward and assumed an uncinate shape. The stomach and small bowel loops were displaced into the chest in the oldest examined fetuses. The first sign of reduction of size of the lung was seen in 16, 5-day old embryos, and at further stages of embryonic development the lung growth impairment strictly paralleled the ingrowth of the liver. The natural history of the right and left CDH were very similar. In fetuses with bilateral CDH, asymmetry regarding size of the defect and volume of intrathoracic hepatic mass was noted with larger defects on the left side in more than 60% of animals. CONCLUSIONS: Pathogenesis of nitrofen-induced diaphragmatic defect in the rat embryo and CDH in the human fetus seem to differ significantly. Nitrofen induces a complex malformation of the embryonic diaphragm and the liver. CDH in rat embryo bears more resemblance to a model of space-occupying lesion than to human CDH. The induction of localized hepatic proliferation may be a result of disturbance of as yet unknown regulatory interaction between hepatic and mesenchymal diaphragmatic cells.

Animals↗
PubMed1983

Retroviruses and mouse embryos: a model system in which to study gene expression in development and differentiation.

Early mouse embryos exposed to Moloney leukaemia virus (M-MuL V) produce substrains of mice, designated Mov-1 to Mov-14, that transmit the virus genetically from one generation to the next. In some substrains the inserted viral genome becomes activated at specific stages of embryogenesis and the available evidence suggests that these viral genomes are developmentally regulated. The effect of cellular differentiation on virus expression was investigated by introducing M-MuL V into preimplantation or postimplantation mouse embryos, or into embryonal carcinoma cells (EC cells) in tissue culture. Whereas preimplantation embryos or EC cells did not permit virus expression, efficient replication occurred in postimplantation embryos or in differentiated cells. The viral genomes introduced into early embryos were highly methylated and non-infectious when analysed in the adult. In contrast, viral genomes introduced into postimplantation embryos remained unmethylated and were infectious in a transfection assay. Similarly, de novo methylation occurred in undifferentiated EC cells but not in differentiated derivatives. These results demonstrate an efficient de novo methylation activity which appears to be involved in the repression of genes introduced into pluripotent embryonic cells and is not observed in cells of the postimplantation embryo or in differentiated cells growing in culture. Integration of M-MuL V into the germ line can lead to recessive lethal mutations. This has been shown for the Mov-13 substrain, as animals homozygous at the Mov-13 locus die between Days 13 and 14 of embryogenesis. This suggests that viral integration occurred in a chromosomal region that is active during, and crucial for, embryonic development.

Animals↗