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At least 433 records · Page 24Linked to original sources
PubMed1995

Late fetal development and selective resorption in Saccostomus campestris (cricetidae).

When female Saccostomus campestris are stressed during pregnancy they may resorb part of the litter. Resorption can take place on more than one occasion during the same pregnancy without affecting the development of the rest of the litter. The last resorption may be initiated as late as 72-48 h before parturition. No other rodents with a similar gestation appear to resorb at this stage. Resorbing fetuses are isolated within uterine compartments from viable fetuses. Ossification occurs at a comparatively late stage of pregnancy in Saccostomus campestris, and there is a lag-period in fetal growth exactly 72-48 h before parturition. These factors may facilitate late resorption in this species. Factors that may cause stress in this species are most likely environmental; in the present study, dipping of the animal colony to treat for a mite infestation may have induced resorption in some of the females.

Animals↗
PubMedDate not supplied

Vascular endothelial growth factor: possible role in fetal development and placental function.

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen with potent permeability properties. This growth factor exists in several isoforms; the most abundant form present in most tissues is VEGF165. The different isoforms exhibit differences in biologic function. During development, VEGF is expressed in multiple embryonic and fetal tissues, with the highest levels found in the lung, kidney, and heart. Vascular endothelial growth factor is also expressed in placental tissues and fetal membranes, and this expression increases with advancing gestation. In the fetal heart and placenta, VEGF expression is inducible by hypoxia. Two receptors, KDR and Flt-1, have been identified for VEGF. They are widely expressed in vascular endothelial cells and are also found in placental tissues where VEGF is localized. In humans, Flt-1 appears to be the predominant receptor, whereas in the cow and sheep, KDR is the major receptor expressed. The presence of VEGF and its receptors in placental tissues throughout gestation strongly suggests that VEGF plays an important role in the development and maintenance of placental vascular function during pregnancy. The localization of VEGF in fetal membranes and the fetal surface of the placenta raises the possibility that VEGF may be involved in the regulation of amniotic fluid volume and composition.

Amino Acid Sequence↗
PubMed1998

Spontaneous mutation during fetal development and post-natal growth.

Somatic mutations seem to accumulate slowly with age during adult life in both mice and men. There is, however, a substantial mutant frequency at birth, suggesting that the rate of accumulation is much higher before birth. This suggests that DNA replication plays an important role in the generation of spontaneous mutations. Since most cell division and accompanying DNA replication occurs early in development, more mutations would arise during growth and development. Indeed, if the mutations are genetically neutral, the mutant frequency would rise very rapidly during early fetal growth, more slowly during later fetal growth and development and still more slowly after birth. To test this hypothesis, we have assayed the mutant frequencies from before birth to 28 days after birth, by which time most growth has occurred. We have used the F1 mice generated by crossing SWR females and MutaMouse males. The MutaMouse has a rescuable lacZ/lambda shuttle vector that can be assayed for an in vivo mutation in an in vitro system. Up to and including birth we assayed the entire animal for mutants; at 14 and 28 days after birth we assayed the small intestine. The data show that, as expected, many mutations arise early in development, by 12.5 days after conception, and confirms the non-linearity of mutation with age. In these mice, about one third of mutations arise before birth, about one third during growth to adulthood and the remaining during the rest of the animal's life, although this depends somewhat on the tissue.

Animals↗
PubMed1998

The EGF system in fetal development.

Immunohistochemical localization of the epidermal growth factor receptor (EGFR) disclosed a wide distribution of this protein in diverse fetal tissues. This review focuses on some of the vast work on the expression and operation of the EGFR and its principal ligands in fetal organogenesis.

Animals↗
PubMed1993

Concanavalin A crossed affinoimmunoelectrophoretic analysis of the major pig serum proteins during fetal development.

The interaction between concanavalin A (Con A) and alpha-fetoprotein (AFP), transferrin (TF), fetuin, alpha 1-antitrypsin (AT) and alpha 1-acid glycoprotein (AGP) has been analyzed by crossed affinoimmunoelectrophoresis (CAIE) in fetal extracts or sera, from 26-day-old porcine fetuses to birth, and in adult pigs. Most of the TF and AFP (100 and 85-90%, respectively) reacted with Con A during the entire developmental period. AGP showed both two reactive and one nonreactive Con A isoforms, whose proportions change greatly during development. In younger fetuses 100% of the protein was Con A-nonreactive. This variant represented 64% in 50-day-old fetuses, 80% in newborn pigs and 20% in adult sera. Fetuin and AT showed a maximum of three Con A-reactive microforms and one Con A-nonreactive microform, which was always a minor form. These microforms were detected mainly in young fetuses. Although the proportion of Con A-reactive variants of fetuin and AT changes during fetal development, the predominant microform was always that with intermediate affinity against Con A. The same microform was also predominant in adult AT, whereas the more reactive microform in respect to Con A predominates in adult fetuin.

Animals↗
PubMed1982

The effect of paternal alcohol consumption on fetal development in mice.

The purpose of this study was to evaluate the effect of chronic paternal alcohol consumption on fetal growth and development in C3H mice. Male mice were pair-fed isocaloric liquid diets containing either 30%, 20%, or 0% ethanol-derived calories, or given free access to lab chow. After four weeks of treatment, all males were allowed to mate with untreated females. No differences were found between the litters of alcohol-treated males and controls in terms of the number of implantation sites, prenatal mortality, fetal weight, sex ratio, or frequency of soft tissue malformations. The results suggest that paternal alcohol consumption does not grossly alter fetal growth and development in C3H mice.

Abnormalities, Drug-Induced↗
PubMed1986

Effect of WR-2721 on fetal development in the rat.

The radioprotector WR-2721 has been shown to radioprotect all tissues studied except the central nervous system. However, it has not yet been used to radioprotect the fetus. In this study we determined that [14C]WR-2721 injected into pregnant rats quickly passed the placenta and was concentrated by the fetus. In addition, we evaluated the toxicity of WR-2721 (2.5-600 mg/kg) to pregnant rats and their fetuses during the period of major organogenesis at Days 9, 11, and 14 postconception. Pregnant animals were only slightly more (10%) sensitive (LD50, 580 mg/kg) to WR-2721 than nonpregnant cohort animals (LD50, 640 mg/kg). At concentrations of 50 mg/kg or less there was a small but statistically significant increase in fetal deaths, while at doses greater than 300 mg/kg a larger degree of fetal mortality occurred. Maximal fetal weight loss, to about 84% of control, was found at 500 mg/kg. No changes in head dimensions or gross malformations of the surviving fetuses were detected at any time or concentration. Of all the parameters measured in this study none demonstrated a predilection for any specific period of major organogenesis. The results of this study indicate that while WR-2721 demonstrates a dose-related embryotoxicity it is not teratogenic.

Amifostine↗
PubMed1987

Maternal toxicity in humans and animals: effects on fetal development and criteria for detection.

Evaluation of published human and animal teratology data revealed associations between maternal toxicity and congenital malformations and embryofetal death. This has been reported elsewhere in detail and is herein summarized. Regarding human data, intrauterine deaths were observed to occur in association with 1) maternal homeostatic changes due to phenylketonuria and diabetes and 2) maternal toxicity resulting from alcohol abuse, use of aminopterin, and, possibly, trimethadione. A pattern of malformations that was similar and thus suggestive of a common cause was noticed among malformations attributed to phenylketonuria, diabetes mellitus, aminopterin, alcohol, warfarin, phenytoin, phenobarbital, trimethadione, and valproic acid. On reviewing 234 studies of agents tested in hamsters, mice, rats and rabbits, a fairly strong association between maternal toxicity and embryo-fetal mortality was observed. Further, a consistent pattern of fetal malformations associated with maternotoxic effects was discovered in a survey of 476 studies of agents tested in these four species. In these reviews, it was postulated that maternal toxicity per se could possibly cause such fetal effects. For evaluating maternotoxic effects in experimental studies, the minimum maternal data required would be frequent measurements of maternal body weight and food consumption, signs of altered behavior, death, and gross lesions at necropsy.

Abnormalities, Drug-Induced↗
PubMed1994

[Fetal development in late gestosis and nicotine consumption].

In pre-eclamptic and in smoking women, the foetus often develops growth retardation. Hence, nicotine as vasoconstrictive substance increases the blood pressure, therefore causes a higher incidence for pre-eclamptic toxaemia in smoking pregnant women. By means of perinatal inquiry in Baden-Württemberg, not only the frequency of preeclamptic toxaemia was proven in smoking women, but also the frequency of toxaemia in mothers with low, of normal and high weight of the newborn. Hypertension is more frequent in mothers with overweight babies than in mothers with babies of normal weight. In case of overweight newborns, toxaemia is less often caused by proteinuria than in underweight babies. Hypertension is less frequent in smoking pregnant women than in non-smoking women. These findings can be explained by a new theory, which interprets pre-eclamptic toxaemia as a compensatory mechanism in foetal growth retardation. For the foetus, which is insufficiently supplied by the placenta, this regulatory mechanism enhances the blood supply of the placenta. The higher incidence of toxaemia in pregnant women with overweight babies is explained by an increased demand on the placenta, which causes a better foetal blood supply of the placenta in developing the toxaemia. In this case, the toxaemia is compensated. In the stage of decompensation with foetal growth retardation, all reserves are mobilised by an increased permeability of the vessels, which leads to an improved passage through the placenta, but also to proteinuria and increased incidence of oedema.(ABSTRACT TRUNCATED AT 250 WORDS)

Birth Weight↗
PubMed2001

Oxytocinase as the most important marker of fetal development.

Enzymes as biochemical markers come within the entire scope of the live mother-fetus system. The most important are the enzymes which regulate physiological processes, of which oxytocinase (a type of aminopeptidase) has a much wider scope of action than its name suggests, as it regulates also the level of aminopeptide hypothalamic hormones. Thus, it determines neurological, endocrinological and immunological regulation of entire steroidogenesis. Under the influence of gestational enlargement of the uterine cavity, the mothers hypothalamus produces an increasing amount of hormones, which in turn induces an increasing oxytocinase synthesis in the placenta in order to prevent the hormone in the blood reaching the level which could bring about uterine contractions. Also, the growing fetus additionally induces the production of oxytocinase by releasing its own hormones. All this occurs in combined action of the mother, fetus, placenta and even fetal membranes in one space-time process called pregnancy. When in the late pregnancy the enzyme remains at constant level or decreases without appearance of uterus contractions, labour induction is necessary due to fetus life hazard of as much as several percent. Reduction in enzyme level and even its insufficient growth in the second trimester of pregnancy, occur several weeks before preterm birth or death of the fetus. On the other hand, in the event of treatment of diseases accompanying the pregnancy,normalization of oxytocynasaemia shows the effectiveness of treatment. With the dominating profile of the steady increase of oxytocinase (>90% of cases), the target values are higher than in the case of irregular growth. Their close values are a result of the hormonal treatment of threatened pregnancies with ACTH depot. In the cases of the primary hypothalamic insufficiency, this treatment reduces the rate of fetal deaths, which would stand at several dozen percent. It is a classical example of biological pregnancy monitoring since the risk of fetal death can be predicted several weeks earlier when assessment of chemical compounds or physical changes still gives accurate results within physiological limits.

Biomarkers↗
PubMed1990

[The effect of dimethoate and vibrations on the fetal development of the rat].

The influence of vibration and organophosphate insecticide dimethoate of rats (Rattus norvegicus Berkenhout) was examined by exposing pregnant dams to these influences on 12 d p.c. After exposures to vibrations for 12 h an increase of the rate of absorption could be ascertained. A dermal absorption of dimethoate (349 mg/kg) resulted in an increase of the rate of absorption, retardation and deformation. Combinations of exposure to vibrations and dimethoate show an intensifying effect.

Abnormalities, Drug-Induced↗
PubMed1991

The effect of maternal administration of captopril on fetal development in rat.

Captopril an angiotensin converting enzyme (ACE) inhibitor, was evaluated for teratogenic potential in Wistar rats. The drug was administered daily from 6 to 15 day of gestation by gavage (0, 3, 10 and 30 mg/kg/day) and perinatal studies were conducted. Captopril decreased food consumption and suppressed gain in body weight. However, no alteration in food efficiency index was observed. The treatment of rats with captopril in doses of 10 and 30 mg/kg, significantly reduced the mean number of implants per litter size and produced intrauterine growth retardation. The incidence of external and visceral malformations were neither dose related nor significantly different from those of controls. In addition, animal treated with these dose levels showed decreased ossification of digits, sternum and skull of the offsprings. The data of the present study indicates that captopril was not found to be teratogenic to Wistar rats. However, adverse effects on intrauterine growth, fetal ossification, neonatal growth and survival rate were seen among the pups.

Abnormalities, Drug-Induced↗