PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Fetal Development”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1993

Embryo-fetal development influenced by lead exposure in iron-deficient rats.

Lead administered (250, 500, 1000 and 2000 ppm Pb as lead nitrate) through drinking water from the 6th to the 14th day of gestation in iron-deficient rats, resulted in a significantly reduced litter size, reduced fetal weight and a reduced crown-rump length, increased resorption and a higher blood-lead uptake in those groups receiving 1000 and 2000 ppm Pb. These animals also had a higher placental lead uptake. However, the level was the same in both groups. Fetal lead uptake remained the same whether or not 2000 ppm lead was given to an iron-deficient or normal iron groups of mothers. This indicates that iron-deficiency renders female rats more susceptible to inducing embryo- and feto-toxicity when given lead through their drinking water.

Animals↗
PubMed1991

Plasma cholesterol and lipoprotein levels during fetal development and infancy.

Intrauterine changes in plasma cholesterol and lipoprotein concentrations have been linked to the development of the adrenal gland (utilization of cholesterol) and liver (production of cholesterol by new synthesis). At term birth, racial and gender differences have been observed with white compared to black, and female compared to male, infants having higher cholesterol concentrations. Within hours of the beginning of oral feeding, total and LDL cholesterol rise significantly. Little further increase occurs after 7 days, and the concentration seen after this time is highly dependent upon the cholesterol and polyunsaturated fat content of the diet. By 12 months of age, investigators cease to find any effect of the milk source fed earlier in infancy on cholesterol and lipoproteins. This is not evidence that diet no longer influences cholesterol and lipoprotein concentrations, but only that individual lipid intakes are varied and difficult to quantitate. Cross-cultural comparisons of infants at this age in fact provide strong suggestive evidence that a large environmental component determines the circulating cholesterol and lipoprotein concentrations seen at one year and beyond.

Cholesterol↗
PubMed1989

A review of experimental studies of iodine deficiency during fetal development.

Iodine deficiency is now recognized as a major international public health problem. It is estimated that 800 million people may be at risk of the effects of iodine deficiency. In humans, the effects occur at all stages of development: the fetus, the neonate, the child and adult. The effects are now denoted by the term iodine deficiency disorders (IDD). They include miscarriages, stillbirths, congenital anomalies, as well as the more familiar goiter, cretinism, impaired brain function, and hypothyroidism in children and adults. In domestic animals, reproductive failure has been reported with the production of aborted, stillborn and weak calves. Experimental studies in animal models have been reviewed to provide evidence of the mechanisms involved, particularly in relation to brain development. The findings in three different species (rat, sheep, monkey) indicate that the effects are mediated by a combination of maternal and fetal hypothyroidism, the effect of maternal hypothyroidism being earlier than the onset of fetal thyroid secretion. The findings suggest that iodine deficiency has an early effect on neuroblast multiplication and, if so, this could be important in the pathogenesis of the neurological form of endemic cretinism. The assessment of the full effects of iodine deficiency on the brain requires further studies in the postnatal period to determine the duration of these effects.

Animals↗
PubMed2004

Gene expression pattern in hepatic stem/progenitor cells during rat fetal development using complementary DNA microarrays.

To identify new and differentially expressed genes in rat fetal liver epithelial stem/progenitor cells during their proliferation, lineage commitment, and differentiation, we used a high throughput method-mouse complementary DNA (cDNA) microarrays-for analysis of gene expression. The gene expression pattern of rat hepatic cells was studied during their differentiation in vivo: from embryonic day (ED) 13 until adulthood. The differentially regulated genes were grouped into two clusters: a cluster of up-regulated genes comprised of 281 clones and a cluster of down-regulated genes comprised of 230 members. The expression of the latter increased abruptly between ED 16 and ED 17. Many of the overexpressed genes from the first cluster fall into distinct, differentially expressed functional groups: genes related to development, morphogenesis, and differentiation; calcium- and phospholipid-binding proteins and signal transducers; and cell adhesion, migration, and matrix proteins. Several other functional groups of genes that are initially down-regulated, then increase during development, also emerged: genes related to inflammation, blood coagulation, detoxification, serum proteins, amino acids, lipids, and carbohydrate metabolism. Twenty-eight genes overexpressed in fetal liver that were not detected in adult liver are suggested as potential markers for identification of liver progenitor cells. In conclusion, our data show that the gene expression program of fetal hepatoblasts differs profoundly from that of adult hepatocytes and that it is regulated in a specific manner with a major switch at ED 16 to 17, marking a dramatic change in the gene expression program during the transition of fetal liver progenitor cells from an undifferentiated to a differentiated state. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).

Aging↗
PubMed1997

Sex hormones regulate CFTR in developing fetal rat lung epithelial cells.

Sex hormones modulate two normal processes of late-gestation mammalian lung development: the onset of augmented production of surfactant phospholipids and the loss of mesenchymal cells. As prenatal lung development advances, epithelial chloride secretory pathways diminish as opposing sodium absorptive pathways increase in expression. We hypothesized that sex hormones may influence both the gene expression and functional activity of the chloride channel known as the cystic fibrosis transmembrane conductance regulator (CFTR) in fetal lung epithelium. We report here that sex hormones exert opposite effects on CFTR. Androgen increases and estrogen decreases CFTR functional activity [as assessed by CFTR antisense (but not sense) oligodeoxynucleotide-sensitive adenosine 3',5'-cyclic monophosphate-stimulated cell volume reduction or by glibenclamide-sensitive, amiloride-insensitive transepithelial electrical potential] in primary cultures of fetal rat lung epithelial cells. No alterations in CFTR mRNA levels measured by quantitative polymerase chain reaction amplification of reverse transcripts) accompanied either the changes in functional activity induced by sex hormones or the changes observed during normal development, suggesting that sex hormone modulation of CFTR in antenatal lung occurs at a posttranscriptional level. Our data are consistent with the hypothesis that both androgen and estrogen contribute to the male disadvantage with respect to fetal lung functional development.

Animals↗
PubMed2006

Fetal development of the hand, digits and digit ratio (2D:4D).

OBJECTIVE: The purpose of this study was to investigate growth patterns in human hands, digits and digit ratio (2D:4D) during the fetal period. METHODS: The study is carried out on 161 human fetuses (83 males, 78 females) free from external pathology or malformation with ages ranging between 9 and 40 weeks of gestation. Following general external measurements, length and width of the hand, digit lengths separate for each hand was measured, hand index and the ratio of the lengths of the 2nd finger to the 4th finger (2D:4D index) was computed. RESULTS: Means and standard deviations of the parameters with respect to gestational weeks, months and trimesters were calculated. There was a significant correlation between all parameters and gestational age (p<0.001). No significant differences were observed between sexes or sides for any of the parameters (p>0.05). 2D:4D ratio was significantly higher in females compared to males (p<0.05) and mean 2D:4D did not change with gestational age. CONCLUSION: Detailed information of hand and digit parameters related to the fetal period will reveal the extent of biological variations of hand and digit parameters to be used in future studies. We hope that data acquired in this study will facilitate other studies on hand and digit anomalies, pathologies and variations as well as diagnoses and treatments of such conditions conducted in obstetrics, perinatology, forensic medicine and fetal pathology departments.

Anthropometry↗
PubMed1989

Differential expression of galactose and N-acetylgalactosamine residues during fetal development and postnatal maturation of rat glomeruli as revealed with lectin conjugates.

A battery of fluorochrome- or peroxidase-coupled lectins, reacting with alpha- or beta-galactose (Gal), terminal N-acetylgalactosamine (GalNAc), or Gal-(beta 1-3)-GalNAc residues, was used to study the emergence and distribution of cellular glycoconjugates in developing and adult rat glomeruli. Neuraminidase pretreatment of the specimens was applied to monitor the maturation of the glomerular sialoglycoprotein coat. In the adult glomeruli, the lectin conjugates applied reacted sparsely or not at all, but most of them showed an increased reactivity with podocytes and/or the glomerular basement membrane after neuraminidase treatment. In the embryonic glomeruli, lectins reacting with beta-Gal residues prominently bound to the basement membranes, as revealed in double-staining with laminin antibodies. This reactivity decreased first during late postnatal development. Some terminal Gal-(beta 1-3)-GalNAc residues were noted in the earliest podocytes, but obviously soon became covered by sialylation. Furthermore, the developing podocytes prominently displayed alpha-Gal residues, as marked by Maclura pomifera (MPA) and Jacalin reactivities but not by the GSA-I conjugates. During postnatal maturation these reactivities also decreased. The GalNAc-specific Helix pomatia (HPA) and Helix aspersa (HAA) agglutinins bound to basement membranes of evolving podocytes but later revealed in the podocytes only a Golgi-like cytoplasmic reactivity. These two lectins showed a marked difference in their binding to tubular basement membranes. In lectin blotting experiments of electrophoretically separated polypeptides transferred onto nitrocellulose, the peanut agglutinin (PNA) and MPA conjugates revealed upon neuraminidase treatment a broad Mr 140,000 polypeptide, compatible with podocalyxin, both in isolated developing and adult glomeruli. The MPA conjugate revealed a similar polypeptide in developing glomeruli, even without neuraminidase treatment. Similar experiments with the HPA and HAA conjugates revealed different polypeptides in both adult and developing glomeruli. Obviously, in the rat kidney the maturation of the podocyte sialoglycoprotein coat and the glomerular basement membranes are multiphasic processes that continue even during late postnatal development.

Acetylgalactosamine↗
PubMed1991

Peptide growth factors: the parallel between fetal development and malignant transformation.

Normal embryonic development and tissue homeostasis depend upon cell-to-cell and tissue-to-tissue communication. Much of this depends upon the production and release of peptide growth regulators such as fibroblast growth factor, epidermal growth factor, etc. As the molecular basis of malignant transformation has been documented, it is apparent that a common means by which a tumor becomes autonomous of external control is by becoming independent of the need for external growth factor stimulation. This can occur through the cell producing and releasing the growth factors needed for its own growth. A similar end result can occur with growth factor receptor mutants in which the receptor gives a positive signal even when no growth factor is bound to the receptor. One potential therapeutic strategy is to interfere with this autocrine loop. Suramin is presented as an example of a drug capable of blocking such autocrine loops. This drug also reverses malignant transformation due to Platelet Derived Growth Factor and K-fgf/hst oncogenes on this basis. Another potential mechanism to accomplish the same end is through the use of monoclonal antibodies to either the growth factor or its receptor. Examples of this are available for TGF-alpha. We have discussed a range of practical issues involved in developing monoclonal antibodies as therapeutic agents.

Antibodies, Monoclonal↗
PubMed2000

Progressive and transient expression of tissue plasminogen activator during fetal development.

In previous studies of the role of tissue plasminogen activator (tPA) in the lung inflammatory response, we observed that tPA expression was present exclusively in the small arteries and arterioles within the lung and absent from the capillaries, veins, and large pulmonary arteries. To define more completely the expression pattern of tPA, we evaluated the distribution of this protein during prenatal and postnatal development. tPA was first observed in the rat fetus at day 13 in the large arteries of both the thoracic and cranial cavities, including the dorsal aortas and pulmonary arteries in the former and the internal carotid and middle cerebral arteries in the latter. By day 15, tPA was no longer detectable in the aortas but appeared throughout the pulmonary, subclavian, vertebral, and basilar arteries. At day 17, tPA had disappeared from the subclavian artery and the proximal portion of the vertebral artery but was found in the smaller arterial branches of these 2 large vessels. By the end of gestation, tPA had also disappeared from the main pulmonary arteries but remained in the branches at the hilus of the lung. At birth, tPA was concentrated in the endothelia of arteries within the pia mater, the basilar and superficial cerebral arteries, and the lung arterial system. As the animals reached maturity, tPA disappeared from the larger cerebral arteries and their cortical branches but continued to be expressed in the vessels of the pia mater and lung. This study indicates that tPA expression is a dynamic process that responds to a changing arterial environment during vascular development.

Animals↗
PubMed1994

Bovine bladder compliance increases with normal fetal development.

In this study we characterized the elastic properties of the normal bovine bladder throughout fetal life, the newborn period and into adulthood. The elasticity of the bladder was measured with a novel circularly clamped bladder testing system. Pressurization of a circularly clamped bladder tissue sample caused the tissue to deflect upward repetitively in the shape of a spherical cap. If the centerline deflection is much larger than the tissue thickness, the elastic modulus, considered the inverse of compliance, can be determined using linear regression techniques. The results of our analyses showed that the elastic modulus decreases in direct proportion with increasing gestational age. These data suggest that during normal development of the bovine fetal bladder there is a progressive change from a rather stiff noncompliant bladder characterized by a high elastic modulus to a compliant bladder with a lower elastic modulus. Moreover, the increase in compliance appears in the developmental period when urine production first occurs. These observations suggest that volume work may be a significant event in the normal development process of the bovine bladder and results in an increase in bladder compliance. Conversely, the poorly compliant fetal bladder may explain some of the transient dilatations of the upper urinary tract which have been documented in utero. Finally, from the newborn period to the mature adult bovine we documented a relatively modest increase in the elastic modulus or decrease in bladder compliance which may reflect the normal aging process.

Animals↗
PubMed1996

Effects of buthionine sulfoximine on the outcome of the in utero administration of alcohol on fetal development.

The adverse effects of the maternal consumption of alcohol on the fetus have been recognized for centuries. Fetal alcohol syndrome is characterized by pre- and postnatal growth retardation, mental retardation, behavioral deficits, and facial deformities. Despite numerous animal studies, the biochemical mechanism(s) by which alcohol produces teratogenic effects on the developing fetus are not well understood. Several studies have shown that administration of alcohol to adult rats produces a decrease in hepatic levels of glutathione (GSH). In utero administration of alcohol has also been shown to produce a decrease in GSH levels, as well as prenatal growth retardation and intrauterine death. In an effort to determine if GSH may have a vital role in protecting the fetus against the teratogenic effects of alcohol, buthionine (SR)-sulfoximine (BSO) was used to deplete GSH levels in the mother and fetus. Timed pregnant Sprague-Dawley rats were placed on a liquid BioServ diet containing either 0%, 11%, 23%, 29%, 31%, 33%, or 35% ethanol-derived calories, with or without BSO (888 mg/kg/24 hr), starting on day 1 of pregnancy. Another set of mothers were fed lab chow and water as a control group for the liquid diet. The mothers were maintained on the diet until gestation day 21 when they were anesthetized with sodium pentobarbital and the pups delivered by cesarean section. The offspring were counted, weighed, killed, and the brain and liver weighed. The effects of BSO on the alcohol dose-response curves (body weights, brain weights, and litter number) were then determined to ascertain if a depletion in GSH potentiated the effects of alcohol. In utero administration of BSO, aside from the depletion of GSH in the liver and brain in the developing fetus, produced a shift to the left in the alcohol dose-response curve.

Animals↗
PubMed1988

Fetal development, and placental and maternal plasma concentrations of progesterone in the little brown bat (Myotis lucifugus).

Progesterone concentrations measured in plasma samples from 280 bats captured during pregnancy or early lactation were related to fetal attributes indicative of stage of pregnancy. Fetal weight increased exponentially from 40 mg at crown-rump length of 6 mm to 2000 mg at 23 mm (term). Fetal weights at term accounted for up to 35% of the weight of intact pregnant animals. Progesterone concentrations increased from less than 5 ng/ml at 2 mm estimated crown-rump length to plateau values of approximately 65 ng/ml (geometric means) from 16 mm crown-rump length until the most advanced stages of pregnancy. Mean concentration in 8 post-partum bats, most of which were actively lactating, was 8.4 ng/ml; 11.6 ng/ml was measured in one animal that was carrying a wet neonate when sampled yet was still pregnant when captured 5 h earlier. Placental concentrations of progesterone ranged from 43 to 964 ng/g wet weight of tissue and mean values increased in a similar fashion though were about 4-fold greater than changes in plasma concentrations of the steroid. The concentrations in placental tissue were at least 15- to 20-fold higher than could be expected from blood contamination, indicating that placental steroidogenesis is likely to occur in this species.

Animals↗