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 703 records · Page 39Linked to original sources
PubMed1987

A fetuin-related glycoprotein (alpha 2HS) in human embryonic and fetal development.

The human plasma protein, alpha 2HS glycoprotein, has an amino acid composition very similar to that of fetuin, the major protein in fetal calf and lamb serum. Immunohistochemical studies of human fetuses (6-33 weeks gestation) showed that alpha 2HS glycoprotein and fetuin have similar distributions in developing brain and several other tissues, e.g., bone, kidney, gonads, gastrointestinal tract, respiratory and cardiovascular systems. There were notable differences in the liver and thymus in the distribution of the two proteins. Fetuin and alpha 2HS glycoprotein are present in plasma and cerebrospinal fluid of both human and sheep fetuses; their concentrations are reciprocally related: in human plasma and cerebrospinal fluid alpha 2HS glycoprotein concentration is high and fetuin low; the reverse is the case in sheep fetuses. Estimates of the concentration of alpha 2HS glycoprotein in human fetal cerebrospinal fluid and plasma were obtained. It is suggested that alpha 2HS glycoprotein may play a role in developing tissues, especially in the human fetus, similar to that of fetuin in other species.

Blood Proteins↗
PubMed1987

The effect of preimplantation culture conditions on murine embryo implantation and fetal development.

Ham's F-10 medium (Gibco, Grand Island, NY) and medium T6 with and without 15% fetal calf serum (FCS) were compared for their ability to support development of murine blastocysts with the capacity to implant and produce normal fetuses when transferred to pseudopregnant females. All media supported equal rates of blastocyst development from 2-cell embryos. In addition, there were no differences in the rates of blastocyst implantation. However, once implanted, blastocysts grown in T6 produced a significantly higher proportion of normal fetuses (58.5% to 65.9%) than blastocysts grown in either Ham's F-10 (2.4%) or T6 with FCS (27.6%). These results demonstrate that the rate of murine blastocyst development from 2-cell embryos in vitro is not a good criterion of healthy embryos. Murine blastocysts transferred in medium with 0% versus 50% FCS implanted and developed into normal fetuses at equal rates.

Animals↗
PubMed1992

[Two cases of acute promyelocytic leukemia in pregnancy and the effect of anthracyclines on fetal development].

Two patients with acute promyelocytic leukemia (APL) in 2nd and 3rd trimester of pregnancy are reported on. Case 1: 38-year-old female consulted our hospital because of bleeding tendency and pancytopenia in April, 1988. She was diagnosed as having APL with disseminated intravascular coagulopathy (DIC) and was found to be in the 14th week of gestation. Combined chemotherapy (BHAC-DMP) including the total dose (440 mg) of daunorubicin (DNR) resulted in intrauterine fetal death at 19 weeks of gestation. The fetus was severely anemic and the bone marrow was hypoplastic. Case 2: A 27-year-old female was diagnosed as having APL with DIC at 29 weeks of gestation. BHAC-DMP including 440 mg DNR achieved complete remission. At 35 weeks of gestation, she delivered a normal infant by Caesarean section. The child had normal hematological findings and showed normal growth. Both cases developed APL accompanied by DIC during pregnancy and were treated with a similar regimen including high dose of anthracyclines. Case 2 treated in the late period of gestation delivered a normal infant, while fetal death resulted in case 1, treated in the early period of gestation. We reviewed the literature regarding chemotherapy using anthracyclines during pregnancy.

Adult↗
PubMed2000

The subarachnoid space: normal fetal development as demonstrated by transvaginal ultrasound.

Enlargement of the subarachnoid spaces can be seen in the following conditions: communicating hydrocephalus, brain atrophy and benign enlargement of the subarachnoid spaces. These disorders may begin in utero. There are no established normograms for the fetal subarachnoid spaces. This study was conducted in order to determine its normal development. Transvaginal sonography was used to examine the subarachnoid space in 80 fetuses between 16 and 40 weeks' gestation. The sinocortical width (SCW) and craniocortical width (CCW) were measured in a coronal plane at the level of the foramen of Monro. The SCW remained relatively constant during the gestational period. The CCW increased in size from the 20th to the 28th week of pregnancy, with a subsequent gradual decrease until term. Determination of fetal subarachnoid space normograms may potentially help in the diagnosis of pathological conditions affecting this space and allow prenatal counselling.

Adult↗
PubMed1996

[The fetal development curves of newborn infants in the Hospital de Cruces (Vizcaya). II. Length, head circumference and ponderal index].

Taking a 27,641 live birth sample, without congenital or genetical malformations and from single pregnancies, delivered at Cruces Hospital (Vizcaya) from February 17 1987 to December 31st 1992, fetal growth curves of length, head circumference and ponderal index, have been developed. For every variable and in every gestational week, percentile distribution, mean and standard deviation and 95% confidence interval of the mean have been calculated. Charts of intrauterine growth in length, head circumference and weight-length ratio must be use in conjunction with intrauterine weight charts allowing the identification of infants with unusual prenatal growth patterns.

Body Height↗
PubMed1988

Patterns of expression of trichocytic and epithelial cytokeratins in mammalian tissues. III. Hair and nail formation during human fetal development.

Cells forming hair and nail material are characterized by the synthesis of members of a particular group of alpha-keratin polypeptides (trichocytic cytokeratins. "T cytokeratins") different from epithelial cytokeratins ("E cytokeratins"). As the precursor cells to trichocytes are derived from fetal epidermal keratinocytes expressing only E cytokeratins, we have studied the patterns of expression of both T and E cytokeratins in developing human hair-and nail-forming tissues of different fetal stages, by immunocytochemistry using antibodies specific for certain T or E cytokeratins and by two-dimensional gel electrophoresis and immunoblotting. In developing hair follicles up to the early bulbous-peg stage (weeks 12-15 of gestational age), only certain E but no T cytokeratins were identified. T cytokeratins were first detected in the late bulbous-peg stage (in week-14 scalp skin) in certain cells of the central part of the hair cone. In hair-producing follicles (weeks 18-25), the lower hair matrix cells were positive for certain E cytokeratins, whereas T cytokeratins appeared in the uppermost portion of the matrix and, most prominently, in the maturing trichocytes. From the late bulbous-peg stage on. E cytokeratin antibody Ks13.1 selectively decorated the inner root sheath. In finger nail "anlagen", T cytokeratins were detected first in week 12 and 13 fetuses, specifically in cells of the lunula region. In more-advanced stages of nail formation, expression of T cytokeratins extended not only to the upper layers of the ventral nail matrix but was also found, albeit more sparsely, in cells of the whole nail-bed epithelium. Throughout these developmental stages, coexpression of T and E cytokeratins was noted in certain cells, including E cytokeratin 19. While in earlier stages E cytokeratins 10/11, characteristic of epidermal-type cornification, were noted in different regions, including the superficial stratum of the nail bed epithelium, they were later restricted to the epithelium of the proximal nail fold. The results show that terminal trichocytic differentiation starts, both in ontogeny and during the steady growth of hairs and nails, in cells expressing E cytokeratins and that coexpression of E and T polypeptides occurs in both kinds of appendages. While in the hair follicle, the change to the exclusive synthesis of T cytokeratins appears to take place relatively abruptly and simply, the development of nail structures from the ventral nail matrix seems to be more gradual and is characterized by more-complex patterns of coexpression of both kinds of cytokeratins.

Antibodies, Monoclonal↗
PubMed1997

Supratentorial parenchyma in the developing fetal brain: in vitro MR study with histologic comparison.

PURPOSE: To assess the in vitro MR signal of the developing brain through histologic comparisons. METHODS: Five healthy fetal specimens aged 16, 19, 22, 27, and 34 gestational weeks were studied in vitro using T1- and T2-weighted sequences in frontal and axial planes. Neuropathologic studies included sections in the same frontal plane. Comparison of histologic sections with measurements of the relative widths of the layers of different signal intensities enabled us to assign cellular correspondence to each MR layer. RESULTS: In the cerebral mantle, a layered pattern was observed on both T1- and T2-weighted images. In the basal ganglia, signal from the pallidum and thalamus was isointense with white matter from 16 to 22 weeks' gestation; then, from 27 and 34 weeks' gestation, the signal was relatively high on T1-weighted images and low on T2-weighted images. The neostriatum had a relatively low signal on T1-weighted images and a high signal on T2-weighted images from 16 to 27 weeks' gestation: then, at 34 weeks' gestation, the signal was relatively high on T1-weighted images and low on T2-weighted images. CONCLUSION: MR imaging can clearly show specific patterns of growing fetal brain in vitro.

Basal Ganglia↗
PubMed1999

Cyclin-dependent kinase inhibitor expression in human heart failure. A comparison with fetal development.

AIMS: Terminal differentiation of cardiac myocyte is associated with their permanent withdrawal from the cell cycle. In adult end-stage heart failure, significant numbers of myocytes express proliferating cell nuclear antigen yet fail to progress to cell division. Cyclin dependent kinase inhibitors are powerful inhibitors of the cell cycle and may play a direct role both in myocyte development and in preventing cell division in the adult. METHODS AND RESULTS: The expression of the CIP/KIP cyclin dependent kinase inhibitors p21, p27, p57 and the retinoblastoma protein was examined in acute (seen in brain dead transplant donors) and end-stage heart failure by Western blot analysis and compared to that seen in human and rat cardiac development. The expression of p21 showed a gradual increase during development in both rat and man, becoming maximal in adulthood p27. levels showed an initial rise with subsequent continual expression throughout life. p57 expression was detectable at only early stages in rat but persisted throughout life in man. In both acute and end-stage heart failure the levels of p21, p27 and p57 reverted to a pattern similar to that observed in human fetal heart: p21 and p27 declined while p57 expression was significantly increased. In contrast, retinoblast protein levels declined during human heart development but were unaltered in heart failure. CONCLUSIONS: The expression of p21, but not p27 or p57, is consistent with a role in the gradual withdrawal of cardiac myocytes from cell cycle during development. In adult heart failure cyclin dependent kinase inhibitor expression reverts to the fetal pattern but is insufficient to initiate cell cycle activation.

Adult↗
PubMed1975

Systemic and pulmonary hemodynamic responses to adrenergic and cholinergic agonists during fetal development.

Systemic and pulmonary hemodynamic responses to adrenergic and cholinergic agonists were investigated in fetal lambs between 60 days and term gestation. The cardiovascular response to these agents increases with fetal age, and the increase is related to maturation of the effector system rather than the vascular receptors. The fetal pulmonary vascular bed and the ductus arteriosus are the primary components responding to acetylcholine; the systemic response is secondary to the occuring in the lung. Both fetal systemic and pulmonary vascular beds are under alpha-adrenergic control whereas the fetal heart is under beta-adrenergic control.

Acetylcholine↗
PubMed2002

Ligand activation of the aromatic hydrocarbon receptor transcription factor drives Bax-dependent apoptosis in developing fetal ovarian germ cells.

We recently reported that a targeted disruption of the gene encoding the aromatic hydrocarbon receptor (AHR) in mice reduces fetal oocyte apoptosis, leading to a 2-fold increase in the number of primordial follicles endowed at birth. Although the identity of the natural ligand(s) for the AHR remains to be unequivocally established, these findings indicate that the level of AHR function is an important physiological determinant of how many oocytes will succumb to apoptosis during development of the fetal ovaries. Furthermore, the AHR is a well established receptor for polycyclic aromatic hydrocarbons (PAHs), a class of ubiquitous environmental chemicals known to cause the death of female germ cells in fetal life. Given the possibility that the AHR serves as a key mediator of fetal oocyte death under both physiological and pathological situations, this study was conducted to more fully examine the impact of PAH-AHR interaction on fetal ovarian germ cells. In addition, experiments were designed to begin identification of the mechanism(s) by which ligand activation of the AHR induces prenatal oocyte depletion after transplacental exposure of fetuses to PAHs in vivo. Embryonic d 13.5 murine fetal ovaries cultured in the presence of PAHs exhibited a high level of germ cell loss via apoptosis that was prevented by the selective AHR antagonist, alpha-napthoflavone (ANF). Immunohistochemical analysis revealed an accumulation of Bax protein in germ cells of fetal ovaries exposed to PAHs before the onset of apoptosis, whereas cotreatment with ANF inhibited the induction of Bax expression. The functional importance of increased Bax expression to the cytotoxic response was confirmed by findings that fetal ovarian germ cell loss caused by in utero exposure of wild-type female fetuses to PAHs was not observed in Bax-deficient female fetuses exposed in parallel. We conclude that a central role exists for the AHR in transducing the actions of PAHs in fetal ovarian germ cells, and that the proapoptotic Bcl-2 family member, Bax, is a required mediator of PAH-induced oocyte loss in female fetuses exposed to PAHs in utero.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2001

[Docosahexaenoic acid (DHA) in fetal development and in infant nutrition].

Docosahexanoic acid (C22:6, DHA) is a highly unsaturated omega-3 fatty acid that forms part of the central nervous and visual system structures. DHA is synthesized from its precursor, alfa-linolenic acid, that is also a omega-3 fatty acid and can be obtained from vegetable oils. Marine organisms, specially fish, are good nutritional sources of DHA and eicosapentanoic acid (EPA), another omega-3 fatty acid that has a role in vascular homeostasis. DHA increases membrane fluidity, improving neurogenesis, synaptogenesis and the activity of retinal photoreceptors. The fetus, specially during the last trimester of pregnancy, has high DHA requirements. It is provided by the mother, since fetal DHA synthesis is negligible in this stage of development. Breast feeding provides DHA to the child, but most replacement artificial formulas do not provide this fatty acid. At the present moment, many products for infant nutrition contain DHA.

Brain↗
PubMed1995

Rodent models for studying steroids and hypertension: from fetal development to cells in culture.

We have used several different approaches to study the role of steroids in hypertension, including rodent in vivo models, transgenic animals, and cell culture systems. Using the developing rodent fetus as a model for the ontogeny of regulation of glucocorticoid and mineralocorticoid synthesis, we found that in the developing rodent fetus, expression of both P450scc (cholesterol side chain cleavage) and P450c11 beta (11 beta-hydroxylase) mRNAs occur early, before there is complete organization of the fetal adrenal. Even after the zones of the adrenal are evident, the fetal adrenal still does not express the glomerulosa-specific P450c11AS (aldosterone synthase) mRNA. Stimulating maternal adrenal mineralocorticoid or glucocorticoid synthesis does not affect accumulation of fetal adrenal steroidogenic mRNAs, suggesting that the rodent fetal adrenal may be somewhat transcriptionally quiescent in vivo. We also used two different transgenic rodent systems to study the roles of steroids in hypertension. Using promoter-directed tumorigenesis in transgenic mice, we created transgenic mice that expressed SV40 T antigen under control of the P450scc promoter. Massive adrenal tumors, but not gonadal tumors, developed in all transgenic mice, and cells from these tumors were easily cultured. Using a novel selection tactic, we obtained several adrenocortical cell lines which have distinct characteristics, suggesting they were locked into various stages of differentiation; both expression of steroidogenic mRNAs and the steroids synthesized differ among the lines. Regulation of steroid synthesis and mRNA abundance also varies among cell lines. Several cell lines also express mouse renin, and its synthesis, secretion, and mRNA abundance is also hormonally regulated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1998

Localization of mRNA expression and activation of signal transduction mechanisms for cannabinoid receptor in rat brain during fetal development.

In the present work, we analyzed cannabinoid receptor mRNA expression, binding and activation of signal transduction mechanisms in the fetal rat brain or in cultures of fetal neuronal or glial cells. Cannabinoid receptor binding and mRNA expression were already measurable at GD14, but they were only located in discrete regions at GD16. Among these, the hippocampus, the cerebellum and the caudate-putamen area, three regions that contain a marked signal for both binding and mRNA in the adult brain. Significant levels of binding and, in particular, of mRNA transcripts were also detected at GD16 in the cerebral cortex, midbrain and brainstem. These structures contain relatively low levels of binding and mRNA in the adult brain, suggesting that cannabinoid receptor gene is transiently expressed in atypical areas during the fetal period. The signal for cannabinoid receptor mRNA in the hippocampus, caudate-putamen and cerebral cortex progressively increased from GD16 up to GD21. At GD18 and GD21, mRNA transcripts could be measured in discrete nuclei, such as septum nuclei, ventromedial hypothalamic nucleus and others. The cerebral cortex exhibited the highest mRNA levels at GD21, although this was not accompanied by a parallel increase in binding. An important aspect is that binding measured at these ages represent binding to functional receptors because their activation by WIN-55,212-2 increased [35S]GTPgammaS binding in the same areas. This increase was reversed by a specific antagonist, SR141716. The areas where the stimulation was more marked were the midbrain and brainstem. Using cell cultures, we have observed that cannabinoid receptor mRNA is present in cortical and hippocampal neuronal cells, but not in the glial cells. However, WIN-55,212-2 was capable of stimulating [35S]GTPgammaS binding in membrane fractions obtained from cortical glial cells and this stimulation was reversed by SR141716. This was not seen with hippocampal glial cell cultures, but occurred in hippocampal and cortical neurons. In addition, the activation of these receptors with Delta9-tetrahydrocannabinol significantly reduced forskolin-stimulated cAMP production in cortical neuronal or glial cell cultures and this effect was reversed by SR141716. In summary, we have detected cannabinoid receptor binding, mRNA expression and activation of signal transduction mechanisms in the fetal rat brain (GD14-GD21), which support the view that the system constituted by these receptors and their putative endogenous ligands might play a role in specific molecular events of the brain development. Of relevance is that binding and mRNA expression appear atypically distributed in the fetal brain as compared with the adult brain, even, that their presence in white-matter-enriched areas might presumably indicate their location in non-neuronal cells. These studies with cell cultures suggest that CB1 receptor subtype is located in neuronal cells obtained from fetal brain, although preliminary evidence is provided of the existence of another receptor subtype operative in glial cells obtained from the cerebral cortex.

Animals↗