Disease relevance of Fetal Development

• MAIN OUTCOME MEASURE: Birth weight, gestation, fetal growth by smoking status and CYP1A1 MspI (AA vs Aa and aa, where Aa and aa were combined because of small numbers of aa and similar results), and GSTT1 (present vs absent) genotypes [1].
• Retinoic acid embryopathy: timing of exposure and effects on fetal development [2].
• Human red cell Aquaporin CHIP. II. Expression during normal fetal development and in a novel form of congenital dyserythropoietic anemia [3].
• In the same experiments, the effect of maternal protein deficiency on fetal development and serum somatomedin levels was examined [4].
• Heme oxygenase expression in human placenta and placental bed: reduced expression of placenta endothelial HO-2 in preeclampsia and fetal growth restriction [5].

Psychiatry related information on Fetal Development

• Maternal smoking, alcohol drinking, caffeine consumption, and fetal growth: results from a prospective study [6].
• Neurodegeneration in fetal development of Down syndrome (DS) patients is proposed to result in apparent neuropathological abnormalities and to contribute to the phenotypic characteristics of mental retardation and premature development of Alzheimer disease [7].
• The availability of choline during critical periods of fetal development alters hippocampal development and affects memory function throughout life [8].

High impact information on Fetal Development

• During mouse embryonic development, PMCA1 is ubiquitously detected from the earliest time points, and all isoforms show spatially overlapping but distinct expression patterns with dynamic temporal changes occurring during late fetal development [9].
• The paternally expressed Igf2 encodes a potent fetal growth factor and the maternally expressed H19 encodes a non-coding RNA (refs 1,2) [10].
• Here we show that Stat5 is essential for the high erythropoietic rate during fetal development [11].
• Fetal insulin secretion in response to maternal glycaemia plays a key role in fetal growth, and adult insulin secretion is a primary determinant of glucose tolerance [12].
• A transcription factor, Cbfa1, which belongs to the runt-domain gene family, is expressed restrictively in fetal development [13].

Chemical compound and disease context of Fetal Development

• Melatonin could be useful in treating preeclampsia and possibly other clinical states involving excess free radical production, such as fetal growth restriction and fetal hypoxia [14].
• Such decrease in fetal insulin secretion may limit the rate of fetal glucose utilization during chronic hyperglycemia and thereby modulate the rate of fetal growth [15].
• We evaluated the involvement of a possible dysfunction of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in the fetal growth retardation and poor growth rates of children born with intrauterine growth retardation (IUGR) [16].
• Poor iron and folic acid status has also been linked to preterm births and fetal growth retardation [17].
• Hypoxia down-regulates placenta growth factor, whereas fetal growth restriction up-regulates placenta growth factor expression: molecular evidence for "placental hyperoxia" in intrauterine growth restriction [18].

Biological context of Fetal Development

• These findings provide a molecular basis for overexpression of IGF-II in Wilms tumors and suggest that WT1 negatively regulates blastemal cell proliferation by limiting the production of a fetal growth factor in the developing vertebrate kidney [19].
• The phenotype of mutant mice suggests that activin beta B (1) plays a role in late fetal development and (2) is critical for female fecundity [20].
• Monogenic diseases that impair sensing of glucose, lower insulin secretion, or increase insulin resistance are associated with impaired fetal growth [21].
• The relative levels of these two transcripts increased during later fetal development; by the 20th day of gestation retinol-binding protein mRNA levels were comparable to those of the adult liver, while the levels of transthyretin mRNA were only 46% of those of the adult liver [22].
• Transferrin as a fetal growth factor: acquisition of responsiveness related to embryonic induction [23].

Anatomical context of Fetal Development

• Here we show that deletion from the Igf2 gene of a transcript (P0) specifically expressed in the labyrinthine trophoblast of the placenta leads to reduced growth of the placenta, followed several days later by fetal growth restriction [24].
• Furthermore, in contrast to IL-7Ralpha-/- mice, FL-/- x IL-7Ralpha-/- mice also lack mature B cells and detectable committed B cell progenitors during fetal development [25].
• These results are consistent with an eventual implication of TRH in the endocrine regulation of metabolism or in the fetal development of pancreas [26].
• The transient expression of AT2 receptors in the mesenchyme of the fetus suggests a role of angiotensin II in fetal development [27].
• Roles of serum thyroxine-binding proteins and maternal thyroid hormones in fetal development [28].

Associations of Fetal Development with chemical compounds

• Effects of maternal marijuana and cocaine use on fetal growth [29].
• Noradrenaline is essential for mouse fetal development [30].
• In addition, vitamin A is involved in fetal development and in the regulation of proliferation and differentiation of cells throughout life [31].
• The response of four of these genes to estradiol is diminished during late fetal development, but the responsiveness is recovered within a week after hatching [32].
• DESIGN, SETTING, and PATIENTS--A cohort of 431 women, enrolled in a multicenter study within 21 days of conception, was monitored throughout pregnancy to determine (1) caffeine exposure, (2) exposure to other risk factors, (3) fetal growth as assessed by ultrasonography, and (4) pregnancy outcome [33].

Gene context of Fetal Development

• Furthermore, they mark the emergence of satellite cells during fetal development, and do not require Pax3 function [34].
• These results show that Igf2r is paternally imprinted and reveal that the receptor is crucial for regulating normal fetal growth, circulating levels of IGF2, and heart development [35].
• However, the absolute number of HSCs increased during fetal development in the Sl/Sl mice [36].
• The result indicates that Grb10 action is essentially independent of insulin-like growth factor 2, providing evidence that imprinting acts on at least two major fetal growth axes in a manner consistent with parent-offspring conflict theory [37].
• To determine the direct effects of PAX2 mutations on kidney development fetal kidneys of mice carrying a Pax2 (1Neu)mutation were examined [38].

Analytical, diagnostic and therapeutic context of Fetal Development

• To assess whether leptin is involved in fetal growth and development we have examined the distribution of mRNAs encoding leptin and the leptin receptor (which has at least six splice variants) in the 14.5-day postcoitus mouse fetus and in the placenta using reverse transcription-PCR and in situ hybridization [39].
• Structure-function analyses of thrombomodulin by gene-targeting in mice: the cytoplasmic domain is not required for normal fetal development [40].
• RESULTS: Immunohistochemistry experiments demonstrated that WISP3 protein is expressed in the midzone chondrocytes of normal adult articular cartilage, in chondrocyte clusters of osteoarthritic cartilage, and in the zone of proliferating chondrocytes of fetal growth cartilage [41].
• To assess the importance of endogenous insulin release in regulation of normal fetal growth, eight fetal lamb pairs were given either an intravenous injection of streptozocin (STZ), a nitrosourea that selectively damages pancreatic beta-cells, or buffer infusion (controls) [42].
• We have investigated the effects of fetal growth restriction, induced by restriction of placental growth and function (PR), on 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD-1) and 11betaHSD-2 messenger RNA (mRNA) expression in fetal tissues in the sheep, using Northern blot analysis [43].

References