Topic
Fetus
About: Fetus is a research topic. Over the lifetime, 21567 publications have been published within this topic receiving 646380 citations. The topic is also known as: foetus & fœtus.
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TL;DR: Using congenital adrenal hyperplasia (CAH) as a model system, this study presents a strategy for the noninvasive prenatal exclusion of an autosomal recessive condition through the detection of fetal DNA in maternal plasma and the approach described in this study may potentially be applicable to other autosome recessive conditions.
Abstract: The presence of fetal DNA in maternal plasma has allowed the development of strategies for noninvasive prenatal diagnosis (1). However, because fetal DNA in maternal plasma circulates among a background of maternal DNA, strategies for noninvasive prenatal diagnosis with applications of fetal DNA in maternal plasma have been confined to the detection of autosomal dominant, paternally inherited genetic traits, such as fetal gender (for sex-linked disorders) (1), rhesus D (2)(3), myotonic dystrophy (4), and achondroplasia (5). Using congenital adrenal hyperplasia (CAH) as a model system, we present a strategy for the noninvasive prenatal exclusion of an autosomal recessive condition through the detection of fetal DNA in maternal plasma. The approach described in this study may potentially be applicable to other autosomal recessive conditions.
More than 90% of cases of CAH are a result of deficiency of 21-hydroxylase, an enzyme of the adrenal gland involved in the synthesis of glucocorticoids and mineralocorticoids. 21-Hydroxylase is encoded by CYP21 , a MHC class III gene located on chromosome 6p21.3. Most mutations causing 21-hydroxylase deficiency are caused by either gene deletions or gene conversions, whereby deleterious mutations are transferred from the nearby pseudogene, CYP21P , which shares 98% homology with CYP21 (6). Consequent to profound deficiency or the complete absence of activity of 21-hydroxylase, severe forms of CAH manifest as salt-wasting attributable to impaired synthesis of mineralocorticoids and glucocorticoids. In addition, the excess buildup of metabolic precursors causes excessive androgen production, leading to virilization of female fetuses (6). Hence, dexamethasone therapy is customarily prescribed prenatally to prevent in utero virilization of an affected female fetus through suppression of the excessive …
143 citations
TL;DR: The results indicate that the placenta is not a major source of leptin production in rats and also suggest the physiological significance of leptin in rat pregnancy.
143 citations
TL;DR: In this article, a longitudinal study in intrauterine growth-restricted fetuses was conducted to determine whether the umbilical vein velocity reduction, which, in turn, reduces blood flow, persists throughout gestation or represents a late event that precedes indicated delivery.
143 citations
TL;DR: Keeping normal maternal thyroid hormone status is likely to be the primary factor in ensuring adequate transplacental thyroid hormone passage and appropriate iodide supply to the fetus.
Abstract: The transplacental passage of thyroid hormones from the maternal circulation to the fetal circulation within the human hemochorial placenta is important for normal fetal development, particularly the development of the central nervous system. The role of maternal thyroid hormones is particularly important in the first half of pregnancy, before the onset of endogenous thyroid hormone production in the fetus. The human placenta regulates the quantity and composition of different forms of transported thyroid hormones to ensure that the requisite levels are present in the fetus for each stage of development. Transplacental thyroid hormone supply to the fetus is modulated by several factors, including the following proteins: plasma membrane transporters, which regulate the passage of thyroid hormones in and out of cells; iodothyronine deiodinases, which metabolize thyroid hormones; and proteins within trophoblast cells, which bind thyroid hormones. In pathological situations of either maternal or fetal thyroid hormone deficiency during pregnancy, the placenta seems to lack the full compensatory mechanisms necessary to optimize maternal-fetal transfer of thyroid hormones. Inadequate passage of thyroid hormones can lead to suboptimal fetal thyroid hormone levels, which might contribute to the neurodevelopmental delay associated with such conditions. Thus, maintaining normal maternal thyroid hormone status is likely to be the primary factor in ensuring adequate transplacental thyroid hormone passage and appropriate iodide supply to the fetus.
143 citations