1,721,176 research outputs found

    Human fetal growth and organ development : 50 years of discoveries

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    Knowledge about human fetal growth and organ development has greatly developed in the last 50 years. Anatomists and physiologists had already described some crucial aspects, for example, the circulation of blood during intrauterine life through the fetal heart, the liver as well as the placenta. However, only in the last century physiologic studies were performed in animal models. In the human fetus, the introduction of ultrasound and Doppler velocimetry has provided data about the growth and development of the fetus and of the circulation through the different fetal districts. Moreover, in the last 2 decades we have learned about fetal oxygenation and fetal nutrient supply caused by the availability of fetal blood samples obtained under relatively steady state conditions. These studies, together with studies using stable isotope methodologies, have clarified some aspects of the supply of the major nutrients for the fetus such as glucose, amino acids, and fatty acids. At the same time, the relevance of placental function has been recognized as a major determinant of fetal diseases leading to intrauterine growth restriction. More recently, the availability of new tools such as 3-dimensional ultrasound and magnetic resonance imaging, have made possible the evaluation of the growth and development of fetal organs. This knowledge in the healthy fetus will improve the ability of clinicians to recognize abnormal phenotypes of the different fetal organs, thus allowing to stage fetal diseases

    Aspetti riproduttivi

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    Undesired effects of steroids during pregnancy

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    Antenatal corticosteroid administration for enhancing fetal lung maturity can be expected to induce negative maternal and fetal side-effects. Maternal short-term effects after multiple courses of corticosteroids are an increase of infections and a higher incidence of endometritis and chorionamnionitis in patients with premature rupture of membranes. A single dose of corticosteroid induces an increase in the count of maternal white blood cells and metabolic effects such as the augmentation of amino acid concentration and of fasting glucose levels in maternal plasma. Negative fetal effects of antenatal corticosteroids are a reduction of fetal body and breathing movements and a reduction of fetal heart rate variation, without any changes in Doppler waveform patterns of fetoplacental vessels. It has been suggested that a multiple course of corticosteroids antenatally might induce negative effects on fetal intrauterine growth and on neonatal birth weight. In addition, multiple courses are associated with an increased risk of early-onset neonatal sepsis

    Placental-fetal interrelationship in IUGR fetuses - A review

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    The role of placental function in maintaining an adequate fetal growth has been addressed by many different laboratories. The relationship between maternal and fetal circulation in the placenta is crucial for efficient exchanges of oxygen and nutrients. Moreover, maturational changes are taking place throughout gestation within the placenta in order to increase the transfer capacities while fetal/placental weight ratio is significantly decreasing. In human pregnancies, an impairment in the invasion of fetal trophoblast cells into the maternal decidua has been hypothesized as a cause of placental insufficiency leading to intrauterine growth restriction (IUGR). This condition has been associated with a number of adaptive changes taking place in both placenta and fetus. Adaptive changes can be followed by pathology leading to fetal death and therefore staging of the disease is fundamental for timing of delivery. A classification of the severity of IUGR in human pregnancies has been proposed based upon fetal heart rate (FHR) and Doppler velocimetry of the umbilical artery (pulsatility index or PI). This classification of clinical severity reflects different degrees of placental insufficiency and is associated with significant differences in placental nutrient exchange. Only those IUGR with pathological PI and FHR are associated with increasing degrees of hypoxemia and lacticacidemia. Furthermore, significant differences are observed in the transplacental glucose gradient in the most severe cases and the placental transport of essential amino acids is significantly reduced both in vivo and in vitro. These findings suggest that both placental metabolism and transport are altered in intrauterine growth restriction in humans
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