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.

Uteroplacental blood flow. The story of decidualization, menstruation, and trophoblast invasion

Abstract: Sexual reproduction in the ocean necessitates only the combination of gametes, followed by absorption of nutrients and oxygen from the surrounding watery medium. As life moved from the sea to the land, reproductive strategies required compensation for the loss of this aquatic environment. For mammals and a few other animals, the solution to this problem was the development of the placenta, the means by which the fetus extracts nutrients from its environment. As the animals that used the placenta evolved from small rodent-like creatures with short gestations to larger animals with prolonged gestations, the demands of the developing fetus grew. Whereas the placenta of the fetal pig, with a gestational period of a little less than 4 months, can extract sufficient nutrients from the mother by simple diffusion across the uterus to the placenta, the human fetus needs a far more complex uteroplacental relationship. Several evolutionary solutions to the increased demands of fetuses can be observed. 1 One approach was a larger placenta. For example, the chinchilla has a neonatal:placental weight ratio of 30:1, whereas the human has a 6:1 ratio. Another means to greater nutritional support for the fetus was to increase the surface area of contact between fetal circulation in the placenta and maternal circulation. The pig fetus has a diffuse placenta that makes contact with the mother’s uterus by a simple folded contact. The human placenta, on the other hand, has a complex villous structure, similar to the sea anemone’s tentacles waving in the sea, that greatly increases the contact surface area between the mother’s blood space and the fetal circulation. Despite this increased fetal-maternal contact, the system is still rather inefficient. We can quantify this by considering the amount of oxygen in the maternal blood that enters the human placenta and the amount of oxygen in the fetal blood that leaves the placenta. Maternal blood has a pO2 of around 100, whereas the pO2 of umbilical vein blood is around 35 to 40. This represents an efficiency of only 35 to 40%. Therefore, it also became necessary to greatly increase the flow of maternal blood into the intervillous space during pregnancy. 2,3 Without this increased maternal blood flow, preterm birth and fetal loss occur. 4 One of two mechanisms can increase maternal flow: increased total body blood flow or increased blood flow to the placental bed through the uterine spiral arteries. For the human, evolution has selected the latter mechanism, limiting the overall systemic effects that increased total body blood flow would produce.

Hormonal regulation of fetal growth.

Abstract: Fetal growth is a complex process depending on the genetics of the fetus, the availability of nutrients and oxygen to the fetus, maternal nutrition and various growth factors and hormones of maternal, fetal and placental origin. Hormones play a central role in regulating fetal growth and development. They act as maturational and nutritional signals in utero and control tissue development and differentiation according to the prevailing environmental conditions in the fetus. The insulin-like growth factor (IGF) system, and IGF-I and IGF-II in particular, plays a critical role in fetal and placental growth throughout gestation. Disruption of the IGF1, IGF2 or IGF1R gene retards fetal growth, whereas disruption of IGF2R or overexpression of IGF2 enhances fetal growth. IGF-I stimulates fetal growth when nutrients are available, thereby ensuring that fetal growth is appropriate for the nutrient supply. The production of IGF-I is particularly sensitive to undernutrition. IGF-II plays a key role in placental growth and nutrient transfer. Several key hormone genes involved in embryonic and fetal growth are imprinted. Disruption of this imprinting causes disorders involving growth defects, such as Beckwith-Wiedemann syndrome, which is associated with fetal overgrowth, or Silver-Russell syndrome, which is associated with intrauterine growth retardation. Optimal fetal growth is essential for perinatal survival and has long-term consequences extending into adulthood. Given the high incidence of intrauterine growth retardation and the high risk of metabolic and cardiovascular complications in later life, further clinical and basic research is needed to develop accurate early diagnosis of aberrant fetal growth and novel therapeutic strategies.

Highly efficient maternal-fetal Zika virus transmission in pregnant rhesus macaques

Abstract: Infection with Zika virus (ZIKV) is associated with human congenital fetal anomalies. To model fetal outcomes in nonhuman primates, we administered Asian-lineage ZIKV subcutaneously to four pregnant rhesus macaques. While non-pregnant animals in a previous study contemporary with the current report clear viremia within 10-12 days, maternal viremia was prolonged in 3 of 4 pregnancies. Fetal head growth velocity in the last month of gestation determined by ultrasound assessment of head circumference was decreased in comparison with biparietal diameter and femur length within each fetus, both within normal range. ZIKV RNA was detected in tissues from all four fetuses at term cesarean section. In all pregnancies, neutrophilic infiltration was present at the maternal-fetal interface (decidua, placenta, fetal membranes), in various fetal tissues, and in fetal retina, choroid, and optic nerve (first trimester infection only). Consistent vertical transmission in this primate model may provide a platform to assess risk factors and test therapeutic interventions for interruption of fetal infection. The results may also suggest that maternal-fetal ZIKV transmission in human pregnancy may be more frequent than currently appreciated.