Fetoplacental inflammation secondary to intra-amniotic (IA) microbial colonization and subclinical chorioamnionitis provide a basis for the development of preterm birth and cerebral palsy (CP) by preferentially affecting the fetal brain tissue.
The larger size placenta and the heavier placenta are demonstrated to have greater number of chorionic villi, this increased number of chorionic villi, increases the surface area of the placenta resulting in better fetoplacental perfusion.
(2015) found through immunohistochemical studies that the placental tissue in DM1, DM2, and GDM presents normal energy levels of vascular endothelial cadherin and b-catenin in the fetoplacental vessels as long as the patient has not been treated with insulin.
As a result of impaired uteroplacental blood flow, manifestations of preeclampsia may be seen in the fetoplacental unit like intrauterine growth restriction (IUGR), oligohydramnios, placental abruption and non-reassuring foetal status (NST).
It was also found that all mothers studied faced gestational toxicosis of various degrees throughout pregnancy; anemia in 67.7%, fetoplacental insufficiency in 87.7%, intrauterine infection in 70.3%, endocrine, nutritional and metabolic diseases in 40%, polyhydramnios in 86.5%, multiple pregnancies in 13.5% and 8.1% of mothers with low weight also gave birth to LBW children.
We also demonstrated that three neonicotinoids (thiacloprid, thiamethoxam, and imidacloprid) increased the production of estrone and estradiol, yet strongly inhibited the production of estriol in a fetoplacental co-culture model of steroidogenesis during pregnancy (Caron-Beaudoin et al.
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