The high vascular resistance outside of the placenta leads to higher maternal blood pressure throughout the body.The fetal cells that implant into the uterine wall are known as the trophoblast. The hemochorial placenta bathes the fetal trophoblast in maternal blood by forming lacunae, or lakes, of the mothers blood that surround fetal tissue. The lacunae are filled by the spiral arteries, which means that the mothers blood pressure is the driving force behind the introduction of new blood, which contains both oxygen and food for the fetus, to the system. It is thought that humans need the increased diffusion provided by the hemochorial placenta in order to grow the large brains compared to their body size that distinguish them from other primates. Incorrect placental implantation
It is thought that "failings" in normal hemochorial placental structure lead to pre-eclampsia and gestational hypertension. The human placenta implants "earlier, deeper, and more extensively" into the uterine wall, which can potentially lead to many problems that are found in human pregnancies, but not as much in other animals. Miscarriage and pre-eclampsia are both very rare in other species, but are two of the most common pregnancy-related diseases in humans. The genetic roots of gestational hypertension and pre-eclampsia are certain, as women with a family history of the condition are three times more likely to develop it when they are pregnant.One of the potential causes of gestational hypertension and pre-eclampsia is when the trophoblast does not invade far enough into the uterine lining.
X-linked endothelial corneal dystrophy (XECD) is a rare form of corneal dystrophy described first in 2006, based on a 4-generation family of 60 members with 9 affected males and 35 trait carriers, which led to mapping the XECD locus to Xq25. It manifests as severe corneal opacification or clouding, sometimes congenital, in the form of a ground glass, milky corneal tissue, and moon crater-like changes of corneal endothelium. Trait carriers manifest only endothelial alterations resembling moon craters.As of December 2014, the molecular basis for this disease remained unknown, although 181 genes were known to be within the XECD locus, of which 68 were known to be protein-coding. References


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