1. The Fetus Doesn’t Accept Complements
The fetus is a semi-allogenic graft in its mother.
It is able to thrive without GVH rejection, is the most enigmatie aspects of reproduction.
The importance of suppressing the innate immune system involving complement mediated cell killing in fetoplaceutal tolerance was suggested by discovery(1).
That the human placenta produces several inhibitors of the complement.
Thus the human placenta is better adapted to prevent maternal complement attack during prepnancy.
Lack of these inhibtors the fetus will be aborted spontaneously.

2. The Placenta PGE2 and Perturition(2)
The placenta, by secreting PGE2 (and possibly other factors such as adenosine), modifies the function of key organ systems allowing the fetus to survive and develop in the aqueous environment of the uterus.

During fetal development, fetal organs and metabolic pathways can mature while their function is suppressed by placental PGE2.
At birth, by ligating the cord and removing the placenta as the source of these inhibitory substances, the newborn is able to adapt readily to its new environment with fully-functional, mature organ systems.

3. Proteome Analysis of Vernix Caseosa
A white creamy substance designated Vernix caseosa (latin for “Cheese-like varnish”) covers the skin of the fetus during the last trimester of pregnancy.
The human is the only species known to produce this substance, and its function has been debated for decades.

Many protective functions have been proposed, such as antimicrobial protection, heat insulation, moisturization and protection of the skin from macerating effects of the amniotic fluid.
Other functions have also been suggested, such as hormonal effects, anti-flammatory effects, nutritive functions, and facilitation of passage through the birth canal.
Furthermore, vernix has been suggested to constitute a mechanical obstruction to bacterial passage.
The composition of vernix is water (81%), lipids (9%), and proteins (10%).
Altogether, 41 proteins were identified by Maria Tollinetal(3).
Of these proteins, 16(39%) are involved in innate immunity and 12(29%) have been demonstrated to have direct antimicrobial activities.

(B) Prematurity and IUGR(Intrauterine Growth Retardation)

1. Fetal biochemisty in Growth Retardation(4)
a. Cytogenetic Studies
A chromosomal abnormality high (17%), triploid (7%), trisomy 18 (6%), trisomy 21 (1%), trisomy 13 (1%) translocation or deletions (2%).
b. Acidosis and hypoxia
c. Hematology
Erythropoietin increases in proportion in the degree of fetal acidemia.
Erythroblast count increase platelet and leucocyte in IUGR may be decreased.
d. Glucose
Glucose decrease due to impaired transfer or increased glycolysis in anaerobic metabolism to lactate.
e. Lipid metabolism
SGA fetuses have high triglyceride levels, reflecting reduced triglyceride oxidation or less incorporation into body fat.
f. Protein metabolism
In growth retardation there are low levels of the essential amino acids.
g. Adrenal steroids
Cortisol and adreno-cortico-trophic hormone (ACTH) appear not to change significantly.
h. Thyroid function
TSH concentration is increased and thyroid hormone concentration are reduced.

2. Intrauterine Growth Restriction Affects the Preterm Infant’s Hippocampus
Thirteen preterm infants born with IUGR after placental insufficiency were compared with 13 infants with normal intrauterine growth age matched for gestational age.
The hippocampal structural differences were defined using voxel-based morphometry and manual segmentation.

The specific neurobehavioral function was evaluated by the Assessment of Preterm Infants.
Voxel-based morphometry detected significant gray matter volume differences in the hippocampus between the two groups.

This finding was confirmed manual segmentation of the hippocampus with a reduction of hippocampal volume after IUGR.

The hippocampal volum reduction was further associated with functional behavioral differences at term-equivalent age in all six subdomains of the Assessment of Preterm Infants.

We conclude that hippocampal development in IUGR is altered and might result from a combination of maternal corticosteroid hormone exposure, hypoxemia, and micronutrient deficiency.

3. Fetal Growth Restriction Is Associated With Prioritization of Umbilical Blood Flow to the Left Hepatic Lobe at the Expense of the Right Lobe
Placental insufficiency is a major cause of impaired fetal growth and premature birth, which, in turn, is associated with an increased risk of chronic disease in later life.
The venous perfusion of the fetal liver differs from that after birth in that, venous blood flows to it both from the splanchnic bed via the portal vein and from the placenta via the umbilical vein (Fig. 4A).

Therefore, we developed a technique for blood flow measurement in the main portal stem and established reference ranges for this flow, showing that in uncompromised fetuses 15-20% of the venous liver perfusion is of splanchnic origin.

In this study, we have gone on to characterize hepatic venous perfusion in FGR and to test the hypothesis that portal blood flow may compensate for insufficient umbilical blood flow to the liver when the latter is diverted through the ductus venosus.
We hypothesized that in growth-restricted fetuses portal blood flow compensates for insufficient umbilical blood flow to the liver.

In 29 fetuses with fetal growth restriction (estimated fetal weight ≦5th percentile), weused ultrasound to measure blood flows in the umbilical vein, ductus venosus, left portal vein, and equally affecting both liver lobes.

However, portal replaced umbilical flow to the right lobe, in a manner graded according to placental vascular resistance; in extreme cases, the right lobe received no umbilical perfusion.

In fetal growth restriction, the liver suffers from venous hypoperfusion, and portal blood partially replaces umbilical flow to the right lobe; this will result in right liver lobe hypoxemia.

This striking prioritization in nutrient delivery of left over right lobes suggests an adaptive response to poor placental perfusion that may have functional consequences.