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The timing of endometrial exposure to estrogen is critical as specific molecular cues associated with uterine receptivity occur simultaneously with conceptus estrogen synthesis and abnormal exposure to estrogen prior to day 12 results in compromised pregnancy establishment [ 13- 15].
For weight at birth, preterm delivery is the end result of a compromised pregnancy, so it is unsurprising that an infant born preterm usually weighs less than a fetus of the same gestational age in utero, indicating that some degree of deceleration in intrauterine growth has occurred.
In addition, treatment × cyclicity and treatment × parity interactions were found to affect pregnancy success, where anovulatory cows and older cows had compromised pregnancy outcomes on the ACT treatment but not on the TAI treatment.
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Since components 2 and 4 in this population most plausibly consist of compromised pregnancies, we see that infants from compromised pregnancies need not share a common birthweight-specific mortality curve.
The framework developed in this paper avoids assuming the existence of an interval of birthweights over which there are no compromised pregnancies and does not constrain birthweights within compromised pregnancies to be normally distributed.
For example, in a 2-component normal mixture describing birthweights for white singletons in the United States, there is not an obvious biological characterization for the two components: we may say that the component with the smaller mean reflects compromised pregnancies, but we cannot immediately attribute the compromised pregnancies to a specific biological mechanism.
Conclusions: Alterations in systemic vascular resistance associated with compromised pregnancies are unlikely to result from or produce an alteration in the structure of omental small arteries.
Aberrant expressions of some miRNAs were reported in the placenta from compromised pregnancies, suggesting that the miRNA profiling of chorionic villi could be related with early recurrent miscarriage (RM).
These biomarkers also represent potential new therapeutic targets to "rescue" placental vascular development and thus fetal growth in compromised pregnancies.
We regard component 3 as most plausibly representing uncompromised pregnancies in this population, so that components 2 and 4 most plausibly consist of compromised pregnancies.
Unlike a contaminated normal model, our approach does not assume the existence of an interval of birthweights over which there are no compromised pregnancies.
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