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Group models of prenatal care continue to grow in popularity.
Therefore in models of prenatal cocaine exposure both migration and maturation of these progenitor cells is delayed.
A causal relationship in this epidemiological link has received considerable support from several experimental models of prenatal infection and/or immune activation.
In addition, many animal experiments have begun to explore mechanistic models of prenatal stress and neurodevelopmental outcomes.
Animal models of prenatal stress (psychological, behavioural, nutritional, or metabolic…) have identified major sex- and time-specific effects on the offspring.
Importantly, the expression of many of these factors that are bivalently marked and regulated by PcG and TrxG is disrupted in various models of prenatal alcohol exposure; moreover, this disruption is associated with profound errors in neuronal patterning.
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Factors that influence the preferred model of prenatal care patients were assessed.
To determine if the CenteringPregnancy model of prenatal care improves maternal health behaviors in adolescent pregnancy.
Results are supportive of a teratological model of prenatal cocaine exposure for infant reactivity/regulation in infancy.
To explore whether the effect (if any) of participation in prenatal care on mode of delivery varies by socioeconomic status, we specify the following model of prenatal care utilization: P left({P}_{ijt}right)=f left({S}_{ijt}/{X}_{ijt},{e}_{ijt}right) (2 where i indexes individuals, j hospitals, and t years.
Here, we combined a neonatal cross-fostering design with a mouse model of prenatal immune challenge induced by maternal gestational treatment with the viral mimetic poly(I C) to dissect the relative contribution of prenatal and postnatal maternal effects on the offspring.
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