Fetal brain development is known to be affected by adverse environmental exposures during pregnancy, including infection, inflammation, hypoxia, alcohol, starvation, and toxins. These exposures are thought to alter autophagy activity in the fetal brain, leading to adverse perinatal outcomes, such as cognitive and sensorimotor deficits. This review introduces the physiologic autophagy pathways in the fetal brain. Next, methods to detect and monitor fetal brain autophagy activity are outlined. An additional discussion explores possible mechanisms by which environmental exposures during pregnancy alter fetal brain autophagy activity. In the final section, a correlation of fetal autophagy activity with the observed postnatal phenotype is attempted. Our main purpose is to provide the current understanding or a lack thereof mechanisms on autophagy, underlying the fetal brain injury exposed to environmental insults.

INTRODUCTION: There is limited information on long-term developmental outcomes in infants with neonatal abstinence syndrome (NAS). We evaluated the infant outcomes of women with opioid use disorder based on newborn pharmacologic treatment of NAS after birth.

INTRODUCTION: One of the early physiologic changes in pre-eclampsia (PE) is increased vascular permeability that can cause hemoconcentration. We hypothesized higher hemoglobin (Hgb) may be an early marker for development of PE. METHODS: During a 3 year period, records of women without known renal disease and a gestational age at delivery (GAD) >24 weeks were evaluated. PE was defined as elevated blood pressure (>140/90) and increased protein: creatinine ratio (PCR>0.29). The Hgb obtained between GA 22-32 weeks were reviewed. In addition to GAD, maternal age (MA) and body mass index (BMI) was recorded. Odds ratios (OR, 95% CI) were determined for the development of PE in women with Hgb >12.9 and >13.9 grams. RESULTS: Of the 10,418 deliveries, 901 (8.6%) were diagnosed with PE. Women with PE delivered earlier (37.2 ± 2.8 vs 38.6 ± 2.1 wks, P<.001) and had higher BMI (35.2 ± 7.1 vs 32.6 ± 6.2 Kg/M2, P<.001). Of the 396 women with a Hgb >12.9, 74 developed PE (OR 2.5, 1.8-3.1, P<.001). Other than GAD (34.4±5.5 vs 37.2±3.6 wks, P<.001), PE with Hgb>12.9 did not differ in MA or BMI. Of 44 women who had Hgb>13.9, 14 developed PE (OR 4.7, 2.5-8.9, P<.001). PE with Hgb>13.9 did not differ in GAD, MA or BMI, however sample size was limited. CONCLUSION: In this retrospective case control study, elevated Hgb was associated with PE. Most pregnant women have Hgb between 24 to 30 weeks. This inexpensive, ubiquitous test may provide an additional warning sign for the development of PE.

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