Objective
This prospective observational study explored the association of hypertensive disorders of pregnancy and small-for-gestational age (SGA) with obstructive sleep apnea (OSA) as determined by screening measures for OSA and sleep studies.
Study Design
Two symptom-based screening questionnaires, the Berlin Questionnaire (BQ) and the Epworth Sleepiness Scale (ESS), were administered to enroll 1509 gravidae. Screen positive subjects were referred for polysomnography (PSG). The primary outcome was the occurrence of either gestational hypertension or preeclampsia. [a1]Generalized linear models (GLM) were used to estimate the relative risks of associations.
Results
1157 subjects were available for outcomes analysis. Screening positive on the BQ was positively associated with hypertensive disorders in GLM models (aRR=1.90, 95%CI 1.52–2.37).
Conclusion
In this large prospective trial, GLM modeling suggest that the BQ but not the ESS demonstrated significant association with measured adverse pregnancy outcomes, and specific items predicted these outcomes better than others. However, causative association of BQ with OSA cannot be assumed.
Human fetuses with Down syndrome demonstrate abnormal brain growth and reduced neurogenesis. Despite the prenatal onset of the phenotype, most therapeutic trials have been conducted in adults. Here, we present evidence for fetal brain molecular and neonatal behavioral alterations in the Ts1Cje mouse model of Down syndrome. Embryonic day 15.5 brain hemisphere RNA from Ts1Cje embryos (n = 5) and wild type littermates (n = 5) was processed and hybridized to mouse gene 1.0 ST arrays. Bioinformatic analyses were implemented to identify differential gene and pathway regulation during Ts1Cje fetal brain development. In separate experiments, the Fox scale, ultrasonic vocalization and homing tests were used to investigate behavioral deficits in Ts1Cje pups (n = 29) versus WT littermates (n = 64) at postnatal days 3–21. Ts1Cje fetal brains displayed more differentially regulated genes (n = 71) than adult (n = 31) when compared to their age-matched euploid brains. Ts1Cje embryonic brains showed up-regulation of cell cycle markers and down-regulation of the solute-carrier amino acid transporters. Several cellular processes were dysregulated at both stages, including apoptosis, inflammation, Jak/Stat signaling, G-protein signaling, and oxidoreductase activity. In addition, early behavioral deficits in surface righting, cliff aversion, negative geotaxis, forelimb grasp, ultrasonic vocalization, and the homing tests were observed. The Ts1Cje mouse model exhibits abnormal gene expression during fetal brain development, and significant neonatal behavioral deficits in the pre-weaning period. In combination with human studies, this suggests that the Down syndrome phenotype manifests prenatally and provides a rationale for prenatal therapy to improve perinatal brain development and post-natal neurocognition.
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