Safety of deep sedation without intubation during surgical abortion in the independent clinic setting.

Objective: To establish the safety of deep sedation without intubation delivered by a certified registered nurse anesthetist (CRNA) in an independent outpatient abortion setting.

Study Design: We performed a review of clinic Quality and Patient Safety Reports, a daily-maintained report of complications at time of all dilation and curettage (D&C) and dilation and evacuation (D&E) procedures performed at an independently operated, urban, high-volume abortion clinic between March 2013 and August 2017. The clinic provided procedures through 23 weeks 6 days gestation to women at low risk for medical or surgical complications, referring high-risk procedures to a nearby hospital.

Demographic, Clinical, and Counseling Factors Associated with the Selection of Pregnancy Termination Method in the Second Trimester for Fetal and Pregnancy Anomalies.

Objective: Despite women's preference for induction of labor (IOL) or dilation and evacuation (D&E) for pregnancy termination in the setting of second trimester fetal or pregnancy abnormality, many women are not given a choice between delivery methods. We investigated patient and clinical related factors associated with selecting IOL or D&E.

Methods: This retrospective cohort experienced pregnancy termination at 17-24 weeks of gestation for fetal anomaly, intrauterine fetal demise, or premature previable rupture.

Global hypermethylation in fetal cortex of Down syndrome due to DNMT3L overexpression.

Down syndrome (DS) is caused by a triplication of chromosome 21 (HSA21). Increased oxidative stress, decreased neurogenesis and synaptic dysfunction from HSA21 gene overexpression are thought to cause mental retardation, dementia and seizure in this disorder. Recent epigenetic studies have raised the possibility that DNA methylation has significant effects on DS neurodevelopment.

OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors.

Mental retardation and early Alzheimer's disease (AD) have generally been attributed to progressive neuronal loss in the developing and mature Down syndrome (DS) brain. However, reduced neuronal production during development could also contribute to the smaller brain size and simplified gyral patterning seen in this disorder. Here, we show impairments in proliferation within the ventricular zone (VZ) of early DS fetal cortex and in cultured early passage DS human neural progenitors (HNPs).