Development and Preliminary Testing of the Withdrawal Assessment Tool-Alpha 2 Agonist: An Assessment Instrument for Monitoring Iatrogenic Withdrawal Symptoms in Children Receiving an Alpha-2 Agonist.

Objectives: To develop and conduct preliminary testing of the Withdrawal Assessment Tool-Alpha 2 Agonist (WAT-A2A) to monitor dexmedetomidine and clonidine withdrawal symptoms in acutely ill children.

Design: Three-phase instrument development study. Phase 1: retrospective chart review of symptoms exhibited by children with documented dexmedetomidine withdrawal; phase 2: WAT-A2A instrument construction based on phase 1 data; and phase 3: prospective testing of the WAT-A2A in children weaning from alpha 2 agonists (A2As).

Effects of maternal exercise modes on infant cord blood proteome.

The aim of this study was to show the effects of different maternal exercise modes on infant cord blood proteome. We used infant cord blood from two randomized controlled trials where women with a wide range of BMI and free of pregnancy complications participated in controlled and supervised aerobic, resistance, or combination (aerobic+resistance) exercise from <16 weeks of gestation until delivery. Results of this study showed that infant cord blood proteome is altered in a maternal exercise mode specific manner.

Placenta-derived SOD3 deletion impairs maternal behavior via alterations in FGF/FGFR-prolactin signaling axis.

Offspring growth requires establishing maternal behavior associated with the maternal endocrine profile. Placentae support the adaptations of the mother, producing bioactive molecules that affect maternal organs. We recently reported that placentae produce superoxide dismutase 3 (SOD3) that exerts sustained effects on the offspring liver via epigenetic modifications.

Exercise activates AMPK in mouse and human pancreatic islets to decrease senescence.

Beta (β)-cell senescence contributes to type 2 diabetes mellitus (T2DM). While exercise is vital for T2DM management and significantly affects cellular ageing markers, its effect on β-cell senescence remains unexplored. Here, we show that short-term endurance exercise training (treadmill running, 1 h per day for 10 days) in two male and female mouse models of insulin resistance decreases β-cell senescence.

Paternal obesity decreases infant MSC mitochondrial functional capacity.

Besides the well-recognized influence of maternal health on fetal in utero development, recent epidemiological studies appoint paternal preconception metabolic health as a significant factor in shaping fetal metabolic programming and subsequently offspring metabolic health; however, mechanisms behind these adaptations remain confined to animal models. To elucidate the effects of paternal obesity (P-OB) on infant metabolism in humans, we examined mesenchymal stem cells (MSCs), which give rise to infant tissue, remain involved in mature tissue maintenance, and resemble the phenotype of the offspring donor. Here, we assessed mitochondrial functional capacity, content, and insulin action in MSC from infants of fathers with overweight [body mass index (BMI: 25-30 kg/m); paternal overweight (P-OW)] or obesity (BMI ≥ 30 kg/m; P-OB) while controlling for maternal intrauterine environment.