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Background Variability in parental leave policies across graduate medical education (GME) programs in the United States complicates efforts to support resident wellness and identify best practices for resident well-being. Objective This review aims to assess how formal parental leave policies affect trainees' well-being, professional satisfaction, and performance during training. Methods A systematic review following the Preferred Reporting Items for Systematic Reviews and Meta Analyses (PRISMA) 2020 guidelines was conducted and registered on PROSPERO in May 2023. Databases searched included MEDLINE, Embase, and Cochrane Central. Studies that evaluated parental leave policies of US-based GME programs and their direct impact on residents and/or fellows were included. Studies were screened for inclusion by 2 independent reviewers, and any conflicts were resolved by a third author. Results Of 1068 articles screened, 43 articles met inclusion criteria. These studies highlighted that leave durations of less than 6 weeks were associated with higher rates of burnout and postpartum depression among trainees. There was no evidence that taking parental leave increased program attrition rate; however, 3 studies reported more than one-third of trainees extended training as a result of taking leave. Trainees who had more than 8 weeks of parental leave reported more successful breastfeeding 6 months out from delivery than those with less than 8 weeks of leave. Conclusions Extended parental leave, notably beyond 6 weeks, improved trainee well-being and professional satisfaction. Based on trainees' perspectives, ideal parental leave policies offer a minimum of 6 to 8 weeks of leave, with a formal and clearly written policy available.

Introduction: The first COVID-19 cases occurred in the US in January of 2020, leading to the implementation of shelter in place. This study seeks to define the impact of shelter in place on the epidemiology of pediatric trauma., Methods: We examined pediatric trauma admissions at 5 Level 1 and 1 Level 2 US pediatric trauma centers between January 1 and June 30, 2017-2020. Demographic and injury data were compared between pre- and post-shelter in place patient cohorts., Results: A total of 8772 pediatric trauma activations were reviewed. There was a 13% decrease in trauma volume in 2020, with a nadir at 16 days following implementation of shelter in place. Injury severity scores were higher in the post-shelter in place cohort. The incidence of nonmotorized vehicle accidents and gunshot wounds increased in the post-shelter in place cohort., Conclusion: We found an overall decrease in pediatric trauma volume following shelter in place. However, injuries tended to be more severe. Our findings help inform targeted injury prevention campaigns during future pandemics., (© 2021 The Authors.)

Background: Pulmonary hypertension (PH) secondary to vascular remodeling contributes to poor outcomes in congenital diaphragmatic hernia (CDH), however mechanisms responsible are unknown. We hypothesized that pulmonary artery endothelial cell (PAEC) dysfunction contributes to smooth muscle cell (SMC) hyperplasia in experimental CDH., Methods: PAEC and SMC were isolated from fetal sheep with experimental CDH and controls. SMC growth was assessed alone and with SOD plus catalase and during coculture with control or CDH PAEC with and without ET-1 siRNA transfection. ET-1 protein was measured in PAEC and SMC lysates and supernatant. ROS production was measured in normal and CDH PAECs with and without ET-1 siRNA. PAEC growth and tube formation were measured with SOD plus catalase., Results: CDH SMC growth was decreased and increased with coculture with CDH PAEC more than control PAEC. Treatment of CDH PAEC with SOD plus catalase or ET-1 siRNA prevented the increase in SMC growth seen with coculture. ET-1 protein was increased in CDH PAEC and SMC. ROS production was increased in CDH PAEC and decreased with ET-1 SiRNA. SOD plus catalase restored CDH PAEC growth and tube formation., Conclusion: PAEC dysfunction in experimental CDH increases SMC proliferation via ET-1 induced ROS production by PAEC.

Decreased lung vascular growth and pulmonary hypertension contribute to poor outcomes in congenital diaphragmatic hernia (CDH). Mechanisms that impair angiogenesis in CDH are poorly understood. We hypothesize that decreased vessel growth in CDH is caused by pulmonary artery endothelial cell (PAEC) dysfunction with loss of a highly proliferative population of PAECs (HP-PAEC). PAECs were harvested from near-term fetal sheep that underwent surgical disruption of the diaphragm at 60-70 days gestational age. Highly proliferative potential was measured via single cell assay. PAEC function was assessed by assays of growth and tube formation and response to known proangiogenic stimuli, vascular endothelial growth factor (VEGF), and nitric oxide (NO). Western blot analysis was used to measure content of angiogenic proteins, and superoxide production was assessed. By single cell assay, the proportion of HP-PAEC with growth of >1,000 cells was markedly reduced in the CDH PAEC, from 29% (controls) to 1% (CDH) (P < 0.0001). Compared with controls, CDH PAEC growth and tube formation were decreased by 31% (P = 0.012) and 54% (P < 0.001), respectively. VEGF and NO treatments increased CDH PAEC growth and tube formation. VEGF and VEGF-R2 proteins were increased in CDH PAEC; however, eNOS and extracellular superoxide dismutase proteins were decreased by 29 and 88%, respectively. We conclude that surgically induced CDH in fetal sheep causes endothelial dysfunction and marked reduction of the HP-PAEC population. We speculate that this CDH PAEC phenotype contributes to impaired vascular growth in CDH.