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Due to the changing complex healthcare environment, educational innovation is essential to meet the needs of current and future neonatal-perinatal medicine (NPM) leaders. Greater clinical demands, decreased academic funding, and expanded graduate medical education program requirements have negatively impacted time for teaching and educational scholarship potentially limiting innovation in the field. By focusing on adult learning principles, embracing technology, and promoting collaboration, today's educators are preparing the next generation of neonatologists. Current innovations include regionalizing simulation boot camps, leveraging virtual learning to increase accessibility, developing niche training opportunities, and incorporating population health principles within existing quality initiatives. Areas in need of additional innovation include faculty and fellow development for teaching skills, expansion of educational networks, and dissemination and financial support of educational scholarship. These efforts and future innovations will require medical institutions and national NPM organizations to further invest in the medical educator as part of their missions.

Neonatal-perinatal medicine fellows must achieve a meaningful accomplishment in scholarly activity as part of their training. Despite the requirement for scholarly training in fellowship, there is a vanishingly small number of MD-only physician-scientists pursuing a research-oriented career. Recent neonatal trainees have identified several factors that preclude their careers in research-focused academic neonatology, including lower pay in academic positions, inadequate training in research techniques, and the perception that individuals in research careers have a poor work-life balance. High competition for limited pediatric research funds also contributes to a diminishing pool of physician-scientists in neonatology. This small number of physician-scientists is threatened by a high rate of attrition among physicians who enter this career path. In order to prevent further declines in the number of neonatal physician-scientists, we need improvements in funding and strong intra- and cross-institutional mentorship to foster individuals interested in a career as a physician-scientist.

Author(s): D'Angio, CT; Wang, H; Hunn, JE; Pryhuber, GS; Chess, PR; Lakshminrusimha, S | Abstract: ObjectiveWe hypothesized that, among parents of potential neonatal research subjects, an accompanying cover sheet added to the permission form (intervention) would increase understanding of the research, when compared to a standard form (control).Study designThis pilot study enrolled parents approached for one of two index studies: one randomized trial and one observational study. A one-page cover sheet described critical study information. Families were randomized 1:1 to receive the cover sheet or not. Objective and subjective understanding and satisfaction were measured.ResultsThirty-two parents completed all measures (17 control, 15 intervention). There were no differences in comprehension score (16.8±5.7 vs 16.3±3.5), subjective understanding (median 6 vs 6.5), or overall satisfaction with consent (median 7 vs 6.5) between control and intervention groups (all Pg0.50).ConclusionA simplified permission form cover sheet had no effect on parents' understanding of studies for which their newborns were being recruited.

Despite American College of Obstetricians and Gynecologists guidelines suggesting that non-urgent planned deliveries be scheduled at/after 39 weeks; elective delivery before 39 weeks occurs often in the United States. The objective of this study is to estimate the elective delivery rate between 36(0/7) and 38(6/7) weeks gestation and compare NICU admission rates between elective and non-elective deliveries. We conducted a retrospective cohort (n = 1,577) study. Charts were reviewed for all singleton deliveries (2006-2007) between 36(0/7) and 38(6/7) weeks gestation taking place at one hospital in NYS to determine delivery status. We computed adjusted relative risks (RR) with 95% confidence intervals (CI) for elective delivery in relation to NICU admission using robust Poisson regression. 32.8% of all births were elective: 20.7% of vaginal and 55.7% of cesarean births. Elective delivery increased with increasing gestational age. After controlling for potential confounders, infants born via a vaginal elective delivery (RR = 1.40, CI: 1.00, 1.94), an elective cesarean (RR = 2.05, CI: 1.53, 2.76), or a non-elective cesarean (RR = 2.00, CI: 1.50, 2.66) are at significantly increased risk of NICU admission compared to infants born via a non-elective vaginal delivery. Elective delivery before 39 weeks is common and increases the risk of infant NICU admission.

Although the endothelial cell is the most abundant cell type in the differentiated lung, little is known about regulation of lung developmental vasculogenesis. Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and angiogenic factor that has putative roles in vascular development. Mitogenic actions of VEGF are mediated by the tyrosine kinase receptor KDR/murine homologue fetal liver kinase Flk-1. HLF (hypoxia-inducible factor-like factor) is a transcription factor that increases VEGF gene transcription. Dexamethasone augments lung maturation in fetal and postnatal animals. However, in vitro studies suggest that dexamethasone blocks induction of VEGF. The objectives for the current study were to measure VEGF mRNA and Flk-1 mRNA in developing mouse lung and to measure the effects of dexamethasone treatment in vivo on VEGF and Flk-1 in newborn mouse lung. Our results show that VEGF and Flk-1 messages increase in parallel during normal lung development (d 13 embryonic to adult) and that the distal epithelium expresses VEGF mRNA at all ages examined. Dexamethasone (0.1-5.0 mg x kg(-1) x d(-1)) treatment of 6-d-old mice resulted in significantly increased VEGF, HLF, and Flk-1 mRNA. Dexamethasone did not affect cell-specific expression of VEGF, VEGF protein, or proportions of VEGF mRNA splice variants. These data suggest that the developing alveolar epithelium has an important role in regulating alveolar capillary development. In addition, unlike effects on cultured cells, dexamethasone, even in relatively high doses, did not adversely affect VEGF expression in vivo. The relatively high levels of VEGF and Flk-1 mRNA in adult lung imply a role for pulmonary VEGF in endothelial cell maintenance or capillary permeability.

Objective. The objective of this case-control study was to develop a screening protocol using head ultrasound (HUS) to detect high-grade intraventricular hemorrhage (IVH) in very-low-birthweight infants with greater specificity than current practice, while maintaining a high degree of sensitivity. Materials and methods. All infants ≤ 32 weeks or ≤ 1500 g admitted to the neonatal intensive care unit between January 1, 1991 and December 31, 1992 were studied. The 1991 cohort was analyzed to identify the factors most sensitive and specific for predicting the occurrence of a high-grade (III or IV) IVH. Results. Eighty-five percent of infants born at 28–32 weeks gestation screened by 2 weeks of age for IVH had normal HUS scans. The factors most predictive of a high-grade IVH were gestational age < 28 weeks, forceps delivery, or any of the following in the first 2 weeks of life: seizures, head circumference increasing by more than 1 cm per week, base deficit ≥ 10, or cardiopulmonary resuscitation in the neonatal intensive care unit. Conclusion. Infants born at 28–32 weeks with a high-grade IVH can be identified with a high degree of sensitivity using refined screening criteria, eliminating 50 % of the HUS scans currently obtained for IVH screening.

Tyrosine kinases are important in the signal transduction of a number of growth factors. As shown previously, transforming growth factor (TGF)-alpha stimulated proliferation of type II cells in vitro. The mitogenic effect of TGF-alpha could be blocked by the addition of the tyrosine kinase inhibitors genistein or tyrphostin. Tyrosine phosphorylation in type II cells exposed to growth factors was examined using an antiphosphotyrosine antibody. After addition of TGF-alpha, phosphorylation of a tyrosine protein with a molecular mass of 170 kD, presumed to be the epidermal growth factor receptor (EGF-R), peaked by 5 min, returning to baseline by 30 min. As expected, genistein or tyrphostin decreased the TGF-alpha-induced phosphorylation of the EGF-R. Addition of TGF-beta resulted in no newly phosphorylated tyrosine proteins. TGF-beta decreased the TGF-alpha-induced phosphorylation of the EGF-R. Previous work has shown that TGF-beta blocks the TGF-alpha stimulation of type II cell proliferation. It appears that TGF-beta interferes with TGF-alpha-induced phosphorylation of the EGF-R.

Embryonic heart cells undergo cyclic strain as the developing heart circulates blood to the embryo. Cyclic strain may have an important regulatory role in formation of the adult structure. This study examines the feasibility of a computerized cell-stretching device for applying strain to embryonic cardiocytes to allow measurement of the cellular response. A primary coculture of myocytes and a secondary culture of nonmyocytes from stage-31 (7 d) embryonic chick hearts were grown on collagen-coated membranes that were subsequently strained at 2 Hz to 20% maximal radial strain. After 24 h, total cell number increased by 37+/-6% in myocyte cocultures and by 26+/-6% in nonmyocyte cultures over unstrained controls. Lactate dehydrogenase and apoptosis assays showed no significant differences in cell viabilities between strained and unstrained cells. After 2 h strain, bromodeoxyuridine incorporation was 38+/-1.2% versus 19+/-0.2% (P < 0.01) in strained versus unstrained myocyte cocultures, and 35+/-2.1% versus 16+/-0.2% (P = 0.01) in nonmyocyte cultures. MF20 antibody labeling and periodic acid-Schiff (PAS) staining estimated the number of myocytes in strained wells as 50-67% larger than in control wells. Tyrosine phosphorylation may play a role in the cellular response to strain, as Western blot analysis showed an increase in tyrosine phosphorylation of two proteins with approximate molecular weights of 63 and 150 kDa within 2 min of strain. The results of this study indicate that embryonic chick cardiocytes can be cultured in an active mechanical environment without significant detachment and damage and that increased proliferation may be a primary response to strain.