Flipping the Teachers: Impact of a Standardized Physiology Curriculum on Neonatology Medical Educators.

OBJECTIVE: Academic physicians must teach elements in an Accreditation Council for Graduate Medical Education (ACGME)-mandated curriculum while balancing career development and clinical workload. Exploring educator perceptions on the learning environment and comparing two instructional methods (traditional didactics [TD] vs. flipped classroom [FC]) in one pediatric subspecialty may elucidate current challenges, barriers, and strategies to optimize learning and educator satisfaction. STUDY DESIGN: A randomized trial comparing effectiveness and learner preference for FC versus TD physiology teaching was conducted in ACGME-accredited neonatal-perinatal medicine (NPM) fellowship programs in 2018 to 2019. Educator preferences were elicited through online surveys pre- and postintervention. Free-text comments were provided for questions exploring strengths, challenges, and opportunities in fellowship education. Statistical analysis included comparisons of demographics and pre-post-intervention educator responses between groups. Thematic analysis of text responses was conducted to identify common subthemes. RESULTS: From 61 participating programs, 114 FC educators and 130 TD educators completed surveys. At baseline, all educators experienced professional satisfaction from teaching fellows, but noted challenges with time available to create and/or deliver educational content, limited content expertise amongst faculty, colleagues' limited enthusiasm toward educating fellows, and lack of perceived value of education by institutions given limited protected time or credit toward promotion. Postintervention, educators in both groups noted a preference to teach physiology using FC due to interactivity, learner enthusiasm, and learner-centeredness. FC educators had a 17% increase in preference to teach using FC (p = 0.001). Challenges with FC included ensuring adequate trainee preparation, protecting educational time, and providing educators with opportunities to develop facilitation skills. CONCLUSION: Overall, NPM educators in a trial evaluating a standardized, peer-reviewed curriculum report professional satisfaction from teaching, but described logistical challenges with developing/delivering content. Educators preferred instruction using FC, but identified challenges with learner preparedness and ensuring adequate educator time and skill. Future efforts should be dedicated to addressing these barriers. KEY POINTS: · Many challenges exist for educators teaching neonatal-perinatal medicine fellows, including time, support, and recognition.. · Many educators preferred using flipped classroom methodology with a standardized curriculum due to interactivity and learner-centeredness.. · Benefits of a standardized, peer-reviewed curriculum include reduced preparation time, adaptability of content, and learning environment enhancement..

Reticular Dysgenesis: A Rare Immunodeficiency in a Neonate With Cytopenias and Bacterial Sepsis.

Severe combined immunodeficiency (SCID) consists of a group of disorders defined by abnormal B and T cell development that typically results in death within the first year of life if undiagnosed or untreated. Reticular dysgenesis (RD) is a rare but especially severe form of SCID that is caused by adenylate kinase 2 deficiency and is characterized not only by lymphopenia but also by profound neutropenia. RD predisposes patients to viral and fungal infections typical of SCID as well as serious bacterial infections atypical in the neonatal period in other SCID types. RD is also associated with sensorineural hearing loss not typically seen in other forms of SCID. Without rapid diagnosis and curative hematopoietic stem cell transplantation, RD is fatal within days to months due to overwhelming bacterial infection. The inclusion of the T cell receptor excision circle assay nationally in 2017 on the newborn screen has facilitated diagnosis of SCID in the neonatal period. This case reports on a male infant with RD who presented after preterm birth with severe cytopenias and a gastrointestinal anomaly and ultimately developed severe bacterial sepsis. Postmortem bone marrow evaluation and panel-based gene sequencing identifying 2 novel variants in the adenylate kinase 2 gene provided confirmation for a diagnosis of RD. This case emphasizes the importance of thorough diagnostic evaluation, including the newborn screen, in neonates and infants with persistent and unexplained cytopenias. Prompt hematology and/or immunology referral is advised for disease management and to facilitate hematopoietic stem cell transplantation to optimize long-term survival.

Mineral Homeostasis and Effects on Bone Mineralization in the Preterm Neonate.

Most bone formation and mineralization occurs late in gestation. Accretion of adequate minerals is a key element of this process and is often interrupted through preterm birth. In utero, mineral transport is accomplished via active transport across the placenta and does not require fetal hormone input. Postnatal mineral homeostasis requires a balance of actions of parathyroid hormone, calcitonin, and vitamin D on target organs. Preterm birth, asphyxia, acidosis, and prolonged parenteral nutrition increase the risk of mineral imbalance and metabolic bone disease (MBD). Aggressive postnatal nutrition is key to preventing and treating MBD in preterm infants.

Nutrition in the Cardiac Newborns: Evidence-based Nutrition Guidelines for Cardiac Newborns.

Both protein and energy malnutrition are common in neonates and infants with congenital heart disease (CHD). Neonates with CHD are at increased risk of developing necrotizing enterocolitis (NEC), particularly the preterm population. Mortality in patients with CHD and NEC is higher than for either disease process alone. Standardized feeding protocols may affect both incidence of NEC and growth failure in infants with CHD. The roles of human milk and probiotics have not yet been explored in this patient population.

Endothelial cell migration during murine yolk sac vascular remodeling occurs by means of a Rac1 and FAK activation pathway in vivo.

The molecular mechanism(s) controlling cell migration during vascular morphogenesis in vivo remain largely undefined. To address this within a physiological context, we used retinaldehyde dehydrogenase-2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Vinculin was increased in Raldh2-/- yolk sacs, and molecular events important for focal adhesion turnover, FAK phosphorylation (Tyr397) and FAK-paxillin association, were decreased. RA-rescue of vascular remodeling down-regulated vinculin and restored FAK phosphorylation (Tyr397) and FAK-paxillin association. Furthermore, vascular rescue with vascular endothelial growth factor-A, Indian hedgehog, and basic fibroblast growth factor restored FAK phosphorylation (Tyr397) in the endothelium of Raldh2-/- yolk sacs. Our results provide new insights into the regulation of endothelial cell migration during vascular remodeling in vivo by adding the Rac1 and FAK activation pathway as a critical mediator of focal adhesion formation and turnover during vascular remodeling.

GLP-2 receptor localizes to enteric neurons and endocrine cells expressing vasoactive peptides and mediates increased blood flow.

BACKGROUND & AIMS: Glucagon-like peptide-2 (GLP-2) is a nutrient-responsive hormone that exerts diverse actions in the gastrointestinal tract, including enhancing epithelial cell survival and proliferation, mucosal blood flow, and nutrient uptake and suppressing gastric motility and secretion. These actions are mediated by the G-protein-coupled receptor, GLP-2R. Cellular localization of the GLP-2R and the nature of its signaling network in the gut, however, are poorly defined. Thus, our aim was to establish cellular localization of GLP-2R and functional connection to vascular action of GLP-2 in the gut. METHODS: Intestinal cellular GLP-2R localization was determined with real-time, quantitative reverse-transcription polymerase chain reaction (qRT-PCR) of laser capture microdissected subtissue and fluorescence in situ hybridization and also with double and/or triple immunostaining of human and pig tissue using a validated GLP-2R polyclonal antibody. Superior mesenteric arterial blood flow and intestinal eNOS expression and phosphorylation were measured in TPN-fed pigs acutely (4 h) infused with GLP-2. RESULTS: We show that the porcine GLP-2R mRNA was expressed in the villus epithelium and myenteric plexus. GLP-2R protein was co-localized by confocal immunohistochemistry with serotonin in enteroendocrine cells and also with endothelial nitric oxide synthase (eNOS)-expressing and vasoactive intestinal polypeptide-positive enteric neurons. In neonatal pigs, GLP-2 infusion dose-dependently stimulated intestinal blood flow and coordinately upregulated the expression of intestinal eNOS mRNA, protein, and phosphorylation (eNOS-Ser1117). CONCLUSIONS: We conclude that the GLP-2-induced stimulation of blood flow is mediated by vasoactive neurotransmitters that are colocalized with GLP-2R in 2 functionally distinct cell types within the gastrointestinal tract.