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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. 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. 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 ( 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.· 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..

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.

Resident/endogenous mesenchymal stromal cells function to promote the normal development, growth, and repair of tissues. Following premature birth, the effects of routine neonatal care (e.g. oxygen support and mechanical ventilation) on the biological properties of lung endogenous mesenchymal stromal cells is (L-MSCs) is poorly understood. New Zealand white preterm rabbits were randomized into the following groups: (i) sacrificed at birth (Fetal), (ii) spontaneously breathing with 50% O2 for 4 hours (SB), or (iii) mechanical ventilation with 50% O2 for 4h (MV). At time of necropsy, L-MSCs were isolated, characterized, and compared. L-MSCs isolated from the MV group had decreased differentiation capacity, ability to form stem cell colonies, and expressed less vascular endothelial growth factor mRNA. Compared to Fetal L-MSCs, 98 and 458 genes were differentially expressed in the L-MSCs derived from the SB and MV groups, respectively. Gene ontology analysis revealed these genes were involved in key regulatory processes including cell cycle, cell division, and angiogenesis. Furthermore, the L-MSCs from the SB and MV groups had smaller mitochondria, nuclear changes, and distended endoplasmic reticula. Short-term hyperoxia/mechanical ventilation after birth alters the biological properties of L-MSCs and stimulates genomic changes that may impact their reparative potential.

To explore interest, feasibility, perceived effectiveness, and acceptability of a standardized, national physiology curriculum for neonatal–perinatal medicine (NPM) fellows using online videos for knowledge acquisition paired with flipped classrooms (FCs) for knowledge application. Two educational programs pairing online videos with FCs were developed and peer-reviewed. These programs were piloted at five institutions. Fellows completed surveys, and fellows and educators participated in focus groups after their FC experiences. Thirty-five fellows responded to the survey. Forty-one fellows and six educators participated in focus groups. Fellows and educators preferred online videos paired with FCs over didactic teaching and perceived them to be effective for knowledge acquisition and application. Fellows and educators preferred FC learning over traditional didactics and reported that FCs facilitated creation of a learning community, fostering active learning. The favorable response toward this pilot project and the feasibility of its use supports further development of a standardized NPM physiology curriculum for fellowship training.

Summary Background Competency rates in neonatal intubation among pediatric residents are low and currently not meeting ACGME/AAP standards. Aims The aim of this study was to compare standard bedside teaching of neonatal endotracheal intubation to a computer module, as well as introduce residents to the emerging technology of videolaryngoscopy. Methods The study population consisted of The University of Texas Health Science Center at San Antonio Pediatric interns/residents and PGY-1 Anesthesia interns rotating through the NICU. Prior to participating in the study, the residents completed a survey addressing past experiences with intubation, comfort level, and prior use of direct and videolaryngoscopy. Participants then performed timed trials of both direct and videolaryngoscopy on the SimNewB®. They had up to three attempts to successfully intubate, with up to 30 s on each attempt. After randomization, participants received one of the following teaching interventions: standard, computer module, or both. This was followed by a second intubation trial and survey completion. Results Thirty residents were enrolled in the study. There was significant improvement in time to successful intubation in both methods after any teaching intervention (direct 22.0 ± 13.4 s vs 14.7 ± 5.9 s, P = 0.002 and videolaryngoscopy 42.2 ± 29.3 s vs 26.8 ± 18.6 s, P = 0.003). No differences were found between the types of teaching. Residents were faster at intubating with direct laryngoscopy compared to videolaryngoscopy before and after teaching. By the end of the study, only 33% of residents preferred using videolaryngoscopy over direct laryngoscopy, but 76% felt videolaryngoscopy was better to teach intubation. Conclusions Both standard teaching and computer module teaching of neonatal intubation on a mannequin model results in improved time to successful intubation and overall improved resident confidence with intubation equipment and technique. Although intubation times were lower with direct laryngoscopy compared to videolaryngoscopy, the participating residents felt that videolaryngoscopy is an important educational tool.

Rigorous medical education research is critical to effectively develop and evaluate the training we provide our learners. Yet many clinical medical educators lack the training and skills needed to conduct high-quality medical education research. We offer guidance on conducting sound quantitative medical education research. Our aim is to equip readers with the key skills and strategies necessary to conduct successful research projects, highlighting new concepts and controversies in the field. We utilize Glassick's criteria for scholarship as a framework to discuss strategies to ensure that the research question of interest is worthy of further study and how to use existing literature and conceptual frameworks to strengthen a research study. Through discussions of the strengths and limitations of commonly used study designs, we expose the reader to particular nuances of these decisions in medical education research and discuss outcomes generally focused on, as well as strategies for determining the significance of consequent findings. We conclude with information on critiquing research findings and preparing results for dissemination to a broad audience. Practical planning worksheets and comprehensive tables illustrating key concepts are provided in order to guide researchers through each step of the process. Medical education research provides wonderful opportunities to improve how we teach our learners, to satisfy our own intellectual curiosity, and ultimately to enhance the care provided to patients.

Respiratory dysfunction in adults has been correlated with neonatal Chlamydia trachomatis pneumonia in several studies, but a causal association has not been clearly demonstrated. In this study, we examined radial alveolar counts (RACs) by microscopy, and airway and parenchymal lung function using a small animal ventilator in juvenile (5 weeks age) and adult (8 weeks age) BALB/c mice challenged as neonates with Chlamydia muridarum (C. mur) on day 1 or day 7 after birth, representing saccular (human pre-term neonates) and alveolar (human term neonates) stages of lung development, respectively. Pups challenged with C. mur on either day 1 or 7 after birth demonstrated significantly enhanced airway hyperreactivity and lung compliance, both as juveniles (5 weeks age) and adults (8 weeks age), compared with mock-challenged mice. Moreover, mice challenged neonatally with Chlamydia displayed significantly reduced RACs, suggesting emphysematous changes. Antimicrobial treatment during the neonatal infection induced early bacterial clearance and partially ameliorated the Chlamydia-induced lung dysfunction as adults. These results suggest that neonatal chlamydial pneumonia, especially in pre-term neonates, is a cause of respiratory dysfunction continuing into adulthood, and that antimicrobial administration may be partially effective in preventing the adverse respiratory sequelae in adulthood. The results of our studies also emphasize the importance of prenatal screening and treatment of pregnant women for C. trachomatis in order to prevent the infection of neonates.

Pica is a significant risk factor for lead exposure during pregnancy and may often go unrecognized. Lead exposure in the pregnant woman may be extremely toxic to the fetus due to unencumbered transport across the placenta. Long term neurological effects of in utero and neonatal lead exposure are largely unknown, and the efficacies of current therapies are controversial. We report a case of a pregnant woman with elevated blood lead levels secondary to pica that was not identified by a routine screening survey. Her full term baby girl had a blood lead level of 70.8 μg/dL. Neonatal therapy with double-volume exchange transfusion followed by a 3 day course of intravenous Edetate Calcium Disodium is described as well as the slow steady decline of her blood lead levels. Neurocognitive development to 18 months is also reported.

Alpha-ENaC expression and activity is regulated by a variety of hormones including beta-adrenergic agonists via the second messenger cAMP. We evaluated the early intermediate pathways involved in the up-regulation of SGK1 by DbcAMP and whether SGK1 is a prerequisite for induction of alpha-ENaC expression. Submandibular gland epithelial (SMG-C6) cells treated with DbcAMP (1 mM) induced both SGK1 mRNA and protein expression. DbcAMP-stimulated SGK1 mRNA expression was decreased by actinomycin D and mRNA and protein expressions were attenuated by PKA inhibitors (H-89 and KT5720). Inhibition of PI3-K with either LY294002 or dominant negative PI3-K reduced DbcAMP-stimulated SGK1 protein and mRNA levels, attenuated the phosphorylation of CREB (a cAMP-activated transcription factor) and decreased alpha-ENaC protein levels and Na(+) transport. In addition, the combination of PKA inhibitors with dominant negative PI3-K synergistically inhibited DbcAMP-induced Na(+) transport. Inhibition of SGK1 expression by siRNA decreased but did not obliterate DbcAMP-induced alpha-ENaC expression. Thus, in a cell line which endogenously exhibits minimal alpha-ENaC expression, induction of SGK1 by DbcAMP occurs via the PI3-K and PKA pathways. Increased alpha-ENaC levels and function are partly dependent upon the early induction of SGK1 expression.

To evaluate the anti-inflammatory effects of exogenous surfactants and surfactant phospholipid without surfactant proteins (SP-A and SP-D) on the lipopolysaccharide- (LPS) stimulated rat alveolar macrophage (AM) cell line NR8383.Exogenous surfactants (beractant, calfactant or colfosceril) and surfactant phospholipid (dipalmitoyl phosphatidylcholine, DPPC), standardized to phospholipid content of 25-1,000 microg/ml were incubated with LPS- (1 microg/ml) stimulated NR8383 AMs.TNF-alpha and IL-1beta secretion and nitric oxide (NO) formation following LPS stimulation were inhibited by treatment with surfactants or DPPC. Furthermore, LPS-dependent NO production and iNOS protein levels were significantly suppressed in cells pretreated for one hour with beractant compared to beractant added simultaneously with or following LPS. Additionally, LPS-stimulated oxidative burst, measured by flow cytometry, was significantly decreased by beractant. Finally, beractant inhibited the translocation of NF-kappaB from cytoplasmic into nuclear extract in LPS-stimulated NR8383 AMs.Exogenous surfactants and surfactant phospholipid inhibit secretion of proinflammatory cytokines and NO in NR8383 AMs. The inhibitory effects of beractant on oxygen radical and LPS-induced NO formation may result from unique mechanisms of decreasing cell signaling. The anti-inflammatory activity of surfactant products used in the treatment of neonatal respiratory distress syndrome (RDS) may depend upon the specific preparation or dose used.

This study compared cytokines (in particular transforming growth factor [TGF]-β2) and lactoferrin in maternal human milk (MHM), human-derived milk fortifier (HDMF), and donor human milk (DHM).MHM was randomly collected from breastfeeding mothers who had no infectious illness at the time of milk expression. HDMF and DHM were products derived from human milk processed by Holder pasteurization. MHM samples were collected at different times (early/late) and gestations (preterm/term). Lactoferrin was analyzed by western blotting, and cytokines were quantified using commercial enzyme-linked immunosorbent assays. Significance was determined using analysis of variance.In the 164 samples analyzed, TGF-β2 concentrations in HDMF and preterm MHM (at all collection times) were fivefold higher than in DHM (p0.05). Early preterm MHM had levels of interleukin (IL)-10 and IL-18, 11-fold higher than DHM (p0.05). IL-6 in DHM was 0.3% of the content found in MHM. IL-18 was fourfold higher in early MHM versus late MHM regardless of gestational age (p0.05). Lactoferrin concentration in DHM was 6% of that found in MHM.Pasteurization decreases concentrations of most cytokines and lactoferrin in DHM. TGF-β2, a protective intestinal cytokine, has comparable concentrations in HDMF to MHM despite pasteurization.

Preterm infants may be at risk of necrotizing enterocolitis (NEC) due to deficiency of transforming growth factor-β 2 (TGF-β2) in the developing intestine. We hypothesized that low epithelial TGF-β2expression in preterm intestine and during NEC results from diminished autocrine induction of TGF-β2in these cells. Premature baboons delivered at 67% gestation were treated per current norms for human preterm infants. NEC was diagnosed by clinical and radiological findings. Inflammatory cytokines, TGF-β2, Smad7, Ski, and strawberry notch N (SnoN)/Ski-like oncoprotein (SKIL) was measured using quantitative reverse transcriptase-polymerase chain reaction, immunoblots, and immunohistochemistry. Smad7 effects were examined in transfected IEC6 intestinal epithelial cells in vitro. Findings were validated in archived human tissue samples of NEC. NEC was recorded in seven premature baboons. Consistent with existing human data, premature baboon intestine expressed less TGF-β2than term intestine. TGF-β2expression was regulated in epithelial cells in an autocrine fashion, which was interrupted in the premature intestine and during NEC due to increased expression of Smad7. LPS increased Smad7 binding to the TGF-β2promoter and was associated with dimethylation of the lysine H3K9, a marker of transcriptional silencing, on the nucleosome of TGF-β2. Increased Smad7 expression in preterm intestine was correlated with the deficiency of SnoN/SKIL, a repressor of the Smad7 promoter. Smad7 inhibits autocrine expression of TGF-β2in intestinal epithelial cells in the normal premature intestine and during NEC. Increased Smad7 expression in the developing intestine may be due to a developmental deficiency of the SnoN/SKIL oncoprotein.

Glucocorticoids and mineralocorticoids modulate Na+ transport via epithelial Na+ channels (ENaC). The rat submandibular epithelial cell line, SMG-C6, expresses α-ENaC mRNA and protein and exhibits amiloride-sensitive Na+ transport when grown in low-serum (2.5%) defined medium, therefore, we examined the effects of altering the composition of the SMG-C6 cell growth medium on ENaC expression and function. No differences in basal or amiloride-sensitive short-circuit current (Isc) were measured across SMG-C6 monolayers grown in the absence of thyroid hormone, insulin, transferrin, or EGF. In the absence of hydrocortisone, basal and amiloride-sensitive Isc significantly decreased. Similarly, monolayers grown in 10% serum-supplemented medium had lower basal Isc and no response to amiloride. Adding hydrocortisone (1.1 μM) to either the low or 10% serum medium increased basal and amiloride-sensitive Isc, which was blocked by RU486, the glucocorticoid and progesterone receptor antagonist. Aldosterone also induced an increase in α-ENaC expression and Na+ transport, which was also blocked by RU486 but not by the mineralocorticoid receptor antagonist spironolactone. Thus, in the SMG-C6 cell line, hydrocortisone and aldosterone increased ENaC expression and basal epithelial Na+ transport. The absence of endogenous ENaC expression in culture conditions devoid of steroids makes the properties of this cell line an excellent model for investigating pathways regulating ENaC expression and Na+ transport.

Background At the time of birth, the major pathway regulating lung fluid absorption is transepithelial Na+ movement via epithelial sodium channels (ENaCs). The density of ENaC proteins is high in the apical membranes of the type II alveolar cells and its expression and function are regulated by many agents, including steroids and growth factors. The rat parotid gland cell line (PAR-C5) expresses all ENaC subunit proteins (α, β, andγ), but monolayers grown in media containing EGF do not demonstrate significant ENaC function. Objective and Methods PAR-C5 cells were studied to examine the effect of EGF on ENaC function and trafficking. Cells were seeded on permeable filter supports in the presence or absence of EGF (20 ng/mL) and/or dexamethasone (0.1 μM). After the monolayers formed tight junctions as demonstrated by transepithelial resistances > 200 Ω.cm2 (mean resistance 513 Ω.cm2), permeable filters were mounted in Ussing chambers and Na+ transport was determined by the amiloride (10 μM)-sensitive component of the short-circuit current (Isc). α-ENaC protein content of similarly treated cells was examined by Western blot. α-ENaC localization in PAR-C5 cells was determined by confocal microscopy following staining with anti-α-ENaC antibody. Results The percent change in amiloride-sensitive Isc was 41.8 ± 5.0% in the absence versus 8.5 ± 5.5% in the presence of EGF (p = .0131). Dexamethasone increased the percent change in amiloride-sensitive Isc to 67.7 ± 12.1% in the absence and 60.3 ± 5.7% in the presence of EGF (p = .234). Despite differences in ENaC function, the amount of α-ENaC protein expression was similar in the presence or absence of EGF. However, PAR-C5 cells grown in the presence of EGF demonstrated less α-ENaC localization in the membrane portion compared with those cells grown in the absence of EGF. Conclusion These results suggest that EGF inhibits the intracellular trafficking of α-ENaC into the plasma membranes in the PAR-C5 cell line. Since animal in utero studies suggest that EGF supplementation may be used to reverse pulmonary hypoplasia, further investigation is needed to characterize the signaling mechanisms whereby EGF and other growth factors modulate intracellular ENaC trafficking in different cell types.

Fluid reabsorption in various epithelia is regulated by Na+ transport via apically located epithelial sodium channels (ENaC). Submandibular gland epithelial (SMG-C6) cells cultured in the absence of hydrocortisone or cAMP demonstrate diminished a-ENaC expression and Na+ transport properties similar to fetal distal lung epithelial cells. Increases in the abundance of the serum and glucocorticoid-regulated protein kinase 1 (sgk1), a phosphatidylinositol 3-kinase (PI3K) activated protein, can suppress ENaC degradation. Since treatment of SMG-C6 cells with dibutyryl cAMP (DbcAMP) for 24 hours increases a-ENaC expression and function, we hypothesized that the up-regulation of a-ENaC expression and amiloride-sensitive Na+ transport by DbcAMP involves an increase in sgk1 via the protein kinase A (PKA) and PI3K pathways. SMG-C6 cells treated with DbcAMP (1 mM) increased both sgk1 RNA levels (peaking at 30 minutes) and protein expression (peaking after 4 h and remained elevated at 24 h). DbcAMP-stimulated sgk1 mRNA expression was decreased by actinomycin D and protein expression was decreased by PKA inhibitors (H-89 and KT5720). Both pharmacological inhibition of PI3K with LY294002 or transfection with dominant negative PI3K construct reduced stimulated sgk1 protein and mRNA levels, attenuated the phosphorylation of CREB (a cAMP-activated transcription factor), and, after 24 h, decreased a-ENaC protein levels and amiloride-sensitive Na+ transport. In addition, the combination of PKA inhibitors with dominant negative PI3K synergistically attenuated all amiloride-sensitive Na+ transport activity. DbcAMP induction of sgk1 acts through the PI3K and PKA pathways and sgk1 may potentiatea-ENaC.