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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.

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.

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.