Pediatric Residency Point-of-Care Ultrasound Training Needs Assessment and Educational Intervention.

Background Prior studies showed that point-of-care ultrasound (POCUS) training is not commonly offered in pediatric residency. We assessed the need for a pediatric POCUS curriculum by evaluating pediatric trainees' attitudes toward the use of POCUS and identifying barriers to training. We also aimed to evaluate the impact of a POCUS educational intervention on self-efficacy and behavior. Methods We conducted a cross-sectional survey of pediatric residents in a single large freestanding children's hospital distributed via an institutional listserv and administered online. The survey included opinion-rating of statements regarding POCUS and barriers to training. We also offered a two-week POCUS course with online modules and hands-on scanning. Participating residents completed pre- and post-course knowledge assessments and follow-up surveys up to 12 months following the course to assess POCUS use and self-report confidence on POCUS indications, acquisition, interpretation, and clinical application. Results Forty-nine respondents were included in the survey representing all three pediatric levels with 16 specialty interest areas. Ninety-six percent of trainees reported that POCUS is an important skill in pediatrics. Ninety-two percent of trainees reported that residency programs should teach residents how to use POCUS. The most important perceived barriers to POCUS training were scheduling availability for POCUS rotations and lack of access to an ultrasound machine. Fourteen participants completed the pre- and post-course knowledge tests, with eight and six participants also completing the six- and 12-month follow-up surveys, respectively. Self-ratings of confidence were significantly improved post-intervention in indications (P = 0.007), image acquisition (P = 0.002), interpretation (P = 0.002), and clinical application (P = 0.004). This confidence improvement was sustained up to 6-12 months (P = 0.004-0.032). Participants also reported higher categorical POCUS use after course completion (P = 0.031). Conclusions Pediatric trainees perceive POCUS as an important skill, hold favorable opinions towards the use of POCUS, and support POCUS training within a pediatric residency. A POCUS course can improve resident POCUS knowledge, instill confidence, and motivate higher POCUS use. Further study is needed to evaluate POCUS applications in pediatric medicine to develop a standardized POCUS curriculum and establish a training guideline for pediatric residency.

STAT3-BDNF-TrkB signalling promotes alveolar epithelial regeneration after lung injury.

Alveolar epithelial regeneration is essential for recovery from devastating lung diseases. This process occurs when type II alveolar pneumocytes (AT2 cells) proliferate and transdifferentiate into type I alveolar pneumocytes (AT1 cells). We used genome-wide analysis of chromatin accessibility and gene expression following acute lung injury to elucidate repair mechanisms. AT2 chromatin accessibility changed substantially following injury to reveal STAT3 binding motifs adjacent to genes that regulate essential regenerative pathways. Single-cell transcriptome analysis identified brain-derived neurotrophic factor (Bdnf) as a STAT3 target gene with newly accessible chromatin in a unique population of regenerating AT2 cells. Furthermore, the BDNF receptor tropomyosin receptor kinase B (TrkB) was enriched on mesenchymal alveolar niche cells (MANCs). Loss or blockade of AT2-specific Stat3, Bdnf or mesenchyme-specific TrkB compromised repair and reduced Fgf7 expression by niche cells. A TrkB agonist improved outcomes in vivo following lung injury. These data highlight the biological and therapeutic importance of the STAT3-BDNF-TrkB axis in orchestrating alveolar epithelial regeneration.

Neutrophils promote alveolar epithelial regeneration by enhancing type II pneumocyte proliferation in a model of acid-induced acute lung injury.

Alveolar epithelial regeneration is essential for resolution of the acute respiratory distress syndrome (ARDS). Although neutrophils have traditionally been considered mediators of epithelial damage, recent studies suggest they promote type II pneumocyte (AT2) proliferation, which is essential for regenerating alveolar epithelium. These studies did not, however, evaluate this relationship in an in vivo model of alveolar epithelial repair following injury. To determine whether neutrophils influence alveolar epithelial repair in vivo, we developed a unilateral acid injury model that creates a severe yet survivable injury with features similar to ARDS. Mice that received injections of the neutrophil-depleting Ly6G antibody had impaired AT2 proliferation 24 and 72 h after acid instillation, which was associated with decreased reepithelialization and increased alveolar protein concentration 72 h after injury. As neutrophil depletion itself may alter the cytokine response, we questioned the contribution of neutrophils to alveolar epithelial repair in neutropenic granulocyte-colony stimulating factor (G-CSF)-/- mice. We found that the loss of G-CSF recapitulated the neutrophil response of Ly6G-treated mice and was associated with defective alveolar epithelial repair, similar to neutrophil-depleted mice, and was reversed by administration of exogenous G-CSF. To approach the mechanisms, we employed an unbiased protein analysis of bronchoalveolar lavage fluid from neutrophil-depleted and neutrophil-replete mice 12 h after inducing lung injury. Pathway analysis identified significant differences in multiple signaling pathways that may explain the differences in epithelial repair. These data emphasize an important link between the innate immune response and tissue repair in which neutrophils promote alveolar epithelial regeneration.