A Novel Simulator for Teaching Endobronchial Ultrasound-guided Needle Biopsy.

BACKGROUND: Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) has become standard for the diagnosis of lung cancer, and there is an increasing need for procedural competence in trainees. We evaluate a low-cost, gelatin-based EBUS-TBNA training simulator to assess pulmonary fellows' baseline skills and facilitate procedural development. METHODS: A low-cost ($30) gelatin-based, high-fidelity simulator was created to represent the airways, major vessels, and lymph node stations essential to identify for EBUS-TBNA. Trainees had a baseline skills assessment using the simulator and were then provided a 1-hour didactic session on EBUS-TBNA and additional practice time with the simulator. Trainees then underwent a postsimulation skills assessment using a modified endobronchial ultrasound (EBUS)-Skills and Tasks Assessment Tool (STAT) performance assessment tool. Simulator fidelity and trainee procedural confidence was assessed using a 10-point scale. RESULTS: Ten fellows received training on the EBUS-TBNA simulator. First-year trainees scored the lowest on the 18-point performance scale with a mean score of 9, while third-year trainees scored highest with a mean score of 17.5. Mean 18-point performance score improvement after simulator training and didactics was 4.31 points for all trainees with the largest change in first-year trainees amounting to 8.25 points. First-year trainees experienced the greatest improvement in EBUS procedural confidence by a mean of 2.5 points on a 10-point confidence survey. CONCLUSION: A low-cost EBUS simulator effectively differentiated early and advanced learners based on graded procedural performance scores. Simulation-based practice significantly improved learners' procedural performance, and the degree of improvement correlated with learner inexperience. The simulation significantly increased early learner confidence in EBUS-TBNA technique.

Brief Glutamine Pretreatment Increases Alveolar Macrophage CD163/Heme Oxygenase-1/p38-MAPK Dephosphorylation Pathway and Decreases Capillary Damage but Not Neutrophil Recruitment in IL-1/LPS-Insufflated Rats.

BACKGROUND: Glutamine (GLN) attenuates acute lung injury (ALI) but its effect on alveolar macrophages is unknown. We hypothesized that GLN pretreatment would induce the anti-inflammatory CD163/heme oxygenase (HO)-1/p38-MAPK dephosphorylation pathway in alveolar macrophages and reduce ALI in rats insufflated with interleukin-1 (IL-1) and lipopolysaccharide (LPS). METHODS: Male Sprague-Dawley rats were randomized to the following groups: GLN-IL-1/LPS-, GLN+IL-1/LPS-, GLN-IL-1/LPS+, and GLN+IL-1/LPS+. GLN pretreatment was given via gavage (1 g/kg L-alanyl-L-glutamine) daily for 2 days. ALI was subsequently induced by insufflating 50 ng IL-1 followed by 5mg/kg E.coli LPS. After 24h, bronchoalveolar lavage (BAL) protein, lactate dehydrogenase (LDH) and neutrophil concentrations were analyzed. BAL alveolar macrophage CD163+ expression, HO-1 and p38-MAPK concentrations were measured, as well as alveolar macrophage tumor necrosis factor (TNF)-α and interleukin (IL)-10 concentrations. Histology and immunofluorescence studies were also performed. RESULTS: Following IL-1/LPS insufflation, GLN pretreated rats had significantly decreased BAL protein and LDH concentrations, but not BAL neutrophil counts, compared to non-GLN pretreated rats. The number of alveolar macrophages and the number of CD163+ macrophages were significantly increased in GLN pretreated IL-1/LPS-insufflated rats compared to non-GLN pretreated, IL-1/LPS-insufflated rats. GLN pretreatment before IL-1/LPS also significantly increased HO-1 concentrations and dephosphorylated p38-MAPK levels but not cytokine levels in alveolar macrophages. Immunofluorescence localized CD163 and HO-1 in alveolar macrophages. CONCLUSION: Short-term GLN pretreatment activates the anti-inflammatory CD163/HO-1/p38-MAPK dephosphorylation pathway of alveolar macrophages and decreases capillary damage but not neutrophil recruitment in IL-1/LPS-insufflated rats.