Explore the vast range of titles available.

Competence-based medical education requires robust data to link competence with clinical experiences. The SARS-CoV-2 (COVID-19) pandemic abruptly altered the standard trajectory of clinical exposure in medical training programs. Residency program directors were tasked with identifying and addressing the resultant gaps in each trainee's experiences using existing tools. This study aims to demonstrate a feasible and efficient method to capture electronic health record (EHR) data that measure the volume and variety of pediatric resident clinical experiences from a continuity clinic; generate individual-, class-, and graduate-level benchmark data; and create a visualization for learners to quickly identify gaps in clinical experiences. This pilot was conducted in a large, urban pediatric residency program from 2016 to 2022. Through consensus, 5 pediatric faculty identified diagnostic groups that pediatric residents should see to be competent in outpatient pediatrics. Information technology consultants used International Classification of Diseases, Tenth Revision (ICD-10) codes corresponding with each diagnostic group to extract EHR patient encounter data as an indicator of exposure to the specific diagnosis. The frequency (volume) and diagnosis types (variety) seen by active residents (classes of 2020-2022) were compared with class and graduated resident (classes of 2016-2019) averages. These data were converted to percentages and translated to a radar chart visualization for residents to quickly compare their current clinical experiences with peers and graduates. Residents were surveyed on the use of these data and the visualization to identify training gaps. Patient encounter data about clinical experiences for 102 residents (N=52 graduates) were extracted. Active residents (n=50) received data reports with radar graphs biannually: 3 for the classes of 2020 and 2021 and 2 for the class of 2022. Radar charts distinctly demonstrated gaps in diagnoses exposure compared with classmates and graduates. Residents found the visualization useful in setting clinical and learning goals. This pilot describes an innovative method of capturing and presenting data about resident clinical experiences, compared with peer and graduate benchmarks, to identify learning gaps that may result from disruptions or modifications in medical training. This methodology can be aggregated across specialties and institutions and potentially inform competence-based medical education.

Endoplasmic reticulum (ER) stress has been implicated in alveolar epithelial type II (AT2) cell apoptosis in idiopathic pulmonary fibrosis. We hypothesized that ER stress (either chemically induced or due to accumulation of misfolded proteins) is also associated with epithelial-mesenchymal transition (EMT) in alveolar epithelial cells (AECs). ER stress inducers, thapsigargin (TG) or tunicamycin (TN), increased expression of ER chaperone, Grp78, and spliced X-box binding protein 1, decreased epithelial markers, E-cadherin and zonula occludens-1 (ZO-1), increased the myofibroblast marker, α-smooth muscle actin (α-SMA), and induced fibroblast-like morphology in both primary AECs and the AT2 cell line, RLE-6TN, consistent with EMT. Overexpression of the surfactant protein (SP)-C BRICHOS mutant SP-C(ΔExon4) in A549 cells increased Grp78 and α-SMA and disrupted ZO-1 distribution, and, in primary AECs, SP-C(ΔExon4) induced fibroblastic-like morphology, decreased ZO-1 and E-cadherin and increased α-SMA, mechanistically linking ER stress associated with mutant SP to fibrosis through EMT. Whereas EMT was evident at lower concentrations of TG or TN, higher concentrations caused apoptosis. The Src inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4]pyramidine) (PP2), abrogated EMT associated with TN or TG in primary AECs, whereas overexpression of SP-C(ΔExon4) increased Src phosphorylation, suggesting a common mechanism. Furthermore, increased Grp78 immunoreactivity was observed in AT2 cells of mice after bleomycin injury, supporting a role for ER stress in epithelial abnormalities in fibrosis in vivo. These results demonstrate that ER stress induces EMT in AECs, at least in part through Src-dependent pathways, suggesting a novel role for ER stress in fibroblast accumulation in pulmonary fibrosis.

Endothelin-1 (ET-1) is implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF), but the cellular mechanisms underlying the role it plays in this disease are not well characterized. Epithelial–mesenchymal transition (EMT), which was recently demonstrated in alveolar epithelial cells (AEC), may play an important role in the pathogenesis of IPF and other forms of pulmonary fibrosis. Whether ET-1 contributes to the induction of EMT in AEC is unknown. The aims of this study were to evaluate AEC production of ET-1 and to determine if ET-1 induces EMT in AEC. We demonstrate that ET-1 is produced at physiologically relevant levels by primary AEC and is secreted preferentially toward the basolateral surface. We also demonstrate that AEC express high levels of endothelin type A receptors (ET-A) and, to a lesser extent, type B receptors (ET-B), suggesting autocrine or paracrine function for alveolar ET-1. In addition, ET-1 induces EMT through ET-A activation. Furthermore, TGF-β1 synthesis is increased by ET-1, ET-1 induces Smad3 phosphorylation, and ET-1–induced EMT is attenuated by a TGF-β1–neutralizing antibody. Thus, ET-1 is an important mediator of EMT in AEC, acting through ET-A–mediated TGF-β1 production. These findings increase our basic understanding of the role of ET-1 in pulmonary fibrosis and suggest potential roles for AEC-derived ET-1 in the pathogenesis of other alveolar epithelial–mediated lung diseases.

Abstract Objective The University of California (UC) leadership sought to develop a robust educational response to the epidemic of opioid-related deaths. Because the contributors to this current crisis are multifactorial, a comprehensive response requires educating future physicians about safe and effective management of pain, safer opioid prescribing, and identification and treatment of substance use disorder (SUD). Methods The six UC medical schools appointed an opioid crisis workgroup to develop educational strategies and a coordinated response to the opioid epidemic. The workgroup had diverse specialty and disciplinary representation. This workgroup focused on developing a foundational set of educational competencies for adoption across all UC medical schools that address pain, SUD, and public health concerns related to the opioid crisis. Results The UC pain and SUD competencies were either newly created or adapted from existing competencies that addressed pain, SUD, and opioid and other prescription drug misuse. The final competencies covered three domains: pain, SUD, and public health issues related to the opioid crisis. Conclusions The authors present a novel set of educational competencies as a response to the opioid crisis. These competencies emphasize the subject areas that are fundamental to the opioid crisis: pain management, the safe use of opioids, and understanding and treating SUD.

(1) To characterise changes in dead space fraction during the first 120 post-operative hours in neonates undergoing stage 1 palliation for hypoplastic left heart syndrome, including hybrid procedure; (2) to document whether dead space fraction varied by shunt type (Blalock-Taussig shunt and Sano) and hybrid procedure; and (3) to determine the association between dead space fraction and outcomes. Retrospective chart review in neonates undergoing stage 1 palliation for hypoplastic left heart syndrome in a cardiac intensive care unit over a consecutive 30-month period. A linear mixed model was used to determine the differences in dead space over time. Multivariable linear regression and a multivariable linear mixed model were used to assess the association between dead space and outcomes at different time points and over time, respectively. Thirty-four neonates received either a Blalock-Taussig shunt (20.5%), Sano shunt (59%), or hybrid procedure (20.5%). Hospital mortality was 8.8%. Dead space fractions in patients undergoing the hybrid procedure were significantly lower on day 1 (p = 0.01) and day 2 (p = 0.02) and increased over time. A dead space fraction >0.6 on post-operative days 3-5 was significantly associated with decreased duration of mechanical ventilation in all surgical groups (p 0.6 on post-operative days 3-5 was associated with lower duration of mechanical ventilation in all surgical groups. A more comprehensive, prospective assessment of dead space in this delicate patient population would likely be beneficial in improving outcomes.

The lymphocytes facilitate activation of macrophages and a variety of other inflammatory cells, with resultant epithelial damage. 5 The critical role of this allogeneic immune response as the initial trigger leading to OB is supported by the fact that the primary risk factors for the development of BOS after lung transplantation are class I and II mismatches between donor and recipient, as well as the number and severity of rejection episodes. 4 Although it has been recognised for over a decade that the airway epithelium is a target of the initial immune response, 6 the pathogenetic pathway that leads to disruption of normal epithelial repair processes, excessive fibroblastic responses and resultant excessive ECM deposition and eventual obliteration of small airways is still incompletely elucidated. [...]they used confocal microscopy to demonstrate co-localisation of epithelial and mesenchymal markers within the epithelium of transplant recipients with OB.

Dexmedetomidine is an alpha2-adrenergic agonist that causes sleep-like sedation and mild analgesia without narcosis or respiratory depression, and has relative cardiovascular stability. Due to these properties, it may be an effective agent for prolonged use in the sedation of patients in the paediatric cardiothoracic intensive care unit. We reviewed our experience with the drug to detail its safety and efficacy. We conducted a retrospective chart review of all patients who received dexmedetomidine over a six month period in a dedicated paediatric cardiothoracic intensive care unit. Patients were identified from pharmacy records showing administration of drugs. We collected demographic data, information relating to doses of dexmedetomidine, physiologic parameters, and clinical outcomes. We identified 54 patients who received the drug. The median age of recipients was 6 months, with a range from 1 day to 16 years. The mean duration of administration was 37.3 hours, with a range from 2 to 177 hours. The mean duration of continuation of administration after extubation was 16.7 hours, with a range from zero to 112.5 hours. Physiologically, there were no clinically significant changes in mean arterial pressure, heart rate, respiratory rate, or saturations of oxygen before, during, or after utilization of the drug. Use of dexmedetomidine significantly reduced the need to administer narcotics, and scores using the COMFORT system were not different between patients who received dexmedetomidine and those who did not. In this limited and retrospective review, dexmedetomidine was found to be safe and efficacious. Its use as a sedative agent for extended periods of time in critically-ill children deserves investigation in a prospective and controlled manner.

Nitric oxide (NO) plays an important role in lung development and perinatal lung function, and pulmonary NO synthases (NOS) are decreased in bronchopulmonary dysplasia (BPD) following preterm birth. Fetal estradiol levels increase during late gestation and estradiol up-regulates NOS, suggesting that after preterm birth estradiol deprivation causes attenuated lung NOS resulting in impaired pulmonary function. To test the effects of postnatal estradiol administration in a primate model of BPD over 14 days after delivery at 125 days of gestation (term = 185 d). Cardiopulmonary function was assessed by echocardiography and whole body plethysmography. Lung morphometric and histopathologic analyses were performed, and NOS enzymatic activity and abundance were measured. Estradiol caused an increase in blood pressure and ductus arteriosus closure. Expiratory resistance and lung compliance were also improved, and this occurred before spontaneous ductal closure. Furthermore, both oxygenation and ventilation indices were improved with estradiol, and the changes in lung function and ventilatory support requirements persisted throughout the study period. Whereas estradiol had negligible effect on indicators of lung inflammation and on lung structure assessed after the initial 14 days of ventilatory support, it caused an increase in lung neuronal and endothelial NOS enzymatic activity. In a primate model of BPD, postnatal estradiol treatment had favorable cardiovascular impact, enhanced pulmonary function, and lowered requirements for ventilatory support in association with an up-regulation of lung NOS. Estradiol may be an efficacious postnatal therapy to improve lung function and outcome in preterm infants.

To compare the pressure-rate products and phase angles of children during minimal support ventilation and after extubation. Prospective, randomized single-center trial in a pediatric intensive care unit in a tertiary children's hospital. Seventeen endotracheally intubated, mechanically ventilated children were placed on T-piece, T-piece with heliox, continuous positive airway pressure, and pressure support in random order. Esophageal pressure swings, phase angles, respiratory mechanics, and physiological parameters were measured on these modes and after extubation. Pressure-rate product postextubation was significantly higher than on support modes. For each mode and after extubation they were: pressure support 198+/-31, continuous positive airway pressure 237+/-30, T-piece 323+/-47, T-piece/heliox 308+/-61, and extubation 378+/-43 cmH2O/min. Phase angles were significantly higher during T-piece ventilation than pressure support but not did not differ significantly from postextubation. Assessment of effort of breathing during even minimal mechanical ventilation may underestimate postextubation effort in children. Postextubation pressure-rate product and hence \"effort of breathing\" in children is best approximated by T-piece ventilation.

Objective: To report two cases of cardiac injury following blunt thoracic trauma without external evidence of injury. Design: Case report and review of the literature. Setting: A 23-bed pediatric intensive care unit in an academic children’s hospital. Interventions: Two children presented following significant thoracic trauma without external evidence of injury. Cardiac injury was not initially suspected, and lack of definitive diagnostic evaluation led to a delay in diagnosis and definitive treatment. Results: A 4-year-old girl presented 6 months after initial injury and evaluation with massive right ventricular dilatation secondary to traumatic tricuspid regurgitation. The second patient, an 11-year-old boy, underwent a laparotomy for suspected abdominal pathology delaying diagnosis of his traumatic ventricular septal defect and definitive repair until clinical hemodynamic deterioration occurred. Conclusion: Clinicians should maintain a high index of suspicion for cardiac injury in patients with a significant mechanism of thoracic trauma despite external evidence. Standard screening tests are often inadequate and echocardiography should be performed for any suspected cardiac trauma.