Addressing unprofessional behaviors in the clinical learning environment: lessons from a multi-year virtual, intergenerational, interdisciplinary workshop.

INTRODUCTION: Optimizing the clinical learning environment (CLE) is a medical education priority nationwide. MATERIALS AND METHODS: We developed a virtual, one-hour workshop engaging students, housestaff and faculty in small-group discussions of five case scenarios adapted from reported unprofessional behaviors in the CLE, plus didactics regarding mistreatment, microaggressions and bystander interventions. RESULTS: Over two sessions (2021-2022), we engaged 340 students and 73 faculty/housestaff facilitators. Post-session surveys showed significant improvement in participants' ability to recognize and respond to challenges in the CLE. DISCUSSION: Our innovative workshop, including scenarios derived from institutional reports of unprofessional behaviors, advanced participants' knowledge and commitment to improve the CLE.

Burn Trauma Acutely Increases the Respiratory Capacity and Function of Liver Mitochondria.

BACKGROUND: A complete understanding of the role of the liver in burn-induced hypermetabolism is lacking. We investigated the acute effect of severe burn trauma on liver mitochondrial respiratory capacity and coupling control as well as the signaling events underlying these alterations. METHODS: Male BALB/c mice (8-12 weeks) received full-thickness scald burns on ∼30% of the body surface. Liver tissue was harvested 24 h postinjury. Mitochondrial respiration was determined by high-resolution respirometry. Citrate synthase activity was determined as a proxy of mitochondrial density. Male Sprague-Dawley rats received full-thickness scald burns to ∼60% of the body surface. Serum was collected 24 h postinjury. HepG2 cells were cultured with serum-enriched media from either sham- or burn-treated rats. Protein levels were analyzed via western blot. RESULTS: Mass-specific (P = 0.01) and mitochondrial-specific (P = 0.01) respiration coupled to ATP production significantly increased in the liver after burn. The respiratory control ratio for ADP (P = 0.04) and the mitochondrial flux control ratio (P = 0.03) were elevated in the liver of burned animals. Complex III and Complex IV protein abundance in the liver increased after burn by 17% and 14%, respectively. Exposure of HepG2 cells to serum from burned rats increased the pAMPKα:AMPKα ratio (P < 0.001) and levels of SIRT1 (P = 0.01), Nrf2 (P < 0.001), and PGC1α (P = 0.02). CONCLUSIONS: Severe burn trauma augments respiratory capacity and function of liver mitochondria, adaptations that augment ATP production. This response may be mediated by systemic factors that activate signaling proteins responsible for regulating cellular energy metabolism and mitochondrial biogenesis.

Race, Income and Insurance Status Affect Neonatal Sepsis Mortality and Healthcare Resource Utilization.

BACKGROUND: Socioeconomic disparities negatively impact neonatal health. The influence of sociodemographic disparities on neonatal sepsis is understudied. We examined the association of insurance payer status, income, race and gender on neonatal sepsis mortality and healthcare resource utilization. METHODS: We used the Kid's Inpatient Database, a nationwide population-based survey from 2006, 2009 and 2012. Neonates diagnosed with sepsis were included in the study. Multivariable logistic regression (mortality) and multivariable linear regression (length of stay and total hospital costs) were constructed to determine the association of patient and hospital characteristics. RESULTS: Our study cohort included a weighted sample of 160,677 septic neonates. Several sociodemographic disparities significantly increased mortality. Self-pay patients had increased mortality (odds ratio 3.26 [95% confidence interval: 2.60-4.08]), decreased length of stay (-2.49 ± 0.31 days, P < 0.0001) and total cost (-$5015.50 ± 783.15, P < 0.0001) compared with privately insured neonates. Additionally, low household income increased odds of death compared with the most affluent households (odds ratio 1.19 [95% confidence interval: 1.05-1.35]). Moreover, Black neonates had significantly decreased length of stay (-0.86 ± 0.25, P = 0.0005) compared with White neonates. CONCLUSIONS: This study identified specific socioeconomic disparities that increased odds of death and increased healthcare resource utilization. Moreover, this study provides specific societal targets to address to reduce neonatal sepsis mortality in the United States.

Race and outcomes in gastroschisis repair: a nationwide analysis.

BACKGROUND: The incidence of gastroschisis has increased 30% between the periods 1995-2005 and 2006-2012, with the largest increase in Black neonates born to Black mothers younger than 20years old. OBJECTIVE: Racial disparities in peri- and post-operative outcomes have been previously identified in several types of adult and pediatric surgical patients. Is there an association between race and clinical outcomes and healthcare resource utilization in neonates with gastroschisis? METHODS: Retrospective study using national administrative data from the Kid's Inpatient Database (KID) from 2006, 2009, and 2012 for neonates (age<28days) with gastroschisis. Multivariable logistic regression was constructed to determine the association of race and socioeconomic characteristics with complications and mortality; linear regression was used for length of stay and hospital charges. RESULTS: We identified 3846 neonates with gastroschisis that underwent surgical repair, including 676 patients with complex gastroschisis. When controlling for birth weight, payer status, socioeconomic status, and hospital characteristics, Black neonates had increased odds of having complex gastroschisis and associated atresias. Mortality was higher in patients with complex gastroschisis, patients from the lowest income quartiles, and patients with Medicaid as primary payer (compared to those with private insurance). Length of stay (LOS) was increased in patients with complex gastroschisis, birth weight <2500g, and Medicaid patients. Hospital charges were higher in complex gastroschisis, Black and Hispanic neonates (as compared to Whites), males, birth weight <2500g, and Medicaid patients. CONCLUSIONS: There is an association between race and complex gastroschisis, associated intestinal atresias, and total charges in neonates with gastroschisis. In addition, income status is associated with mortality and hospital charges while payer status is associated with complications, mortality, LOS, and hospital charges. Public health and prenatal interventions should target at-risk populations to improve clinical outcomes. PROGNOSIS STUDY: Level of Evidence: II.

Sporadic Burkitt Lymphoma Presenting as Acute Pancreatitis, Concurrent Sinusitis, and Enlarged Adenoids.

Pancreatitis and sinusitis as presentations of Burkitt lymphoma are uncommon and rarely described in children. We describe here the case of a child who presented with symptoms suggestive of sinusitis unresponsive to antibiotics, with subsequent development of abdominal symptoms due to pancreatitis. He was eventually diagnosed with Burkitt lymphoma.

STAT3 Inhibition Suppresses Hepatic Stellate Cell Fibrogenesis: HJC0123, a Potential Therapeutic Agent for Liver Fibrosis.

Hepatic Stellate Cells (HSCs) are the major source of the excessive extracellular matrix (ECM) production that replaces liver parenchyma with fibrous tissue during liver fibrosis. The signal transducer and activator of transcription 3 (STAT3) promotes HCSs survival, proliferation, and activation contributing to fibrogenesis. We have previously used a fragment-based drug design approach and have discovered a novel STAT3 inhibitor, HJC0123. Here, we explored the biological effects of HJC0123 on the fibrogenic properties of HSCs. HJC0123 treatment resulted in the inhibition of HSCs proliferation at submicromolar concentrations. HJC0123 reduced the phosphorylation, nuclear translocation, and transcriptional activity of STAT3. It decreased the expression of STAT3-regulated proteins, induced cell cycle arrest, promoted apoptosis and downregulated SOCS3. HJC0123 treatment inhibited HSCs activation and downregulated ECM protein fibronectin and type I collagen expression. In addition, HJC0123 increased IL-6 production and decreased TGF-ß induced Smad2/3 phosphorylation. These results demonstrate that HJC0123 represents a novel STAT3 inhibitor that suppresses the fibrogenic properties of HSCs, suggesting its therapeutic potential in liver fibrosis.