Apoptosis, programmed cell death, eliminates injured or harmful cells. It can mediate its response through the actions of death ligands including TRAIL. TRAIL, a member of TNF superfamily, induces apoptosis of transformed cells through the action of death domain receptors DR-4 and DR5. It directly induces apoptosis through an extrinsic pathway, which involves the activation of caspases. TRAIL also is able to prevent apoptosis through the actions of its decoy receptors DcR-1 and DcR-2. Various regulators of TRAIL include FADD, IAPs, Bcl-2s, p53, and FLIPs. TRAIL is present in cells involved in asthma including eosinophils, mast cells, fibroblasts, and airway epithelial cells. It is expressed in airway remodeling and may be linked with the pathways of transforming growth factor-beta1, which is thought to cause damage to the epithelium. The repair process of the epithelium is hindered as a result of increased apoptosis induced by TGF-beta1, which overlaps with the pathways of TRAIL. Analogs of TRAIL could have therapeutical applications for asthma. TRAIL is also seen as the basis for a "miracle" drug for cancer because of its ability to selectively kill cancer cells.
Background The association between physician self-reported empathy and burnout has been studied in the past with diverse findings. We aimed to determine the association between empathy and burnout among United States emergency medicine (EM) physicians using a novel combination of tools for validation. Methods This was a prospective single-center observational study. Data were collected from EM physicians. From December 1, 2018 to January 31, 2019, we used the Jefferson scale of empathy (JSE) to assess physician empathy and the Copenhagen burnout inventory (CBI) to assess burnout. We divided EM physicians into different groups (residents in each year of training, junior/senior attendings). Empathy, burnout scores and their association were analyzed and compared among these groups. Results A total of 33 attending physicians and 35 EM residents participated in this study. Median self-reported empathy scores were 113 (interquartile range (IQR): 105 - 117) in post-graduate year (PGY)-1, 112 (90 - 115) in PGY-2, 106 (93 - 118) in PGY-3 EM residents, 112 (105 - 116) in junior and 114 (101 - 125) in senior attending physicians. Overall burnout scores were 43 (33 - 50) in PGY-1, 51 (29 - 56) in PGY-2, 43 (42 - 53) in PGY-3 EM residents, 33 (24 - 47) in junior attending and 25 (22 - 53) in senior attending physicians separately. The Spearman correlation (ρ) was -0.11 and β-weight was -0.23 between empathy and patient-related burnout scores. Conclusion Self-reported empathy declines over the course of EM residency training and improves after graduation. Overall high burnout occurs among EM residents and improves after graduation. Our analysis showed a weak negative correlation between self-reported empathy and patient-related burnout among EM physicians.
Widespread damage of airway epithelium and defective epithelial repair are hallmarks of chronic asthma. Growth factors and cytokines spatially and temporally regulate epithelial shedding and repair. Within this context, a key function is exerted by transforming growth factor (TGF)-beta. Recent growing evidence suggests that chloride (Cl(-)) channels are critical to cell apoptosis. We examined the effects of TGF-beta1 on Cl(-) channel expression and activity and its relationship with apoptosis in human bronchial epithelial cells (HBECs). The small interfering RNA (siRNA) approach was used to investigate the potential role of CLC-3, a member of the volume-regulated Cl(-) channel family, in apoptosis of HBECs. TGF-beta1 significantly induced HBEC apoptosis, which paralleled to a significant decrease in the endogenous expression of CLC-3 protein and mRNA transcripts. Outward rectifying and voltage-dependent CLC-3-like Cl(-) currents in HBECs were diminished by TGF-beta1. siRNA for CLC-3 abolished Cl(-) current and enhanced TGF-beta1-induced cell apoptosis. Overexpression of CLC-3 in HBECs inhibited TGF-beta1-induced cell apoptosis. Bcl-2 was also downregulated after TGF-beta stimulation. TGF-beta1-induced cell apoptosis was suppressed in Bcl-2-transfected HBECs. Our data demonstrate that CLC-3-like voltage-gated chloride channels play a critical role in TGF-beta-induced apoptosis of human airway epithelial cells.
Background Healthcare provider wellness have been reported to correlate with patient care outcomes. It is not understood whether synergistic effects may exist between them. Objective We aim to investigate three provider wellness markers and determine their associations with provider self-reported medical errors and intent-to-leave outcomes among Emergency Department (ED) providers. Design This is a multi-center retrospective study. Method Three wellness domains include professional fulfillment (PF), burnout (BO), and personal resilience (PR). Two outcomes measured as provider self-reported medical errors and provider intent-to-leave. Correlations between wellness markers and outcomes were analyzed. When adjusted for other confounders (provider demographics, provider experience, and operational environment), a multivariate logistic regression analysis was performed to further determine the interactions among these three domains on provider wellness affecting patient and provider related outcomes. Results Total 242 surveys were collected from providers at 16 different EDs. The median score of PF were 2.83 among physicians and 2.67 among APPs, BO were 1.00 (physicians) and 0.95 (APPs), and PR were 0.88 (physicians) and 0.81 (APPs). The median scores of selfreported medical errors were 1.50 (physicians) and 0.95 (APPs), and intent-to-leave were 1.00 (physicians and APPs). High correlations occurred among PF, BO, and PR. When
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