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Objectives:. The research question asked to what extent do self-rated performance scores of individual surgeons correspond to assessed procedural performance abilities and to peer ratings of procedural performance during a mass casualty (MASCAL) event? Background:. Self-assessment using performance rating scales is ubiquitous in surgical education as a proxy for direct measurement of competence. The validity and reliability of self-ratings as competency measures are susceptible to cognitive biases such as Dunning-Kruger effects, which describe how individuals over/underestimate their own performance compared to assessments from independent sources. The ability of surgeons to accurately self-assess their procedural performance remains undetermined. Methods:. A purposive sample of military surgeons (N = 13) who collectively cared for trauma patients during a MASCAL event participated in the study. Pre-event performance assessment scores for 32 trauma procedures were compared with post-event self and peer performance ratings using F tests (P < 0.05) and effect sizes (Cohen’s d). Results:. There were no significant differences between peer ratings and performance assessment scores. There were significant differences between self-ratings and both peer ratings (P < 0.001) and performance assessment scores (P < 0.001). Effect sizes were very large for self to peer rating comparison (Cohen’s d = 2.34) and self to performance assessment comparison (Cohen’s d = 2.77). Conclusions:. The outcomes demonstrate that self-ratings were significantly lower than the independently determined assessment scores for each surgeon, revealing a Dunning-Kruger effect for highly skilled individuals underestimating their abilities. These outcomes underscore the limitations of self-assessment for measuring competence.

Objectives: The research question asked to what extent do self-rated performance scores of individual surgeons correspond to assessed procedural performance abilities and to peer ratings of procedural performance during a mass casualty (MASCAL) event?, Background: Self-assessment using performance rating scales is ubiquitous in surgical education as a proxy for direct measurement of competence. The validity and reliability of self-ratings as competency measures are susceptible to cognitive biases such as Dunning-Kruger effects, which describe how individuals over/underestimate their own performance compared to assessments from independent sources. The ability of surgeons to accurately self-assess their procedural performance remains undetermined., Methods: A purposive sample of military surgeons (N = 13) who collectively cared for trauma patients during a MASCAL event participated in the study. Pre-event performance assessment scores for 32 trauma procedures were compared with post-event self and peer performance ratings using F tests ( P < 0.05) and effect sizes (Cohen's d )., Results: There were no significant differences between peer ratings and performance assessment scores. There were significant differences between self-ratings and both peer ratings ( P < 0.001) and performance assessment scores ( P < 0.001). Effect sizes were very large for self to peer rating comparison (Cohen's d = 2.34) and self to performance assessment comparison (Cohen's d = 2.77)., Conclusions: The outcomes demonstrate that self-ratings were significantly lower than the independently determined assessment scores for each surgeon, revealing a Dunning-Kruger effect for highly skilled individuals underestimating their abilities. These outcomes underscore the limitations of self-assessment for measuring competence., (Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc.)

TNF inhibits serine protease inhibitor 2.1 (Spi 2.1) and IGF-I gene expression by GH in CWSV-1 hepatocytes. The current study describes construction of a GH-inducible IGF-I promoter construct and investigates mechanisms by which TNF and nuclear factor-kappaB (NFkappaB) inhibit GH-inducible gene expression. CWSV-1 cells were transfected with GH-inducible Spi 2.1 or IGF-I promoter luciferase constructs, incubated with TNF signaling inhibitors (fumonisin B1 for sphingomyelinase and SP600125 for c-Jun N-terminal kinase), treated with or without TNF, and then stimulated with recombinant human GH. The 5- to 6-fold induction of Spi 2.1 and IGF-I promoter activity by GH was inhibited by TNF. Neither fumonisin B1 nor SP600125 prevented the inhibitory effects of TNF on GH-inducible promoter activity. Dominant-negative inhibitor-kappaBalpha (IkappaBalpha) expression vectors (IkappaBalphaS/A or IkappaBalphaTrunc), p65 and p50 expression vectors, and p65 deletion constructs were used to investigate the NFkappaB pathway. IkappaBalphaS/A and IkappaBalphaTrunc ameliorated the inhibitory effects of TNF on GH-inducible Spi 2.1 and IGF-I promoter activity. Cotransfection of CWSV-1 cells with expression vectors for p65 alone or p50 and p65 together inhibited GH-inducible Spi 2.1 and IGF-I promoter activity. Cotransfection with a C-terminal p65 deletion (1-450) enhanced GH-inducible promoter activity, whereas the N-terminal deletion (31-551) was inhibitory for IGF-I but not Spi 2.1. Cycloheximide did not antagonize the inhibitory effects of TNF on GH-inducible IGF-I expression. We conclude the inhibitory effects of TNF on GH-inducible promoter activity are mediated by NFkappaB, especially p65, by a mechanism that does not require protein synthesis.

During systemic inflammation, the liver becomes unresponsive to growth hormone (GH), resulting in decreased plasma insulin-like growth factor-I (IGF-I) with concomitant reductions in lean body mass. Transgenic mice that overexpress IL-6 also demonstrate impaired growth and decreased IGF-I. To determine whether IL-6 directly inhibits GH-inducible gene expression, CWSV-1 hepatocytes were incubated with IL-6 (10 ng/ml), then stimulated with recombinant human GH (500 ng/ml, 18 h). The increase in IGF-I and serine protease inhibitor 2.1 (Spi 2.1) mRNA in GH-treated cells was inhibited by treatment with IL-6 for 24 h. To investigate potential mechanisms, we examined the effects of IL-6 on GH receptor (GHR) expression and GH signaling via the JAK/signal transducer and activator of transcription (STAT) and MAP kinase pathways. Incubation of cells with IL-6 (10 ng/ml, 24 h) had no effect on GHR abundance or signaling proteins JAK2, STAT5b, and ERK1/2. Although GH transiently increased (2- to 5-fold) the tyrosine phosphorylation of GHR, JAK2, STAT5b, and ERK1/2, IL-6 did not alter these phosphorylation events. However, nuclear protein from IL-6-treated cells demonstrated reduced STAT5 DNA binding (by EMSA) at 15 min (-20%) and 60 min (-43%) after GH stimulation. To determine whether IL-6 inhibits GH-inducible promoter activity, CWSV-1 cells were transfected with Spi 2.1 or prolactin receptor promoter luciferase vectors, incubated with or without IL-6, then stimulated with GH. The induction of both Spi 2.1 (7.5-fold) and prolactin receptor (4-fold) promoter activity by GH was inhibited by IL-6. In summary, IL-6 mediates hepatic GH resistance by a time-dependent inhibition of GH-inducible promoter activity that is associated with reductions in STAT5 DNA binding.