Gender Disparity in Non-ACGME (Accreditation Council for Graduate Medical Education) Otolaryngology Fellowship Leadership.

OBJECTIVE: Women are underrepresented among practicing otolaryngology physicians with increasing disparities in leadership roles and higher levels of professional attainment in academic medicine. The purpose of this study is to determine the gender gap among fellowship directors within specific otolaryngology subspecialties, and how this compares to disparities among all academic appointments held by otolaryngologists. Additionally, we seek to better understand how years practiced, H-index, professorship status, and academic productivity differ between men and women in fellowship director roles. DESIGN: Cross-sectional. Publicly available data from non-ACGME accredited otolaryngology fellowships was collected from department websites and Doximity including gender, years of practice, and professor status of fellowship directors. Scopus was used to find H-index for identified fellowship directors. Fisher's Exact tests were used to determine if significant gender disparity existed between each fellowship and academic otolaryngology as whole. H-index and years of practice were plotted for men and women comparing the slope of lines of best fit as a measure of academic productivity. SETTING: Non-ACGME accredited otolaryngology fellowships in the US. PARTICIPANTS: Fellowship directors in non-ACGME accredited otolaryngology fellowships. RESULTS: Among 174 fellowship positions in our analysis, head and neck (17.3% women), laryngology (17.2% women), rhinology (5.7% women), and facial plastics (8.1% women) had significantly lower overall women representation compared to academic otolaryngology (36.6% women) (p < 0.05). As fellowship directors, women were significantly more productive than men given years practiced and H-index (p = 0.008). CONCLUSIONS: Gender disparities among otolaryngologists are amplified in the role of fellowship directors compared to broader academic otolaryngology. This is true despite women in these roles demonstrating higher academic productivity.

Endothelial SOCS3 maintains homeostasis and promotes survival in endotoxemic mice.

SOCS3 is the main inhibitor of the JAK/STAT3 pathway. This pathway is activated by interleukin 6 (IL-6), a major mediator of the cytokine storm during shock. To determine its role in the vascular response to shock, we challenged mice lacking SOCS3 in the adult endothelium (SOCS3iEKO) with a nonlethal dose of lipopolysaccharide (LPS). SOCS3iEKO mice died 16-24 hours postinjection after severe kidney failure. Loss of SOCS3 led to an LPS-induced type I IFN-like program and high expression of prothrombotic and proadhesive genes. Consistently, we observed intraluminal leukocyte adhesion and neutrophil extracellular trap-osis (NETosis), as well as retinal venular leukoembolization. Notably, heterozygous mice displayed an intermediate phenotype, suggesting a gene dose effect. In vitro studies were performed to study the role of SOCS3 protein levels in the regulation of the inflammatory response. In human umbilical vein endothelial cells, pulse-chase experiments showed that SOCS3 protein had a half-life less than 20 minutes. Inhibition of SOCS3 ubiquitination and proteasomal degradation led to protein accumulation and a stronger inhibition of IL-6 signaling and barrier function loss. Together, our data demonstrate that the regulation of SOCS3 protein levels is critical to inhibit IL-6-mediated endotheliopathy during shock and provide a promising therapeutic avenue to prevent multiorgan dysfunction through stabilization of endothelial SOCS3.