Analysis of Gender-based Differences in Surgery Faculty Compensation, Promotion, and Retention: Establishing Equity.

OBJECTIVES: The objectives of this study were to evaluate gender-based differences in faculty salaries before and after implementation of a university-wide objective compensation plan, Faculty First (FF), in alignment with Association of American Medical Colleges regional median salary (AAMC-WRMS). Gender-based differences in promotion and retention were also assessed. SUMMARY BACKGROUND DATA: Previous studies demonstrate that female faculty within surgery are compensated less than male counterparts are and have decreased representation in higher academic ranks and leadership positions. METHODS: At a single institution, surgery faculty salaries and work relative value units (wRVUs) were reviewed from 2009 to 2017, and time to promotion and retention were reviewed from 1998 to 2007. In 2015, FF supplanted specialty-specific compensation plans. Salaries and wRVUs relative to AAMC-WRMS, time to promotion, and retention were compared between genders. RESULTS: Female faculty (N = 24) were compensated significantly less than males were (N = 62) before FF (P = 0.004). Female faculty compensation significantly increased after FF (P < 0.001). After FF, female and male faculty compensation was similar (P = 0.32). Average time to promotion for female (N = 29) and male faculty (N = 82) was similar for promotion to associate professor (P = 0.49) and to full professor (P = 0.37). Promotion was associated with significantly higher retention for both genders (P < 0.001). The median time of departure was similar between female and male faculty (P = 0.73). CONCLUSIONS: A university-wide objective compensation plan increased faculty salaries to the AAMC western region median, allowing correction of gender-based salary inequity. Time to promotion and retention was similar between female and male faculty.

Stimulation of the interleukin-1 receptor and Toll-like receptor 2 inhibits hepatitis B virus replication in hepatoma cell lines in vitro.

BACKGROUND: Toll-like receptors (TLRs) are a key component of the innate immune system and TLR2 has been shown to be involved in the immunopathogenesis of hepatitis B virus (HBV) infection in vivo. We investigated the role of TLR2 stimulation of virus-infected hepatocyte cell lines as a potential antiviral mechanism in vitro. METHODS: The hepatoblastoma cell line HepG2 was transduced with recombinant HBV baculoviruses and the hepatoma cell line Huh-7 was transiently transfected with complimentary DNA clones of HBV. HBV viral replication was quantified after stimulation with interleukin (IL)-1beta and Pam-2-Cys, a synthetic TLR2 ligand, by measuring intracellular core-associated single-stranded HBV DNA using Southern blot hybridization, as well as viral nucleocapsid formation using a non-denaturing immunoblot method. RESULTS: Stimulation of both cell lines in vitro with IL-1beta and Pam-2-Cys, both known to induce expression of the pro inflammatory cytokines tumour necrosis factor-alpha and IL-8 via a nuclear factor-kappaB dependent pathway, resulted in the inhibition of HBV DNA replication in the transduced HepG2 cells by up to 90% and nucleocapsid formation in the transiently transfected Huh-7 cells by up to 30%, when compared with mock-treated cells. CONCLUSIONS: Hepatoma cell lines expressed functional IL-1 receptor and TLR2 receptors, which when stimulated led to a signalling cascade that inhibited HBV replication. These data support an active role for hepatocytes in inhibiting HBV replication and provide a rationale for the development of TLR agonists as potentially novel antiviral agents.

Regulation of Toll-like receptor-2 expression in chronic hepatitis B by the precore protein.

UNLABELLED: Toll-like receptors (TLRs) play a key role in the innate immune response. The aim of this study was to examine the expression of TLR2 and TLR4 in chronic hepatitis B (CHB). The TLR2 and TLR4 expression on hepatocytes and Kupffer cells from fresh liver biopsies was measured from 21 patients with untreated hepatitis B e antigen (HBeAg)-positive and HBeAg-negative CHB. Parallel studies were also undertaken on monocytes from their peripheral blood. Expression of TLR2 on hepatocytes, Kupffer cells, and peripheral monocytes was significantly reduced in patients with HBeAg-positive CHB in comparison with HBeAg-negative CHB and controls, whereas it was significantly increased in HBeAg-negative CHB compared with controls. The level of TLR4 expression did not differ significantly between the groups. These results were confirmed in vitro using hepatic cell lines transduced with recombinant HBV baculovirus expressing wild-type HBV (HBeAg-positive), precore stop codon (G1896A) mutant HBV (HBeAg-negative). The functional relevance of these findings was established by the demonstration of significantly reduced cytokine production (TNF-alpha) and phospho-p38 kinase expression in the presence of the HBeAg. In the absence of HBeAg, HBV replication was associated with up-regulation of the TLR2 pathway leading to increased TNF-alpha production. CONCLUSION: This study demonstrates a potentially important interaction between HBeAg, HBV, and the innate immune response.