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Background Scholarly activity is expected of program directors of the Accreditation Council for Graduate Medical Education (ACGME)-accredited residency training programs. Anesthesiology residency programs are cited more often than surgical programs for deficiencies in academic productivity. We hypothesized that this may in part reflect differences in scholarly activity between program directors of anesthesiology and surgical trainings programs. To test the hypothesis, we examined the career track record of current program directors of ACGME-accredited anesthesiology and surgical residency programs at the same institutions using PubMed citations and funding from the National Institutes of Health (NIH) as metrics of scholarly activity. Methods Between November 1, 2011 and December 31, 2011, we obtained data from publicly available websites on program directors at 127 institutions that had ACGME-accredited programs in both anesthesiology and surgery. Information gathered on each individual included year of board certification, year first appointed program director, academic rank, history of NIH grant funding, and number of PubMed citations. We also calculated the h-index for a randomly selected subset of 25 institution-matched program directors. Results There were no differences between the groups in number of years since board certification (P = 0.42), academic rank (P = 0.38), or years as a program director (P = 0.22). However, program directors in anesthesiology had less prior or current NIH funding (P = 0.002), fewer total and education-related PubMed citations (both P < 0.001), and a lower h-index (P = 0.001) than surgery program directors. Multivariate analysis revealed that the publication rate for anesthesiology program directors was 43% (95% CI 0.31–0.58) that of the corresponding program directors of surgical residency programs, holding other variables constant. Conclusions Program directors of anesthesiology residency programs have considerably less scholarly activity in terms of peer-reviewed publications and federal research funding than directors of surgical residency programs. As such, this study provides further evidence for a systemic weakness in the scholarly fabric of academic anesthesiology.

Complement is an important mediator of vascular injury following oxidative stress. We recently demonstrated that complement activation following endothelial oxidative stress is mediated by mannose-binding lectin (MBL) and activation of the lectin complement pathway. Here, we investigated whether nine plant lectins which have a binding profile similar to that of MBL competitively inhibit MBL deposition and subsequent complement activation following human umbilical vein endothelial cell (HUVEC) oxidative stress. HUVEC oxidative stress (1% O 2 , 24 hr) significantly increased Ulex europaeus agglutinin II (UEA-II) binding by 72 ± 9% compared to normoxic cells. UEA-II inhibited MBL binding to HUVEC in a concentration-dependent manner following oxidative stress. Further, MBL inhibited UEA-II binding to HUVEC in a concentration-dependent manner following oxidative stress, suggesting a common ligand. UEA-II (Յ 100 mol/L) did not attenuate the hemolytic activity, nor did it inhibit C3a des Arg formation from alternative or classical complement pathway-specific hemolytic assays. C3 deposition (measured by ELISA) following HUVEC oxidative stress was inhibited by UEA-II in a concentration-dependent manner (IC 50 ‫ס‬ 10 pmol/L). UEA-II inhibited C3 and MBL co-localization (confocal microscopy) in a concentration-dependent manner on HUVEC following oxidative stress (IC 50 ≈ 1 pmol/L). Finally, UEA-II significantly inhibited complement-dependent neutrophil chemotaxis, but failed to inhibit fMLP-mediated chemotaxis, following endothelial oxidative stress. These data demonstrate that UEA-II is a novel, potent inhibitor of human MBL deposition and complement activation following human endothelial oxidative stress. Keywords: Hypoxia, reoxygenation, mannose-binding lectin, neutrophils, chemotaxisEndothelial cells are important in the regulation of coagulation, vascular permeability, vasomotor tone and inflammation. Oxidative stress may result in complement activation and endothelial dysfunction. Endothelial dysfunction and complement activation are thought to be involved in human pathology including myocardial infarction (Weisman et al. 1990;Tsao et al. 1990), lung injury , sepsis , and gut ischemia (Siegfried et al. 1992). Indeed, inhibition of complement attenuates tissue injury in patients undergoing cardiopulmonary bypass (Fitch et al. 1999) and in several experimental models of human disease (Weisman et al. 1990;Vakeva et al. 1998;Zhou et al. 2000). Complement is known to interact with the vascular endothelium and initiate a variety of proinflammatory signals, including leukocyte adhesion molecule expression, pro-inflammatory cytokine secretion, and Abbreviations: fMLP, formyl methionine leucine phenylalanine; GlcNAc, N-acetylglucosamine; GVB, gelatin veronal buffer; HRP, horseradish peroxidase; HS, human serum; HUVEC, human umbilical vein endothelial cells; mAb, monoclonal antibody; MBL, mannose-binding lectin; pAb, polyclonal antibody; UEA-II, Ulex europaeus agglutinin II.Article and publication are at www.proteinsci...