Introduction: The number of female residents in orthopaedic surgery is rising; however, orthopaedics currently has the lowest percentage of women among all medical specialties. The Hirsch index (h-index) is a metric used to determine research productivity, an important factor for academic promotion in the field of orthopaedics. The purpose of this study was to compare research productivity (using the h-index) among male and female orthopaedic surgeons at academic residency programs within the United States. Methods: The websites for all Accreditation Council for Graduate Medical Education-accredited orthopaedic surgery residency programs in the United States were evaluated and the following information was collected: geographic region of the institution, sex, specialty, academic rank, and institutional leadership positions of faculty members. The h-index for each faculty member was collected from the Web of Science Database. Results: H-indices of 4,323 academic orthopaedic surgeons from 160 residency programs in the United States were collected. In total, 1,587 faculty members were assistant professors (220, 13.9% women), 839 were associate professors (91, 10.8% women), 902 were professors (50, 5.5% women), and academic rank was not specified for 991 (74, 7.5% women). One hundred forty-three faculty members held the position of department chair (2, 1.4% women) and 701 were division chiefs (58, 8.3% women). In geographic regions with a greater proportion of female orthopaedic faculty members, women had greater research productivity. Among Department Chairs, associate professors, and professors there was no difference in research productivity between male and female academic orthopaedic surgeons. By contrast, among assistant professors, there was a significant difference in research productivity. Conclusion: A higher proportion of female faculty in an orthopaedic department was positively associated with increased female research productivity. Female faculty at the highest ranks and leadership positions are as academically productive as their male counterparts. Despite similar research productivity, female orthopaedic surgeons are not nearly as well represented as their male counterparts in orthopaedics in general and in leadership positions within the field. In addition, a significantly smaller research productivity among female assistant professors disappears at the higher ranks in comparison to their male counterparts. This indicates a critical gap in factors that influence research productivity according to sex at the most junior faculty rank. Level of Evidence: Level III

BACKGROUND Ischemia/reperfusion injury (IRI) has been shown to cause endothelial glycocalyx (EG) damage. Whether the hypoxic/ischemic insult or the oxidative and inflammatory stress of reperfusion plays a greater part in glycocalyx damage is not known. Furthermore, the mechanisms by which IRI causes EG damage have not been fully elucidated. The aims of this study were to determine if hypoxia alone or hypoxia/reoxygenation (H/R) caused greater damage to the glycocalyx, and if this damage was mediated by reactive oxygen species (ROS) and Ca2+ signaling. METHODS Human umbilical vein endothelial cells were cultured to confluence and exposed to either normoxia (30 minutes), hypoxia (2% O2 for 30 minutes), or H/R (30 minutes hypoxia followed by 30 minutes normoxia). Some cells were pretreated with ROS scavengers TEMPOL, MitoTEMPOL, Febuxostat, or Apocynin, or with the Ca2+ chelator BAPTA or Ca2+ channel blockers 2-aminoethoxydiphenyl borate, A967079, Pyr3, or ML204. Intracellular ROS was quantified for all groups. Endothelial glycocalyx was measured using fluorescently tagged wheat germ agglutinin and imaged with fluorescence microscopy. RESULTS Glycocalyx thickness was decreased in both hypoxia and H/R groups, with the decrease being greater in the H/R group. TEMPOL, MitoTEMPOL, BAPTA, and 2-aminoethoxydiphenyl borate prevented loss of glycocalyx in H/R. The ROS levels were likewise elevated compared with normoxia in both groups, but were increased in the H/R group compared with hypoxia alone. BAPTA did not prevent ROS production in either group. CONCLUSION In our cellular model for shock, we demonstrate that although hypoxia alone is sufficient to produce glycocalyx loss, H/R causes a greater decrease in glycocalyx thickness. Under both conditions damage is dependent on ROS and Ca2+ signaling. Notably, we found that ROS are generated upstream of Ca2+, but that ROS-mediated damage to the glycocalyx is dependent on Ca2+.

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