Department of Orthopaedic Surgery

ABSTRACT Why do women remain underrepresented in positions of power? The present work leverages four studies ( N = 99,293) spanning archival, qualitative, and experimental methods to surface one novel antecedent to this gender gap. Men (vs. women) tend to perceive their organizations as more meritocratic as a function of their structural power (Studies 1–2). This gender difference is statistically accounted for by the fact that men's power is more often accompanied by perceived resource sufficiency , or the appraisal that one has adequate instrumental and material resources to meet role demands and exercise authority effectively (Studies 1–3). A preregistered experiment finds that higher (vs. lower) perceived resource sufficiency increases meritocracy perceptions, which in turn increase career investment intentions but weaken support for equity‐enhancing initiatives (Study 4). Together, these findings reveal that structural power's psychological consequences are not uniform across gender but depend on whether authority is accompanied by the resources needed to exercise power. The gender gap in power may thus reproduce itself, as women become less convinced that the system rewards their effort, whereas men with the authority to change organizational systems become least likely to see the need for change.

BACKGROUND: Developmental control of jaw size is crucial to prevent birth defects and facilitate evolutionary adaptation. We have shown that jaw size is established by neural crest mesenchyme (NCM), which are progenitor cells that migrate into the mandibular primordia and produce the jaws. NCM relies on multiple signaling pathways including Sonic Hedgehog (SHH) to mediate interactions with mandibular epithelium and promote jaw outgrowth. We investigated if NCM-mediated regulation of the SHH pathway underlies species-specific evolution of jaw size. RESULTS: We analyze expression of SHH pathway members over time and find that Growth Arrest-Specific 1 (GAS1), which is a SHH co-receptor, is expressed 20-75-fold higher in mandibular primordia of duck relative to those of quail. We generate quail-duck chimeras and demonstrate Gas1 expression is NCM-regulated. Gain- and loss-of-function experiments reveal species-specific sensitivity to SHH signaling, especially for Gas1. Gas1 overexpression and knockdown in NCM alters cell number and jaw size, and differentially affects genes involved in the SHH and WNT pathways, the cell cycle, and others. We also uncover intriguing differences in the Gas1 promoter and coding sequence between duck and quail. CONCLUSIONS: Our work suggests changes to Gas1 expression and function may modulate jaw size during development, disease, and evolution.

While gender and economic outcomes in negotiation have been studied for decades, much less is known about gender differences in subjective outcomes, such as trust, rapport, and willingness to negotiate again, despite their importance for long-term success. In a series of studies with over 2,000 participants, we find that people consistently report better subjective outcomes when negotiating with women. This preference persists even in anonymous negotiations where gender is unknown and cannot be inferred from behavior, as well as in conditions where negotiation partner gender is randomly assigned. Importantly, we find no gender difference in economic outcomes. To understand why, we analyzed transcripts of real negotiations for any behavioral differences. These findings reveal an overlooked gender dynamic: While men and women achieve similar economic results, women foster stronger interpersonal relationships, which in turn lead to greater satisfaction and greater desire for future negotiations with women.

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Despite decades of progress, gender inequalities in workplace authority and compensation persist. This review reveals recent advances in understanding how gendered careers emerge through three psychological mechanisms prevalent in organizations: (i) intrapersonal gender biases, (ii) interpersonal power dynamics, and (iii) intergroup gender relations. Because power is perceived as masculine, women in authority face systematic backlash. While status offers women an alternative leadership route, it proves less valuable than power - lacking resource control and requiring constant social validation rather than conferring formal authority. We suggest that mindsets about human malleability moderate these dynamics: fixed mindsets amplify stereotyping and power-based challenges for women leaders, while growth mindsets attenuate barriers. Our framework aims to illuminate gender disparities and to suggest promising intervention pathways.

Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls (p < 0.01) and a significant rise in PDGFRα-GFP + FAPs (p < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including Cxcl13, Cxcl3, Ly6d, Klk1, Fgf23, Serpinb2, Mmp13, Ccl17, Postn, and Adam12. PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies.

BackgroundChildren's media both reflects and shapes societal attitudes toward physical disability. Despite its potential impact on self-concept and stigma, longitudinal, data-driven analysis of these portrayals remains scarce. This study aimed to quantify longitudinal trends in the tone and framing of physical disability representation in children's media and to explore implications for pediatric rehabilitation.MethodsA quantitative content analysis was conducted on 68 children's media productions (1933-2025) sourced from the Vanderbilt Peabody database. Content was filtered to age-appropriate ratings (G, PG, PG-13, TV-14). Three trained reviewers classified depictions of physical disability by clinical category (e.g., spinal cord injury, limb difference) and tone (Positive, Neutral, Negative) and coded for the presence of rehabilitation themes. Inter-rater reliability (κ = 0.83) was achieved. Statistical testing included Mann-Kendall trend analysis and Fisher's exact tests to compare pre-2000 vs post-2000 portrayals.ResultsPositive portrayals increased significantly from pre-2000 (63%) to post-2000 (90%) (p = 0.01). A consistent upward trend across decades was confirmed (Z = 3.47, p < 0.01). Spinal cord injury was the most frequently depicted disability (40%); rehabilitation themes appeared in 24% of productions, more commonly post-2000. Productions with rehabilitation content were more likely to feature positive portrayals (94% vs 89%).ConclusionsOver nine decades, children's media has shifted toward more affirming representations of physical disability, particularly after 2000. Findings suggest that pediatric rehabilitation providers can use positive media examples to reinforce therapeutic engagement, normalize assistive devices, and address stigma in age-appropriate ways.

BACKGROUND: Rotator cuff (RC) tears are among the most common causes of shoulder dysfunction in sports medicine. Muscle atrophy and degeneration are important risk factors for RC tendon retearing and suboptimal recovery of shoulder function after tendon repair. Although blood flow restriction (BFR) can stimulate muscle regeneration after lower extremity trauma and anterior cruciate ligament reconstruction, the mechanisms that underlie BFR remain unknown, and its application to RC tears has not yet been explored. HYPOTHESIS: The authors hypothesized that BFR induces transfer of mitochondria from intramuscular fibro-adipogenic progenitors (FAPs) to myocytes, enhances muscle regeneration, and improves shoulder function after RC injury. STUDY DESIGN: Controlled laboratory study. METHODS: To assess mitochondrial transfer after BFR, the authors used Prrx1-Cre/MitoTag reporter mice, in which FAP mitochondria are labeled. Mice underwent unilateral forelimb BFR, and supraspinatus (SS) muscles were collected at baseline and days 1, 2, 3, 5, and 7 for histology. To model massive RC tears, mice received unilateral SS and infraspinatus tendon transection with denervation (TT+DN) and then were randomized to a BFR (every 3 days) or control group. At 2 or 6 weeks after surgery, SS muscles were analyzed for mitochondrial transfer, fiber size, and fiber-type distribution. Additionally, forelimb gait and weightbearing were captured using the Blackbox system. RESULTS: BFR was associated with increased FAP-mediated mitochondrial transfer in healthy SS muscle as early as 1 day after BFR treatment and lasted for up to 3 days after BFR. The authors observed an enhanced effect of BFR-induced FAP mitochondrial transfer in SS muscle after RC injury, compared with the control, at both 2 and 6 weeks after TT+DN. BFR-treated mice had significantly reduced muscle atrophy, fatty infiltration, and fibrosis after RC injury. They also observed a significant improvement in forepaw weightbearing ratio and ipsilateral forepaw stride length at 6 weeks after injury in BFR-treated mice compared with controls. CONCLUSION: BFR significantly improves muscle quality and shoulder function after RC injury. These effects occur alongside increased mitochondrial transfer from FAPs to myocytes. CLINICAL RELEVANCE: Understanding the mechanism of BFR by which BFR enhances muscle regeneration could pave the way for its use as a novel rehabilitation strategy to improve recovery in patients with RC injuries and other muscle-related conditions.