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Background: Recent data show that aesthetic surgery research is lagging compared with reconstructive surgery: research funding and institutional disparities within aesthetic surgery are potential factors in this trend.Objectives: The authors sought to determine if disparities exist in aesthetic surgery research based on funding sources or practice settings.Methods: The authors reviewed Aesthetic Surgery Journal articles from 2009 to 2019. Chi-square, t test, bivariate, and multivariate regression analyses were employed to evaluate research trends.Results: A total of 2262 publications were identified, with 318 funded articles meeting inclusion criteria. The majority of studies (294, 92%) received external funding, with 281 (88%) being supported solely by external funds. Externally funded studies were financed by private industry (194, 66%), foundations/societies (53, 18%), government grants (23, 8%), or a combination of agencies (24, 8%). The majority of funded studies were at academic institutions (266, 84%), followed by private practice (46, 14%) and private industry (6, 2%). Analysis of annual publications revealed a rising percentage of academic-based research, which correlated with decreasing research from private practice (r = -0.95, r2 = 0.89, P < 0.001). Compared with academic institutions, private practice relied more heavily on industry funding (55% vs 87%, respectively, P = 0.001), exhibiting lower rates of foundational/societal (20% vs 2%), governmental (9% vs 0%), combined (8% vs 7%), and internal department funding (8% vs 4%). Article citations and level of evidence were unaffected by funding source, agency, or practice setting.Conclusions: Lack of diversity in research funding among private practice surgeons may explain the reported discrepancies that currently exist between aesthetic and reconstructive surgery research. [ABSTRACT FROM AUTHOR]

Cellular lipid metabolism, lipoprotein interactions, and liver X receptor (LXR) activation have been implicated in the pathophysiology and treatment of cancer, although findings vary across cancer models and by lipoprotein profiles. In this study, we investigated the effects of human‐derived low‐density lipoproteins (LDL), high‐density lipoproteins (HDL), and HDL‐associated proteins apolipoprotein A1 (apoA1) and serum amyloid A (SAA) on markers of viability, cholesterol flux, and differentiation in K562 cells—a bone marrow‐derived, stem‐like erythroleukemia cell model of chronic myelogenous leukemia (CML). We further evaluated whether lipoprotein‐mediated effects were altered by concomitant LXR activation. We observed that LDL promoted higher K562 cell viability in a dose‐ and time‐dependent manner and increased cellular cholesterol concentrations, while LXR activation by the agonist TO901317 ablated these effects. LXR activation in the presence of HDL, apoA1 and SAA‐rich HDL suppressed K562 cell viability, while robustly inducing mRNA expression of ATP‐binding cassette transporter A1 (ABCA1). HDL and its associated proteins additionally suppressed mRNA expression of anti‐apoptotic B‐cell lymphoma‐extra large (BCL‐xL), and the erythroid lineage marker 5′‐aminolevulinate synthase 2 (ALAS2), while SAA‐rich HDL induced mRNA expression of the megakaryocytic lineage marker integrin subunit alpha 2b (ITGA2B). Together, these findings suggest that lipoproteins and LXR may impact the viability and characteristics of CML cells. [ABSTRACT FROM AUTHOR]