Introduction Health outcomes research has gained considerable traction over the past decade as the medical community attempts to move beyond traditional outcome measures such as morbidity and mortality. Since its inception in 2009, the BREAST-Q has provided meaningful and reliable information regarding health related – quality of life (HR-QOL) and patient satisfaction for use in both clinical practice and research. Now five years from its initial publication, we review how researchers have utilized the BREAST-Q and how it has enhanced our understanding and practice of plastic and reconstructive breast surgery. Methods An electronic literature review was performed to identify publications that used the BREAST-Q to assess patient outcomes. Studies developing and/or validating the BREAST-Q or an alternate patient reported outcome measure (PROM), review papers, conference abstracts, discussions, comments and/or responses to previously published papers, studies that modified a version of BREAST-Q, and studies not published in English were excluded. Results Our literature review yielded 214 unique articles, 49 of which met our inclusion criteria. Important trends and highlights were further examined. Discussion The BREAST-Q has provided important insights in breast surgery highlighted by literature concerning autologous reconstruction, implant type, fat grafting, and patient education. The BREAST-Q has increased the use of PROMs in breast surgery and provided numerous important insights in its brief existence. The increased interest in PROMs as well as the under utilized potential of the BREAST-Q should permit its continued use and ability to foster new innovations and improve quality of care.

Lysozyme is an abundant, cationic antimicrobial protein that plays an important role in pulmonary host defense. Increased concentration of lysozyme in the airspaces of transgenic mice enhanced bacterial killing whereas lysozyme deficiency resulted in increased bacterial burden and morbidity. Lysozyme degrades peptidoglycan in the bacterial cell wall leading to rapid killing of Gram-positive organisms; however, this mechanism cannot account for the protective effect of lysozyme against Gram-negative bacteria. The current study was therefore designed to test the hypothesis that the catalytic activity (muramidase activity) of lysozyme is not required for bacterial killing in vivo. Substitution of serine for aspartic acid at position 53 (D53S) in mouse lysozyme M completely ablated muramidase activity. Muramidase-deficient recombinant lysozyme (LysMD53S) killed both Gram-positive and Gram-negative bacteria in vitro. Targeted expression of LysMD53S in the respiratory epithelium of wild-type (LysM+/+/LysMD53S) or lysozyme Mnull mice (LysM−/−/LysMD53S) resulted in significantly elevated lysozyme protein in the airspaces without any increase in muramidase activity. Intratracheal challenge of transgenic mice with Gram-positive or Gram-negative bacteria resulted in a significant increase in bacterial burden in LysM−/− mice that was completely reversed by targeted expression of LysMD53S. These results indicate that the muramidase activity of lysozyme is not required for bacterial killing in vitro or in vivo.

Note: The term "resident" in this document refers to both specialty residents and subspecialty fellows. Once the Common Program Requirements are inserted into each set of specialty and subspecialty requirements, the terms "resident" and "fellow" will be used respectively. Where applicable, text in italics describes the underlying philosophy of the requirements in that section. These philosophic statements are not program requirements and are therefore not citable.