Context Rib raising is an osteopathic manipulative treatment modality that can help patients with various respiratory conditions to improve their work of breathing. However, the tolerance of this technique in hospitalized patients has not been assessed in a systematic manner. We hypothesized that rib raising would be a well-tolerated treatment modality for hospitalized patients admitted for asthma, pneumonia, chronic obstructive pulmonary disease, and/or congestive heart failure. Objective To determine hospitalized patients’ tolerance of rib raising through a prospective pilot study. Methods The study included patients at University Hospitals–Richmond Medical Center and University Hospitals–Bedford Medical Center who were admitted for asthma, pneumonia, chronic obstructive pulmonary disease, and/or congestive heart failure between November 1, 2016, and October 31, 2017. Each patient was treated with rib raising, which was performed in a standardized fashion. Immediately after treatment, patients were asked to rate their tolerance of the procedure on a scale of 0 to 10, where 0 represented no discomfort and 10 represented maximum discomfort. Results The study population consisted of 87 hospitalized, non–intensive care unit patients. The mean tolerance score for rib raising was 1.18, and the median score was 0. The score was between 0 and 3 in 80 patients (92.0%), between 4 and 6 in 6 patients (6.9%), and between 7 and 10 in 1 patient (1.1%). Conclusion Rib raising was shown to be well tolerated by the majority of the patients in the study population.

BAG3, a BAG co-chaperone family member, co-localizes with actin microfilaments and influences processes that involve actin function, including adhesion and migration. Because actin function regulates cell division, we hypothesized that the BAG3 WW-domain regulates cellular division through its cytoskeletal association. We show that BAG3 co-localizes with leading lamellipodia exclusively during G2 and mitosis phases. Co-immunoprecipitation of BAG3 and pulldown of GST-tagged BAG3 WW-domain confirmed that BAG3 WW-domain association with actin increased during G2 and mitosis relative to asynchronous cells. Deletion of the BAG3 WW-domain caused an abnormal cellular morphology, degenerate F-actin organization, longer doubling time (p<0.05, n=4), and three-fold increase in polynucleated cells relative to empty vector and full length-BAG3 (FL-BAG3; p<0.001, n=3). We confirmed polyploidy development and absence of cytokinesis in αWW-BAG3 cells by live-cell imaging, and observed mitotic delay relative to control and FL-BAG3 cells. To identify a potential regulation mechanism for BAG3-actin binding, we identified WBP2 as a novel BAG3 WW domain interacting protein in a yeast two-hybrid assay. BAG3 and WBP2 co-immunoprecipitated only in G1 and S phases, indicating cell cycle-specific BAG3-WBP2 binding. WBP2 silencing caused indiscriminate BAG3 co-immunoprecipitation with actin across all cell cycle phases, suggesting that association with WBP2 prevents BAG3-actin binding. We are the first to identify a function for WBP2, which our data show regulates BAG3 WW-domain association with actin in a cell cycle-specific manner. Because actin dysfunction has been proposed to contribute to chromosomal instability and tumor formation, the WW-domain of BAG3 is a potential target to reduce abnormal cell division. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2032. doi:1538-7445.AM2012-2032