Outliers of total shoulder arthroplasty in the bundled payment era.

Background: The Centers for Medicare & Medicaid Services implemented the Bundled Payments for Care Improvement Advanced (BPCIA) Model that covers 90-day care episodes after select orthopedic procedures including anatomic or reverse ball-and-socket total shoulder arthroplasty (TSA/rTSA). This study investigated whether patients undergoing TSA/rTSA for nondegenerative processes incur higher costs than patients undergoing arthroplasty for degenerative processes.

Methods: A retrospective review was conducted of all patients at a single academic medical center enrolled in the BPCIA model for TSA/rTSA from October 1, 2018, through December 31, 2022.

Mapping the Energetic Epitope of an Antibody/Interleukin-23 Interaction with Hydrogen/Deuterium Exchange, Fast Photochemical Oxidation of Proteins Mass Spectrometry, and Alanine Shave Mutagenesis.

Epitope mapping the specific residues of an antibody/antigen interaction can be used to support mechanistic interpretation, antibody optimization, and epitope novelty assessment. Thus, there is a strong need for mapping methods, particularly integrative ones. Here, we report the identification of an energetic epitope by determining the interfacial hot-spot that dominates the binding affinity for an anti-interleukin-23 (anti-IL-23) antibody by using the complementary approaches of hydrogen/deuterium exchange mass spectrometry (HDX-MS), fast photochemical oxidation of proteins (FPOP), alanine shave mutagenesis, and binding analytics.

Responses to altered oxygen tension are distinct between human stem cells of high and low chondrogenic capacity.

Background: Lowering oxygen from atmospheric level (hyperoxia) to the physiological level (physioxia) of articular cartilage promotes mesenchymal stem cell (MSC) chondrogenesis. However, the literature is equivocal regarding the benefits of physioxic culture on preventing hypertrophy of MSC-derived chondrocytes. Articular cartilage progenitors (ACPs) undergo chondrogenic differentiation with reduced hypertrophy marker expression in hyperoxia but have not been studied in physioxia.

The related transcriptional enhancer factor-1 isoform, TEAD4(216), can repress vascular endothelial growth factor expression in mammalian cells.

Increased cellular production of vascular endothelial growth factor (VEGF) is responsible for the development and progression of multiple cancers and other neovascular conditions, and therapies targeting post-translational VEGF products are used in the treatment of these diseases. Development of methods to control and modify the transcription of the VEGF gene is an alternative approach that may have therapeutic potential. We have previously shown that isoforms of the transcriptional enhancer factor 1-related (TEAD4) protein can enhance the production of VEGF.