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Epithelial remodeling is a histopathologic feature of chronic inflammatory airway diseases including chronic rhinosinusitis (CRS). Cell-type shifts and their relationship to CRS endotypes and severity are incompletely described. We sought to understand the relationship of epithelial cell remodeling to inflammatory endotypes and disease outcomes in CRS. Using cell-type transcriptional signatures derived from epithelial single-cell sequencing, we analyzed bulk RNA-sequencing data from sinus epithelial brushings obtained from patients with CRS with and without nasal polyps in comparison to healthy controls. The airway epithelium in nasal polyposis displayed increased tuft cell transcripts and decreased ciliated cell transcripts along with an IL-13 activation signature. In contrast, CRS without polyps showed an IL-17 activation signature. IL-13 activation scores were associated with increased tuft cell, goblet cell, and mast cell scores and decreased ciliated cell scores. Furthermore, the IL-13 score was strongly associated with a previously reported activated ("polyp") tuft cell score and a prostaglandin E2 activation signature. The Lund-Mackay score, a computed tomographic metric of sinus opacification, correlated positively with activated tuft cell, mast cell, prostaglandin E2, and IL-13 signatures and negatively with ciliated cell transcriptional signatures. These results demonstrate that cell-type alterations and prostaglandin E2 stimulation are key components of IL-13–induced epithelial remodeling in nasal polyposis, whereas IL-17 signaling is more prominent in CRS without polyps, and that clinical severity correlates with the degree of IL-13–driven epithelial remodeling. [Display omitted] [ABSTRACT FROM AUTHOR]

Surgical site infections (SSIs) are a significant complications in total knee arthroplasty (TKA). The purpose of this study was to evaluate if traditional vs. single-use instrumentation had an effect on SSI's. We compared SSI rates and costs of TKAs performed with single-use (449) and traditional (169) TKA instrumentation trays. Total OR Time was, on average, 30 min less when single-use instrumentation was used. SSIs decreased in the single-use group (n=1) compared to the traditional group (n=5) (P=0.006). Single-use instrumentation added $490 in initial costs; however it saved between $480 and $600. Single-use instrumentation may provide a benefit to the patient by potentially decreasing the risk of infection and reducing the overall hospital costs. [ABSTRACT FROM AUTHOR]

The article discusses a research which examines the role of GATA-binding factor 6 (GATA6) in cardiac conduction system (CCS) and embryonic heart. It indicates that myocardial-specific deletion of the carboxyl zinc-finger of Gata6 alters the CCS in postnatal life and reduces cell-cycle exit of TBX3+ myocytes in the developing atrioventricular bundle. It reveals that GATA6 contributes to the atrioventricular node's development and postnatal function.

Background IL-25 can function as an early signal for the respiratory type 2 response characteristic of allergic asthma and chronic rhinosinusitis with nasal polyps (CRSwNP). In the mouse gut, tuft cells are the epithelial source of IL-25. However, the source of human airway epithelial IL-25 has remained elusive. Objective In this study we sought to determine whether the solitary chemosensory cell (SCC) is the predominant source of IL-25 in the sinonasal epithelium. Method Flow cytometry and immunofluorescence for SCCs and IL-25 were used to interrogate polyp and turbinate tissue from patients with CRSwNP. Mucus was collected during acute inflammatory exacerbations from patients with CRSwNP or chronic rhinosinusitis without nasal polyps and IL-25 levels determined by using ELISA. Lastly, sinonasal epithelial cultures derived from polyp and turbinate tissue were stimulated with IL-13 and analyzed for SCC proliferation and IL-25 production. Results This study demonstrates that a discrete cell type, likely an SCC, characterized by expression of the taste-associated G protein gustducin and the intestinal tuft cell marker doublecortin-like kinase 1, is the predominant source of IL-25 in the human upper airway. Additionally, we show that patients with CRSwNP have increased numbers of SCCs in nasal polyp tissue and that in vitro IL-13 exposure both increased proliferation and induced apical secretion of IL-25 into the mucosal layer. Conclusions Inflammatory sinus polyps but not adjacent turbinate tissue show expansion of the SCC population, which is the source of epithelial IL-25. [ABSTRACT FROM AUTHOR]