Description: In austral winter, biological productivity at the Angolan shelf reaches its maximum. The alongshore winds, however, reach their seasonal minimum suggesting that processes other than local wind‐driven upwelling contribute to near‐coastal cooling and upward nutrient supply, one possibility being mixing induced by internal tides (ITs). Here, we apply a three‐dimensional ocean model to simulate the generation, propagation, and dissipation of ITs at the Angolan continental slope and shelf. Model results are validated against moored acoustic Doppler current profiler and other observations. Simulated ITs are mainly generated in regions with a critical/supercritical slope typically between the 200‐ and 500‐m isobaths. Mixing induced by ITs is found to be strongest close to the coast and gradually decreases offshore thereby contributing to the establishment of cross‐shore temperature gradients. The available seasonal coverage of hydrographic data is used to design simulations to investigate the influence of seasonally varying stratification characterized by low stratification in austral winter and high stratification in austral summer. The results show that IT characteristics, such as their wavelengths, sea surface convergence patterns, and baroclinic structure, have substantial seasonal variations and additionally strong spatial inhomogeneities. However, seasonal variations in the spatially averaged generation, onshore flux, and dissipation of IT energy are weak. By evaluating the change of potential energy, it is shown, nevertheless, that mixing due to ITs is more effective during austral winter. We argue that this is because the weaker background stratification in austral winter than in austral summer acts as a preconditioning for IT mixing.

Description: Background: Phenotype of chronic rhinosinusitis (CRS) may be an important determining factor of the efficacy of anti-inflammatory treatments. Although both glucocorticoids and macrolide antibiotics have been recommended for the treatment of CRS, whether they have different anti-inflammatory functions for distinct phenotypic CRS has not been completely understood. The aim of this study is to compare the anti-inflammatory effects of clarithromycin and dexamethasone on sinonasal mucosal explants from different phenotypic CRS ex vivo. Methods: Ethmoid mucosal tissues from CRSsNP patients (n = 15), and polyp tissues from eosinophilic (n = 13) and non-eosinophilic (n = 12) CRSwNP patients were cultured in an ex vivo explant model with or without dexamethasone or clarithromycin treatment for 24 h. After culture, the production and/or expression of anti-inflammatory molecules, epithelial-derived cytokines, pro-inflammatory cytokines, T helper (Th)1, Th2 and Th17 cytokines, chemokines, dendritic cell relevant markers, pattern recognition receptors (PRRs), and tissue remodeling factors were detected in tissue explants or culture supernatants by RT-PCR or ELISA, respectively. Results: We found that both clarithromycin and dexamethasone up-regulated the production of anti-inflammatory mediators (Clara cell 10-kDa protein and interleukin (IL)-10), whereas down-regulated the production of Th2 response and eosinophilia promoting molecules (thymic stromal lymphopoietin, IL-25, IL-33, CD80, CD86, OX40 ligand, programmed cell death ligand 1, CCL17, CCL22, CCL11, CCL5, IL-5, IL-13, and eosinophilic cationic protein) and Th1 response and neutrophilia promoting molecules (CXCL8, CXCL5, CXCL10, CXCL9, interferon-γ, and IL-12), from sinonasal mucosa from distinct phenotypic CRS. In contrast, they had no effect on IL-17A production. The expression of PRRs (Toll-like receptors and melanoma differentiation-associated gene 5) was induced, and the production of tissue remodeling factors (transforming growth factor-β1, epidermal growth factor, basic fibroblast growth factor, platelet derived growth factor, vascular endothelial growth factor, and matrix metalloproteinase 9) was suppressed, in different phenotypic CRS by dexamethasone and clarithromycin in comparable extent. Conclusions: Out of our expectation, our explant model study discovered herein that glucocorticoids and macrolides likely exerted similar regulatory actions on CRS and most of their effects did not vary by the phenotypes of CRS.