Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. PM induces innate immune responses and contributes to allergic sensitization, although the mechanisms governing this process remain unclear. Lung mucosal uric acid has also been linked to allergic sensitization. The links among PM exposure, uric acid, and allergic sensitization remain unexplored. We therefore investigated the mechanisms behind PM-induced allergic sensitization in the context of lung mucosal uric acid. PM10 and house dust mite exposure selectively induced lung mucosal uric acid production and secretion in vivo, which did not occur with other challenges (lipopolysaccharide, virus, bacteria, or inflammatory/fibrotic stimuli). PM10-induced uric acid mediates allergic sensitization and augments antigen-specific T-cell proliferation, which is inhibited by uricase. We then demonstrate that human airway epithelial cells secrete uric acid basally and after stimulation through a previously unidentified mucosal secretion system. Our work discovers a previously unknown mechanism of air pollution-induced, uric acid-mediated, allergic sensitization that may be important in the pathogenesis of asthma.
Monodisperse Ca-alginate microspheres were prepared using the membrane emulsification method. Three ionic types of drugs (anionic, cationic and non-ionic) were incorporated into the microspheres, and the effects of sodium alginate concentration and the pressure applied during the dispersing process on the properties of the microspheres were examined. Monodisperse microspheres were obtained when the concentration of alginate solution was 2 wt% and the pressure applied was 0.4 x 10(5) Pa. The mean size of microspheres was approximately 4 microm. Lidocaine x HCl (cationic), sodium salicylate (anionic) and 4-acetamidophenol (non-ionic) were selected as ionic model drugs and included in the alginate microspheres. Lidocaine x HCl (cationic drug) release was more retarded than that of the anionic drug, because of the electrostatic attraction between the negative charge of the ionized carboxyl group in the alginate chain and the positive charge of the cationic drug. In acidic release medium, a slow release was observed due to the low swelling characteristic and the increased viscosity of alginate, regardless of ionic type of drug.
Background: Surgery is the mainstay of treatment for non-small cell lung cancer, but the decline in pulmonary function after surgery is noticeable and needs attention. The aim of this study was to evaluate longitudinal changes in pulmonary function and its integrated patient-reported outcomes (PROs) after lung cancer surgery.Methods: The data were obtained from a prospective cohort study, Coordinate Approach to Cancer Patients' Health for Lung Cancer. Changes in forced vital capacity (FVC) and forced expiratory volume in 1s (FEV 1 ) 2 weeks, 6 months, and 1 year after surgery and the corresponding modi ed Medical Research Council (mMRC) dyspnea scale and chronic obstructive lung disease assessment test (CAT) score were evaluated. Mixed effect models were used to investigate the changes in pulmonary function and PROs.Results: Among 620 patients, 477 (76.9%) underwent lobectomy, while 120 (19.4%) and 23 (3.7%) were treated with limited resection and bilobectomy/pneumonectomy, respectively. Both FVC and FEV 1 markedly decreased 2 weeks after surgery and improved thereafter but did not recover to baseline values.The corresponding mMRC dyspnea scale and CAT score also showed worsening immediately after surgery. The dyspnea scale was still higher, while the CAT score returned to baseline 1 year after surgery, although the breathlessness and lack of energy persisted. Patients treated with bilobectomy/pneumonectomy showed -2.3%, -6.8%, and -6.0% more decrease in FEV 1 (% predicted) compared to the patients who underwent lobectomy at each time point. Moreover, worsening quality of life including dyspnea was also robust in patients treated with pneumonectomy/bilobectomy. Conclusions: After lung cancer surgery, pulmonary function and PROs was remarkable decreased at immediate post-operative period and improved thereafter except for dyspnea and lack of energy. The proper information on timeline of change in lung function and symptoms following lung cancer surgery could guide patient care approach following lung cancer surgery.
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