Mossbeard0592

s, had a lower risk of all-cause mortality. Blood eosinophilia can be used as a biomarker in hospitalized COPD exacerbations for predicting the risk of all-cause mortality.Purpose Cognitive dysfunction is a common impairment associated with COPD. However, little is known about 1) its prevalence among those subjects referred for pulmonary rehabilitation (PR), 2) how it may affect the benefit of PR, 3) whether PR improves cognitive function and 4) whether cognitive dysfunction affects the usability of telehealth technology usually used to deliver in-home PR. Patients and methods Fifty-six subjects with stable COPD (54% females, mean age 62 years (SD 9) and median FEV1 0.9 L (IQR 0.7 to 1.1)) participated in this multicenter observational study and performed 24 sessions of PR. The Montreal Cognitive Assessment tool (MoCA) was used to assess the occurrence of mild cognitive dysfunction (using a screening cutoff less then 26) at baseline, completion of PR and 3 months of follow-up. Results Mild cognitive dysfunction was found in 41 subjects (73% [95% CI 60 to 83%]). The MoCA score significantly improved following PR for those people with baseline mild cognitive dysfunction (p less then 0.01). There was no significant difference in clinical outcomes between those people with or without mild cognitive dysfunction following PR nor in the proportion of subjects who were autonomous in using the telemonitoring system (83% compared with 71%, p=0.60). β-Estradiol purchase Conclusion Mild cognitive dysfunction is highly prevalent among those people with COPD referred for PR but does not affect the benefits of PR nor the usability of a telemonitoring system. PR may improve short- and mid-term cognitive function for those people who experience mild cognitive dysfunction at the time they are referred to PR.Background Disease-specific knowledge is associated with outcomes of patients, but the knowledge level of chronic obstructive pulmonary disease (COPD) patients is known to be low. Objective We measured the level of disease-specific knowledge and defined factors associated with poor disease knowledge in COPD patients. Materials and methods A cross-sectional survey was performed in five hospitals in South Korea. At enrolment, all patients completed the Bristol COPD Knowledge Questionnaire (BCKQ), Satisfaction with Life Scale (SWLS), Personal Resource Questionnaire (PRQ), St. George's Respiratory Questionnaire (SGRQ), 36-item Short-Form Health Survey (SF-36), and the Hospital Anxiety and Depression Scale (HADS). The data were analyzed via linear regression to identify factors associated with low-level knowledge of COPD. Results A total of 245 COPD patients were enrolled in this study. The mean total BCKQ score was 28.1 (SD, 7.4). The lowest scores were seen for items exploring knowledge of "Oral steroids" and "Inhaled steroids". In univariate analysis, higher level of education (r = 0.17), low income (r = 0.13), the post-bronchodilator FEV1, % predicted (r = -0.24), the post-bronchodilator FEV1/FVC ratio (r = -0.13), SWLS (r = 0.15), PRQ (r = 0.16), SF-36 MCS (r = 0.13), HADS-A (r = -0.17), and HADS-D (r = -0.28) scores correlated with the BCKQ score (all p less then 0.05). FEV1 (r = -0.25, p less then 0.001) and HADS-D score (r = -0.29, p less then 0.001) were significantly associated with the total BCKQ score in multivariate analysis. Conclusion Our Korean patients with COPD lacked knowledge on oral and inhaled steroid treatments. In particular, patients with higher-level lung function and/or depressive symptoms exhibited poorer disease-specific knowledge; such patients may require additional education.Introduction Cigarette smoke (CS)-induced inflammation in macrophages is involved in the pathological process of chronic obstructive pulmonary disease (COPD). Necroptosis, which is a form of programmed necrosis, has a close relationship with robust inflammation, while its roles in COPD are unclear. Materials and methods Necroptosis markers were measured in mouse alveolar macrophages and cultured bone marrow-derived macrophages (BMDMs). Necroptosis inhibitors were used to block necroptosis in BMDMs, and inflammatory cytokines were detected. We further explored the related signaling pathways. Results In this study, we demonstrated the way in which necroptosis, in addition to its upstream and downstream signals, regulates CS-induced inflammatory responses in macrophages. We observed that CS exposure caused a significant increase in the levels of necroptosis markers (receptor interacting kinases [RIPK] 1 and 3) in mouse alveolar macrophages and BMDMs. Pharmacological inhibition of RIPK1 or 3 caused a significant suppression in CS extract (CSE)-induced inflammatory cytokines, chemokine ligands (CXCL) 1 and 2, and interleukin (IL)-6 in BMDMs. CSE-induced necroptosis was regulated by mitochondrial reactive oxygen species (mitoROS), which also promoted inflammation in BMDMs. Furthermore, necroptosis regulated CSE-induced inflammatory responses in BMDMs, most likely through activation of the nuclear factor-κB pathway. Conclusion Taken together, our results demonstrate that mitoROS-dependent necroptosis is essential for CS-induced inflammation in BMDMs and suggest that inhibition of necroptosis in macrophages may represent effective therapeutic approaches for COPD patients.Introduction The vitamin D binding protein (VDBP, also known as GC-globulin) and vitamin D deficiency have been associated with chronic obstructive pulmonary disease (COPD). rs7041 and rs4588 are two single nucleotide polymorphisms of the VDBP gene, including three common allelic variants (GC1S, GC1F and GC2). Previous studies primarily assessed the serum levels of vitamin D and VDBP in COPD. However, less is known regarding the impact of the local release of VDBP on COPD lung function. Thus, we examined the association of sputum and plasma VDBP with lung function at baseline and at four years, and examined potential genetic polymorphism interactions. Methods The baseline levels of sputum VDBP, plasma VDBP and plasma 25-OH vitamin D, as well as the GC rs4588 and rs7041 genotypes, were assessed in a 4-year Finnish follow-up cohort (n = 233) of non-smokers, and smokers with and without COPD. The associations between the VDBP levels and the longitudinal decline of lung function were further analysed. Results High frequencies of the haplotypes in rs7041/rs4588 were homozygous GC1S/1S (42.