A high participation rate is warranted in order to ensure validity in surveys of the general population. However, participation rates in such studies have declined during the last decades.

To evaluate the reasons for and potential effects of non-response in a large population-based survey about asthma and respiratory symptoms in Northern Sweden.

Within the Obstructive Lung Disease In Norrbotten (OLIN) studies, a random sample of 12,000 adults aged 20-79 was invited to a postal questionnaire survey about asthma, allergic rhino-conjunctivitis and respiratory symptoms in 2016. Three reminders were sent. A random sample of 500 non-responders was invited to a telephone interview.

The participation rate in the initial mailing was 41.4%, and 9.2%, 5.0%, and 2.6% in the subsequent three reminders and totally 58.3% (n=6854) responded. Of 500 non-responders selected for telephone interviews, 320 were possible to reach and 272 participated. Male sex, younger age, and current smoking were associated with both late and non-response. The prevalence of asthma and most respiratory symptoms did not differ significantly between responders and non-responders while allergic rhino-conjunctivitis and smoking was more common among non-responders. Reminders increased the participation rate but did not alter risk ratios for smoking and occupational exposures. Reasons for non-response were mainly lack of time and having forgotten to answer.

With a response rate of 58.3%, neither the prevalence estimates of asthma, respiratory symptoms nor the associations to risk factors were affected by non-response, while allergic rhino-conjunctivitis and smoking was underestimated in this Swedish population.

With a response rate of 58.3%, neither the prevalence estimates of asthma, respiratory symptoms nor the associations to risk factors were affected by non-response, while allergic rhino-conjunctivitis and smoking was underestimated in this Swedish population.

Chronic obstructive pulmonary disease (COPD) is a leading cause of unplanned readmission. There is need to identify risk factors for, and strategies to prevent readmission in patients with COPD.

To systematically review and summarise the prevalence, risk factors and outcomes associated with rehospitalisation due to COPD exacerbation.

The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed. Five databases were searched for relevant studies.

Fifty-seven studies from 30 countries met the inclusion criteria. The prevalence of COPD-related readmission varied from 2.6 to 82.2% at 30 days, 11.8-44.8% at 31-90 days, 17.9-63.0% at 6 months, and 25.0-87.0% at 12 months post-discharge. There were differences in the reported factors associated with readmissions, which may reflect variations in the local context, such as the availability of community-based services to care for exacerbations of COPD. Hospitalisation in the previous year prior to index admission was the key prtions should be tailored to the local healthcare environment.Biomolecular corona formed on nanoparticles (NPs) influences the latter’s in vivo biological effects. Nanomaterials with different physicochemical properties exert similar adverse effects, such as cytotoxicity, suggesting the existence of ubiquitous signals during various corona formations that mediate common and fundamental cellular events. Here, we discover the involvement of the unfolded protein response (UPR) and recruited chaperones in the corona. selleck inhibitor Specially, heat shock protein 90 kDa α class B member 1 (Hsp90ab1) is abundantly enriched in the corona, accompanied by substantial aggregation of misfolded protein on particles intracellularly. Further analysis reveals the particulate matter 2.5 (PM2.5) and metal-containing particles are more capable of denaturing proteins. The recruited Hsp90ab1 activates diverse NPs’ pathological behaviour by heat stress response (HSR), which were significantly reversed by geldanamycin (GA), the inhibitor of Hsp90ab1. Murine lung inflammation induced by PM2.5 and iron oxide NPs (Fe3O4NPs) is suppressed by GA, highlighting that Hsp90ab1-mediated UPR is a potential target for the treatment of environmental pollution-related illnesses. Based on our findings, the UPR and Hsp90ab1 presented in the corona of particles initiate fundamental intracellular reactions that lead to common pathological outcomes, which may provide new insights for understanding nanotoxicity and designing therapeutic approaches for diseases associated with environmental pollution.Throughout the process of metastatic dissemination, tumor cells are continuously subjected to mechanical forces resulting from complex fluid flows due to changes in pressures in their local microenvironments. While these forces have been associated with invasive phenotypes in 3D matrices, their role in key steps of the metastatic cascade, namely extravasation and subsequent interstitial migration, remains poorly understood. In this study, an in vitro model of the human microvasculature was employed to subject tumor cells to physiological luminal, trans-endothelial, and interstitial flows to evaluate their effects on those key steps of metastasis. Luminal flow promoted the extravasation potential of tumor cells, possibly as a result of their increased intravascular migration speed. Trans-endothelial flow increased the speed with which tumor cells transmigrated across the endothelium as well as their migration speed in the matrix following extravasation. In addition, tumor cells possessed a greater propensity to migrate in close proximity to the endothelium when subjected to physiological flows, which may promote the successful formation of metastatic foci. These results show important roles of fluid flow during extravasation and invasion, which could determine the local metastatic potential of tumor cells.Mast cells and IgE are most familiar as the effectors of type I hypersensitivity reactions including anaphylaxis. It is becoming clear however that this pair has important immunomodulatory effects on innate and adaptive cells of the immune system. In this purview, they act as endogenous adjuvants to ignite evolving immune responses, promote the transition of allergic disease into chronic illness and disrupt the development of active mechanisms of tolerance to ingested foods. Suppression of IgE-mediated mast cell activation can be exerted by molecules targeting IgE, FcɛRI or signaling kinases including Syk, or by IgG antibodies acting via inhibitory Fcγ receptors. In 2015 we reviewed the evidence for the adjuvant functions of mast cells. This update includes the original text, incorporates some important developments in the field over the past five years and discusses how interventions targeting these pathways might have promise in the development of strategies to treat allergic disease.